The Cavendish

Glowing Cats to Fight FIV

2011-09-18T07:19:00.002-04:00

GMO Corn

2011-09-08T06:40:00.000-04:00

Worries about Climate Change

2011-09-07T06:52:00.001-04:00

Origins of Intelligence

2011-09-07T06:32:00.000-04:00

And another regrettable thing about deathis the ceasing of your own brand of magic,which took a whole life to develop and market-the quips, the witticisms, the slantadjusted to a few, those loved ones nearest the lip of the stage, their soft faces blanchedin the footlight glow, their laughter close to tears,their tears confused with their diamond earrings,their warm pooled breath in and out with your heartbeat,their response and your performance twinned.The jokes over the phone. The memories packedin rapid-access file. The whole act.Who will do it again? That's it: no one;imitators and descendants aren't the same. - John Updike who passed away on 1/30/09

Greatest Discoveries in Genetics

2011-09-06T16:00:00.000-04:00

Lab Safety

2011-09-06T10:00:00.002-04:00

Microscope Lab

2011-09-02T17:53:00.000-04:00

Tree Identification

2011-09-02T17:47:00.001-04:00

Tree Identification

2011-09-02T17:47:00.000-04:00

Carbon Dioxide Lab

2011-09-02T17:41:00.004-04:00

Martha Chase and Alfred Hershey

2011-07-22T11:00:00.002-04:00

Education Notes

2011-06-22T06:45:00.001-04:00

Wll It's Just a Theory

2011-06-16T06:31:00.000-04:00

Doctors believe in Climate Change

2011-06-16T06:28:00.000-04:00

Drosophila Database

2011-06-15T15:25:00.000-04:00

Ecological Cycles

2011-06-15T08:54:00.006-04:00

Owl Pellet Lab

2011-06-08T14:51:00.006-04:00

Climate Crisis in Education

2011-05-25T06:37:00.000-04:00

Alu PCR Insert- Chromosome 16

2011-05-23T13:55:00.009-04:00

Allium Assay 1:80 Roundup

2011-05-23T13:33:00.017-04:00

Cytogenetic Activities

2011-05-16T10:18:00.003-04:00

Leprosy Transmission

2011-05-04T06:37:00.001-04:00

DNA Replication

2011-05-02T07:55:00.004-04:00

National Center for Biotechnology Information

2011-04-10T16:46:00.000-04:00

Chernobyl's Victims: Slide Presentation

2011-04-09T10:19:00.002-04:00

X Chromosome Deactivation

2011-03-31T08:26:00.001-04:00

Erythtoblastosis fetalis

2011-03-29T10:39:00.004-04:00

Honors Biotechnology Debate

2011-01-09T18:13:00.001-05:00

Honors Biotechnology: Debate Topics and Format

Aim above morality. Be not simply good, be good for something. -Henry David Thoreau

Debates will consist of groups of four with two members taking the affirmative position on a topic and two members taking the opposing view. Each group will have a period to present their case to the class. The class will b e the representative jury and determine which team best presented their case. The more meticulous, well thought out, and nuanced arguments will most likely sway the class. The presentations must be given equally by each team member. My expectation is that both members will be equally knowledgeable about their topic and will be able to intelligently address questions directed to them from me or the audience.

Arguments defending each team’s position must be supported by evidence. All evidence used must be based on current science from respected sources. Teams will be challenged by the instructor or audience to clarify or explain the relevance, meaning, and veracity of any information presented to support or negate a team’s position.

The debates will begin with a ten slide PowerPoint presentation of the affirmative position lasting ten minutes. This will be followed by a ten slide PowerPoint presentation by the opposing view also lasting ten minutes. After both presentations, eight minutes will be provided for questions from the instructor/audience. Upon completion of the first round of questions each team will be provided five minutes for rebuttal presentations beginning with affirmative side. The remaining time will be devoted to a final round of questions. The audience and instructor will then choose by secret ballot the team that was most persuasive and knowledgeable.

Given the relatively short period of time for each presentation it will be essential that each presentation is compactly choreographed so that the debate format can proceed without delays. It is also important that each team provide authentic information and answer questions based on diligent research and a thorough grasp of the topic. Please do not try to invent answers to questions you are not able to answer and ABOVE ALL do not waste my time. I fully expect that your debates will be conducted with focus, comprehensive knowledge, and an appropriate demeanor and delivery.

The Debate Forum:
1. Ten minutes for pro presentation
2. 10 minutes for con presentation
3. 5 minutes audience questions
4. 5 minutes pro rebuttal
5. 5 minutes con rebuttal
6. Audience questions
7. Vote of audience

Debate Issues:
Team I
Government is currently involved in health care reform. Debate the following: With limited numbers of transplants available rationing systems must be established for determining who will receive transplants. On what basis should rationing systems be based?
A. First come, first serve
B. The wealthiest
C. The youngest
D. Those who have the highest IQ
E. Those with genetic defects favored over those whose unhealthy lifestyle has produced organ failure.

Team II
Embryonic stem cells have been advertised as the beginning of a new medical revolution. The excitement has been caused by the totipotency demonstrated by these cells. As a result, they have the potential to cure a number of diseases such as Parkinson’s, Type I Diabetes, and Multiple Sclerosis. Some believe that using embryonic stem cells in research and future treatment protocols poses insurmountable bioethical and moral concerns. Should embryonic stem cells be used in the research and treatment of disease?

Team III.
Should a woman be held responsible if her drinking alcohol, smoking or abusing drugs during pregnancy harms her child? Should she be held liable for harm coming to her fetus from any of these substances? Should she be held legally accountable for abusing illegal substances such as crack or heroin during her pregnancy? Is there a moral difference between the use of harmful legal substances or harmful illegal substances while pregnant?

Suicides Among Indian Farmers

2011-01-03T05:58:00.002-05:00

Bring 'Em Home Lyrics

2010-11-25T11:51:00.003-05:00

Bring 'Em Home Lyrics
If you love your Uncle Sam,Bring them home, bring them home.
Support our boys in Vietnam,Bring them home, bring them home.
It'll make our generals sad, I know,Bring them home, bring them home.
They want to tangle with the foe,Bring them home, bring them home.

They want to test their weaponry,Bring them home, bring them home.
But here is their big fallacy,Bring them home, bring them home.
I may be right, I may be wrong,Bring them home, bring them home.
But I got a right to sing this song,Bring them home, bring them home.

There's one thing I must confess,Bring them home, bring them home.
I'm not really a pacifist,Bring them home, bring them home.
If an army invaded this land of mine,Bring them home, bring them home.
You'd find me out on the firing line,Bring them home, bring them home.

Even if they brought their planes to bomb,Bring them home, bring them home.
Even if they brought helicopters and napalm,Bring them home, bring them home.
Show those generals their fallacy:Bring them home, bring them home.
They don't have the right weaponry,Bring them home, bring them home.

For defense you need common sense,Bring them home, bring them home.
They don't have the right armaments,Bring them home, bring them home.
The world needs teachers, books and schools,Bring them home, bring them home.
And learning a few universal rules,Bring them home, bring them home.

So if you love your Uncle Same,Bring them home, bring them home.
Support our boys in Vietnam,Bring them home, bring them home.

Bring 'Em Home Lyrics
If you love your Uncle Sam,Bring them home, bring them home.
Support our boys in Vietnam,Bring them home, bring them home.
It'll make our generals sad, I know,Bring them home, bring them home.

They want to tangle with the foe,Bring them home, bring them home.
They want to test their weaponry,Bring them home, bring them home.But here is their big fallacy,Bring them home, bring them home.
I may be right, I may be wrong,Bring them home, bring them home.

But I got a right to sing this song,Bring them home, bring them home.
There's one thing I must confess,Bring them home, bring them home.
I'm not really a pacifist,Bring them home, bring them home.
If an army invaded this land of mine,Bring them home, bring them home.
You'd find me out on the firing line,Bring them home, bring them home.
Even if they brought their planes to bomb,Bring them home, bring them home.
Even if they brought helicopters and napalm,Bring them home, bring them home.

Show those generals their fallacy:Bring them home, bring them home.
They don't have the right weaponry,Bring them home, bring them home.
For defense you need common sense,Bring them home, bring them home.They don't have the right armaments,Bring them home, bring them home.

The world needs teachers, books and schools,Bring them home, bring them home.
And learning a few universal rules,Bring them home, bring them home.
So if you love your Uncle Same,Bring them home, bring them home.
Support our boys in Vietnam,Bring them home, bring them home.

Stem Cells

2010-11-17T06:32:00.001-05:00

Rosalind Franklin

2010-11-08T07:03:00.000-05:00

Balancing the Budget by Cutting Science

2010-11-08T07:00:00.002-05:00

What Do the 2010 Election Results Mean for Federal Science Budgets?
Agencies are likely to see smaller budgets in the wake of Republican gains in the House of Representatives, but drastic cuts are unlikely
By John Matson November 5, 2010 3

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CASH OUT? What will a party shift in the House of Representatives spell for the budgets of U.S. science agencies? Image: © iStockphoto/spxChrome
November 2 midterm elections marked a shift of power in Washington, D.C. The Republican Party wrested control of the U.S. House of Representatives from the Democrats, who had held power across both houses of Congress and the White House since President Barack Obama's election in 2008.Just days after the midterm elections, a report from the American Association for the Advancement of Science (AAAS) and a related story in The New York Times examined what would happen to federal science agencies if the GOP carried through on their planned budget cuts. The 2010 Republican agenda, "A Pledge to America," proposed rolling back discretionary spending to 2008 levels, with exceptions for seniors and the military. (Discretionary spending makes up roughly one third of the federal budget; the rest goes to mandatory programs such as Social Security and Medicare.)The plan, if executed, would cut more than $8 billion in federal research and development from what Obama had proposed for 2011, according to the AAAS analysis. Nearly $3 billion of that would come from the National Institutes of Health (NIH); NASA, the National Science Foundation and the Department of Energy would lose more than $1 billion apiece.But how realistic are those kinds of cuts, considering that Democrats still control the Senate and the White House? To find out what the coming years have in store for science agencies, we spoke to Allen Schick, a professor of public policy at the University of Maryland, College Park.[An edited transcript of the interview follows.]Do you think this campaign promise to roll back discretionary spending across the board to 2008 levels is feasible?In the magnitude that they're talking about, cutting about $100 billion in nondefense spending, it's feasible, but it would generate an enormous amount of conflict between Democrats and Republicans, between the House and Senate, and most importantly within Republican ranks.In other words, even Republicans who don't want to spend have things they want to spend on. One example might be the NIH, which has a big bioterrorism budget and a big cancer research budget.Implementing these kinds of cuts would generate a lot of pressure. So I can't promise you that these cuts will materialize, certainly not to the degree that the Republicans have been talking about up to the election. That level would generate enormous conflicts.What is a realistic scenario for these agency budgets?At the very least, these budgets will be frozen. In other words, incremental increases that you get from year to year and the bigger increases that some of them got during the Obama period, those are out the window for at least the next year.If you look at 1994 to 1996 as a precedent, you see an interesting pattern. In the period immediately after the [midterm] election, appropriations were cut, and that generated a lot of conflict. But after Clinton was elected to his second term, things normalized somewhat. That could be where we're headed here.One of the cards that Obama has is that the Republicans do not want to be blamed for a shutdown of government. When that happened last time [1995–1996], it worked against them.Can we expect to see conflicts between the House and Senate on these issues?Well, we've had that problem in the last few years, even when the Democrats controlled the House and the Senate. Those two chambers are wired fundamentally differently. In the House the majority always wins, except in those rare circumstances where the majority is fractured. And the Republicans have a big margin now, so they don't have to worry about that—at least not right away.The Senate is a very different story. You look at so much recent legislation—the health care legislation, financial services legislation, appropriations legislation—the biggest conflicts in recent years have been between the House and the Senate.How much leverage does the president have in terms of resolving conflicts between the houses of Congress?Well, he has veto power, which can be very powerful. And he has what is called the bully pulpit. He can tell the American people, "Look how they're devastating the crown jewel of biomedicine at the NIH," or "For America to prosper we need to retain our scientific lead, and the Republicans are squandering it."He does have some weapons, but given the deficit and the election returns, this president is not going to be able to come up with a budget that shows big increases, as he did the past two years.As for the budget that is in the works now, some of these science agencies already have authorization bills but not appropriations bills. Does that protect them from budget cuts at all?No. First of all, some agencies have expired authorizations. And in terms of appropriated funds, the authorizations are only a hunting license to get appropriations. You can't cash in a discretionary authorization. The amount of money you have to spend is the amount appropriated.What happens after the appropriations bills come through?In past situations like this, for example when Clinton was president, you can look for what you call "niche initiatives". A niche is an isolated program where you can say that you're doing something at $10 million, $20 million, and you can issue a daily press release on each of these initiatives, but they don't add up to a lot of money. It's very different from Congress, say, giving the NIH a $5-billion increase.I think you're going to see a lot of these niche programs for this kind of research or that kind of scientific endeavor or this kind of infrastructure. In the face of cuts, it looks like you're doing something. In Congress they call them sweeteners—a spoonful of sugar helps the medicine go down.Americans want to get rid of the deficit, they want smaller government, but they want bigger benefits from government. So the niche programs are kind of a way of reconciling these conflicting views.If you were working for one of these agencies that relies on discretionary funding, how would you be feeling right now?I'd be feeling nervous. An agency with a frozen budget regards it as a cutback, because certain expenses rise, such as payroll. In the scientific area, which is different than a lot of the rest of government, most of the money goes out the door in the form of grants and contracts. So what we might call intramural research—the research done inside the NIH—is a small part of the NIH budget. So what you can see is that the people who would be worried the most are the recipients of these grants and contracts, like universities or medical centers.So freezing or even cutting these budgets somewhat will have an impact across the country?That's right. The effect is not going to be isolated inside the Beltway.

Genes Become more Mysterious

2010-11-08T06:58:00.000-05:00

Skin Cells to Blood

2010-11-08T06:56:00.001-05:00

Suddenly Susceptible

2010-10-17T17:41:00.003-04:00

Permanent Address: http://www.scientificamerican.com/blog/post.cfm?id=from-chytrid-to-ranavirus-another-d-2010-10-14
From chytrid to ranavirus: Another disease is devastating frog populations
By John Platt Thursday, October 14, 2010 1

The chytrid fungus (Batrachochytrium dendrobatidis) isn't the only thing killing frogs and amphibians around the world. Now we have word that a disease from the genus Ranavirus is devastating frog populations in the U.K. According to research published in the October 2010 issue of Animal Conservation, the rapidly spreading ranavirus is killing common frogs (Rana temporaria) in areas where it has never been seen before. And where ranavirus is present in the U.K., common frog populations have dropped 81 percent in the last 12 years. The disease causes infected frogs to bleed to death through hemorrhaging organs and skin ulcerations.
Previously restricted to southeast England, and possibly introduced to the U.K. through imported frogs or fish, ranavirus has now spread to Lancashire in the west, Yorkshire in the north, and the south coast of the country. "[What] we desperately need to solve is how the disease spreads," co-author Trent Garner of the Zoological Society of London (ZSL) said in a prepared statement.
"Our findings show that ranavirus not only causes one-off mass-mortality events, but is also responsible for long-term population declines," lead author Amber Teacher, also from ZSL, said. "We need to understand more about this virus if we are to minimize the serious threat that it poses to our native amphibians."
According to the paper's abstract, this is the first study to examine the long-term impacts of ranavirus, although other studies (such as this one from the Archives of Virology or this one in the Journal of Wildlife Diseases) have looked at mass mortality events associated with the disease. Ranavirus has also been linked to mass deaths of salamanders, turtles and other amphibians worldwide.
There is good news amidst the bad: Some U.K. common frog populations managed to bounce back from ranavirus infections. This, the authors say, suggests that there may be some ranavirus immunity already present in some frogs.
Photo: Common frog (Rana temporaria), via Wikipedia
© 2010 Scientific American, a Division of Nature America, Inc. All Rights Reserved.
About Scientific American

Socialism to the Rescue

2010-10-17T17:36:00.001-04:00

Saved, In Essence, By Socialism
The drama that unfolded in Chile as 33 miners were miraculously, meticulously rescued from the depths was riveting. It was not, however, "a smashing victory for free-market capitalism," as claimed by a surreal op-ed in the Wall Street Journal, but a victory for faith, technology and especially competent, caring governance.
"The miners were employees of...an out-of-control, anti-union, government-regulation-defying, safety nightmare corporation...The miners were rescued by a government-sponsored intervention supervised by the state's copper company (and) the expertise of an American government agency."

What Happened to the Bees

2010-10-17T17:31:00.000-04:00

Stem Developments

2010-10-17T10:42:00.001-04:00

Carbon Dioxide and Climate Change

2010-10-16T16:21:00.003-04:00

Carbon dioxide (chemical formula CO2) is a chemical compound composed of two oxygen atoms covalently bonded to a single carbon atom. It is a gas at standard temperature and pressure and exists in Earth's atmosphere in this state. CO2 is a trace gas comprising 0.039% of the atmosphere.
Carbon dioxide is used by plants during photosynthesis to make sugars, which may either be consumed in respiration or used as the raw material to produce other organic compounds needed for plant growth and development. It is emitted during respiration by plants, and by all animals, fungi and microorganisms that depend either directly or indirectly on plants for food. It is thus a major component of the carbon cycle. Carbon dioxide is generated as a by-product of the combustion of fossil fuels or the burning of vegetable matter, among other chemical processes. Amounts of carbon dioxide are emitted from volcanoes and other geothermal processes such as hot springs and geysers and by the dissolution of carbonates in crustal rocks. High levels of CO2 are used to increase plant growth in some tightly closed commercial greenhouses.[1][2][3]
As of October 2010[update], carbon dioxide in the Earth's atmosphere is at a concentration of 388 ppm by volume.[4] Atmospheric concentrations of carbon dioxide fluctuate slightly with the change of the seasons, driven primarily by seasonal plant growth in the Northern Hemisphere. Concentrations of carbon dioxide fall during the northern spring and summer as plants consume the gas, and rise during the northern autumn and winter as plants go dormant, die and decay. Taking all this into account, the concentration of CO2 grew by about 2 ppm in 2009.[5] Carbon dioxide is a greenhouse gas as it transmits visible light but absorbs strongly in the infrared and near-infrared.
Before the advent of human-caused release of carbon dioxide to the atmosphere, concentrations tended to increase with increasing global temperatures, acting as a positive feedback for changes induced by other processes such as orbital cycles.[6] There is a seasonal cycle in CO2 concentration associated primarily with the Northern Hemisphere growing season.[7]
Carbon dioxide has no liquid state at pressures below 5.1 atmospheres. At 1 atmosphere (near mean sea level pressure), the gas deposits directly to a solid at temperatures below −78 °C (−108 °F; 195.1 K) and the solid sublimes directly to a gas above −78 °C. In its solid state, carbon dioxide is commonly called dry ice.
CO2 is an acidic oxide: an aqueous solution turns litmus from blue to pink. It is the anhydride of carbonic acid, an acid which is unstable in aqueous solution, from which it cannot be concentrated. In organisms carbonic acid production is catalysed by the enzyme, carbonic anhydrase.
CO2 + H2O H2CO3
CO2 is toxic in higher concentrations: 1% (10,000 ppm) will make some people feel drowsy.[8] Concentrations of 7% to 10% cause dizziness, headache, visual and hearing dysfunction, and unconsciousness within a few minutes to an hour.[9]

Element Quiz

2010-10-08T05:52:00.001-04:00

Biology : Element Quiz

Calcium __________

Fluorine __________

Argon __________

Chlorine __________

Phosphorus ____________

Magnesium __________

Silicon ___________

Aluminum _________

Sodium __________

Nitrogen __________

Potassium _________

Neon __________

Oxygen _________

Carbon __________

Boron ________

Beryllium __________

Lithium _________

Helium ___________

Hydrogen _________

Sulfur __________

Chapter 1

2010-09-22T08:50:00.019-04:00

Viruses: Are They Living Organisms?

2010-09-15T07:07:00.003-04:00

Are viruses living organisms? They are not made of cells. According to the Cell Theory, all living things are made of cells. The cell is the basic unit of structure and function. However, if a virus infects a compatible cell they can reproduce themselves in great numbers using the reproductive machinery of that cell. Anyone who has had the flu or the common cold has experienced this process. Viruses are obligate intracellular parasites which is a fancy way of saying that they require a living cell to survive. Otherwise they remain dormant, in the air or on a surface waiting to meet the right cell. Can you name some diseases caused by viruses?

Sean Hannity - Science ILLiterate

2010-09-13T12:12:00.006-04:00

This link will provide you with an opportunity to tell Sean Hannity that his lack of knowledge on climate science makes him eminently unqualified to speak on the subject. It is perfectly okay to have opinions based on facts, but it is irresponsible to lie night after night to the American people. Climate Change is based on a bedrock of robust science. Hannity's pronouncements on the subject are embarrasing and dangerous because he can actually influence people who know even less than he does, if that is possible. Hannnity, like his stablemate, OReilly is a "bloviator" who abuses the public airwaves to promulgate rightwing and corporate extremism. They transform mendacity into peevish propaganda. Their intellectual creed is identical to Joseph Goebbels': tell the lie often enough and the people will believe it. Why this kind of pandemic dishonesty and manipulation of facts has been allowed to contine is testamony to the sorry state of public discourse in this country. It is time Americans demanded authentic information from their media instead of the pernicious and vituperative pulp Hannity excretes on his radio and television "shows" ( Fox, of course) every day without any informed rebuttal.

Louis Pasteur

2010-09-12T09:59:00.005-04:00

Louis Pasteur (pahs TOOR) was born to a tanner, Jean Joseph Pasteur and his wife Jeanne in France in the ancient town of Dole. His father had been a soldier in Napoleon's army. They sent Louis to a school in Arbois (Ahr-bwah) when he was six. He enjoyed drawing portraits of his family and friends. At that time his skill seemed to be in the field of art without a hint of his future fame as a scientist. After he graduated he went to the Royal College in Besancon (bih zan SAH(N) where he earned his B.A. and then a Bachelor of Science degree two years later at the age of twenty. In 1847 he received a doctorate degree and became a professor at age twenty-six. He fell in love with and married Marie Laurent and they had five children, but only two of them survived.

He began to study fermentation and how it related to alcoholic drinks. His research led to the process of pasteurization* of milk to kill viruses and harmful bacteria. The milk is not heated to the boiling point which would change the flavor, but is heated to a temperature sufficient to kill the bacteria which would cause it spoil easily or cause disease. It is then chilled and must be kept cold until used.
He named the new science bacteriology* and suggested a new theory, The Germ Theory of Disease. He believed that diseases were caused by germs attacking the body from the outside. The raising of silkworms was a large industry in France at that time. People raised them in their homes or in large sheds. The silk worms constantly ate mulberry leaves, so the owners would even get up in the night to feed them. The silkworm would spin a cocoon and become a chrysalis. Then the cocoons were put in a steam stove, dried in the sun and handed over to the weavers to unravel the silk threads. Each cocoon would be composed of a single silk thread 1000-3000 feet long. A few of the cocoons would be saved to develop into the moths which lay the eggs which hatched into silkworms and start the cycle all over again. In 1849 the worms were hit with a disease and began to die. It first started in France and spread worldwide to every country except Japan. In 1865 at the request of the government Pasteur performed experiments to find the cause of the malady. Using the microscope he determined that corpuscles in the infected worms were causing them to die. The worms would infect each other. He helped the growers to find a way to isolate and then use eggs that were not infected. At the end of this arduous* task he suffered a stroke and paralysis. For several months he was completely paralyzed. He was only 45 years old. After two years he began to recover the use of his body. His next task was to try and find the cause of disease in the body. He developed a vaccine for a disease in chickens, fowl cholera, and a disease in animals, splenic fever. After proving its success he began to prepare a vaccine for large numbers of animals and by 1883 the number of animals vaccinated against the disease called anthrax* reached nearly 500,000.

Pasteur devoted the rest of his life developing vaccines for people against such diseases as cholera, diphtheria, tuberculosis and smallpox.
The idea of immunization* with a weakened version of a disease was not new. As early as 1774 a vaccine for smallpox* had been discovered, and Edward Jenner before 1800 was vaccinating people against smallpox. He found that if he inoculated people with cowpox, they got the less severe disease which prevented them from getting smallpox.
He is especially remembered for the case in which he vaccinated* a nine-year-old boy, Joseph Meister, who had been bitten by a dog that had rabies.* The boy recovered after receiving the vaccine from Pasteur. When he grew up he became a caretaker at the Pasteur Institute.

Thousands of people since that time have received rabies vaccinations and been saved from getting the disease which is almost always fatal. The Pasteur Institute was founded in 1888 in Paris. When he died he was buried there in a fine tomb.

Whither Turtles

2010-09-12T08:44:00.001-04:00

What IS IT?

2010-09-09T19:21:00.003-04:00

Characteristics of Living Things

2010-09-07T14:23:00.001-04:00

Problems with Induced Pleuripotent Stem Cells

2010-02-11T08:00:00.002-05:00

Cell-Off: Induced Pluripotent Stem Cells Fall Short of Potential Found in Embryonic Version
It was hoped using reprogrammed mature cells would be a noncontroversial alternative to embryo-derived stem cells. But problems like low replication rates and early senescence have impeded their efficacy in generating differentiated cells
By Charles Q. Choi
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Scientific American magazine on Facebook
The act of reprogramming cells to make them as capable as ones from embryos apparently can result in aberrant cells that age and die abnormally, suggesting there is a long way to go to prove such cells are really like embryonic stem cells and can find use in therapies.Embryonic stem cells are pluripotent, able to create all cell types, save more embryonic tissue. To avoid the controversy surrounding these cells, scientists around the world have explored reprogramming mature cells to make them just as potent, with the hope being that such induced pluripotent stem (iPS) cells might one day help replace diseased or damaged tissue. Rapid progress is being made toward controlled differentiation of human iPS cells into specific tissue types, such as heart, neuron, liver, pancreas and eye."You hear all this dialogue in the media and scientific community about how iPS cells are just the same as embryonic stem cells, how they can solve the whole controversy by removing the need for embryos," says stem cell scientist Robert Lanza, chief scientific officer at Advanced Cell Technology in Worcester, Mass. "There's a lot of excitement about iPS cells, but no one wants to hear about the problems."Lanza and his colleagues investigated a range of cell types derived from eight human iPS cell lines and 25 embryonic stem cell lines. At first they found that human iPS cells could indeed generate blood vessel, blood precursor and retinal cells with characteristics similar to ones derived from embryonic stem cells, albeit with significantly reduced efficiency.Further study, however, revealed cells derived from iPS cells had significantly higher rates of cell death, or apoptosis, than ones from embryonic stem cells. Moreover, whereas the blood vessel cells that resulted could also form capillarylike structures, they and the retinal cells aged prematurely, losing their ability to divide.In addition, where cells derived from embryonic stem cells are great at proliferating—a potentially critical feature if one wants to grow sufficient numbers of cells for clinical use—ones from the iPS lines were much feebler. "It's not just a little difference, but up to 1,000- to 5,000-fold less activity, the difference between not having enough to coat the tip of a pen to enough to fill a whole test tube," Lanza says."We were devastated to find this out," Lanza adds. He notes his company had planned this year to apply to the U.S. Food and Drug Administration to use red blood cells and platelets derived from iPS cells in clinical trials, but "at this point, therapies with these cells are years off."There were already concerns surrounding the use of iPS cells in therapies because prior studies suggested they were prone to forming cancers. "What our findings show is that the problems with iPS cells don't just involve one or two or a few abnormal iPS cells escaping into the body and forming tumors, but that the whole population of cells is screwed up," Lanza says.Although no clinical trials involving therapies derived from iPS cells are on the books, researchers are currently testing drugs on them. "Our results are saying that if cells in these experiments are senescing and undergoing apoptosis, any conclusions we draw from that might not apply to what drugs are being tested on them, but from how the cells were derived," Lanza says.The abnormalities seen with the iPS cells may be related to viruses used to create them. Unpublished results from the researchers hint that significantly fewer anomalies are seen in iPS cells created via virus-free reprogramming strategies, such as ones that use proteins or small-molecule drugs. "The most obvious explanation there is that one cannot slice up DNA with viruses and not expect consequences," Lanza says. He and his colleagues detailed their findings online February 11 in the journal Stem Cells."This shows iPS cells have a lot of problems, but that doesn't mean they don't have potential—just not with the established methodologies used to create them," says tissue engineer Anthony Atala, director of Wake Forest University Baptist Medical Center's Institute for Regenerative Medicine in Winston–Salem, N.C. "It's a solvable problem, but it looks as if one should look away from methods that don't genetically modify the cell."Future research should not only compare how embryonic stem cells, iPS cells and adult stem cells differentiate, but focus on what effects the niche in which these cells will reside, when transplanted, will have on their characteristics, including tendencies to mutate into cancer cells, notes cell and stem cell biologist Olga Genbacev at the University of California, San Francisco, (U.C.S.F.) School of Medicine. "The major obstacle for this research is time: We need time and coordinated international efforts," she says."Rather than being gloom and doom with these results, we should think of them pointing us toward things that are going to have to be fixed," commented developmental and stem cell biologist Susan Fisher at U.C.S.F. "For instance, these undergo senescence early. Well, there are major pathways known to control senescence. We'll want to look at those pathways to understand what's going on in these iPS cells and see if we can repair them."

Romanticism Hit by Climate Change

2010-02-11T07:53:00.004-05:00

Romanticism undone: Invasive species, global warming taking toll on plants at Thoreau's Walden Pond
By John Platt

Henry David Thoreau famously catalogued the plants around Walden Pond more than 150 years ago, and the information he gathered then is helping to illustrate the effects of invasive species and global warming on the area today.According to a paper published January 26 in the journal PLoS ONE, climate change has given invasive and nonnative species a leg up in the Walden Pond area, and native species are suffering the losers. (A nonnative species is considered invasive if it has the potential to disperse widely and rapidly, especially within habitats that are minimally maintained by humans. Some nonnative species do not spread quickly enough to qualify as invasive.)Researchers compared Thoreau's information with data on temperature and plant populations from this century as well as full information on plant phenology (flowering time, germination, migration and other seasonal activities). They found that the average temperature in Concord, Mass., has increased 2.4 degrees Celsius since Thoreau's time, and that some nonnative plants have adapted by flowering as much as three weeks earlier than they used to. Some native species, by contrast, were less flexible and have not been able to adjust their flowering times. As a result, their populations have dropped."These results demonstrate for the first time that climate change likely plays a direct role in promoting nonnative species success," lead author Charles C. Davis, an assistant professor of organismic and evolutionary biology at Harvard University, said in a prepared statement. "Our research suggests quite decisively that nonnative and invasive species have been the climate change winners. Climate change will lead to an as yet unknown shuffling of species, and it appears that invasive species will become more dominant."The team didn't just count the plants to come up with this observation. They also examined "habit, plant height at maturity, leaf mass per area, flower diameter, pollination syndrome and seed weight" to come up with a full picture of the health of the species in the area.This isn't the first time that Davis and his colleagues have studied Walden's plants. Two years ago, they found that 27 percent of the plant species Thoreau recorded from 1851 to 1858 are now locally extinct. Another 36 percent "are so sparse that extinction may be imminent," they wrote in a previous paper. At that time, species like lilies, orchids, violets, roses and dogwoods were shown to have seen the biggest losses.Image: Cover to Walden by Henry David Thoreau, via Wikipedia

Allium Assay

2010-01-14T11:19:00.015-05:00

1:20 dilution

1:320 dilution: slide #1

Cytoplasm heavily vessicled

Karyorrhexis - nuclear fragmentation

pyknosis- nuclear shrinkage

POEA- change cell's permeability

Amlifies toxicity

Adjuvants not inerts

hanging chromosomes in two metphase photographs

prophase breakup

scattered anaphase

Genetics -U.Cal

2010-01-14T10:02:00.002-05:00

RFLPs

2010-01-11T16:18:00.005-05:00

Restriction Fragment Length Polymorphisms (RFLPs)Restriction enzymes cut DNA at precise points producing
a collection of DNA fragments of precisely defined length.
These can be separated by electrophoresis, with the smaller fragments migrating farther than the larger fragments.
One or more of the fragments can be visualized with a "probe" — a molecule of single-stranded DNA that is
complementary to a run of nucleotides in one or more of the restriction fragments and is
radioactive (or fluorescent).
If probes encounter a complementary sequence of nucleotides in a test sample of DNA, they bind to it by Watson-Crick base pairing and thus identify it.
Polymorphisms are inherited differences found among the individuals in a population. RFLPs have provided valuable information in many areas of biology, including:
screening human DNA for the presence of potentially deleterious genes ("Case 1");
providing evidence to establish the innocence of, or a probability of the guilt of, a crime suspect by DNA "fingerprinting" ("Case 3").
Case 1: Screening for the sickle-cell gene Sickle cell disease is a genetic disorder in which both genes in the patient encode the amino acid valine (Val) in the sixth position of the beta chain (betaS) of the hemoglobin molecule. "Normal" beta chains (betaA) have glutamic acid at this position.
The only difference between the two genes is the substitution of a T for an A in the middle position of codon 6. This
converts a GAG codon (for Glu) to a GTG codon for Val and
abolishes a sequence (CTGAGG, which spans codons 5, 6, and 7) recognized and cut by one of the restriction enzymes.
When the normal gene (betaA) is digested with the enzyme and the fragments separated by electrophoresis, the probe binds to a short fragment (between the red arrows).
However, the enzyme cannot cut the sickle-cell gene at this site, so the probe attaches to a much larger fragment (between the blue arrows).
The figure (from data provided by S. E. Antonarakis) shows the pedigree of a family whose only son has sickle-cell disease. Both his father and mother were heterozygous (semifilled box and circle respectively) as they had to be to produce an afflicted child (solid box). The electrophoresis patterns for each member of the family are placed directly beneath them. Note that the two homozygous children (1 and 3) have only a single band, but these are more intense because there is twice as much DNA in them.
In this example, a change of a single nucleotide produced the RFLP. This is a very common cause of RFLPs and now such polymorphisms are often referred to as single nucleotide polymorphisms or SNPs. (However, not all RFLPs arise from SNPs. Link to an example of one that didn't.)
How can these tools be used?
By testing the DNA of prospective parents, their genotype can be determined and their odds of producing an afflicted child can be determined. In the case of sickle-cell disease, if both parents are heterozygous for the genes, there is a 1 in 4 chance that they will produce a child with the disease. Amniocentesis and chorionic villus sampling make it possible to apply the same techniques to the DNA of a fetus early in pregnancy. The parents can learn whether the unborn child will be free of the disease or not. They may choose to have an abortion rather than bring an afflicted child into the world. Three problems:
The mutations that cause most human genetic diseases are more varied than the single mutation associated with sickle-cell disease. Over a thousand different mutations in the cystic fibrosis gene can cause the disease. A probe for one will probably fail to identify a second. A mixture of probes, one for each of the more common mutations, can be used. But there remains the problem of "false negatives": people who are falsely told they do not carry a mutant gene.
There are many diseases which result from several mutant genes working together to produce the disease phenotype.
There are still genetic diseases for which no gene has yet been discovered. Until the gene can be located, cloned, and sequenced, no probe can be made to detect it directly. However, it is sometimes possible to find a genetic "marker" that can serve as a surrogate for the gene itself. Let's see how.
Case 2: Screening for a RFLP "marker"
If a particular RFLP is usually associated with a particular genetic disease, then the presence or absence of that RFLP can be used to counsel people about their risk of developing or transmitting the disease. The assumption is that the gene they are really interested in is located so close to the RFLP that the presence of the RFLP can serve as a surrogate for the disease gene itself. But people wanting to be tested cannot simply walk in off the street. Because of crossing over, a particular RFLP might be associated with the mutant gene in some people, with its healthy allele in others. Thus it is essential to examine not only the patient but as many members of the patient's family as possible.
The most useful probes for such analysis bind to a unique sequence of DNA; that is, a sequence occurring at only one place in the genome. Often this DNA is of unknown, if any, function. This can actually be helpful as this DNA has been freer to mutate without harm to the owner. The probe will hybridize (bind to) different lengths of digested DNA in different people depending on where the enzyme cutting sites are that each person has inherited. Thus a large variety of alleles (polymorphisms) may be present in the population. Some people will be homozygous and reveal a single band; others (e.g., all the family members shown below) will be heterozygous with each allele producing its band.
The pedigree shows the inheritance of a RFLP marker through three generations in a single family. A total of 8 alleles (numbered to the left of the blots) are present in the family. The RFLPs of each member of the family are placed directly below his (squares) or her (circles) symbol and RFLP numbers.
If, for example, everyone who inherited RFLP 2 also has a certain inherited disorder, and no one lacking RFLP 2 has the disorder, we deduce that the gene for the disease is closely linked to this RFLP. If the parents decide to have another child, prenatal testing could reveal whether that child was apt to come down with the disease.
But note, that crossing over during gamete formation could have moved the RFLP to the healthy allele. So the greater the distance between the RFLP and the gene locus, the lower the probability of an accurate diagnosis.
Link to discussion of genetic linkage.
Case 3: DNA "typing" Each human cell contains 6 x 109 base pairs of DNA. Some of this represents structural genes (e.g., for the beta chain of hemoglobin) that are identical in a large proportion of people. But long stretches of DNA do not encode for anything and are free to mutate extensively. It seems certain that if we could read the entire sequence of DNA in each human, we would never find two that were identical (unless the samples were from identical siblings; i.e., derived from a single zygote).
So each person's DNA is as unique as a fingerprint. This truth has not escaped the law enforcement and legal professions. Analysis of DNA, called DNA typing, is widely used to
identify rapists and other criminals;
determine paternity; that is, who the father of the child really is;
determine whether a hopeful immigrant is, as he or she claims, really a close relative of already established residents.
The image (courtesy of Lifecodes Corporation) shows the test results in a rape case. Two probes were used: one revealing the bands at the top, the other those at the bottom. DNA was tested from
semen removed from the vagina of the rape victim (EVIDENCE #2);
a semen stain left on the victim's clothing (EVIDENCE #1);
the DNA of the victim herself (VICTIM) to be sure that the DNA didn't come from her cells;
DNA from two suspects (SUSPECT #1, SUSPECT #2);
a set of DNA fragments of known and decreasing length (MARKER). They provide a built-in ruler for measuring the exact distance that each fragment travels.
the cells of a previously-tested person to be sure the probes are performing properly (CONTROL).
One the basis of this test, suspect #2 can clearly be ruled out. None of his bands matches the bands found in the semen. Is suspect #1 guilty?
We can never be certain. The best we can do is to estimate the probability that another person, picked at random, could provide the same DNA fingerprint.
As a conservative estimate, a given allele (band) might be found in 25% of the people tested. The probability of a random match of two alleles is (0.25)2 or 1 in 16. The probability that 6 alleles match, as in this case, is (0.25)6 or 1 in 4096.
But the suspect was not picked at random, so you may feel that the evidence of guilt is strong.
The more probes you use, the more confident you can be that you have gotten the right man. If, for example, a set of probes revealed 14 bands in a suspect's DNA identical to those in the semen sample, the probability that you have the wrong man drops to less than 1 in 268 million (0.25)14 = 1/268,435,456, which is more than the entire population, males and females, in the United States.
Starting in 1999, law enforcement agencies in both Great Britain and the United States began switching to a new version of RFLP analysis using shorter sequences called STRs ("Short Tandem Repeats").
STRs are repeated sequences of a few (usually four) nucleotides, e.g., TCATTCATTCATTCAT. They often occur in the untranslated parts of known genes (whose sequence can be used for the PCR primers). The exact number of repeats (6, 7, 8, 9, etc.) varies in different people (and, often, in the gene on each chromosome; that is, people are often heterozygous for the marker).
In the U.S., where 13 STRs — scattered over different chromosomes — are examined, the chance that two people picked at random have the same pattern is less than 1 in 1 trillion.

Those Darn Feedbacks Are What Get You Every Time

2010-01-06T13:05:00.002-05:00

Methane release 'looks stronger' By Michael Fitzpatrick Science reporter, BBC News
Scientists have uncovered what appears to be a further dramatic increase in the leakage of methane gas that is seeping from the Arctic seabed.
Methane is about 20 times more potent than CO2 in trapping solar heat.
The findings come from measurements of carbon fluxes around the north of Russia, led by Igor Semiletov from the University of Alaska at Fairbanks.
"Methane release from the East Siberian Shelf is underway and it looks stronger than it was supposed [to be]," he said.
Professor Semiletov has been studying methane seepage in the region for the last few decades, and leads the International Siberian Shelf Study (ISSS), which has launched multiple expeditions to the Arctic Ocean.
The preliminary findings of ISSS 2009 are now being prepared for publication, he told BBC News.
Methane seepage recorded last summer was already the highest ever measured in the Arctic Ocean.
High seepage
Acting as a giant frozen depository of carbon such as CO2 and methane (often stored as compacted solid gas hydrates), Siberia's shallow shelf areas are increasingly subjected to warming and are now giving up greater amounts of methane to the sea and to the atmosphere than recorded in the past.
METHANE HYDRATES
Methane gas is trapped inside a crystal structure of water-ice
The gas is released when the ice melts, normally at 0C
At higher pressure, ie under the ocean, hydrates are stable at higher temperatures
This undersea permafrost was until recently considered to be stable.
But now scientists think the release of such a powerful greenhouse gas may accelerate global warming.
Higher concentrations of atmospheric methane are contributing to global temperature rise; this in turn is projected to cause further permafrost melting and the release of yet more methane in a feedback loop.
A worst-case scenario is one where the feedback passes a tipping point and billions of tonnes of methane are released suddenly, as has occurred at least once in the Earth's past.
Such sudden releases have been linked to rapid increases in global temperatures and could have been a factor in the mass extinction of species.
According to a report by the US National Oceanic and Atmospheric Administration (Noaa), the springtime air temperature across the region in the period 2000-2007 was an average of 4C higher than during 1970-1999.
That is the fastest temperature rise on the planet, claims the university.
The recent thaw over the last decade means that some of the large reserve of carbon from organic material such as dead animals and plants in sediments is now being released into the sea and into our atmosphere.
Trapped below that is the methane hydrate now warming and leaking through holes in the defrosting sediments.
1. Methane hydrate is stable at high pressure and low temperature
2. Nearer the surface, where water pressure is lower, hydrates break down earlier than at greater depth as temperatures rise
3. Gas rises from the sea-bed in plumes of bubbles - some of it dissolves before it reaches the surface
4. The ISSS team says it has detected methane breaking the ocean surface
Previously it was thought much of this gas was absorbed into the sea.
But according to a recent report that Professor Semiletov and his team compiled for the environmental group WWF, the shallow depth of arctic shelves means that methane is reaching the atmosphere without reacting to become CO2 dissolved in the ocean.
Professor Semiletov's fellow researcher aboard the Russian icebreaker that carries the ISSS team each year is Professor Orjan Gustafsson from Stockholm University in Sweden.
He said that methane measured in the atmosphere around the region is 100 times higher than normal background levels, and in some cases 1,000 times higher.
'No alarm'
Despite the high readings, Professor Gustafsson said that so far there was no cause for alarm, and stressed that further studies were still necessary to determine the exact cause of the methane seepage.
"It is important now to understand how fast it is being released and how much is being released," he said.
However, there is a real fear that global warming may cause Siberia's subsea permafrost to thaw.
Some estimates put the amount of carbon trapped in shelf permafrost at 1,600 billion tonnes - roughly twice as much carbon as in the atmosphere now.
The release of this once captive carbon from destabilised ocean sediments and permafrost would have catastrophic effect on our climate and life on Earth, warn the scientists.

Allium Assay

2010-01-04T20:19:00.001-05:00

Protocol no. 8
ALLIUM TEST
The Allium test provides a rapid screening procedure for chemicals, pollutants contaminants, etc. which may represent environmental hazards. Root growth inhibition and adverse effects upon chromosomes provide an indication of likely toxicity.

RATIONALE
The root tip is often the first part of any plant which is likely to come into contact with chemicals and pollutants to be found in soil and water supplies. Observation of the root tip system of the onion, Allium cepa, has shown that this plant is particularly sensitive to the harmful effects of such environmental contaminants. Gross effects can be quantified by measurement of inhibition of growth of the newly developing root system, whereas examination of the chromosomes of the individual cells of the root tip can indicate likely mutagenic effects.
BASIC PROCEDURE
Twelve onions (Allium cepa) are prepared by removal of the outer scales and brownish bottom plate and placed onto test tubes filled with test liquids for 4 days, the liquid being changed every day. A further series of twelve onions are similarly prepared and maintained on pure water to provide a control population. The ten onions which appear to be developing the best in each series are selected for examination. On day 2 one root tip from each of 5 onions is prepared for microscopic examination. One hundred mitoses are scored from each of the 5 slides, as is the mitotic index (MI) for 400 cells. On day 4 the root length of each bulb is measured and the series photographed. (A recovery experiment can be performed by changing the medium for 5 of the 10 onions of each test series to control water after measurement on day 4, replenishing the liquid on day 5 and, finally, measuring the root length and photographing the series on day 6). Toxicity is measured by both macroscopic parameters (e.g. growth inhibition), where the degree of damage is used to assess the toxic status of the chemical tested, and microscopic parameters, where the rate of chromosome breakage and damage may be used to predict mutagenesis.
CRITICAL ASSESSMENT
Plants are easy to store and handle, and are plentiful and inexpensive. In general the chromosome condition of plant cells is good, thus providing a high standard in control conditions. The Allium test is a relatively rapid, easy to perform test as well as being both highly sensitive and reproducible. It also provides comparable results to a number of other test systems. Both macroscopic and microscopic effects may be observed and there appears to be a good correlation between the two. The macroscopic effect (inhibition of root growth) appears to be the most sensitive parameter. This is to be expected as any deleterious effect, direct or indirect, is likely to result in inhibition of growth. Microscopic examination allows assessment of chromosome damage and cell division disturbances, thus providing additional information as to the severity or mechanism of the toxic effect, or potential mutagenicity. The root cells possess certain enzymes, the mixed function oxidases, which are instrumental in the activation of many promutagens to mutagens. This activating system will improve the detection of those chemicals which exert their toxic effect via a reactive metabolite. The system has a wide range of applications, e.g. for testing pure chemicals, drinking water, natural water, industrial waste, etc., and is useful for evaluating and ranking environmental chemicals with reference to toxicity. The test can also be used to measure the relative toxicities of non-water soluble compounds, provided they can be dissolved in a suitable solvent and then diluted in water so that the final concentration does not exceed certain limits. In cases such as these solvent controls must also be incorporated into the test regime. The system operates over a wide pH range (3.5-11.0) without any obvious effects upon the growth of the root systems. Thus moderately acidic/alkali water samples, chemical solutions, etc. can readily be tested without pH correction being necessary. N.B. Although the pH itself may not affect the growth of the roots, it should be taken into consideration when assessing the toxicity of compounds as, in many cases, the pH can dramatically alter the toxic potential of these, e.g. by changing the state of ionisation. Disadvantages of the system concern problems associated with the state of compounds being tested. The influence of pH upon compounds present in solution and the resultant change in toxic profiles has already been mentioned. Another problem concerns the presence of insoluble compounds in water-ways, industrial effluent, etc.. It is very difficult to look at the biological effect of such complex mixtures in the Allium system as particulate matter may exert indirect harmful effects such as the prevention of uptake of nutrients etc.. It is therefore recommended that samples such as these are also chemically analysed. The Allium test is highly sensitive and, as such, positive toxic effects may result for a number of compounds which would not necessarily be deemed harmful when tested in other systems (especially higher organisms such as fish). Although this may occasionally result in false positives it also ensures that contaminations will not be overlooked; this is especially important when complex mixtures are to be tested. A positive result in this test system should, therefore, be taken to indicate a potential biological hazard. False negatives, on the other hand, have been shown to rarely occur in either the Allium test or other similar plant tests (Ennever et al., 1988), therefore, any compound tested giving a negative result can be reliably considered nonmutagenic. An extrapolation of results from one test system to another (and eventually to humans) should, however, be based on the results of a battery of tests and with due consideration to the metabolic pathways of the compound tested. Development of the test The Allium test system was first used in 1938 to examine the effect of colchicine (Levan, 1938; Östergren, 1944) and has received much attention since that time (for review, see Grant, 1982). Certain modifications of the basic test system have been introduced to enable environmental monitoring of complex mixtures such as those present in river water, industrial waste, etc. (Fiskesjö, 1985a). The major modifications include the use of a series of bulbs (i.e. 10) for each condition tested (thus permitting an EC50 determination), and the immediate exposure of bulbs to test solutions (the old test allowed an initial growth period in pure water until roots reached an appropriate length, 1-2 cm, after which they were exposed to test compounds). Comparison to other short-term alternative toxicity test systems This test has shown good agreement with results from other test systems, using many different organisms, eukaryotic as well as prokaryotic. Results of such comparisons are summarised below (taken from Fiskesjö, 1985a). Chinese hamster cell line V79 In the absence of a metabolic activating system V79 cells appear less sensitive than the Allium test in response to organic mercury compounds. The relative sensitivity is reversed when the cells are incubated in the presence of mixed function oxidases. Despite changes in sensitivities the overall results between the two systems are comparable. Human lymphocytes The Allium test seems slightly more sensitive to the effects of organic mercury compounds than do human lymphocytes, although the overall ranking of chemicals by toxicity is similar. It should also be noted that when studied microscopically both cell types respond in a similar way (c-mitosis). Autotrophic algae, heterotrophic microorganisms and activated sludge A number of chemicals have been tested in the Allium test and the results compared to those found using 16 different plankton algae (green algae and silicious algae), yeast (Saccharomyces cerevisiae), protozoa (Tetrahymena pyriformis) and activated sludge (composition of bacteria, yeast and protozoa). The tests were all comparable when the rank ordering of chemicals according to toxicity was examined, although differences in sensitivities were apparent. The majority of the algae were more sensitive than the Allium test whereas the yeast, protozoa, and activated sludge were less sensitive. Aquatic animals (Daphnia magna, Brachydario rerio - egg or spawn & Microtox bacteria test) and plants (Lens & Unicellular algae) A number of aquatic plants and animals appear to be less sensitive to certain classes of compound compared to the Allium test e.g. fish (Gasterosteus aculeatus). The Allium test, in this case, is probably a better test for environmental screening due to its higher sensitivity. Other animals (e.g. the crustacean Nitocra spinipes) and plants (e.g. Lens and unicellular algae) give comparable results to the Allium test.
CHEMICALS TESTED
Wide range of metals, industrial pollutants, compounds, etc. have been tested. Water from a variety of sources has also been examined. For examples see references below.
REFERENCES
1. Berggren, D. & Fiskesjö, G. (1987) Aluminum toxicity and speciation in soil liquids - experiments with Allium cepa L. Environ. Tox Chem., 6, 771-779.
2. Ennever, F.K.; Andreano, G. & Rosenkranz, H.S. (1988) The ability of plant genotoxicity assays to predict carcinogenicity. Mut. Res., 205, 99-105
3. Fiskesjö, G. (1981) Allium test on copper in drinking water. Vatten, 17(3), 232-240.
4. Fiskesjö, G. (1981) Benzo(a)pyrene and N-methyl-N-nitro-N-nitrosguanidine in the Allium test. Hereditas, 95, 155-162
5. Fiskesjö, G., Lassen, C. & Renberg, L. (1981) Chlorophenoxyacetic acids and chlorophenols in the modified Allium test. Chem. Biol. Interac., 34, 333-344
6. Fiskesjö, G. (1982) Evaluation of short-term tests for toxicity and mutagenicity with special reference to mercury and selenium. Ph.D. thesis, Inst. of Genetics, Univ. of Lund, Sweden. Fiskesjö, G. (1983) Nucleolar dissolution induced by aluminium in root cells of Allium. Physiologica plantarum, 59, 508-511.
7. Fiskesjö, G. (1985a) The Allium as a standard in environmental monitoring. Hereditas, 102, 99-102 Fiskesjö, G. (1985b) Allium test on river water from Bra n and Sax n before and after closure of a chemical factory. Ambio, 14(2), 99-103
8. Fiskesjö, G. (1987) The Allium test - an alternative. ATLA, 15, 33-35. Fiskesjö, G. (1988) The Allium test - an alternative in environmental studies: the relative toxicity of metal ions. Mut. Res., 197(2), 243-260. Grant, W.F. (1982) Chromosome aberration assays in Allium. Mut. Res., 99, 273-291.
9. Levan, A. (1938) The effect of colchicine on root mitoses in Allium. Hereditas 24, 471-486. Östergren, G (1944) Colchicine mitosis, chromosome contraction, narcosis and protein chain folding. Hereditas 30, 429-467.

Sequencing Neanderthal DNA

2010-01-04T07:30:00.005-05:00

DNA analysed from early European By Paul Rincon Science reporter, BBC News
Scientists have analysed DNA extracted from the remains of a 30,000-year-old European hunter-gatherer.
Studying the DNA of long-dead humans can open up a window into the evolution of our species ( Homo sapiens ).
But previous studies of this kind have been hampered by scientists' inability to distinguish between the ancient human DNA and modern contamination.
In Current Biology journal, a German-Russian team details how it was possible to overcome this hurdle.
Svante Paabo, from the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany, and colleagues used the latest DNA sequencing techniques to study genetic information from human remains unearthed in 1954 at Kostenki, Russia.
Excavations at Kostenki, on the banks of the river Don in southern Russia, have yielded large concentrations of archaeological finds from the Palaeolithic (roughly 40,000 years ago to 10,000 years ago). Some of the finds date back as far as 45,000 years.
“ The ironic thing is that our group has been one of those that raised this issue ” Professor Svante Paabo, Max Planck Institue
The DNA analysed in this study comes from a male aged 20-25 who was deliberately buried in an oval pit some 30,000 years ago.
Known as the Markina Gora skeleton, it was found lying in a crouched position with fists reaching upwards and a face orientated down towards the dirt. The bones were covered in a pigment called red ochre, thought to have been used in prehistoric funeral rites.
The type of DNA extracted and analysed is that stored in mitochondria - the "powerhouses" of cells. This mitochondrial DNA (mtDNA) is passed down from a mother to her offspring, providing a unique record of maternal inheritance.
Using technology pioneered in the study of DNA from Neanderthal bones, they were able to distinguish between ancient genetic material from the Kostenki male and contamination from modern people who handled the bones, or whose DNA reached the remains by some other means.
The new approach, developed by Professor Paabo and his colleagues, exploits three features which tend to distinguish ancient DNA from modern contamination. One of these is size; fragments of ancient DNA are often shorter than those from modern sources.
Previous ancient DNA studies used the widespread polymerase chain reaction (PCR) technology. PCR amplifies a few pieces of genetic material, generating thousands to millions of copies of a sequence. But the researchers found many fragments of ancient DNA were too small to be amplified by PCR.
A second characteristic of ancient DNA was its tendency to show particular changes, or mutations, in the genetic sequence at the ends of DNA molecules.
A third feature was a characteristic breakage of molecules at particular positions in the DNA strand.
Trust issues
The apparent ease with which modern DNA can infiltrate ancient remains has led many researchers to doubt even those studies employing the most rigorous methods to weed out contamination by modern genetic material.
"The ironic thing is that our group has been one of those that raised this issue," Professor Paabo told BBC News.
"To take animal studies on cave bears, for example, if we use PCR primers specific for human DNA on cave bear bones, we can retrieve modern human DNA on almost every one. That has made me think: 'how can I trust anything on this'."
Using the new techniques, the researchers were able to sequence the entire mitochondrial genome of the Markina Gora individual.
Future studies like the one in Current Biology could help shed light on whether the humans living in Europe 30,000 years ago are the direct ancestors of modern populations or whether they were replaced by immigrants who introduced farming to the continent several thousand years ago.
The modern gene pool contains a wide variety of mtDNA lineages. Studying these maternal lineages provides scientists with clues to the origins and histories of human populations.
Scientists look for known genetic signatures in order to classify an individual's mtDNA into different types, or "haplogroups". These haplogroups represent major branches on the family tree of Homo sapiens .
Early arrival
The researchers were able to assign the Kostenki individual to haplogroup "U2", which is relatively uncommon among modern populations.
U2 appears to be scattered at low frequencies in populations from South and Western Asia, Europe and North Africa.
Despite its rarity, the very presence of this haplogroup in today's Europeans suggests some continuity between Palaeolithic hunters and the continent's present-day inhabitants, argue the authors of the latest study.
U2, along with closely related haplogroups such as U5, are among those which could plausibly have arrived in Europe during the Palaeolithic.
Geneticists use well-established techniques to "date" particular genetic events, such as when a haplogroup first diversified. The "U" branch (comprising haplogroups U1, U2, U3 and so on) appears to be more ancient than many other genetic lineages found in Europe.
A recent study found a very high percentage of U types in the skeletal remains of ancient hunter-gatherers from Central Europe compared with later farming immigrants and modern people from the region.
Meanwhile, an analysis last year of mtDNA from 28,000-year-old remains unearthed at Paglicci Cave in Italy showed this individual belonged to haplogroup "H" - the most common type found in modern Europeans.

Long Term Fitness and Telomeres

2010-01-04T07:11:00.002-05:00

Long-term fitness 'fights ageing'
Long-term physical activity has an anti-ageing effect at the cellular level, a German study suggests.
Researchers focused on telomeres, the protective caps on the chromosomes that keep a cell's DNA stable but shorten with age.
They found telomeres shortened less quickly in key immune cells of athletes with a long history of endurance training.
The study, by Saarland University, appears in the journal Circulation.
“ This is direct evidence of an anti-ageing effect of physical exercise ” Dr Ulrich Laufs Saarland University
In a separate study of young Swedish men, cardiovascular fitness has been linked to increased intelligence and higher educational achievement.
Telomeres are relatively short sections of specialised DNA that sit at the ends of all our chromosomes.
They have been compared to the plastic tips at the ends of shoelaces that prevent the laces from unravelling.
Each time a cell divides, its telomeres shorten and the cell becomes more susceptible to dying.
National athletes
The researchers measured the length of telomeres in blood samples from two groups of professional athletes and two groups of people who were healthy non-smokers, but who did not take regular exercise.
One group of professional athletes included members of the German national track and field athletics team, who had an average age of 20.
The second group was made up of middle-aged athletes who had regularly run long distances - an average of 80km a week - since their youth.
The researchers found evidence that the physical exercise of the professional athletes led to activation of an enzyme called telomerase, which helped to stabilise telomeres.
This reduced the telomere shortening in leukocytes, a type of white blood cell that plays a key role in fighting infection and disease.
The most pronounced effect was found in athletes who had been regularly endurance training for several decades.
Potency of training
Lead researcher Dr Ulrich Laufs said: "This is direct evidence of an anti-ageing effect of physical exercise.
"Our data improves the molecular understanding of the protective effects of exercise and underlines the potency of physical training in reducing the impact of age-related disease."
“ It is still difficult to separate cause and effect from these studies - as longer telomeres may still be a marker of fitness ” Professor Tim Spector Kings College London
Professor Tim Spector, an expert on genetics and ageing at Kings College London, said other studies had suggested more moderate exercise had a beneficial effect on ageing.
He said: "It is still difficult to separate cause and effect from these studies - as longer telomeres may still be a marker of fitness.
"Nevertheless - this is further evidence that regular exercise may retard aging."
Professor Kay-Tee Khaw, of the University of Cambridge, an expert on ageing, said: "The benefits of physical activity for health are well established from many large long-term population studies.
"Even moderate levels of physical activity are related to lower levels of many heart disease risk factors such as blood pressure and cholesterol and lower risk of many chronic diseases associated with ageing such as heart disease, stroke, diabetes and some cancers."
Intelligence link
In the second study, published in Proceeding of the National Academy of Sciences, a team from the University of Gothenburg analysed data on more than 1.2 million Swedish men born from 1950-1976 who enlisted for military service at age 18.
They found that good heart health was linked to higher intelligence, better educational achievement and raised status in society.
By studying twins in the study, the researchers concluded that environmental and lifestyle factors were key, rather than genetics.
They said the findings suggested that campaigns to promote physical exercise might help to raise standards of educational achievement across the population.
Lead researcher Professor Georg Kuhn said cardiovascular exercise increased blood flow to the brain, which in turn might help forge more and stronger connections between nerve cells.
However, he said it was also possible that intelligent people tended to make more exercise.
Story from BBC NEWS:

Limbaugh Hospitalized with Chest Pains: The Best of Care in th Worst of Times

2009-12-31T10:05:00.005-05:00

I am reluctant to kick anyone when they are down, even Rush Limbaugh. Limbaugh has a daily radio audience of 25 million people aptly known as "dittoheads". This is perhaps do to their avid willingness to rescind all responsibilty for critical analysis, compassion, and even minimal levels of cognition. They, like Limbaugh, have repudiated all responsibility for the troubled legacy we will pass on to future generations. Daily, for example, he mocks the "envirowhackos" and socialists who are propagating the lie of climate change. Rush would have us believe that the science supporting concerns about warming and rapidly changing planet are nothing but a liberal ( enunciated with a sneer and protracted disdain) scam and "hoax". Two years ago Limabaugh admitted to being addicted to the pain medication OxyContin. The investigation into how the great one obtained his stash mysteriously disappeared from the "drive by " media for which Limbaugh proclaims so much loathing. El Rushbo's felonious behaviors were quietly forgiven and forgotten. Had the same favor been been granted to an African-American star in the NFL, I am certain Rush would have many sermons on the subject of personal responsibility, accountability, and the permissiveness of the Obama Administration as a causal antecedent. In addition to his daily rants against science Rush has allocated much time deriding attempts to reform the dysfuntional American healthcare system. If you are fortunate enough to have health insurance, don't have the temerity to get sick. The American system, based on the "anything for a buck" foundation of capitalism, does not want to insure sick people. Bad for profits. Thank God Rush has the best of the best insurance. As a result, he will no doubt survive his encounter with mortality and continue telling lies to his legions of flatliners. Many Americans without Rush's resources and close relationship with Mammon would not have been so fortunate.

Telomere Length in Cancer Cells and Abuse Victims

2009-12-16T07:38:00.010-05:00

The Natural World: Love It or Lose It

2009-12-16T07:32:00.006-05:00

Many Thanks to Chloe Cullen for these fine

photographs.

What is it? Where Did It Come rom?

2009-12-16T06:48:00.003-05:00

Florida manatees generally grow to around 3 metres (10 feet) but range in length from about 2.5 to 3.9 metres (8 to 13 feet) and weigh up to 1,655 kg (3,650 pounds). The Antillean subspecies is very similar but is distinguishable from the Florida manatee by certain skull features. West African manatees closely resemble West Indian manatees and are similar in size. Amazonian manatees are smaller, reaching a length of 2.8 metres (9.2 feet) and a weight of 480 kg (1,056 pounds), and, unlike the other two species, they are more blackish in colour, commonly have a white patch on the chest, and lack nails on the flippers. The flippers are used by all species for sculling, turning, bottom walking, and manipulating food.
Manatees are uniquely adapted for eating aquatic plants. The manatee’s large lips are prehensile and studded with specialized sensory bristles and hairs (vibrissae) for discriminating between and manipulating food plants. Compared with the fish and krill eaten by other marine mammals, most aquatic plants are low in energy value and protein. Manatees must therefore eat large amounts of this bulky, low-energy food to satisfy their dietary requirements. To handle such a diet, manatees are hindgut digesters (like horses) and have intestines as long as 30 metres (100 feet). The teeth have also evolved in response to dietary demands. To counter abrasion from ingested sand and silica, manatees constantly grow new molars. These teeth progress from the rear of the jaws forward as older, worn teeth drop out at the front of the mouth. Unlike almost all other mammals, tooth replacement occurs throughout life.
The lungs are oriented parallel to the water’s surface, and the ribs lack marrow, which makes them unusually dense and heavy. These traits, along with the manatee’s ability to control the volume of small air spaces in the lungs, permit the animal to maintain a horizontal orientation anywhere in the water from the bottom to the surface. Manatees can remain submerged for up to 20 minutes. With each breath they replenish about 90 percent of the air in the lungs. (Humans, by contrast, replenish only about 10 percent.) This set of diverse adaptations enables foraging on a variety of plant forms, including submerged sea grasses, floating plants, mangrove leaves, and grasses along banks.
Manatees have unusually low metabolic rates, which probably makes possible their long fasting periods and subsistence on low-energy food. Although they can deposit large stores of fat, manatees’ capacity to generate and retain body heat in cool water is poor. The brain is very small in comparison with those of other mammals of similar body size. Although the cerebrum lacks marked convolutions, the proportion of the brain devoted to higher functions is comparable to that of primates.

2009-12-07T16:13:00.005-05:00

The Corporate Assault on Amphibians Continues

2009-12-07T14:23:00.003-05:00

Published on Monday, December 7, 2009 by Reuters
Study Finds Weed Killer Affects Frogs Sexually
by Reuters
OTTAWA - The widely used weed killer atrazine affects the sexual development of frogs, raising questions about the effects of its use in the environment, the University of Ottawa said on Thursday.
The widely used weed killer atrazine affects the sexual development of frogs, raising questions about the effects of its use in the environment, the University of Ottawa said on Thursday. (Reuters image)A study by researchers at the university found that at low levels comparable to those measured in the Canadian environment, fewer tadpoles reached the froglet stage and the ratio of females to males increased.
"Atrazine is one of the top-selling herbicides used worldwide and was designed to inhibit weed growth in cornfields," the university said in a statement.
"It is so widely used that it can be detected in many rivers, streams and in some water supplies. This has raised the alarm on the possibility of other serious detrimental environmental effects."
Syngenta AG, a major Swiss manufacturer of atrazine, has long defended its safety. The company has said it is one of the best-studied herbicides available and pointed to previous safety reviews from the U.S. Environmental Protection Agency (EPA) and World Health Organization, among others.
The EPA said in October that it was reviewing the health impacts of the herbicide. Some studies have tied it to birth defects, low birth weight and premature babies.
(Reporting by Randall Palmer; editing by Peter Galloway)

© 2009 Reuters
Article printed from www.CommonDreams.org
URL to article: http://www.commondreams.org/headline/2009/12/07-4

Feminized Fish and Skewed Gender Ratios

2009-11-28T18:18:00.007-05:00

Gene Structure

2009-11-22T16:12:00.004-05:00

Transformation Powerpoint

2009-11-19T08:51:00.001-05:00

Carbohydrates

2009-11-16T08:15:00.000-05:00

And another regrettable thing about death
is the ceasing of your own brand of magic,
which took a whole life to develop and market-
the quips, the witticisms, the slant
adjusted to a few, those loved ones nearest
the lip of the stage, their soft faces blanched
in the footlight glow, their laughter close to tears,
their tears confused with their diamond earrings,
their warm pooled breath in and out with your heartbeat,
their response and your performance twinned.
The jokes over the phone. The memories packed
in rapid-access file. The whole act.
Who will do it again? That's it: no one;
imitators and descendants aren't the same.
- John Updike who passed away on 1/30/09

Picture of the Day: What is it?

2009-11-10T06:46:00.000-05:00

And another regrettable thing about death
is the ceasing of your own brand of magic,
which took a whole life to develop and market-
the quips, the witticisms, the slant
adjusted to a few, those loved ones nearest
the lip of the stage, their soft faces blanched
in the footlight glow, their laughter close to tears,
their tears confused with their diamond earrings,
their warm pooled breath in and out with your heartbeat,
their response and your performance twinned.
The jokes over the phone. The memories packed
in rapid-access file. The whole act.
Who will do it again? That's it: no one;
imitators and descendants aren't the same.
- John Updike who passed away on 1/30/09

Stem Cell Rip-Off?

2009-11-10T06:40:00.003-05:00

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CDC Recommendations for Booster

2009-11-09T08:37:00.003-05:00

Prevention of Pneumococcal Disease: Recommendations of the Advisory Committee on Immunization Practices (ACIP)
Summary
This report updates the last recommendations by the Advisory Committee on Immunization Practices (ACIP) concerning pneumococcal polysaccharide vaccine (MMWR 1989;38:64-8,73-6). ACIP recommends that the vaccine be used more extensively and administered to all persons in the following groups: a) persons aged greater than or equal to 65 years, b) immunocompetent persons aged greater than or equal to 2 years who are at increased risk for illness and death associated with pneumococcal disease because of chronic illness, c) persons aged greater than or equal to 2 years with functional or anatomic asplenia, d) persons aged greater than or equal to 2 years living in environments in which the risk for disease is high, and e) immunocompromised persons aged greater than or equal to 2 years who are at high risk for infection. This report contains updated information regarding a) antimicrobial resistance among pneumococci, b) vaccine effectiveness and cost-effectiveness, c) indications for vaccination, d) guidelines for revaccination, e) strategies for improving delivery of vaccine, and f) development of pneumococcal conjugate vaccine.
INTRODUCTION
Streptococcus pneumoniae (pneumococcus) is a bacterial pathogen that affects children and adults worldwide. It is a leading cause of illness in young children and causes illness and death among the elderly and persons who have certain underlying medical conditions. The organism colonizes the upper respiratory tract and can cause the following types of illnesses: a) disseminated invasive infections, including bacteremia and meningitis; b) pneumonia and other lower respiratory tract infections; and c) upper respiratory tract infections, including otitis media and sinusitis. Each year in the United States, pneumococcal disease accounts for an estimated 3,000 cases of meningitis, 50,000 cases of bacteremia, 500,000 cases of pneumonia, and 7 million cases of otitis media (1-4). The focus of this report is the prevention of invasive pneumococcal disease (i.e., bacteremia, meningitis, or infection of other normally sterile sites) through the use of pneumococcal polysaccharide vaccine. This vaccine protects against invasive bacteremic disease, although existing data suggest that it is less effective in protecting against other types of pneumococcal infections.
BACKGROUND Incidence of Invasive Disease
Severe pneumococcal infections result from dissemination of bacteria to the bloodstream and the central nervous system. Data from community-based studies indicate that overall annual incidence of pneumococcal bacteremia in the United States is an estimated 15-30 cases per 100,000 population; the rate is higher for persons aged greater than or equal to 65 years (50-83 cases per 100,000 population) and for children aged less than or equal to 2 years (160 cases per 100,000 population) (5-9). In adults, 60%-87% of pneumococcal bacteremia is associated with pneumonia (10-12); in young children, the primary sites of infection are frequently not identified.
In the United States, the risk for acquiring bacteremia is lower among white persons than among persons in other racial/ethnic groups (i.e., blacks, Alaskan Natives, and American Indians). Black adults have a threefold to fivefold higher overall incidence of bacteremia (49-58 cases per 100,000 population) than whites (5-8). Rates of invasive pneumococcal disease are exceptionally high among Alaskan Natives and American Indians. The age-adjusted annual incidence of invasive pneumococcal infection among Alaskan Natives and Alaskan Native children aged less than 2 years was determined by a prospective surveillance study to be 74 cases and 624 cases per 100,000 population, respectively; rates for meningitis and bacteremic pneumonia are eightfold to tenfold higher for Alaskan Natives of all ages than for other U.S. population groups (13). The highest incidence rates for any U.S. population have been reported among specific American Indian groups (e.g., Apache) (14). The overall annual incidence for such groups is 156 cases per 100,000 population; the incidence for children aged 1-2 years in these groups is 2,396 cases per 100,000 population.
In the United States, the estimated overall annual incidence of pneumococcal meningitis is one to two cases per 100,000 population (15). The incidence of pneumococcal meningitis is highest among children aged 6-24 months and persons aged greater than or equal to 65 years; rates for blacks are twice as high as those for whites and Hispanics. Because the incidence of Haemophilus influenzae type b (Hib) meningitis in children rapidly decreased following the introduction of Hib conjugate vaccines, S. pneumoniae has become the most common cause of bacterial meningitis in the United States (CDC, unpublished data).
Other Pneumococcal Infections Lower Respiratory Tract Infections
S. pneumoniae is the most common cause of community-acquired bacterial pneumonia, occurring most frequently among the elderly and young children. The precise incidence of pneumococcal pneumonia is difficult to ascertain because routine diagnostic tests are insufficiently specific and sensitive. Nonetheless, at least 500,000 cases of pneumococcal pneumonia are estimated to occur annually in the United States; S. pneumoniae accounts for approximately 25%-35% of cases of community-acquired bacterial pneumonia in persons who require hospitalization (16-19). Concomitant bacteremia occurs in approximately 10%-25% of adult patients who have pneumococcal pneumonia (17,20).
Acute Otitis Media and Other Upper Respiratory Tract Infections
S. pneumoniae is a substantial cause of acute otitis media (AOM) and other upper respiratory tract infections (e.g., sinusitis). Although these types of infections usually do not progress to invasive disease, they cause considerable morbidity and medical cost. In the United States, AOM results in more than 24 million visits to pediatricians per year (21); approximately 30%-50% of AOM infections are caused by S. pneumoniae (22). AOM infection most often occurs in children aged less than 4 years. In the United States, 62% of children experience an episode of AOM during their first year of life, and nearly half have had three or more episodes before their third birthday (23).
Mortality
Pneumococcal infection causes an estimated 40,000 deaths annually in the United States (1,2,24), accounting for more deaths than any other vaccine-preventable bacterial disease (25). Approximately half of these deaths potentially could be prevented through the use of vaccine. Case-fatality rates are highest for meningitis and bacteremia, and the highest mortality occurs among the elderly and patients who have underlying medical conditions. Among children, death from pneumococcal infection is relatively uncommon, except among those who a) have meningitis, b) are immunocompromised, or c) have undergone splenectomy and have severe bacteremia. Despite appropriate antimicrobial therapy and intensive medical care, the overall case-fatality rate for pneumococcal bacteremia is 15%-20% among adults. Among elderly patients, this rate is approximately 30%-40% (5-7,15,26-28). An overall case-fatality rate of 36% was recently documented for adult inner-city residents who were hospitalized for pneumococcal bacteremia (12).
Risk Factors
Children aged less than 2 years and adults aged greater than or equal to 65 years are at increased risk for pneumococcal infection. Persons who have certain underlying medical conditions also are at increased risk for developing pneumococcal infection or experiencing severe disease and complications. Adults at increased risk include those who are generally immunocompetent but who have chronic cardiovascular diseases (e.g., congestive heart failure or cardiomyopathy), chronic pulmonary diseases (e.g., chronic obstructive pulmonary disease {COPD} or emphysema), or chronic liver diseases (e.g., cirrhosis). Diabetes mellitus often is associated with cardiovascular or renal dysfunction, which increases the risk for severe pneumococcal illness. The incidence of pneumococcal infection is increased for persons who have liver disease as a result of alcohol abuse (10,20,29,30). Asthma has not been associated with an increased risk for pneumococcal disease, unless it occurs with chronic bronchitis, emphysema, or long-term use of systemic corticosteroids.
Persons with functional or anatomic asplenia (e.g., sickle cell disease or splenectomy) are at highest risk for pneumococcal infection, because this condition leads to reduced clearance of encapsulated bacteria from the bloodstream. Children who have sickle cell disease or have had a splenectomy are at increased risk for fulminant pneumococcal sepsis associated with high mortality. Before the widespread use of penicillin chemoprophylaxis for these patients, children with sickle cell disease were 600-fold more likely than children without this disease to develop pneumococcal meningitis (24).
The risk for pneumococcal infection is high for persons who have decreased responsiveness to polysaccharide antigens or increased rate of decline in serum antibody concentrations as a result of a) immunosuppressive conditions (e.g., congenital immunodeficiency, human immunodeficiency virus {HIV} infection, leukemia, lymphoma, multiple myeloma, Hodgkins disease, or generalized malignancy); b) organ or bone marrow transplantation; c) therapy with alkylating agents, antimetabolites, or systemic corticosteroids (31); or d) chronic renal failure or nephrotic syndrome (20,30). S. pneumoniae is the most commonly identified bacterial pathogen that causes pneumonia in HIV-infected persons (32). In children, invasive pneumococcal disease is often the first clinical manifestation of HIV infection. The annual attack rate of pneumococcal bacteremia is as high as 1% (940 cases per 100,000 population) among persons with acquired immunodeficiency syndrome (AIDS) (33). As many as 91% of adults who have invasive pneumococcal infection have at least one of the previously mentioned underlying medical conditions, including age greater than or equal to 65 years (6,9,24,27). Recurrent pneumococcal meningitis may occur in patients who have chronic cerebrospinal fluid (CSF) leakage resulting from congenital lesions, skull fractures, or neurosurgical procedures.
A case-control study conducted in Finland identified day care center attendance among children aged less than 2 years as a major risk factor for invasive pneumococcal disease (34). Although the risk for invasive pneumococcal infection associated with day care center attendance was significantly higher (i.e., 36-fold) among children aged less than 2 years compared with those who did not attend day care, the risk among children aged greater than or equal to 2 years (the age group in which pneumococcal polysaccharide vaccine could potentially prevent disease) was not significantly different from that for those who did not attend day care. Studies conducted in the United States also have indicated that children aged less than 2 years who attend day care are at higher risk for infection than are those who do not (35). In addition, clusters of invasive pneumococcal disease have been reported among children who attend day care (36,37).
Antimicrobial Resistance
Strains of drug-resistant S. pneumoniae (DRSP) have become increasingly common in the United States and in other parts of the world (38,39). In some areas, as many as 35% of pneumococcal isolates have been reported to have intermediate- (minimum inhibitory concentration {MIC}=0.1-1.0 ug/mL) or high-level (MIC greater than or equal to 2 ug/mL) resistance to penicillin (CDC, unpublished data;8,40,41). Many penicillin-resistant pneumococci are also resistant to other antimicrobial drugs (e.g., erythromycin, trimethoprim-sulfamethoxazole, and extended-spectrum cephalosporins). High-level penicillin resistance and multidrug resistance often complicate the management of pneumococcal infection and make choosing empiric antimicrobial therapy for suspected cases of meningitis, pneumonia, and otitis media increasingly difficult (42). Treating patients infected with nonsusceptible organisms may require the use of expensive alternative antimicrobial agents and may result in prolonged hospitalization and increased medical costs. The impact of antimicrobial resistance on mortality is not clearly defined. Emerging antimicrobial resistance further emphasizes the need for preventing pneumococcal infections by vaccination.
PNEUMOCOCCAL POLYSACCHARIDE VACCINE
The currently available pneumococcal vaccines, manufactured by both Merck and Company, Inc. (Pneumovax 23) and Lederle Laboratories (Pnu-Immune 23), include 23 purified capsular polysaccharide antigens of S. pneumoniae (serotypes 1, 2, 3, 4, 5, 6B, 7F, 8, 9N, 9V, 10A, 11A, 12F, 14, 15B, 17F, 18C, 19A, 19F, 20, 22F, 23F, and 33F). These vaccines were licensed in the United States in 1983 and replaced an earlier 14-valent formulation that was licensed in 1977. One dose (0.5 mL) of the 23-valent vaccine contains 25 ug of each capsular polysaccharide antigen dissolved in isotonic saline solution with phenol (0.25%) or thimerosal (0.01%) added as preservative and no adjuvant. The 23 capsular types in the vaccine represent at least 85%-90% of the serotypes that cause invasive pneumococcal infections among children and adults in the United States (43-45). The six serotypes (6B, 9V, 14, 19A, 19F, and 23F) that most frequently cause invasive drug-resistant pneumococcal infection in the United States are represented in the 23-valent vaccine (8,39).
Immunogenicity
Pneumococcal capsular polysaccharide antigens induce type-specific antibodies that enhance opsonization, phagocytosis, and killing of pneumococci by leukocytes and other phagocytic cells. After vaccination, an antigen-specific antibody response, indicated by a twofold or greater rise in serotype-specific antibody, develops within 2-3 weeks in greater than or equal to 80% of healthy young adults (46); however, immune responses may not be consistent among all 23 serotypes in the vaccine. The levels of antibodies that correlate with protection against pneumococcal disease have not been clearly defined.
Antibody responses also occur in the elderly and in patients who have alcoholic cirrhosis, COPD, and insulin-dependent diabetes mellitus (20,24,46); however, antibody concentrations and responses to individual antigens may be lower among such persons than among healthy young adults. Persons aged greater than or equal to 2 years with anatomic or functional asplenia (e.g., from splenectomy or sickle cell disease) generally respond to pneumococcal vaccination with antibody levels comparable with those observed in healthy persons of the same age (47).
In immunocompromised patients, antibody responses to pneumococcal vaccination are often diminished or absent. In patients with leukemia, lymphoma, or multiple myeloma, antibody response to pneumococcal vaccination is substantially lower than response among patients who are immunocompetent. Patients who have chronic renal failure requiring dialysis, renal transplantation, or nephrotic syndrome have a diminished immune response to vaccination, resulting in lower antibody concentrations than those observed in healthy adults (24). In patients with Hodgkins disease, the antibody response to pneumococcal vaccination is greater if the vaccine is administered before splenectomy, radiation, or chemotherapy; however, during chemotherapy, preexisting pneumocococcal antibodies may decrease, and responses to pneumococcal vaccine may be diminished (48). Patients who have AIDS may have a diminished antibody response to pneumococcal vaccine (49,50). The reduction in titers of antibody corresponds to the degree of immunosuppression; some asymptomatic HIV-infected persons or those with only generalized lymphadenopathy respond to the 23-valent polysaccharide vaccine (51). HIV-infected patients with CD4+ T-lymphocyte counts less than 500 cells/uL often have lower responses to pneumococcal vaccination than either HIV-infected persons with higher CD4+ T-lymphocyte counts or persons who are not HIV-infected (52).
Bacterial capsular polysaccharides induce antibodies primarily by T-cell- independent mechanisms. Therefore, antibody response to most pneumococcal capsular types is generally poor or inconsistent in children aged less than 2 years whose immune systems are immature. Age-specific immune responses also vary by serotype, and the response to some common pediatric pneumococcal serotypes (e.g., 6A and 14) also is decreased in children aged 2-5 years (53-55).
Duration of Antibody Levels
Levels of antibodies to most pneumococcal vaccine antigens remain elevated for at least 5 years in healthy adults. In some persons, antibody concentrations decrease to prevaccination levels by 10 years (56,57). A more rapid decline (i.e., within 3-5 years after vaccination) in antibody concentrations may occur in certain children who have undergone splenectomy following trauma and in those who have sickle cell disease (58,59). Similar rates of decline can occur in children with nephrotic syndrome (60). Antibody concentrations also have declined after 5-10 years in elderly persons, persons who have undergone splenectomy, patients with renal disease requiring dialysis, and persons who have received transplants (24,56,57,61-63). Low or rapidly declining antibody concentrations after vaccination also have been noted among patients with Hodgkins disease (64) and multiple myeloma (65). However, these quantitative measurements of antibodies do not account for the quality of the antibody being produced and the level of functional immune response. Tests measuring opsonophagocytic activity and the quality of antibodies produced (i.e., avidity for pneumococcal antigens) may ultimately be more relevant for evaluating response to pneumococcal vaccination (66).
Precautions and Contraindications
The safety of pneumococcal polysaccharide vaccine during the first trimester of pregnancy has not been evaluated, although no adverse consequences have been reported among newborns whose mothers were inadvertently vaccinated during pregnancy. For additional information about precautions and contraindications, the vaccine manufacturer's package insert should be reviewed.
Side Effects and Adverse Reactions
Pneumococcal polysaccharide vaccine generally is considered safe based on clinical experience since 1977, when the pneumococcal polysaccharide vaccine was licensed in the United States. Approximately half of persons who receive pneumococcal vaccine develop mild, local side effects (e.g., pain at the injection site, erythema, and swelling). These reactions usually persist for less than 48 hours. Moderate systemic reactions (e.g., fever and myalgias) and more severe local reactions (e.g., local induration) are rare. Intradermal administration may cause severe local reactions and is inappropriate. Severe systemic adverse effects (e.g., anaphylactic reactions) rarely have been reported after administration of pneumococcal vaccine (20,24). In a recent meta-analysis of nine randomized controlled trials of pneumococcal vaccine efficacy, local reactions were observed among approximately one third or fewer of 7,531 patients receiving the vaccine, and there were no reports of severe febrile or anaphylactic reactions (67). No neurologic disorders (e.g., Guillain-Barre syndrome) have been associated with administration of pneumococcal vaccine. Although preliminary data have suggested that the pneumococcal vaccine may cause transient increases in HIV replication (68), the importance of this occurrence is unknown. Pneumococcal vaccination has not been causally associated with death among vaccine recipients. Health-care providers should report suspected adverse events after administration of pneumococcal polysaccharide vaccine to the Vaccine Adverse Event Reporting System (VAERS) by calling (800) 822-7967, a 24-hour, toll-free telephone number.
Vaccine Efficacy, Effectiveness, and Cost-Effectiveness
Several clinical trials have been conducted evaluating the efficacy of vaccine against pneumonia and pneumococcal bacteremia. In addition, multiple case-control and serotype prevalence studies have provided evidence for pneumococcal vaccine effectiveness against invasive disease ((Table_1) {44,69-80}).
Efficacy Against Nonbacteremic Pneumococcal Disease
Prelicensure randomized controlled trials (RCTs) of pneumococcal vaccine efficacy were conducted in the 1970s among young, healthy gold miners in South Africa who had high rates of pneumococcal pneumonia and bacteremia; a multivalent polysaccharide vaccine significantly reduced the occurrence of radiographically diagnosed pneumonia in this group (71,72). In non-epidemic situations in the United States, most pneumococcal disease in adults occurs in the elderly or in persons with chronic medical conditions. Vaccine efficacy for nonbacteremic pneumonia was not demonstrated for these populations in two postlicensure RCTs conducted in the United States (74,76). However, these studies may have lacked sufficient statistical power to detect a difference in the incidence of laboratory-confirmed, nonbacteremic pneumococcal pneumonia between the vaccinated and nonvaccinated study groups (81). A meta-analysis evaluating pneumococcal vaccine efficacy by combining the results of nine randomized, controlled trials also did not demonstrate a protective effect for nonbacteremic pneumonia among persons in high-risk groups (67). The ability to evaluate vaccine efficacy in these studies is limited because of the lack of specific and sensitive diagnostic tests for nonbacteremic pneumococcal pneumonia. The pneumococcal polysaccharide vaccine is not effective for the prevention of common upper respiratory diseases (e.g., sinusitis or AOM) in children (82).
Effectiveness Against Invasive Disease
Effectiveness in case-control studies generally has ranged from 56% to 81% (75,78-80). Only one case-control study did not document effectiveness against bacteremic disease (77) -- possibly because of study limitations, including small sample size and incomplete ascertainment of vaccination status of patients. In addition, case-patients and persons who served as controls may not have been comparable regarding the severity of their underlying medical conditions, potentially creating a biased underestimate of vaccine effectiveness (81).
A serotype prevalence study based on CDC's pneumococcal surveillance system demonstrated a 57% (95% confidence interval {CI}=45%-66%) overall protective effectiveness against invasive infections caused by serotypes included in the vaccine among persons aged greater than or equal to 6 years (44). Vaccine effectiveness of 65%-84% also was demonstrated among specific patient groups (e.g., persons who have diabetes mellitus, coronary vascular disease, congestive heart failure, chronic pulmonary disease, and anatomic asplenia). Effectiveness in immunocompetent persons aged greater than or equal to 65 years was 75% (95% CI=57%-85%). Vaccine effectiveness could not be confirmed for certain groups of immunocompromised patients (e.g., those with sickle cell disease, chronic renal failure, immunoglobulin deficiency, Hodgkins disease, non-Hodgkins lymphoma, leukemia, or multiple myeloma). However, this study could not accurately measure effectiveness in each of these groups because of the minimal numbers of unvaccinated patients with these illnesses. In an earlier study, vaccinated children and young adults aged 2-25 years who had sickle cell disease or who had undergone splenectomy experienced significantly less bacteremic pneumococcal disease than patients who were not vaccinated (47). A meta-analysis of nine randomized controlled trials of pneumococcal vaccine concluded that pneumococcal vaccine is efficacious in reducing the frequency of bacteremic pneumococcal pneumonia among adults in low-risk groups (67). However, the vaccine is not effective in preventing disease caused by non-vaccine serotype organisms (79).
Cost-Effectiveness
Preliminary results of a cost-effectiveness analysis indicate that pneumococcal polysaccharide vaccine is cost-effective and potentially cost-saving among persons aged greater than or equal to 65 years for prevention of bacteremia (83). The vaccine compares favorably with other standard preventive practices.
VACCINE ADMINISTRATION
Pneumococcal vaccine is administered intramuscularly or subcutaneously as one 0.5-mL dose. Pneumococcal vaccine may be administered at the same time as influenza vaccine (by separate injection in the other arm) without an increase in side effects or decreased antibody response to either vaccine (62,84). Pneumococcal vaccine also may be administered concurrently with other vaccines. The administration of pneumococcal vaccine with combined diphtheria, tetanus, and pertussis (DTP); poliovirus; or other vaccines does not increase the severity of reactions or diminish antibody responses (85).
RECOMMENDATIONS FOR VACCINE USE Immunocompetent Persons
The vaccine is both cost effective and protective against invasive pneumococcal infection when administered to immunocompetent persons aged greater than or equal to 2 years. Therefore, all persons in the following categories should receive the 23-valent pneumococcal polysaccharide vaccine (Table_2). If earlier vaccination status is unknown, persons in these categories should be administered pneumococcal vaccine.
Persons Aged greater than or equal to 65 Years
All persons in this category should receive the pneumococcal vaccine, including previously unvaccinated persons and persons who have not received vaccine within 5 years (and were less than 65 years of age at the time of vaccination). All persons who have unknown vaccination status should receive one dose of vaccine (Figure_1).
Persons Aged 2-64 Years Who Have Chronic Illness
Persons aged 2-64 years who are at increased risk for pneumococcal disease or its complications if they become infected should be vaccinated. Persons at increased risk for severe disease include those with chronic illness such as chronic cardiovascular disease (e.g., congestive heart failure {CHF} or cardiomyopathies), chronic pulmonary disease (e.g., COPD or emphysema, but not asthma), diabetes mellitus, alcoholism, chronic liver disease (cirrhosis), or CSF leaks.
Persons aged 50-64 years commonly have chronic illness, and 12% have pulmonary risk factors for invasive pneumococcal disease. Therefore, persons in this age group who have these risk factors should receive the vaccine (86). Persons aged 50 years should have their overall vaccination status reviewed to determine whether they have risk factors that indicate a need for pneumococcal vaccination (87). Vaccination status also should be assessed during the adolescent immunization visit at 11-12 years of age (88).
Persons Aged 2-64 Years Who Have Functional or Anatomic Asplenia
Persons aged 2-64 years who have functional or anatomic asplenia (e.g., sickle cell disease or splenectomy) also should be vaccinated. Persons with such a condition should be informed that vaccination does not guarantee protection against fulminant pneumococcal disease, for which the case-fatality rate is 50%-80%. Asplenic patients with unexplained fever or manifestations of sepsis should receive prompt medical attention, including evaluation and treatment for suspected bacteremia. Chemoprophylaxis also should be considered in these patients (see Other Methods of Prevention). When elective splenectomy is being planned, pneumococcal vaccine should be administered at least 2 weeks before surgery.
Persons Aged 2-64 Years Who Are Living in Special Environments or Social Settings
Persons aged 2-64 years who are living in environments or social settings in which the risk for invasive pneumococcal disease or its complications is increased (e.g., Alaskan Natives and certain American Indian populations) should be vaccinated. In addition, because of recently reported outbreaks of pneumococcal disease (89), vaccination status should be assessed for residents of nursing homes and other long-term-care facilities.
Available data do not support routine pneumococcal vaccination of healthy children attending day care facilities. Recurrent upper respiratory tract diseases, including otitis media and sinusitis, are not specific indications for pneumococcal vaccine.
Immunocompromised Persons
Persons who have conditions associated with decreased immunologic function that increase the risk for severe pneumococcal disease or its complications should be vaccinated. Although the vaccine is not as effective for immunocompromised patients as it is for immunocompetent persons, the potential benefits and safety of the vaccine justify its use.
The vaccine is recommended for persons in the following groups: immunocompromised persons aged greater than or equal to 2 years, including persons with HIV infection, leukemia, lymphoma, Hodgkins disease, multiple myeloma, generalized malignancy, chronic renal failure, nephrotic syndrome, or other conditions associated with immunosuppression (e.g., organ or bone marrow transplantation); and persons receiving immunosuppressive chemotherapy, including long-term systemic corticosteroids. If earlier vaccination status is unknown, immunocompromised persons should be administered pneumococcal vaccine.
Persons with asymptomatic or symptomatic HIV infection should be vaccinated as soon as possible after their diagnosis is confirmed. Plasma HIV levels have been found to be transiently elevated after pneumococcal vaccination in some studies (68); other studies have not demonstrated such an elevation (90). However, no adverse effects of pneumococcal vaccination on patient survival have been detected (68,90). When cancer chemotherapy or other immunosuppressive therapy is being considered (e.g., for patients with Hodgkins disease or those who undergo organ or bone marrow transplantation), the interval between vaccination and initiation of immunosuppressive therapy should be at least 2 weeks. Vaccination during chemotherapy or radiation therapy should be avoided.
REVACCINATION Duration of Immunity
Following pneumococcal vaccination, serotype-specific antibody levels decline after 5-10 years and decrease more rapidly in some groups than others (56,57,61-63), which suggests that revaccination may be indicated to provide continued protection. However, data concerning serologic correlates of protection are not conclusive, which limits the ability to precisely define indications for revaccination based on serologic data alone. Polysaccharide vaccines, including the currently available pneumococcal vaccine, do not induce T-cell-dependent responses associated with immunologic memory. Antibody levels increase after revaccination, but an anamnestic response does not occur (91). The overall increase in antibody levels among elderly persons has been determined to be lower after revaccination than following primary vaccination (92). Long-term follow-up data concerning antibody levels in persons who have been revaccinated are not yet available.
Data from one epidemiologic study have suggested that vaccination may provide protection for at least 9 years after receipt of the initial dose (44). Decreasing estimates of effectiveness with increasing interval since vaccination, particularly among the very elderly (i.e., persons aged greater than or equal to 85 years), have been reported (79).
Adverse Reactions Following Revaccination
Early studies have indicated that local reactions (i.e., arthus-type reactions) among adults receiving the second dose of 14-valent vaccine within 2 years after the first dose are more severe than those occurring after initial vaccination (20,93). However, subsequent studies have suggested that revaccination after intervals of greater than or equal to 4 years is not associated with an increased incidence of adverse side effects (20,94,95). Although severe local reactions may occur following a second dose of pneumococcal vaccine, the rate of adverse reactions is no greater than the rate after the first dose. An evaluation of 1,000 elderly Medicare enrollees who received a second dose of pneumococcal vaccine indicated that they were not significantly more likely to be hospitalized in the 30 days after vaccination than were the approximately 66,000 persons who received their first dose of vaccine (96). No data are available to allow estimates of adverse reaction rates among persons who received more than two doses of pneumococcal vaccine.
Indications for Revaccination
Routine revaccination of immunocompetent persons previously vaccinated with 23-valent polysaccharide vaccine is not recommended. However, revaccination once is recommended for persons aged greater than or equal to 2 years who are at highest risk for serious pneumococcal infection and those who are likely to have a rapid decline in pneumococcal antibody levels, provided that 5 years have elapsed since receipt of the first dose of pneumococcal vaccine. Revaccination 3 years after the previous dose may be considered for children at highest risk for severe pneumococcal infection who would be aged less than or equal to 10 years at the time of revaccination. These children include those with functional or anatomic asplenia (e.g., sickle cell disease or splenectomy) and those with conditions associated with rapid antibody decline after initial vaccination (e.g., nephrotic syndrome, renal failure, or renal transplantation). Revaccination is contraindicated for persons who had a severe reaction (e.g., anaphylactic reaction or localized arthus-type reaction) to the initial dose they received.
Persons at highest risk and those most likely to have rapid declines in antibody levels include persons with functional or anatomic asplenia (e.g., sickle cell disease or splenectomy), HIV infection, leukemia, lymphoma, Hodgkins disease, multiple myeloma, generalized malignancy, chronic renal failure, nephrotic syndrome, or other conditions associated with immunosuppression (e.g., organ or bone marrow transplantation), and those receiving immunosuppressive chemotherapy (including long-term systemic corticosteroids). If vaccination status is unknown, patients in these categories should be administered pneumococcal vaccine.
Persons aged greater than or equal to 65 years should be administered a second dose of vaccine if they received the vaccine greater than or equal to 5 years previously and were aged less than 65 years at the time of primary vaccination. Elderly persons with unknown vaccination status should be administered one dose of vaccine (Figure_1).
The need for subsequent doses of pneumococcal vaccine is unclear and will be assessed when additional data become available. Because data are insufficient concerning the safety of pneumococcal vaccine when administered three or more times, revaccination following a second dose is not routinely recommended.
Persons with Uncertain Vaccination Status
To help avoid the administration of unnecessary doses, every patient should be given a record of the vaccination. However, providers should not withhold vaccination in the absence of an immunization record or complete medical record. The patient's verbal history should be used to determine prior vaccination status. When indicated, vaccine should be administered to patients who are uncertain about their vaccination history.
OTHER METHODS OF PREVENTION Chemoprophylaxis
Oral penicillin V (125 mg, twice daily), when administered to infants and young children with sickle cell disease, has reduced the incidence of pneumococcal bacteremia by 84% compared with those receiving placebo (97). Therefore, daily penicillin prophylaxis for children with sickle cell hemoglobinopathy is recommended beginning before 4 months of age. Consensus on the age at which prophylaxis should be discontinued has not been achieved. However, children with sickle cell anemia who had received prophylactic penicillin for prolonged intervals (but who had not had a prior severe pneumococcal infection or a splenectomy) have stopped prophylactic penicillin therapy at 5 years of age without increased incidence of pneumococcal bacteremia or meningitis (98).
Oral penicillin G or V is recommended for prevention of pneumococcal disease in children with functional or anatomic asplenia (85). Antimicrobial prophylaxis against pneumococcal infection may be particularly useful for asplenic children not likely to respond to the polysaccharide vaccine (e.g., those aged less than 2 years or those receiving intensive chemotherapy or cytoreduction therapy). However, the impact of the emergence of drug-resistant S. pneumoniae on the effectiveness of antimicrobial prophylaxis is not known.
Passive Immunization
Intramuscular or intravenous immunoglobulin administration may be useful for preventing pneumococcal infection in children with congenital or acquired immunodeficiency diseases, including those with HIV infection, who have recurrent, serious bacterial infections (i.e., two or more serious bacterial infections {e.g., bacteremia, meningitis, or pneumonia} in a 1-year period) (85,99). Data are inadequate to evaluate the utility of intravenous immunoglobulin administration in the prevention of pneumococcal disease among HIV-infected adults.
STRATEGIES FOR IMPLEMENTING RECOMMENDATIONS FOR THE USE OF VACCINE
The use of pneumococcal polysaccharide vaccine consistently has been recommended by ACIP (20,100), the American Academy of Pediatrics (85), the American College of Physicians (87), and the American Academy of Family Physicians. In addition, Medicare has provided a payment for pneumococcal vaccine since 1981 and a specific billing code (i.e., G009) for its administration since 1994. Roster billing for pneumococcal vaccination was authorized in August 1996. Hospitals may receive a separate payment for pneumococcal vaccination of Medicare beneficiaries independent of reimbursement based on prospective payment systems for services provided for other conditions. Despite these factors, the vaccine remains underutilized.
Pneumococcal vaccine is recommended for approximately 31 million persons aged greater than or equal to 65 years and approximately 23 million persons aged less than 65 years who are at high risk for pneumococcal disease (U.S. Immunization Survey, 1985). The year 2000 objectives of the Public Health Service call for vaccinating at least 60% of persons at risk for influenza and pneumococcal disease (and 80% of the institutionalized elderly) by the year 2000 (101). Most persons considered at risk for pneumococcal infection also should receive annual influenza vaccinations. However, as of 1993, only 28% of persons aged greater than or equal to 65 years had ever received the pneumococcal vaccine. This percentage is considerably lower than the reported annual influenza vaccination rates (52%) for the same population (102).
Barriers to achieving high pneumococcal vaccination levels among adults include a) missed opportunities to vaccinate adults during contacts with health-care providers in offices, outpatient clinics, and hospitals; b) lack of vaccine delivery systems in the public and private sectors that can reach adults in different settings (e.g., health-care, workplace, and college or university settings); c) patient and provider fears concerning adverse events following vaccination; and d) lack of awareness among both patients and providers of the seriousness of pneumococcal disease and benefits of pneumococcal vaccination (2,103). Because pneumococcal vaccine effectively reduces the incidence of bacteremia, the use of vaccine must be increased in accordance with recommendations.
Age-Based Strategies
Persons aged 50-64 years commonly have chronic illness, and 12% have pulmonary conditions that place them at increased risk for pneumococcal disease (86). However, less than 20% of those with risk factors are estimated to have received pneumococcal vaccine. A specific age-based standard should improve vaccination rates among persons with high-risk conditions. Therefore, age 50 years has been established as a time to review the overall immunization status of patients; risk factors that indicate the need to administer pneumococcal vaccine should be evaluated at this visit (86,87). Vaccination status also should be assessed during the adolescent immunization visit at age 11-12 years (88). This visit provides an opportunity to review the need for pneumococcal vaccine; adolescents with high-risk conditions should be vaccinated.
Organizational Strategies
Organizational strategies (e.g., standing orders {rather than requiring a physician's order} for pneumococcal vaccination of high-risk patients who are eligible to receive vaccine) are the most effective methods for increasing pneumococcal vaccination rates among persons at high risk (104). In a New York hospital, instituting standing orders for pneumococcal vaccination of the elderly and at-risk patients increased the pneumococcal vaccination rate from zero to 78% (105). Similar increases were achieved for influenza vaccination in community hospitals in Minnesota (106). The Health Care Financing Administration recently has approved a regulation that permits the use of standing orders to administer pneumococcal vaccine to Medicare patients (103). Pneumococcal vaccination also should be routinely provided for residents of nursing homes and other long-term-care facilities.
High vaccination coverage rates can be achieved when pneumococcal vaccination programs are targeted to hospitalized patients at high risk (104). A hospital-based immunization strategy is effective and capable of reaching those patients most likely to develop pneumococcal disease (106-109). Two thirds of persons with serious pneumococcal disease had been hospitalized within the previous 4 years before their pneumococcal illness, yet few had received pneumococcal vaccine (109). Among these patients, 87% had one or more high-risk conditions. Administration of pneumococcal vaccine should be included in routine clinical practice, and the vaccine, when indicated, should be administered before discharge to hospitalized patients to prevent subsequent admissions for pneumococcal disease. Eligible patients in high-risk groups can be identified by physicians, infection-control practitioners, nurse specialists, and clinical pharmacists.
Community-Based Vaccination Programs
Vaccination coverage rates increase when public health departments promote and offer the vaccine. A community-based immunization program implemented in public health jurisdictions by the California State Department of Health Services resulted in a 33% higher rate of pneumococcal vaccination than jurisdictions without such immunization programs (110). This program included interventions such as a) promoting and providing pneumococcal vaccine at health-department-sponsored outreach clinics, health-center clinics, and nursing and convalescent homes and b) promoting pneumococcal vaccine through leaflets, posters, and other material and referring persons to specific clinics for vaccination. Because rates of pneumococcal disease are high among blacks, particularly those of lower socioeconomic status, community outreach programs that are focused on underserved, often inner-city populations could be effective in preventing life-threatening pneumococcal disease among persons in these groups.
A community-based pneumococcal vaccine campaign was conducted as part of the Hawaii Pneumococcal Disease Initiative, which employed public and private sector partnerships to substantially increase vaccine delivery and improve vaccination levels among persons aged greater than or equal to 65 years (111). This public vaccination program was considered cost-effective for vaccinating substantial numbers of adults and stimulated vaccination activity among private health-care providers.
Provider-Based Strategies
Provider-based strategies that have proved effective in increasing adult vaccination rates include practice-based tracking systems and physician reminder systems. In practice-based tracking systems, providers identify the total number of their patients who are at risk and maintain rosters showing the proportion of patients who receive vaccination. Physicians using such a tracking system have administered 30% more influenza vaccine than those not using the system (112).
Physician reminder systems consisting of charts, computers, or preventive-health checklists remind physicians to review the need for pneumococcal vaccine for each patient and to administer the vaccine to those at risk for pneumococcal disease. Staff in physicians' offices, clinics, health maintenance organizations, and employee health clinics can be instructed to identify and label the medical records of patients who should receive the vaccine. The use of preventive-health checklists has increased pneumococcal vaccination rates fourfold (113) and from 5% to 42% (114). In one hospital, implementation of a computer reminder system that prompted physicians to review pneumococcal vaccination status before discharge increased pneumococcal vaccination rates from less than 4% to 45% (115).
Health-care providers in facilities providing episodic or acute care (e.g., emergency rooms and walk-in clinics) should be familiar with pneumococcal vaccine recommendations. They should offer vaccine to persons in high-risk groups or provide written information concerning why, where, and how to obtain the vaccine.
Simultaneous Administration of Pneumococcal and Influenza Vaccines
Because the indications for pneumococcal and influenza vaccines are similar, the time of administration of influenza vaccine -- including mass vaccination at outpatient clinics -- should be used as an opportunity to identify and vaccinate patients with pneumococcal vaccine. However, influenza vaccine is administered each year, whereas pneumococcal vaccine typically is administered only once for persons in most groups (see Revaccination).
CONJUGATE VACCINE DEVELOPMENT
Additional immunogenic pneumococcal vaccines that provide long-term immunity are needed -- especially for children aged less than 2 years, because incidence of disease is high and antibody responses to the polysaccharide vaccine antigens are poor in this age group. The most promising approach is the development of a protein-polysaccharide conjugate vaccine for selected serotypes, which improves the immunogenicity and potentially the protective efficacy of pneumococcal vaccination -- especially in young children. Immune response to many capsular polysaccharides can be improved by covalent coupling of the polysaccharide antigen to a carrier protein (116,117). Current conjugate vaccine development has focused on the serotypes most commonly causing infections in childhood. Candidate vaccine formulations in development and evaluation phases include at least seven serotypes of pneumococcal polysaccharides conjugated to one or several protein carriers. An effective conjugate vaccine protecting against the seven most common serotypes (4, 6B, 9V, 14, 18C, 19F, and 23F and serologically cross-reactive serotypes {e.g., 6A}) could potentially prevent 86% of bacteremia, 83% of meningitis, and 65% of otitis media cases among children aged less than 6 years in the United States (45). In persons aged greater than or equal to 6 years, these serotypes have accounted for 50% of the cerebrospinal fluid and blood isolates (44). Preliminary results obtained in phase I and phase II studies suggest that these vaccines generally are safe and induce primary and booster antibody responses in children aged 2-5 years and infants aged 2 months (118-121). Multicenter trials to evaluate conjugate vaccine efficacy against acute pneumococcal otitis media and invasive disease in children are ongoing.
The polysaccharide vaccine has not reduced nasopharyngeal carriage of S. pneumoniae among children (122). However, preliminary data suggest that conjugate vaccines may reduce nasopharyngeal carriage of the pneumococcal serotypes included in the vaccine (123). Reduction in carriage rates of S. pneumoniae would potentially increase the overall impact of the vaccine by reducing transmission and, consequently, disease incidence. Prospective randomized trials are required to demonstrate the protective efficacy of conjugate vaccines against invasive pneumococcal infections. These vaccines also should be evaluated for utility in preventing pneumococcal disease in immunocompromised adults who respond poorly to the current 23-valent polysaccharide vaccine.
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Douglas RM, Paton JC, Duncan SJ, Hansman DJ. Antibody response to pneumococcal vaccination in children younger than five years of age. J Infect Dis 1983;148:131-7.
Mufson MA, Krause HE, Schiffman G. Long-term persistence of antibody following immunization with pneumococcal polysaccharide vaccine. Proc Soc Exp Biol Med 1983;173:270-5.
Mufson MA, Krause HE, Schiffman G, Hughey DF. Pneumococcal antibody levels one decade after immunization of healthy adults. Am J Med Sci 1987;293:279-89.
Giebink GS, Le CT, Schiffman G. Decline of serum antibody in splenectomized children after vaccination with pneumococcal capsular polysaccharides. J Pediatr 1984;105:576-84.
Weintrub PS, Schiffman G, Addiego JE Jr., et al. Long-term follow-up and booster immunization with polyvalent pneumococcal polysaccharide in patients with sickle cell anemia. J Pediatr 1984;105:261-3.
Spika JS, Halsey NA, Le CT, et al. Decline of vaccine-induced antipneumococcal antibody in children with nephrotic syndrome. Am J Kidney Dis 1986;7:466-70.
Vella PP, McLean AA, Woodhour AF, Weibel RE, Hilleman MR. Persistence of pneumococcal antibodies in human subjects following vaccination. Proc Soc Exp Biol Med 1980;164:435-8.
Hilleman MR, Carlson AJ, McLean AA, Vella PP, Weibel RE, Woodhour AF. Streptococcus pneumoniae polysaccharide vaccine: age and dose responses, safety, persistence of antibody, revaccination, and simultaneous administration of pneumococcal and influenza vaccines. Rev Infect Dis 1981;3(suppl):S31-S42.
Kraus C, Fischer S, Ansorg R, Hðttemann U. Pneumococcal antibodies (IgG, IgM) in patients with chronic obstructive lung disease 3 years after pneumococcal vaccination. Med Microbiol Immunol 1985;174:51-8.
Minor DR, Schiffman G, McIntosh LS. Response of patients with Hodgkin's disease to pneumococcal vaccine. Ann Intern Med 1979;90:887-92.
Schmid GP, Smith RP, Baltch AL, Hall CA, Schiffman G. Antibody response to pneumococcal vaccine in patients with multiple myeloma. J Infect Dis 1981;143:590-7.
Romero-Steiner S, Pais L, Holder P, Carlone GM, Keyserling, H. Opsonophagocytosis of Streptococcus pneumoniae as an indicator of functional antibody activity in adults vaccinated with a 23-valent polysaccharide vaccine {Abstract}. Program and Abstracts of American Society for Microbiology. 98th Annual Meeting, Washington, DC, May 21-25, 1995.
Fine MJ, Smith MA, Carson CA, et al. Efficacy of pneumococcal vaccination in adults: a meta-analysis of randomized controlled trials. Arch Intern Med 1994;154:2666-77.
Brichacek B, Swindells S, Janoff EN, Pirruccello S, Stevenson M. Increased plasma HIV-1 burden following antigenic challenge with pneumococcal vaccine. J Infect Dis 1996;174:1191-9.
MacLeod CM, Hodges RG, Heidelberger M, Bernhard WG. Prevention of pneumococcal pneumonia by immunization with specific capsular polysaccharides. J Exp Med 1945;82:445-65.
Kaufman P. Pneumonia in old age: active immunization against pneumonia with pneumococcus polysaccharide -- results of a six year study. Arch Intern Med 1947;79:518-31.
Austrian R, Douglas RM, Schiffman G, et al. Prevention of pneumococcal pneumonia by vaccination. Trans Assoc Am Physicians 1976;89:184-9.
Smit P, Oberholzer D, Hayden-Smith S, Koornhof HJ, Hilleman MR. Protective efficacy of pneumococcal polysaccharide vaccines. JAMA 1977;238:2613-6.
Riley ID, Tarr PI, Andrews M, et al. Immunisation with a polyvalent pneumococcal vaccine. Lancet 1977;1:1338-41.
Broome CV. Efficacy of pneumococcal polysaccharide vaccines. Rev Infect Dis 1981;3(suppl):S82-S96.
Shapiro ED, Clemens JD. A controlled evaluation of the protective efficacy of pneumococcal vaccine for patients at high risk of serious pneumococcal infections. Ann Intern Med 1984;101:325-30.
Simberkoff MS, Cross AP, Al-Ibrahim M, et al. Efficacy of pneumococcal vaccine in high-risk patients: results of a Veterans Administration cooperative study. N Engl J Med 1986;315: 1318-27.
Forrester HL, Jahnigen DW, LaForce FM. Inefficacy of pneumococcal vaccine in a high-risk population. Am J Med 1987;83:425-30.
Sims RV, Steinmann WC, McConville JH, King LR, Zwick WC, Schwartz JS. The clinical effectiveness of pneumococcal vaccine in the elderly. Ann Intern Med 1988;108:653-7.
Shapiro ED, Berg AT, Austrian R, et al. The protective efficacy of polyvalent pneumococcal polysaccharide vaccine. N Engl J Med 1991;325:1453-60.
Farr BM, Johnston BL, Cobb DK, et al. Preventing pneumococcal bacteremia in patients at risk: results of a matched case-control study. Arch Intern Med 1995;155:2336-40.
Spika JS, Fedson DS, Facklam RR. Pneumococcal vaccination -- controversies and opportunities. Infect Dis Clin North Am 1990;4:11-27.
Klein JO, Teele DW, Sloyer JL, et al. Use of pneumococcal vaccine for prevention of recurrent episodes of otitis media. In: Weinstein L, Fields BN, eds. Seminars in infectious disease. New York: Thieme-Stratton Inc, 1982;305-10.
Lin JD, Sisk JE, Moskowitz A, Fedson DS. The cost effectiveness of pneumococcal vaccination {Abstract}. Abstracts of the American Public Health Association 124th Annual Meeting and Exposition. New York, NY, November 17-21,1996, p. 328.
DeStefano F, Goodman RA, Noble GR, McClary GD, Smith SJ, Broome CV. Simultaneous administration of influenza and pneumococcal vaccines. JAMA 1982;247:2551-4.
American Academy of Pediatrics. 1994 Red book: report of the Committee on Infectious Diseases. Elk Grove Village, IL: American Academy of Pediatrics 1994:371-5.
CDC. Assessing adult vaccination status at age 50 years. MMWR 1995;44:561-3.
American College of Physicians Task Force on Adult Immunization, Infectious Diseases Society of America. Guide for adult immunization. 3rd ed. Philadelphia, PA: American College of Physicians, 1994;107-14.
CDC. Immunization of adolescents: recommendations of the Advisory Committee on Immunization Practices (ACIP), the American Academy of Pediatrics, the American Academy of Family Physicians, and the American Medical Association. MMWR 1996;45(No. RR-13).
CDC. Outbreaks of pneumococcal pneumonia among unvaccinated residents in chronic-care facilities -- Massachusetts, October 1995, Oklahoma, February 1996, and Maryland, May-June 1996. MMWR 1997;46:60-2.
Katzenstein TL, Gerstoft J, Nielsen H. Assessments of plasma HIV RNA and CD4 cell counts after combined Pneumovax and tetanus toxoid vaccination: no detectable increase in HIV replication 6 weeks after immunization. Scand J Infect Dis 1996;28:239-41.
Garner CV, Pier GB. Immunologic considerations for the development of conjugate vaccines. In: Cruse JM, Lewis RE, eds. Conjugate vaccines. Basel, Switzerland: Karger, 1989;11-7.
Mufson MA, Hughey DF, Turner CE, Schiffman G. Revaccination with pneumococcal vaccine of elderly persons 6 years after primary vaccination. Vaccine 1991;9:403-7.
Borgoåo JM, McLean AA, Vella PP, et al. Vaccination and revaccination with polyvalent pneumococcal polysaccharide vaccines in adults and infants. Proc Soc Exp Biol Med 1978;157:148-54.
Mufson MA, Krause HE, Schiffman G. Reactivity and antibody responses of volunteers given two or three doses of pneumococcal vaccine. Proc Soc Exp Biol Med 1984;177:220-5.
Rigau-Perez JG, Overturf GD, Chan LS, Weiss J, Powars D. Reactions to booster pneumococcal vaccination in patients with sickle cell disease. Pediatr Infect Dis 1983;2:199-202.
Snow R, Babish JD, McBean AM. Is there any connection between a second pneumonia shot and hospitalization among Medicare beneficiaries? Pub Hlth Rep 1995;110:720-5.
Gaston MH, Verter JI, Woods G, et al. Prophylaxis with oral penicillin in children with sickle cell anemia. N Engl J Med 1986;314:1593-9.
Faletta JM, Woods GM, Verter JI, et al. Discontinuing penicillin prophylaxis in children with sickle cell anemia. J Pediatr 1995;127:685-90.
Mofenson LM, Moye J, Bethel J, et al. Prophylactic intravenous immunoglobulin in HIV-infected children with CD4+ counts of 0.20x10 9/L or more: effect on viral, opportunistic, and bacterial infections. JAMA 1992;268:483-8.
CDC. Update on adult immunization: recommendations of the Immunization Practices Advisory Committee (ACIP). MMWR 1991;40(No. RR-12):42-4.
U.S. Department of Health and Human Services. Healthy People 2000: National health promotion and disease prevention objectives. Washington, DC: Public Health Service, 1991.
CDC. Influenza and pneumococcal vaccination coverage levels among persons aged greater than or equal to 65 years. MMWR 1995;44:506-7,513-5.
CDC. Increasing pneumococcal vaccination rates -- United States, 1993. MMWR 1995;44:741-4.
Gyorkos TW, Tannenbaum TN, Abrahamowicz M, et al. Evaluation of the effectiveness of immunization delivery methods. Can J Public Health 1994;85(suppl):S14-S30.
Klein RS, Adachi N. An effective hospital-based pneumococcal immunization program. Arch Intern Med 1986;146:327-9.
Crouse BJ, Nichol K, Peterson DC, Grimm MB. Hospital-based strategies for improving influenza vaccination rates. J Fam Pract 1994;38:258-61.
Schwartz B, Breiman R. Pneumococcal immunization: from policy to practice {Editorial}. JAMA 1990;264:1154-5.
Fedson DS. Improving the use of pneumococcal vaccine through a strategy of hospital-based immunization: a review of its rationale and implications. J Am Geriatr Soc 1985;33:142-50.
Fedson DS, Harward MP, Reid RA, Kaiser DL. Hospital-based pneumococcal immunization. Epidemiologic rationale from the Shenandoah study. JAMA 1990;264:1117-22.
CDC. Pneumococcal immunization program -- California, 1986-1988. MMWR 1989;38:517-9.
Campbell JF, Donohue MA, Nevin-Woods C, et al. The Hawaii pneumococcal disease initiative. Am J Public Health 1993;83:1175-6.
Buffington J, Bell KM, LaForce FM, et al. A target-based model for increasing influenza immunizations in private practice. J Gen Intern Med 1991;6:204-9.
Cheney C, Ramsdell JW. Effect of medical records' checklists on implementation of periodic health measures. Am J Med 1987;83:129-36.
Cohen DI, Littenberg B, Wetzel C, Neuhauser D. Improving physician compliance with preventive medicine guidelines. Med Care 1982;20:1040-5.
Clancy CM, Gelfman D, Poses RM. A strategy to improve the utilization of pneumococcal vaccine. J Gen Intern Med 1992;7:14-8.
Baltimore RS. New challenges in the development of a conjugate pneumococcal vaccine {Editorial}. JAMA 1992;268:3366-7.
Robbins JB, Schneerson R. Polysaccharide-protein conjugates: a new generation of vaccines. J Infect Dis 1990;161:821-32.
Steinhoff MC, Edwards K, Keyserling H, et al. A randomized comparison of three bivalent Streptococcus pneumoniae glycoprotein conjugate vaccines in young children: effect of polysaccharide size and linkage characteristics. Pediatr Infect Dis J 1994;13:368-72.
Kayhty H, Ahman H, R½nnberg P-R, Tillikainen R, Eskola J. Pneumococcal polysaccharide-meningococcal outer membrane protein complex conjugate vaccine is immunogenic in infants and children. J Infect Dis 1995;172:1273-8.
Leach A, Ceesay SJ, Banya WA, Greenwood BM. Pilot trial of a pentavalent pneumococcal polysaccharide/protein conjugate vaccine in Gambian infants. Pediatr Infect Dis J 1996;15:333-9.
Anderson EL, Kennedy DJ, Geldmacher KM, Donnelly J, Mendelman PM. Immunogenicity of heptavalent pneumococcal conjugate vaccine in infants. J Pediatr 1996;128:649-53.
Douglas RM, Hansman D, Miles HB, Paton JC. Pneumococcal carriage and type-specific antibody. Failure of a 14-valent vaccine to reduce carriage in healthy children. Am J Dis Child 1986;140:1183-5.
Dagan RR, Melamed M, Muallem L, et al. Reduction of nasopharyngeal carriage of pneumococci during the second year of life by a heptavalent conjugate pneumococcal vaccine. J Infect Dis 1996;174:1271-8.

Experience is the Great Teacher

2009-11-09T08:00:00.006-05:00

The new field of epigenetics is redefining the field of genetics and molecular biology. No longer can we say that the presence of a gene is predetermined destiny. On the contrary, the once clear demarcations between genotypye and phenotype have been blurred into the gray realms of question and uncertainty. This is the proper terrain for good science to take place. The hard and fast domains of truth will always lead us into facile acceptance and sclerotic cognition. These are not realms where imagination or science can can work their magic. jj

Early life stress 'changes' genes
By Victoria Gill Science reporter, BBC News

Mice that are abandoned as pups have behavioural problems later on
A study in mice has hinted at the impact that early life trauma and stress can have on genes, and how they can result in behavioural problems.
Scientists described the long-term effects of stress on baby mice in the journal Nature Neuroscience.
Stressed mice produced hormones that "changed" their genes, affecting their behaviour throughout their lives.
This work could provide clues to how stress and trauma in early life can lead to later problems.
The study was led by Christopher Murgatroyd, a scientist from the Max Planck Institute of Psychiatry in Munich, Germany.
He told BBC News that this study went into "molecular detail" - showing exactly how stressful experiences in early life could "programme" long-term behaviour.
To do this, the researchers had to cause stress to newborn mouse pups and monitor how their experiences affected them throughout their lives.
"We separated the pups from their mothers for three hours each day for ten days," Dr Murgatroyd explained.
"It was a very mild stress and the animals were not affected at a nutritional level, but they would [have felt] abandoned."
The team found that mice that had been "abandoned" during their early lives were then less able to cope with stressful situations throughout their lives.
The stressed mice also had poorer memories.
Programming genes
Dr Murgatroyd explained that these effects were caused by "epigenetic changes", where the early stressful experience actually changed the DNA of some of the animals' genes.
"This is a two-step mechanism," Dr Murgatroyd explained.
When the baby mice were stressed, they produced high levels of stress hormones.
These hormones "tweak" the DNA of a gene that codes for a specific stress hormone - vasopressin.
"This leaves a permanent mark at the vasopressin gene," said Dr Murgatroyd. "It is then programmed to produce high levels [of the hormone] later on in life."
The researchers were able to show that vasopressin was behind the behavioural and memory problems. When the adult mice were given a drug that blocked the effects of the hormone, their behaviour returned to normal.
This work was carried out in mice, but scientists are also investigating how childhood trauma in humans can lead to problems such as depression.
Professor Hans Reul, a neuroscientist from the University of Bristol, UK, said that this was "a very valuable addition to the body of work on the long-term effects of early-life stress".
"There is strong evidence that adversities such as abuse and neglect during infancy contribute to the development of psychiatric diseases such as depression," he told BBC News.
"This underscores the importance of the study of epigenetic mechanisms in stress-related disorders."

Achorn's Myopia

2009-11-09T07:52:00.000-05:00

[GPRI] Fine Letter by Longtime Green Jeff JohnsonRichard Walton richard at soup.org Wed Mar 28 19:08:17 PST 2007
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Hi: This is a fine letter by longtime Green [and once our candidate for
lieutenant governor and other offices] Jeff Johnson. It is unusually long
for a Letter to the Editor so the editors must have thought highly of it.
As I certainly did. Peace. Richard.

Wednesday, March 28, 2007 10:06 p.m.
Kerry s gaffes vs. Bush s high crimes
01:00 AM EDT on Wednesday, March 28, 2007
Edward Achorn s accusation, in his Feb. 6 column Politicians are all too
human, that John Kerry is a hypocrite is certainly reasonable. We all
might justly be accused of occasionally being hypocritical. However, the
Kerry critique is too simplistic in its partisan focus. Whether Kerry is
bashing America is not really relevant. The U.S. deserves to be
criticized. We are fighting a war that has been responsible for the deaths
of thousands of innocent human beings.
This war was sold like toothpaste to the American people with a series of
blatant lies emanating from the executive branch. The human and financial
costs of this illegal war are too numerous to count, but one very high
price, not often discussed, is blowback. We are considered a rogue nation
by the majority of the world s people.
By many accounts, we have energized, if not emboldened terrorism, with
policies that demonstrate contempt for human life. The face of Bush is a
recruiting poster for all of the people of the world who hate America not
because we get to watch American Idol on television but because of the
terrible things we have done to them. And Bush s mendacity seems to lack
any boundary or constraint whatsoever. While he was supposedly listening
to advisers on the advisabilty of his surge, he was already implementing
this flawed policy that will only result in more death, hatred and
carnage.
As for Kerry s vote against the Kyoto protocol, Achorn makes another valid
point, but it certainly does not diminish Bush s responsibilities to this
nation to act on global warming. For six years and change, Bush has denied
the irrefutable and unambiguous science supporting the anthropogenic
causes of global warming.
Bush s science adviser, a lawyer, even altered a recent EPA report on the
seriousness of global warming to make its findings sound less ominous.
The first installment of the 2007 IPCC report (Intergovernmental Panel on
Climate Change) is positively chilling in its forecasts for the not too
distant future. Climate change is the biggest threat not only to our
nation s security, but to the security of our species. And what has Bush
done? Nothing, unless you call coal gasification and learning how to
pronounce cellulosic inspired leadership.
Don t get me wrong, I am not a Kerry supporter. In fact, I have equal
loathing for both of the mainstream political parties that have been
complicit in plotting the suicidal foreign and domestic policies of the
last two decades. But Bush is in a league of his own. Negligence and lies
have been the hallmark of his reign of errors. John Kerry may indeed have
gaffed again, but at least he is not guilty, as Bush is, of high crimes.
JEFF JOHNSON
Wakefield
"The only way out of our crisis (terrorism) is to reduce the anger of the
most rational, thus also reducing the constituency of the least rational."
Sam Smith.
"When they come for the innocent without crossing over
your body, cursed be your religion and your life." Anon. But often
quoted by Dorothy Day.
--
-----------------------------------------------------------
"Richard Walton" <richard at soup.org>

Proteins,Lipids,Carbohydrates

2009-11-03T20:26:00.003-05:00

Seahorse Reproduction

2009-11-02T07:07:00.003-05:00

Peer at a seahorse, briefly hold one up to the light, and you will see a most unlikely creature; something you would hardly believe was real were it not lying there in the palm of your hand. Should we presume these odd-looking creatures were designed by a mischievous god who had some time on her hands? Rummaging through a box labelled "spare parts", she finds a horse's head and, feeling a desire for experimentation, places it on top of the pouched torso of a kangaroo.
Poseidon's Steed
by Helen Scales
272pp,
GOTHAM BOOKS,
£15.99
Buy Poseidon's Steed at the Guardian bookshop
This playful god adds a pair of swivelling chameleon eyes and the prehensile tail of a tree-dwelling monkey for embellishment – then stands back to admire her work. Not bad, but how about a suit of magical colour-changing armour, and a crown shaped as intricately and uniquely as a human fingerprint? Shrink it all down to the size of a chess piece and the new creature is complete.
No matter how tempting such a strange tale of creation may be, seahorses are real creatures, a product of natural selection and an endangered species. They inhabit a wide stretch of the oceans and are not, as we might suppose, restricted to warm azure waters that lap on equatorial shores. If you stand with your toes dabbling in shallow sea almost anywhere in the world there is a chance you might see a seahorse. Not a very great chance, admittedly, but a chance nonetheless.
Right now, somewhere in the world, sunbeams pierce through shallow water and cast pools of brightness on the seagrass meadow below. The night shift has ended, and diurnal creatures begin to emerge from sleeping hideaways: rabbitfish, parrotfish, damselfish.
Suddenly, two tiny silhouettes come together like a pair of knights on a chessboard. The seahorses greet each other with a nose-to-nose caress and, wrapping their tails around a single blade of grass, they begin a seductive dance, spiralling round and round each other. Blushes of orange and pink give away their emotions and, for a moment, the seahorses swim together, heads tucked down, tails entwined. A gentle humming and clicking from the male is the soundtrack to their flirting.
The first time a seahorse couple meet, this gentle courtship carries on for hours, days even, and it is a risky time. Driven by hormones that interfere with the instinct to hide, they abandon the camouflaged safety of their seagrass home. The female initiates sex by reaching up toward the surface, stretching her body as straight as it will go. This proves quite irresistible to the male, who immediately responds by pumping his tail vigorously up and down.
The couple halt in the open water column and hold their bodies close, forming a heart shape with their touching snouts and bellies. Their first attempt isn't quite right, so they break apart and try again several times until their position is perfected, the female just above the male. Then an extraordinary thing happens. A short hollow tube emerges from the female, which she pushes into an opening in her partner's belly. The couple raise their heads and arch their backs as the female shoots an egg-laden liquid into the male.
Copulation is perfunctory, taking just six or seven seconds. When the male is full with the precious cargo, he wanders off, his bright mating costume already fading. He sways and wiggles his body, settling the eggs into position where they will remain for the next few weeks, growing in a protected internal pond.
The strangest thing about seahorses is that their males are the only ones in the world who experience – firsthand – the agonies of childbirth. Admittedly, there are many fathers who do a great job of helping out with the youngsters. In eastern Australia's rainforests, tadpoles of the marsupial frog wriggle into special pouches slung on their fathers' hind legs. Six weeks later, out hop the next generation of miniature frogs.
These, and many other caring males – including pipefishes and seadragons – deserve praise for their efforts, but only male seahorses become truly pregnant, nurturing their young inside their bodies, providing them with food and oxygen, whisking away waste products. This is all the more remarkable when we consider that pregnancy is a rare occurrence in fish, even among females.
When people first hear about seahorse males getting pregnant, the question that naturally follows is, "So what makes them male?" The simple answer is sperm. The distinction between scarce round eggs and prolific tadpole-like sperm is essentially all that separates woman from man, doe from buck, mare from stallion, and so on.
Yet despite such a clear definition, it took marine biologists a long time to understand what was going on with seahorse sex. The ancient Greek philosopher Aristotle first wrote about the unusual reproductive habits of the Syngnathidae family, to which seahorses belong, in the third century BC. In his book, On The History of Animals, Aristotle went into extraordinary detail about the lives of many fish species he encountered while staying on the Mediterranean island of Lesbos. But it wasn't until the 18th century that scientists finally realised something strange was going on, and began to study syngnathid sex in detail.
For four decades, arguments flared over which sex carried the eggs during a seahorse pregnancy. Everyone agreed that the females produced the eggs, but it wasn't clear whether or not they handed them over to their male partners to look after. The academic tussle was played out on the pages of specialist journals, until the debate was finally laid to rest in the 1870s, when several scientists observed pairs of seahorses engaging in tight embraces within the confines of the laboratory. Those watching closely enough witnessed the transfer of eggs.
Females of most species make a limited number of eggs and tend to look after them well before they hatch, while males make torrents of sperm. This means that pregnancy isn't usually a great option for males. Why should a male spend time looking after a single brood of young, when he could be roaming around, fertilising many more broods elsewhere?
For mammals, there is only one contender for who is best suited to do the childcare: the female nurtures young inside her womb, leaving the male pacing about with few options to help except fending off predators, and bringing them food. Female fish, however, usually carry out external rather than internal fertilisation. So they can abandon their eggs to concentrate on feeding, in order that next time they make bigger, better eggs.
Male fish, on the other hand, can boost their credentials by hanging around. By claiming and defending a piece of prime territory, a male can look after several clutches at once and, in doing so, become irresistible to the ladies who prefer responsible, caring types to father their children.
When evolutionary biologists discovered that male seahorses become truly pregnant, they rubbed their hands in anticipation. It gave them a perfect opportunity to test out their theories of how differences between the sexes evolve. They expected to find that the females, unshackled from the toils of pregnancy, had kicked up their heels and adopted a typically male habit, spreading their gametes as far and wide as possible. But no, most female seahorses are loyal to one male throughout his pregnancy, and do not mate again until he is ready. In fact, many seahorses are monogamous throughout whole breeding seasons, returning to the same partner time and again. Some may even stay in devoted couplings for much of their lives.
So what benefits do females gain by abandoning pregnancy while at the same time sticking with one mate? The answer could lie in their rarity. Seahorses don't live in crowded neighbourhoods, possibly because their plankton food is too scarce to support more than a handful of adults in a habitat the size of a tennis court. With such limited social opportunities and meagre swimming skills, seahorses can't rely on finding a new partner every time they are ready to breed. As soon as they have found a suitable mate, it pays off in the long run for both males and females to stay together.
Equally, if males are unlikely to find a profusion of other mates, it isn't a huge sacrifice to settle down, be faithful, and become pregnant. And taking on the reins of pregnancy gives male seahorses one last added benefit: full reassurance that all the babies he is caring for are definitely his own – something other males, most notoriously human beings, can't be absolutely sure of without a DNA test.
And so, eventually, a cloud of transparent specks like a swarm of apostrophes is launched into the sea: a herd of miniature seahorses with huge snouts too big for their spindly bodies but with all the necessary features already in place.
The brand-new foals, each the size of a flea, swim upward, inflating their swim bladders with a gulp of fresh air before drifting away to begin life with no more help from father or mother. They will settle down in different seagrass patches and, after six months of feeding and growing, they will – all being well – find a partner and start a family of their own.
As for the fathers, their work is never finished. As soon as the arduous birth is over, the female returns and their courtship ritual resumes. The male may already be pregnant again by the next day – a tiresome life indeed, but one that maximises the output of offspring. Which is, ultimately, all that really counts.

Tiger Skin Trade in China

2009-10-26T06:27:00.003-04:00

Tiger skin trade in China exposed
By Jody Bourton Earth News reporter
Advertisement
Skins for sale
An undercover investigation has revealed the continued trade in tiger skins in China.
Covert filming by the Environment Investigation Agency shows traders selling skins of tigers and other rare animals such as snow leopards.
The skins are sold as luxury items and are used for clothes and home decor.
The campaigning group has published its investigation a few days before an international summit on big cat conservation in Kathmandu, Nepal.
Buying and selling big cat skins and body parts is illegal in China.
People are buying them for prestige, skins are very expensive and tend to cost around 20,000 US dollars each
Alasdair CameronEnvironmental Investigation Agency
However, a team from the Environmental Investigation Agency (EIA), based in London, UK and Washington DC, US says its investigations reveal the trade in big cats still occurs in many parts of the country, including Tibet.
Between 25 July and 19 August 2009 the EIA carried out investigations in markets in five cities in western China.
Skin sale
In just 21 days the team was offered four full tiger skins, 12 leopard skins, 11 snow leopard skins and two clouded leopard skins as well as associated bones and teeth from the species.
"It's really quite significant," says EIA spokesperson Alasdair Cameron.
"What's interesting is the market has changed. Previously the market was for skins amongst the Tibetan community, that market has largely collapsed and what we're seeing now is skins bought for decoration and taxidermy amongst Chinese businesspeople," he says.
"People are buying them for prestige, skins are very expensive and tend to cost around 20,000 US dollars each," Mr Cameron explains.
Advertisement
Other rare cat skins offered
"We're also being told skins are being used for non-financial bribery within China, so the demand is increasing outside of the Tibetan areas."
The EIA says the animals are being smuggled into China from various places including Tibet, India, Nepal, Pakistan and Afghanistan.
Covert operation
The team captured the illegal trade on film using a hidden camera while they enquired about animal skins on sale.
What surprised the team was how easy it was to find and purchase the endangered animal products.
"There is some law enforcement in China, in a few regions, but there are whole swathes of the country where this trade is allowed to carry on with almost no fear of detection," Mr Cameron says.
"Some of the places we have been to, skins are openly displayed in shop windows while police cars drive past."
Debbie Banks, lead campaigner of the EIA, believes not is enough is being done by the Chinese authorities to combat the trade.
"If China can put a man into space, they can do more to save the wild tiger," she says.
Tiger meet
On the 27 October a summit is being held in Kathmandu, Nepal to discuss how best to save wild tigers from extinction.
The Kathmandu Global Tiger Workshop will bring together tiger experts and conservation organisations from around the world to further efforts to protect the animal, especially running up to the Chinese calendar's year of the tiger in 2010.
However, Mr Cameron has mixed feelings about the forthcoming year of the tiger.
"We're hoping to use the year of the tiger as a way to highlight the threats faced by the animal but traders in China are actually saying that next year is going to be great because people will want to get a piece of the tiger in the year of the tiger."
"There could actually be a spike in demand."

Respiration

2009-10-21T07:05:00.004-04:00

Aerobic respiration
Respiration is a process which releases energy inside each of the body's cells. It is not, as many people think, simply breathing - but see below.
Equation for the reaction
Reactants i.e. needed to take part in the process
Products i.e. made by the process
Not "made" but released from molecules of reactant
Glucose
+ oxygen
carbon dioxide
+ water
+ energy
From digestion of food especiallycarbohydrates
From air breathed in
Into air breathedout
Left in cell/blood/breathed out as vapour
More efficient than anaerobic respirationEnergy is trapped in the molecular structure of ATP
Delivered to cells in bloodstream
Removed from cells in blood stream
Used to power all the cell's processes-movement, electrical activity, synthesisThe energy is actually contained in the bonds between the atoms of the glucose molecule C6H12O6 which is the basic "fuel" for most cells in the body. This comes from carbohydrates in food which are processed by the digestive system, absorbed into the blood and passed around the body. The energy release is most efficient when the glucose is oxidised using oxygen derived from air, producing CO2 and H2O which are much simpler compounds. Aerobic respiration is an almost universal process - carried out by most animals and plants. It consists of several stages, the first of which is shared with anaerobic respiration and takes place in the cytoplasm of cells. The purely aerobic reactions take place inside mitochondria, small specialised organelles within the cytoplasm of all body cells. More active cells have more mitochondria.
Click for more information about the glycolysis, link reaction, Krebs/citric acid cycle and electron transport processes.Green plants carry out respiration 24 hours of the day, but in the light it is masked by photosynthesis which seems to put it in reverse. Some organisms can also perform anaerobic repiration as a less efficient alternative. In the bodies of most (higher) animals, aerobic respiration is assisted by muscular movement performed by the breathing system (also known as the respiratory system) and the circulatory system, but at the single cell level diffusion takes over.

Barnacle Glue and Penises

2009-10-19T07:16:00.003-04:00

Barnacles are able to attach themselves to almost anything.
They are found clinging to the hulls of ships, the sides of rock pools and even to the skin of whales.
Just how they stick so steadfastly whilst underwater has remained a biochemical puzzle for scientists for many years.
Now researchers have solved this mystery, showing that barnacle glue binds together exactly the same way as human blood does when it clots.
Barnacles are crustaceans that live in shallow ocean environments.
We've found homologous enzymes in barnacles and humans
Dr Gary DickinsonDuke University, US
As larvae they affix to hard substrates, then remain stationary for the rest of their lives.
To attach themselves to a surface, the barnacles secrete an adhesive substance.
Scientist knew the chemical properties of this glue, but not how these chemicals interact to create a sticky effect.
Now researchers reveal all in The Journal of Experimental Biology.
Sticking point
Actually obtaining some barnacle glue proved an initial hurdle.
"No one really knew how to work with barnacle glue before this study," says Dr Gary Dickinson, a member of the research team from Duke University's Marine Laboratory in Durham, North Carolina, US.
"Most people try to cut it off the bottom of a barnacle and then dissolve it, but we knew this does not work well, and this approach has limited potential," he explains.

Sticking around
So Dr Dickinson and his colleagues learnt how to gently remove glue from the barnacles (Amphibalanus amphitrite) as they secreted it.
They were then able to deconstruct the glue to find out exactly how it works.
The team initially compared the glue to another substance which clots in solution; red blood cells.
They expected the mechanism by which glue particles bind, and red blood cells bind, to be different.
However, they found they are remarkably similar.
In blood, a number of enzymes work to create long protein fibres that bind red blood cells, or platelets, together into a clot and create a scab.
Using techniques including atomic force microscopy and mass spectrometry, the team found that very similar enzymes, known as trypsin-like serine proteases, are at work in barnacle glue.
One of these glue enzymes is remarkably like Factor XIII, an essential blood clotting agent in human blood.
The enzymes are highly conserved because they are very effective at what they do
Dr Gary DickinsonDuke University, US
"We've found homologous enzymes in barnacles and humans, which serve the same function of clotting proteins underwater, despite roughly a billion years of evolutionary separation," says Dr Dickinson.
However, this surprising result does make evolutionary sense, says team member Professor Dan Rittschof, also from Duke University's Marine Laboratory.
"Virtually no biochemical pathway is brand new. Everything is related and really important pathways are used over and over," he explains.
"Really key parts of those pathways can't change because if they do, the pathway fails and the animal dies."
Glue potential
Dr Dickinson believes other organisms might also use this glue.
"The enzymes are highly conserved because they are very effective at what they do."
"There are bound to be a number of other organisms that use the same enzymes for the same purpose," he says.
His team hopes that further research might lead to a solution to the problem of marine fouling, where barnacles stick to boat hulls creating drag.
Many anti-fouling compounds used to paint the undersides of boats are toxic, so Dr Dickinson's team hopes to find a more environmentally-friendly solution.

Washington: Barnacles can totally change the size and shape of their penises to battle the waves and have sex, a new study has found.Graduate student Christopher Neufeld and Dr. Richard Palmer from the Department of Biological Sciences at the University of Alberta discovered that these distant relatives of crabs and lobsters can alter the size of their penises up to 8 times their body length, in order to mate.The authors said that barnacles want to mate but are permanently bound to whatever rock or hull they once latched onto. Because of this condition, barnacles have evolved the longest penises of any creature for their size to seek out and have sex with their neighbors.Neufeld and Palmer have shown that barnacles appear to have acquired the capacity to change the size and shape of their penises to closely match local wave conditions.
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"Barnacles have evolved the longest penises of any creature for their size to seek out and have sex.."
When wave action is light, a longer (thinner) penis can reach more mates, but at times of higher wave action, a shorter (stouter) penis is more manoeuvrable in flow and therefore can reach more mates.The research suggests that sexual selection, competition with other males, female choice, sexual conflict between males and females, is not required to explain variation in genital form.In barnacles, this variation appears to be driven largely by the hydrodynamic conditions experienced under breaking waves, the authors said.The study is published in Proceedings of the Royal Society B.

Salt Tolerant Tomato

2009-10-14T06:49:00.002-04:00

GM Tomato Plant Doesn't Shrink from Salty Water
By Kate Wong
Each year, nearly 25 million acres of once-farmable land are lost to salty irrigation water. The salts deposited in the fields disrupt a plant's ability to soak up water through the roots, lowering productivity and sometimes even dehydrating the plant entirely. Scientists have tried for decades to develop salt-tolerant crops through selective breeding but to no avail. Now findings described in the August issue of the journal Nature Biotechnology are offering the first seeds of hope. According to the report, researchers have genetically engineered tomato plants that flourish in salty water.
Earlier research had identified a plant protein that isolates salt, stowing it in intracellular compartments where it cannot upset the plant's normal biochemical routine. Building on that work, Eduardo Blumwald of the University of California at Davis and University of Toronto postdoctoral fellow Hong-Xia Zhang genetically manipulated tomato plants to manufacture more of this so-called transport protein. The resulting plants grow and produce fruit even when irrigated with water that's 50 times saltier than normal¿more than a third as salty as seawater.
The researchers grew the salt-tolerant plants in greenhouses, but Blumwald hopes to conduct field trials in salt-damaged soils in the future. If all goes as planned, he notes, scientists could develop commercially useful versions of these transgenic tomato plants within three years.

Scientists Successfully Clone an Endangered Mammal
By Kate Wong
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Though it remains a topic of controversy among conservation biologists, the idea of using cloning technology to preserve endangered species has received serious consideration ever since the cloning of Dolly the sheep in 1997. But recent attempts to clone endangered mammals such as the argali and the gaur have failed to yield viable offspring. Now a European research team has met with success. According to a report in the October issue of the journal Nature Biotechnology, the same technique used to replicate Dolly¿somatic cell nuclear transfer¿has produced an apparently healthy mouflon lamb, a member of an endangered species of sheep found on Sardinia, Corsica and Cyprus.
Pasqualino Loi of the University of Teramo in Italy and his colleagues recovered so-called somatic granulosa cells from the ovaries of two female mouflons found dead in a Sardinian pasture and injected their nuclei into domestic sheep egg cells that had had their nuclei removed. The resulting embryos were then surgically implanted in four domestic ewes, one of which delivered a cloned baby mouflon after 155 days. At 25 days old, the time at which the researchers submitted their report, the little mouflon appeared normal.
"Although the nuclear donor cells were recovered from dead animals and considered nonviable, they were able to generate normal embryos and offspring," the team writes. "Our findings support the use of cloning for the expansion of critically endangered populations, both within a concerted conservation program and in extreme situations involving sudden death.

Why are Red Pines Dieing in Northeastern Forests

2009-10-12T08:12:00.004-04:00

Red pines are in rapid decline. This Fact Sheet from Cornell discusses possible reasons for the die off such as " wet feet" syndrome". Red pine used to be considered an ideal tree for timber as it grew rapidly in relatively poor soils. Are the reasons for red pine's demise more complex than those at Cornell seem to think. Are our summers and winters changing so dramatically that the resiliance of many organisms is impaired resulting in deleterious impacts on their immune systems and consequent susceptibility to disease? I hope that the policymakers soon to be treking to Copenhagen are listening to the cries of nature. The survival of thousands of species, including our own, depends on rapid and judicious action to reduce greenhouse emissions. jj

RED PINE DECLINE

IntroductionRed or Norway pine (Pinus resinosa) is a favored timber tree in the northeast and north central states. It grows rapidly, has a straight, clear trunk, and seems to thrive on a variety of soils. In addition the species has few serious insect and disease pests. Because of this, red pine is as popular for shade and ornamental purposes as it is for reforestation. Unfortunately, as more trees have been planted in increasingly diverse sites, unforeseen problems in cultivation of red pine have become apparent.Symptoms
One problem is the decline and sudden death of red pine. Mature, stately trees in apparently excellent health "suddenly" die. Usually trees begin to decline for several years before they die. This decline in growth may be so gradual that it is undetected by the casual observer. There may be no obvious insects problems or evidence of disease on trees in the early stages of infection, however trees that die are quickly colonized by secondary bark beetles and woodboring insects.
Figure 1: Row of dead and recently killed red pine.
Figure 2: Declining red pine.
Causes
Several factors may be to blame, and may vary across the range of red pine. In the northeastern states, the decline and death of red pine appears to be associated with what is called "wet feet. There, soils in which the affected root systems are growing are invariably shallow and poorly drained regardless of soil type. In such soils most of the roots are confined to the upper 6 inches of soil. Typically these root systems are in various stages of deterioration. There are few feeder roots, and most of these are devoid of mycorrhizae, (beneficial fungus/root associations). Furthermore, the root system may show symptoms of root decay and rot caused by various fungi such as Leptographium spp. and Phytophthora spp.
The shallow and poorly drained topsoil appears to be responsible for triggering the decline of the trees. In years of high spring rainfall, soil on these sites becomes so saturated that roots are starved of oxygen and literally suffocate. As the soil dries later in the summer, recovery of the root system is possible. However, when prolonged periods of high spring soil moisture continue for several consecutive years, the diminished root system eventually loses its ability to nourish the growing crown, and decline begins. Older trees are more likely to suffer because their crowns are larger and their dependence on the entire root system is greater than it might be with younger trees. Furthermore, the longer the tree has grown on the adverse site, the more injury its root system may accumulate.
In some north central states, drought appear to be the factor that predisposes trees to decline. Drought stressed trees are also more susceptible to invasion by bark beetles, some of which help to spread root rot pathogens such as Leptographium spp. from tree to tree. When trees succomb, it is likely to be from a combination of these factors. In either case, the effect is the about same. Extended periods where trees have too much or too little water around the root system appears to lead to dieback of roots, decreased crown growth, and increased stress on the tree which throws it into a state of decline.Management Strategies
"Wet feet" can be prevented by not planting red pines on poorly drained, shallow soils. Unfortunately, trees that have already been planted on such high hazard sites are not easy to save. In some cases, diversion ditches, drains, or furrows have been used to improve soil drainage, and save declining trees. These techniques may not be practical in forest or woodlot situations but could be used to prolong lives of highvalued shade and ornamental trees. No other preventative or therapeautic actions are known to be effective.
Updated, SLJ, 3/05
This publication may contain pesticide recommendations. Changes in pesticide regulations occur constantly, some materials mentioned may no longer be available, and some uses may no longer be legal. All pesticides distributed, sold, and/or applied in New York State must be registered with the New York State Department of Environmental Conservation (DEC). Questions concerning the legality and/or registration status for pesticide use in New York State should be directed to the appropriate Cornell Cooperative Extension Specialist or your regional DEC office. READ THE LABEL BEFORE APPLYING ANY PESTICIDE. __________________________________________________________________________________The Plant Disease Diagnostic Clinic at Cornell University is located at 334 Plant Science Building, Ithaca, NY, 14853. Phone: 607-255-7850, Fax: 607-255-4471, Email: kls13@cornell.edu or slj2@cornell.edu

Amphibian Crisis- The Tip of the Extinction Iceberg

2009-10-12T07:57:00.005-04:00

Crisis for the worlds amphibians
VIEWPOINT Helen Meredith
It is a time of crisis for the world's amphibians, says Helen Meredith. In this week's Green Room she says we may be facing our last chance to save this important group of animals.
“ They consume huge quantities of invertebrates, including humanity's most vilified pests and their crucial role in global ecosystems helps maintain healthy functioning environments ”
A third of all species of amphibian are threatened with extinction; nearly half are in decline, and they are the most threatened of all the vertebrate groups.
If allowed to continue, the projected losses would constitute the largest mass extinction since the disappearance of the dinosaurs.
But first things first; what are amphibians and why should we care about their decline?
Amphibians are one of nature's less familiar groups - an issue that presents major challenges to establishing the conservation action they so urgently require.
They have been around on the planet for about 360 million years, arising over 100 million years before the first mammal and 200 million years before the first bird.
Great survivors
Modern amphibians comprise frogs, toads, salamanders, newts and caecilians (limbless amphibians), and number in excess of 6,000 species to date.
More than 20% are not understood well enough to be assigned any conservation status and it is estimated that up to 10,000 species may exist in total.
WHAT ARE AMPHIBIANS?
First true amphibians evolved about 250m years ago
There are three orders: frogs (including toads), salamanders (including newts) and caecilians, which are limbless
Adapted to many different aquatic and terrestrial habitats
Present today on every continent except Antarctica
Many undergo metamorphosis, from larvae to adults
They are found on every continent except Antarctica, ranging from the Arctic Circle to the tropical deserts.
Of all the vertebrates, amphibians lead some of the strangest lives. Various species can survive partial freezing, 10 years without food, long droughts and temperatures of up to 40C (104F).
They are among life's great survivors, enduring mass extinction events that have wiped out the dinosaurs and whole swathes of mammals and birds. In this light, their current extinction crisis seems all the more troubling.
Although they may not seem to have an impact upon the daily lives of many cultures, they provide numerous essential services to mankind.
They consume huge quantities of invertebrates, including humanity's most vilified pests.
Their crucial role in global ecosystems, both as predator and prey, helps maintain healthy functioning environments. Frogs are an important protein source in many subsistence cultures and are traded in their millions as food and pets.
The skin secretions that protect amphibians against predation and infection have been found to contain important pharmaceutical compounds that show potential in treating a variety of illnesses from HIV to cancer.
The most famous case is that of the phantasmal poison frog (Epipedobates tricolor) . Skin secretions from this frog yielded the compound epibatidine, which is a painkiller 200 times more effective than morphine.
“ The fight to save the world's amphibians shouts into a howling gale of climate change, war, overpopulation, economic crises, and countless other global disasters ”
Amphibians are repositories of potentially life-saving chemicals and are key model organisms in scientific research.
Witnessing the precipitous decline of the amphibians is sobering. Why now, after hundreds of millions of years of survival, are they bowing out?
As always, the reasons are diverse and complex. The usual suspects of habitat destruction, climate change, invasive species, environmental contaminants and overexploitation represent key interrelated factors.
Additionally, a disease called chytridiomycosis or "chytrid" (caused by the fungus Batrachochytrium dendrobatidis ) infects a wide range of amphibians globally and is capable of driving species to extinction.
Exacerbated by the other issues impacting amphibians, chytrid has emerged as one of the major threats to their survival. This disease can kill amphibians in otherwise pristine habitats or provide the final nail in the coffin for species already pushed to the brink of extinction.
The fight to save the world's amphibians shouts into a howling gale of climate change, war, overpopulation, economic crises, and countless other global disasters, rendering their plight (just like many other aspects of biodiversity) somewhat low on the agenda of global priorities; they are slipping away almost unnoticed.
What can be done?
A recent IUCN amphibian conservation summit held at the Zoological Society of London (ZSL) highlighted plans to launch the Amphibian Survival Alliance, which will unite existing organisations and projects working on amphibian conservation (like ZSL's EDGE Amphibians Project), creating a mutually supportive network.
This initiative is still woefully underfunded given the urgent need for action, but represents a major step towards consolidating worldwide conservation activities to protect as many species as possible.
We hope this will improve and expand the movement to protect amphibians, boosting the fundraising and publicity drive necessary to raise concern over amphibian declines and put vital conservation strategies into practice.
To lend perspective, the original cost of the global Amphibian Conservation Action Plan was equivalent to about one and a half Boeing 747 aeroplanes.
The latest plans drawn up at the summit would cost just one tenth of this sum, and would at least make progress towards saving a third of the world's amphibians.
Initially tackling the two main threats to amphibian survival, disease and habitat destruction, the Amphibian Survival Alliance will require major political backing and financial support if it is to achieve its objectives.
It represents the best hope for amphibians at this most critical and desperate time.
Amphibians are widely viewed as the "canaries in the coalmine" for environmental change.
Despite their glorious past, they simply cannot withstand the current onslaught.
Tellingly, the very same factors that threaten amphibians also endanger all other life on Earth, not least humans.
If we cannot rectify the amphibian extinction crisis, then what does this mean for the future of mankind?
Saving the world's amphibians is a crucial part of the puzzle in guaranteeing our own sustainable existence.
I hope we will act before it is too late for us all.
Helen Meredith is a conservation scientist from the Zoological Society of London (ZSL)
The Green Room is a series of opinion articles on environmental topics running weekly on the BBC News website

Do you agree with Helen Meredith? Should we take action to prevent the decline of amphibian species? Does their survival matter? Who should provide financial support for their conservation?
It is our responsibility as a species to help the amphibians, as well as all animal and plant species, to recover as it is mostly our fault for their decline. Joe Wright, Canterbury, England
'Of course amphibians need to be saved, we treat the world and its other inhabitants in such a cavalier fashion that we have destroyed much of its habitat and, inhabitants. Sooner or later it will no longer be able to support the Human population due to our own greed, and lack of consideration for other life forms. Who should pay to save the amphibians, we should through our governments and taxes. Its about time we started putting things right not talking about it. Big businesses should pay the most because they are the ones who have benefited most from the rape, and destruction of the world's resources.' Totally agreed. Couldn't have put it better myself! And on top of amphibians, there's such crisis in seemingly every animal group [human AND natural] right now. It's almost as if nature itself is taking back everything before we can deal the fatal blow, leaving us to die out alone [which, we kind of deserve by now]. Globally, more money needs to actually go towards people and the environment, and not to war, weaponry, fossil fuels and government / bank's pockets... Daniel Bevis, Fleet, Hampshire, UK
It's still the same long term solution.Too many people!When will a politician have the guts to break rank and tell it like it is! steve johnson, whitwick,leics
Obviously,it is very essential to save amphibians in our planet. As an civil engineer I am to count biodiversity while any development of infrastructure works. In view of above contexts, we treat the world and its other inhabitants in such a cavalier fashion that we have destroyed much of its habitat and, inhabitants.We should take action to prevent the decline of amphibian species.Their survival in the world is vulnerable. Richer countries are more responsible for their survival. Its about time we begun putting things right not talking about it. A government or a large business should provide financial support for their conservation. Engr Salam, Kushtia,Bangladesh
Mankind really is flying without a net. The way we assume we know it all even when a whole class of life like the amphibians is in great distress. Creatures we can hardly list let alone know how they interact and play their part in Nature facing extinction. Dismissed with hardly a thought. We talk a lot here in the US about security. Health care security through medical insurance, security from terrorists by having a strong defense, economic security but how has that worked out? Hasn't it in truth amounted to a failure of the highest order to think small like this and to continue to dump resources into propping up failed policy. Our ability to fund important research and conservation efforts let alone start new businesses is gutted by seeking false security. Investment should be shifted to helping protect nature itself. It's got to be better than having an insurance policy that's hardly worth the paper it's written on, a military that has smart bombs that wind up making enemies or a monetary policy that let derivatives trading run rampant so a few people could get rich. Dale Lanan, Longmont, Colorado, USA
it is important the amphibian [all species] be given the pretective knowledge required. They were here first. so there it is, gavin hall , wellington new zealand
100% agreed, with the concerns of the Helen. Funding amphibian protection efforts is quite necessary to enhance their numbers and to check their business in the commercial world. It's an important but a temporary solution. Unless we do not protect the wells, ponds, rivers, oceans, fields, forests and atmosphere, we would not be able to give enough space to the amphibians, necessary for their survival. If we allow our population and present form of activities to grow, with the current pace, there wouldn't be sufficient space and healthy environment left for these precious species. It's not an isolated challenge. It is 100% related with the human population and their anti-natural activities. We are relaxed by believing there are different levels of the 'catastrophes'. Those species which have already extinct from the planet, catastrophe 'started and concluded'. For the endangered specie the catastrophe is 'going on' and we are still busy in current trends by not acknowledging the catastrophe trends of the climate change. If, we can sense danger for the amphibians and other species, then, there is absolute need of urgency for human beings too. Sanjay Singh Thakur, Indore,India
It remains a mystery to me why it took so long for the scientific community to become aware of this catastrophe. I am not a trained scientist, but I became aware of a severe crash in frog populations during the middle to late 1970's. I only noticed that biologists began to mention this in print sometime in the late 1990's. No matter how many resources, financial and otherwise, can now be brought to bear on the problem, I fail to see exactly what can be done; especially in combating Chytrid fungus. What specific suggestions are there? This is not to suggest that nothing should be done, but what? I hate to be the pessimist, but I fear that humanity has progressed past the point of rescue of our fellow biological travelers upon this earth, and that we are doomed to follow them into oblivion. And it will be deservedly so. tom, castleton, NY USA
We need to let the wilds become wild again, which means moving all human encroachment: summer homes, boating, vacation lodges. We need to recognize the finiteness of our planet and live accordingly, by recognizing not one of us owns any of the space over anybody else. When we go into the wilds we minimize our footprints, like when they climb Antarctic Mountains, even your excrement must return, and they all do this in hanging tents. At the beginning of the wilderness, we may have structured camping, with walkin as opposed to drive-in. We need an ecologically sustainable Global Societal model, where no one lives in destitution. Check out paradigmshift2011.ning.com Let's change our world to show consideration for the quality of life for the next generation. Cheers, Chris Curpen Chris Curpen, Winnipeg, Manitoba, Canada
Of course amphibians need to be saved, we treat the world and its other inhabitants in such a cavalier fashion that we have destroyed much of its habitat and, inhabitants. Sooner or later it will no longer be able to support the Human population due to our own greed, and lack of consideration for other life forms. Who should pay to save the amphibians, we should through our governments and taxes. Its about time we started putting things right not talking about it. Big businesses should pay the most because they are the ones who have benefited most from the rape, and destruction of the world's resources. Arthur Griffiths, Capel Iwan, Carmarthenshire, Wales
although I am very sympathetic to the plight of amphibians and quite passionate about our "own" newt here, the rough skinned newt, I really cannot see fromthe article how "a mutually suportive network" is going to make much of a difference in a direct sense. It rather reminds me of the money-making "portal" idea of the great internet boom/bust period which was supposed to provide coordinated access to other individual and network sites but contributed very little by itself (and largely became extinct during the bust). More funding for amphibians, yes by all means. But the irony is that, if we include time and effort by e.g. volunteers and concnerned citizens in the $$ figure of money already expended on amphibian rescue, the bulk of it is used (and quite effectively)for amphibians in areas in what we used to call the developed world. And I cannot see that changing through the proposed effort, even if it becomes fully funded. Paul van Poppelen, Gibsons, BC, Canada
Helen, Great article, please look at our blog, we're in this fight together! http://frogsaregreen.com Susan Susan Newman, Jersey City, NJ USA
A weekly series of thought-provoking opinion pieces on environmental topics
Story from BBC NEWS:http://news.bbc.co.uk/go/pr/fr/-/2/hi/science/nature/8292690.stmPublished: 2009/10/06 14:11:05 GMT© BBC MMIX
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Chromatin Packaging

2009-10-11T18:49:00.004-04:00

Revealed: The human genome in 3D
Scientists have worked out the 3D structure of the human genome.
Their findings, published in Science magazine, reveal how long strands of DNA code are folded and tightly packed into the nucleus of a human cell.
Unfolded, the cell's genome - those strands of DNA code - would be approximately 2m in length.
The team showed how this is organised into a tight ball to fit inside a nucleus, which is about one hundredth of a millimetre in diameter.
The US-based research team developed improved DNA sequencing and computational methods to build a model of the genome.
“ This is the first glimpse we're getting of a whole genome in 3D ” Job Dekker University of Massachusetts
Job Dekker, from the University of Massachusetts Medical School, led the research.
He explained to BBC News that, with its new approach, his team had discovered important patterns in the shape of the genome.
"For a given part of the genome, we can determine its neighbours," he said.
"And if you can do that for every gene - if you know which other genes surround it - you can work your way back computationally to calculate the structure.
"This is the first glimpse we're getting of a whole genome in 3D."
DNA is bundled into chromosomes. The combination of DNA and protein that makes up these chromosomes is called chromatin.
Dr Dekker explained how a 3D view showed how chromatin's complicated folding pattern was important in the regulation of genes.
"We now see that things that are far apart along the linear sequence of the genome are actually next to each other in the folded structure," he said.
"They're close together in the structure, and they're talking to each other."
This constant communication is the basis of the regulation that keeps a cell healthy and functional.
This means that a detailed view of the genome's structure could provide a new window into diseases such as cancer, which is caused by errors in the genetic code.
"Maybe we will be able to predict these [disease-causing] changes better now," said Dr Dekker.
The team also discovered that the human genome is organised into two separate compartments, keeping active genes accessible while keeping inactive DNA in a sort of storage compartment.
The chromosomes snake in and out of the two compartments - separating their active and inactive sections

http://news.bbc.co.uk/1/hi/sci/tech/8294817.stm

NOVA Episodes

2009-10-09T10:51:00.002-04:00

http://www.pbs.org/wgbh/nova/archive/int_heal.html

Influenza
18 Ways to Make a Baby
Ageing
Anthrax
Judah Folkman
Cracking the Code of Life
Epigenetics
The Family that Walks on all Fours
Ghost in Your Genes
DNA Testing

DNA Sequencing

2009-10-07T06:03:00.002-04:00

IBM will announce on Tuesday how it intends to hold DNA molecules in tiny holes in silicon in an effort to decode their genetic secrets letter by letter.
Their microelectronic approach solves one of two long-standing problems in "nanopore" DNA sequencing: how to stop it flying through too quickly.
The aim is to speed up DNA sequencing in a push toward personalised medicine.
IBM's chief executive Sam Palmisano will announce the plans to the Medical Innovation Summit in the US on Tuesday.
While sequencing the genomes of humans and animals has become relatively routine in a laboratory setting, the ability to quickly and cheaply sequence genomes of individuals remains out of reach.
That widely available genetic information will help bring about the era of "personalised medicine" - in which preventative or therapeutic approaches can be tailored to individuals based on their specific genetic makeup.
All-electronic
"There have been a number of attempts to sequence DNA much faster than it was sequenced when the first human genome was announced," said Gustavo Stolovitzky, a computational biologist from IBM.

Individual genetic information will lead to more directed therapies
"All of them use some complicated sample preparation - chopping the DNA, amplifying, reverse transcribing - and some sophisticated and labour-intensive optics," Dr Stolovitzky told BBC News.
"All this makes sequencing faster, but still slower and more expensive than it needs to be before it could be used for personalised medicine."
Instead, Dr Stolovitzky and colleagues are pursuing a method involving silicon peppered with holes just three billionths of a metre across - 20,000 times thinner than a human hair and just wide enough for one strand of DNA to pass through.
Researchers have been looking into using such nanopores for a number of years - mimicking the proteins in cell membranes that perform the same trick - because using a semiconductor offers significant advantages over biochemical and optical techniques.
"DNA nanopore sequencing continues to be one of the great candidates to do fast and cheap DNA sequencing without sample preparation or sophisticated optics, using only electronics to fetch the signal out," Dr Stolovitzky said.
Moreover, the approach could be done in a "massively parallel" way - that is, with hundreds or thousands of DNA strands passing through an array of holes on a single chip.
Trap stack
The idea is conceptually simple but devilishly difficult to carry out. Because DNA naturally carries a net electric charge, simply applying a voltage across the two sides of the chip drives the DNA strands through the holes.
However, the DNA tends to pass through too quickly to decode the identities of the individual nucleotides - letters of the genetic code - as they pass.
More than that, until they can study DNA strands moving at a more carefully controlled pace, researchers cannot develop the techniques to query the precise nucleotide they have trapped in place.

The Blue Gene supercomputer simulated the nanopores' every atom
The IBM team have now hit on the idea of a chip composed of a stack of layers, each of which can hold a precisely-controlled voltage in a thin layer inside the nanopore.
These smaller voltages trap the negatively charged chemical groups called phosphates that separate individual nucleotides.
By cycling this internal voltage, the DNA strand can be made to advance one nucleotide at a time.
The team has used IBM's Blue Gene supercomputer to simulate the process in order to ensure it would work, and the team has built prototypes of the trapping nanopore. Tuesday's announcement marks the beginning of the testing and refinement stages of the process.
What remains is to investigate the means to identify the individual nucleotides trapped inside the nanopores, which is likely to rest on measuring some electrical or electronic property of each as it passes.
Stas Polonsky, another IBM researcher working on the project, remains convinced that with the benefit of a trapping mechanism, this last problem is tractable.
"As a company we have a lot of expertise with electrical measurements," he said.
"We have nanopores plus the whole arsenal of microelectronics - we can integrate all these ultrasensitive circuits right on a chip, which will boost the sensitivity for measurements tremendously."

Nobel Prize in Physiology - Telemorase

2009-10-05T08:39:00.000-04:00

(Reuters) - Elizabeth Blackburn, Carol Greider and Jack Szostak won the 2009 Nobel prize for medicine or physiology on Monday for their work on chromosomes.
Here are some details about the winners:
* ELIZABETH H. BLACKBURN:
-- Elizabeth Helen Blackburn is a molecular biologist and biochemist who conducted ground-breaking research on DNA (deoxyribonucleic acid) and cell division that has provided a new line of inquiry into the chemical bases of life.
-- Her discovery of a key enzyme, telomerase, which is necessary for chromosomes to make copies of themselves before cell division, has been applied to the study of chromosome behavior and of certain diseases, such as fungal infections and cancer.
-- Blackburn, who has U.S. and Australian citizenship, was born in Hobart, Australia in November 1948. Blackburn's interest in medicine and biology was influenced early on by her parents, both of whom were physicians.
-- Blackburn graduated from the University of Melbourne in 1970 and with a MS degree in 1971.
-- She went to Cambridge University, where she obtained a Ph.D. in molecular biology in 1975. She then went to the United States, drawn by professional and personal reasons. While attending Cambridge, Blackburn met and married John Sedat, an American postdoctoral researcher in biology. -- Blackburn then began her work with telomeres, which help chromosomes to remain stable and whole, thereby ensuring completion of the DNA replication cycle. In 1978 she became assistant professor at the University of California, Berkeley, where she was to make her ground-breaking discoveries concerning chromosomes and DNA.
-- In 1990 she went to the University of California at San Francisco. She is currently the Morris Herzstein Professor of Biology and Physiology at UCSF.
-- She was fired in 2004 from then-President George W. Bush's Council on Bioethics for her criticism of his restrictive policy on embryonic stem cell research. Earlier this year she said "The previous administration had this strange impression that science was the enemy of morality."
* CAROL W. GREIDER:
-- Greider began with her adviser, Elizabeth Blackburn, to investigate how a certain single-celled pond organism maintained the tens of thousands of caps on the ends of its mini-chromosomes - specialized structures known as telomeres that protect against DNA damage.
-- Greider is a U.S. citizen and was born in 1961 in San Diego, near the University of California, Davis campus, where her father was a physics professor.
-- Greider received her Ph.D. from University of California, Berkeley, in 1987 in molecular and cell biology. After postdoctoral research at Cold Spring Harbor Laboratory, she was appointed professor in the department of molecular biology and genetics at Johns Hopkins University School of Medicine in Baltimore in 1997.
-- Greider was credited with helping co-discover telomerase, an enzyme that maintains the length and integrity of telomeres. She has continued her work on telomeres and documented a mouse model for dyskeratosis congenital, a rare, inherited disorder related to stem cell failure.
-- Greider shared the 2006 Albert Lasker Award for Basic Medical Research with Blackburn and Szostak. Continued...

Rutherford Model

2009-10-04T15:12:00.003-04:00

Background Information
In order to have a phase change in matter heat must be either gained or lost. Phase changes occur all around us in everday life. For instance, ice melts when a drink is left in a room at normal temperature; conversely, water freezes when place in a really cold temperature (the freezer). In this experiment we see how heat is lost in order to change the milk from a liquid state to a solid state. This is also an example of a physical change in matter.
Students will also be able to observe how adding solute (ice cream salt) to a solvent (ice) changes the physical properties of that solvent. In this case the freezing point of the ice is lowered allowing for the milk to turn into ice cream.
For a group of about 150 students this lab cost around $35- $40.

Student Activity
To print out the Student Copy only, click here.
Materials
240 mL milk
45 mL sugar
cups
80 mL ice cream
salt
2.5 mL vanilla or chocolate flavoring
50 mL beaker
100 mL graduated cylinder
ice
400 mL beaker
3.8 L zipper bag (gallon); freezer quality
gloves
0.95 L zipper bag (quart); freezer quality
dish towel
spoons
Celsius thermometer

Procedure:
Find a partner to work with.
Place a dishtowel over your work area. Keep your work on the towel.
Pour 240 mL milk, 45 mL sugar, and 2.5 mL vanilla or chocolate flavoring into the 0.95 L zipper bag. CAREFULLY seal the bag and shake up the mixture thoroughly.
Put this small zipper bag inside the much larger 3.8 L zipper bag.
In the 3.8 L bag add enough ice to cover the 0.95 L bag and add 80 mL of ice cream salt. Take the temperature of the ice:______ C
CAREFULLY SEAL THE BAG!
Put your gloves on and get ready to make a phase change!
Take turns flipping the bag. Hold the bag by its corners. Keep the bag flipping over and over. Remember to keep the bag over the towel at all times. It should take 10 to 15 minutes to freeze. Take the temperature of the ice/water mixture again: ________ C
When you have ice cream, take the smaller bag out and rinse it off with cold water. One partner needs to take the larger bag and it's contents to the trash bag. DO NOT DUMP IT DOWN THE SINK!!!
Dish out the ice cream equally into the cups, and ENJOY! (You may rinse the cup out and use it for water if you are thirsty.)
Please clean up your area. (Leave it neater than you found it.)
Student Questions
Student Questions are included on the Student Copy of the activity. To print out the Student Copy only, click here.
Answer the following on a separate sheet of paper:
What state of matter was the milk when you began?
What state of matter was the milk when you were done?
In order to change the phase of the milk, what had to be removed?
What happened to the heat energy that left the milk?
Why was the salt added to the ice?
If you did not add sugar would the ice cream have frozen faster? Why?
Why did the outside of the bag get wet? (Assume that your bag did not spring a leak.)
http://www.unit5.org/chemistry/Atom.htm

Gaia's Acid Reflux

2009-10-04T14:17:00.006-04:00

Arctic Seas Turn to Acid, Putting Vital Food Chain at Risk
With the world's oceans absorbing six million tonnes of carbon a day, a leading oceanographer warns of eco disaster
by Robin McKie
Carbon-dioxide emissions are turning the waters of the Arctic Ocean into acid at an unprecedented rate, scientists have discovered. Research carried out in the archipelago of Svalbard has shown in many regions around the north pole seawater is likely to reach corrosive levels within 10 years. The water will then start to dissolve the shells of mussels and other shellfish and cause major disruption to the food chain. By the end of the century, the entire Arctic Ocean will be corrosively acidic.
"This is extremely worrying," Professor Jean-Pierre Gattuso, of France's Centre National de la Recherche Scientifique, told an international oceanography conference last week. "We knew that the seas were getting more acidic and this would disrupt the ability of shellfish – like mussels – to grow their shells. But now we realise the situation is much worse. The water will become so acidic it will actually dissolve the shells of living shellfish."
Just as an acid descaler breaks apart limescale inside a kettle, so the shells that protect molluscs and other creatures will be dissolved. "This will affect the whole food chain, including the North Atlantic salmon, which feeds on molluscs," said Gattuso, speaking at a European commission conference, Oceans of Tomorrow, in Barcelona last week. The oceanographer told delegates that the problem of ocean acidification was worse in high latitudes, in the Arctic and around Antarctica, than it was nearer the equator.
"More carbon dioxide can dissolve in cold water than warm," he said. "Hence the problem of acidification is worse in the Arctic than in the tropics, though we have only recently got round to studying the problem in detail."
About a quarter of the carbon dioxide pumped into the atmosphere by factories, power stations and cars now ends up being absorbed by the oceans. That represents more than six million tonnes of carbon a day.
This carbon dioxide dissolves and is turned into carbonic acid, causing the oceans to become more acidic. "We knew the Arctic would be particularly badly affected when we started our studies but I did not anticipate the extent of the problem," said Gattuso.
His research suggests that 10% of the Arctic Ocean will be corrosively acidic by 2018; 50% by 2050; and 100% ocean by 2100. "Over the whole planet, there will be a threefold increase in the average acidity of the oceans, which is unprecedented during the past 20 million years. That level of acidification will cause immense damage to the ecosystem and the food chain, particularly in the Arctic," he added.
The tiny mollusc Limacina helicina, which is found in Arctic waters, will be particularly vulnerable, he said. The little shellfish is eaten by baleen whales, salmon, herring and various seabirds. Its disappearance would therefore have a major impact on the entire marine food chain. The deep-water coral Lophelia pertusa would also be extremely vulnerable to rising acidity. Reefs in high latitudes are constructed by only one or two types of coral – unlike tropical coral reefs which are built by a large variety of species. The loss of Lophelia pertusa would therefore devastate reefs off Norway and the coast of Scotland, removing underwater shelters that are exploited by dozens of species of fish and other creatures.
"Scientists have proposed all sorts of geo-engineering solutions to global warming," said Gattuso. "For instance, they have proposed spraying the upper atmosphere with aerosol particles that would reduce sunlight reaching the Earth, mitigating the warming caused by rising levels of carbon dioxide.
"But these ideas miss the point. They will still allow carbon dioxide emissions to continue to increase – and thus the oceans to become more and more acidic. There is only one way to stop the devastation the oceans are now facing and that is to limit carbon-dioxide emissions as a matter of urgency."
This was backed by other speakers at the conference. Daniel Conley, of Lund University, Sweden, said that increasing acidity levels, sea-level rises and temperature changes now threatened to bring about irreversible loss of biodiversity in the sea. Christoph Heinze, of Bergen University, Norway, said his studies, part of the EU CarboOcean project, had found that carbon from the atmosphere was being transported into the oceans' deeper waters far more rapidly than expected and was already having a corrosive effect on life forms there.
The oceans' vulnerability to climate change and rising carbon-dioxide levels has also been a key factor in the launching of the EU's Tara Ocean project at Barcelona. The expedition, on the sailing ship Tara, will take three years to circumnavigate the globe, culminating in a voyage through the icy Northwest Passage in Canada, and will make continual and detailed samplings of seawater to study its life forms.
A litre of seawater contains between 1bn and 10bn single-celled organisms called prokaryotes, between 10bn and 100bn viruses and a vast number of more complex, microscopic creatures known as zooplankton, said Chris Bowler, a marine biologist on Tara.
"People think they are just swimming in water when they go for a dip in the sea," he said. "In fact, they are bathing in a plankton soup."
That plankton soup is of crucial importance to the planet, he added. "As much carbon dioxide is absorbed by plankton as is absorbed by tropical rainforests. Its health is therefore of crucial importance to us all."
However, only 1% of the life forms found in the sea have been properly identified and studied, said Bowler. "The aim of the Tara project is to correct some of that ignorance and identify many more of these organisms while we still have the chance. Issues like ocean acidification, rising sea levels and global warming will not be concerns at the back of our minds. They will be a key focus for the work that we do while we are on our expedition."
The toll by 2100
■ The Intergovernmental Panel on Climate Change forecast in 2007 that sea levels would rise by 20cm to 60cm by 2100 thanks to global warming caused by man-made carbon-dioxide emissions. This is now thought to be an underestimate, however, with most scientific bodies warning that sea levels could rise by a metre or even higher. Major inundations of vulnerable regions such as Bangladesh would ensue.

■ The planet will be hotter by 3C by 2100, most scientists now expect, though rises of 4.5C to 5C could be experienced. Deserts will spread and heatwaves will become more prevalent. Ice-caps will melt and cyclones are also likely to be triggered.

■ Weather patterns across the globe will become more unstable, numbers of devastating storms will increase dramatically while snow will disappear from all but the highest mountains.

When the Pollinators Disappear...

2009-10-04T14:13:00.002-04:00

Beekeepers Tell Pesticide Firm to Buzz Off
by Rob Edwards
One of the world's biggest pesticide companies, Syngenta, has been accused of a "howling conflict of interest" for funding research into the disappearance of honeybees - a problem which some people claim it may have helped cause.
A bumblebee rests on a sunflower. The 41st world apiculture congress, where 10,000 beekeepers, entomologists and other actors in the honey business are gathered, will try to understan what is killing bees. (AFP/File/Karen Bleier)Syngenta, based in Basel, Switzerland, last year clocked up £7.3 billion worth of sales in more than 90 countries. Among the products it markets to farmers are insecticides which have been blamed for harming honeybees.
It now also co-funds a £1m project in the UK, announced last week, to research the decline of the bees. But the company has dismissed criticisms of its role in the project as "perverse".
A film due to open in cinemas this week highlights the global plight of the honeybee and argues that insecticides are partly to blame. Called Vanishing Of The Bees, it is backed by the Co-operative retail group, which has a strict policy on the use of pesticides on the fruit and vegetables it sells, including a total ban on the use of several chemicals.
According to beekeepers, honeybee populations in the UK crashed by nearly a third in 2008. The implications are alarming, as bees contribute £200m a year to the UK economy, pollinating a third of our food.
Scientists speculate that a combination of factors may be involved, including disease, mites, weather and modern farming practices. But some argue that a group of widely-used nicotine-based insecticides known as neonicotinoids could be inflicting neural damage on bees, and contributing to their demise. Syngenta sells two products containing neonicotinoids, Actara and Cruiser.
To protect bee populations, some such insecticides have been banned or restricted in France, Germany, Italy and Slovenia. But they can still be used in other countries, including the UK and the United States.
A coalition of environmental groups has launched a campaign for a ban on neonicotinoids in the UK. The group includes the Soil Association, which certifies organic food.
Its Scottish director, Hugh Raven, said Syngenta had made its position clear by opposing a ban on neonicotinoids.
"The taint of commercial interest has undermined this research before it's even started," he said.
The research is also supported by the government's Biotechnology and Biological Sciences Research Council. "The BBSRC should think again, and get a co-funder without this howling conflict of interest," said Raven.
Professor Andrew Watterson, head of the occupational and environmental health research group at Stirling University, agreed there were "potential conflicts of interest in the project which may affect the credibility of the findings".
Graham White, a beekeeper in the Scottish Borders and an environmental author, was scathing about Syngenta's role: "Putting Syngenta in charge of UK research into the causes of honeybee deaths is arguably the equivalent of putting the tobacco companies in charge of research into lung cancer."
But Andrew Coker, Syngenta's head of corporate affairs in the UK, said: "It seems perverse that we put our money into researching bee health and then get criticised for it."
Dr Celia Caulcott, BBSRC's director of innovation and skills, also defended the research. She said: "The use of insecticides in agriculture is just one possible reason for the problems bees are facing. The most important thing to do right now is to understand what is happening and then translate that knowledge into actions to address the decline."