A team of scientists has documented that Yasuní National Park, in the core of the Ecuadorian Amazon, shatters world records for a wide array of plant and animal groups, from amphibians to trees to insects. The authors also conclude that proposed oil development projects represent the greatest threat to Yasuní and its biodiversity.

"This study demonstrates that Yasuní is the most diverse area in South America, and possibly the world," said Dr. Peter English of The University of Texas at Austin. "Amphibians, birds, mammals and vascular plants all reach maximum diversity in Yasuní."

The study is published in the open-access scientific journal PLoS ONE.

"We have so far documented 596 bird species occurring in Yasuni," said English, a bird specialist. "That's incredible diversity to find in just one corner of the Amazon rainforest and rivals any other spot on the planet."

Other specialists joined in to give the first complete picture of the extraordinary diversity found in Yasuní National Park.

"The 150 amphibian species documented to date throughout Yasuní is a world record for an area of this size," said Shawn McCracken of Texas State University. "There are more species of frogs and toads within Yasuní than are native to the United States and Canada combined."

The scientists also confirmed that an average upland hectare (2.47 acres) in Yasuní contains more tree species, 655, than are native to the continental United States and Canada combined. The number of tree species rises to more than 1,100 for an area of 25 hectares.

"In just one hectare in Yasuní, there are more tree, shrub and liana (woody vines) species than anywhere else in the world," said Gorky Villa, an Ecuadorian botanist working with both the Smithsonian Institution and Finding Species.

Perhaps the most impressive statistic of all is that a single hectare of forest in Yasuní is projected to contain 100,000 insect species. According to eminent entomologist Dr. Terry Erwin, that is the highest estimated diversity per unit area in the world for any plant or animal group.

"One of our most important findings about Yasuní is that small areas of forest harbor extremely high numbers of animals and plants," said lead author Margot Bass, president of Finding Species, a non-profit with offices in Maryland and Quito, Ecuador. "Yasuní is probably unmatched by any other park in the world for total numbers of species."

The extraordinary diversity of Yasuní is best exemplified at the 1,600-acre Tiputini Biodiversity Station on the northern edge of the park.

"The Tiputini Biodiversity Station is home to 247 amphibian and reptile species, 550 bird species and around 200 mammal species," said Dr. Kelly Swing of the University of San Francisco in Quito, Ecuador.

"What makes Yasuní especially important is its potential to sustain this extraordinary biodiversity in the long term," said Dr. Matt Finer of Save America's Forests. "For example, the Yasuní region is predicted to maintain wet, rainforest conditions as climate change-induced drought intensifies in the eastern Amazon."

The paper concludes with a number of science-based policy recommendations. One key recommendation is a moratorium on new oil exploration or development projects within the park, particularly in the remote and relatively intact—but oil rich—northeast corner that contains oil blocks 31 and ITT.

The Ecuadorian government is promoting a revolutionary plan, known as the Yasuní-ITT Initiative, which would leave the park's largest oil reserves in the ITT block permanently under the ground. A lack of funding commitments, however, now threatens the proposal.

"The Yasuní-ITT Initiative urgently needs international funders to step up and make it a success, or else more drilling in the core of Yasuní may become a tragic reality," concluded Finer.

As Americans begin the process of breaking their New Year's resolutions - sure, one king-sized Kit Kat won't hurt anyone - they can forgive themselves with a consolation: Hormones may be to blame.

In a new study, which was published online Dec. 24 in the journal Biological Psychiatry, researchers have found that the hormone ghrelin causes mice to search out food - even when they weren't hungry.

"We've shown that ghrelin affects behaviors related to eating and that it may consequently lead to overeating," said study researcher Dr. Jeffrey Zigman, assistant professor of internal medicine and psychiatry at University of Texas Southwestern Medical Center.

The results could apply to us, as we also have this hormone, which has been shown in the past to activate the same brain regions excited by cocaine in humans.

In the experiments, Zigman and colleagues trained mice to remember that a room with striped walls held a high-calorie treat, while a chamber with gray walls contained a low-calorie snack. After the training, satiated mice were given the opportunity to wander to whatever room they wanted. Those mice that were injected with a dose of ghrelin preferred the room known for calorie-infused goodies, even if the room was empty of food. Mice that were ghrelin-free had no preference.

"The mice's behavior had nothing to do with eating," Zigman said. "Their behavior was linked to obtaining the more pleasurable thing."

Ghrelin is not the only factor involved with overeating, however. Here are other reasons some folks just can't stop chowing down:

Genetics: A 2003 study from Imperial College London revealed that people who carried the gene GAD2 were more likely to be obese. GAD2 speeds up the production of a neurotransmitter in the brain, which in turn stimulates us to eat.

Dopamine: In a study published in 2007 in the journal Behavioral Neuroscience, participants with low levels of the neurotransmitter dopamine were more likely to overeat in an attempt to stimulate pleasurable feelings.

Larger portions: Genetics aside, all people are induced to eat more if they are given larger portions. A 2005 Cornell University study found when moviegoers were served stale popcorn in big buckets they ate 34 percent more than those given the same stale popcorn in medium-sized containers.

Creatures of habit: If you always eat a box of Milk Duds at the movie theatre, there's a good chance when you go to see "Avatar" you'll order some, even if you aren't hungry.

Finally, there's the problem of limited willpower. If we ask the brain to do too many things at once, we simply won't have the energy left to either stop ourselves from overeating (ghrelin or no ghrelin) or from imbibing in other activities we find rewarding, according to a 1999 study by Stanford University's Baba Shiv.

Turning grape juice into wine is a stressful business for yeasts. Dr Agustin Aranda from the University of Valencia, Spain has identified the genes in yeast that enable it to respond to stress and is investigating ways to improve yeast performance by modifying its stress response mechanism.

Speaking at the Society for General Microbiology meeting at Heriot-Watt University, Edinburgh, Sept. 9, Dr Aranda described the stresses that wine yeasts undergo in the fermentation process. Industrial wine making involves adding dried yeast starter cultures to the juice; both the drying and reactivating processes cause stress damage to the yeast cells. As the juice is fermented into wine the rising ethanol (alcohol) levels also damage the yeast cells and oxidation causes further damage.

By manipulating the genes that control the stress response of the yeast, the researchers found that they could improve its performance in industrial fermentation processes. They found that a family of enzymes called sirtuins had an important role in controlling wine yeast lifespan.

"Our research aimed to improve winemaking techniques but our findings on oxidative stress and ageing in yeast could be potentially useful in understanding the positive roles of antioxidants present in grapes and grape juice," said Dr Aranda.

Biologists at the University of California, Riverside report new evidence for evolutionary change recorded in both the fossil record and the genomes (or genetic blueprints) of living organisms, providing fresh support for Charles Darwin's theory of evolution.

The researchers were able to correlate the progressive loss of enamel in the fossil record with a simultaneous molecular decay of a gene, called the enamelin gene, that is involved in enamel formation in mammals.

Enamel is the hardest substance in the vertebrate body, and most mammals have teeth capped with it.

Examples exist, however, of mammals without mineralized teeth (e.g., baleen whales, anteaters, pangolins) and of mammals with teeth that lack enamel (e.g., sloths, aardvarks, and pygmy sperm whales). Further, the fossil record documents when enamel was lost in these lineages.

"The fossil record is almost entirely limited to hard tissues such as bones and teeth," said Mark Springer, a professor of biology, who led the study. "Given this limitation, there are very few opportunities to examine the co-evolution of genes in the genome of living organisms and morphological features preserved in the fossil record."

In 2007, Springer, along with Robert Meredith and John Gatesy in the Department of Biology at UC Riverside, initiated a study of enamelless mammals in which the researchers focused on the enamelin gene. They predicted that these species would have copies of the gene that codes for the tooth-specific enamelin protein, but this gene would show evidence of molecular decay in these species.

"Mammals without enamel are descended from ancestral forms that had teeth with enamel," Springer said. "We predicted that enamel-specific genes such as enamelin would show evidence in living organisms of molecular decay because these genes are vestigial and no longer necessary for survival."

Now his lab has found evidence of such molecular "cavities" in the genomes of living organisms. Using modern gene sequencing technology, Meredith discovered mutations in the enamelin gene that disrupt how the enamelin protein is coded, resulting in obliteration of the genetic blueprint for the enamelin protein.

Results of the study appear in the Sept. 4 issue of the open-access journal PLoS Genetics.

Darwin argued that all organisms are descended from one or a few organisms and that natural selection drives evolutionary change. The fossil record demonstrates that the first mammals had teeth with enamel. Mammals without enamel therefore must have descended from mammals with enamel-covered teeth.

"We could therefore predict that nonfunctional vestiges of the genes that code for enamel should be found in mammals that lack enamel," Springer said. "When we made our predictions, however, we did not have sequences for the enamelin gene in toothless and enamelless mammals. Since then my lab worked on obtaining these sequences so we could test our prediction."

Previous studies in evolutionary biology have provided only limited evidence linking morphological degeneration in the fossil record to molecular decay in the genome. The study led by Springer takes advantage of the hardness of enamel and teeth to provide more robust evidence for the linkage.

"The molecular counterpart to vestigial organs is pseudogenes that are descended from formerly functional genes," Springer explained. "In our research we clearly see the parallel evolution of enamel loss in the fossil record and the molecular decay of the enamelin gene into a pseudogene in representatives of four different orders of mammals that have lost enamel."

Broadly, the research involved the following steps: First, Meredith collected the DNA sequences for the enamelin gene in different mammals. Next, the researchers analyzed sequences using a variety of molecular evolutionary methods, including new approaches developed by Springer's group. Finally, the group used the results of their analyses to test previous hypotheses and generate new ones.

"Currently, we are actively engaged in deciphering the evolutionary history of other genes that are involved in enamel formation," Springer said.

Authors of the study are Springer; Meredith, a postdoctoral scholar in Springer's lab; Gatesy, an associate professor of biology; William Murphy of Texas A&M University; and Oliver Ryder of the San Diego Zoo's Institute for Conservation Research, Calif. Meredith, the first author of the research paper, performed all the lab work and, under guidance from Springer and Gatesy, ran most of the computer analyses.

The research was supported in part by an Assembling the Tree of Life grant to Springer and Gatesy from the National Science Foundation.

Scientists at UC Santa Barbara have discovered a potential new drug delivery system. The finding is a biological mechanism for delivery of nanoparticles into tissue. The results are published in the Proceedings of the National Academy of Sciences.

"This work is important because when giving a drug to a patient, it circulates in the blood stream, but often doesn't get into the tissue," said senior author Erkki Ruoslahti, of the Burnham Institute for Medical Research at UCSB. "This is especially true with tumors.

"We believe this method will lead to better, more efficient delivery of drugs," he said. In this study, the scientists used prostate cancer cells as their target, but the method could apply to any type of cell.

The scientists developed a peptide, a small piece of protein that can carry "cargo" for delivery into the cell. The cargo could be a nanoparticle, or even a cell. Riding on the peptide, the cargo gets out of the blood vessel and penetrates the tissue.

The drug is located at one end of the peptide. At the other is the "C terminal," which has the "motif" –– an amino acid sequence including arginine or lysine, that causes the tissue penetration. This terminal has to be open, the researchers found. The strict requirement for the C terminal led the group to coin a new name, the "C-end rule," or CendR, pronounced "sender."

Ruoslahti explained that another exciting aspect of the study is the discovery that viruses appear to use this "CendR" system to get into cells. "It's a natural system," he said. "We're not quite clear what the exact function is, but viruses appear to take advantage of it."

Ongoing research in the Ruoslahti lab is understanding how viruses use this system, and then working to develop inhibitors to prevent viruses from entering the cell.

The two first authors on the paper are Tambet Teesalu and Kazuki N. Sugahara, both of the Burnham Institute for Medical Research at UCSB. Third author Venkata Ramana Kotamraju, of the same institute, made the peptides. Ruoslahti is also affiliated with the Burnham Institute for Medical Research in La Jolla, Calif.

Mammals and many species of birds and fish are among evolution's "winners," while crocodiles, alligators and a reptile cousin of snakes known as the tuatara are among the losers, according to new research by UCLA scientists and colleagues.

"Our results indicate that mammals are special," said Michael Alfaro, a UCLA assistant professor of ecology and evolutionary biology and lead author of the research.

The study, published July 24 in the early online edition of Proceedings of the National Academy of Sciences, also shows that new species emerge nearly as often as they die off.

Alfaro and his colleagues analyzed DNA sequences and fossils from 47 major vertebrate groups and used a computational approach to calculate whether the "species richness" of each group was exceptionally high or low. The research allows scientists to calculate for the first time which animal lineages have exceptional rates of success.

Among the evolutionary winners are most modern birds, including the songbirds, parrots, doves, eagles, hummingbirds and pigeons; a group that includes most mammals; and a group of fish that includes most of the fish that live on coral reefs, said Alfaro, an evolutionary biologist.

A group with the scientific name Boreoeutheria, which consists of many mammals, has diversified about seven times faster than scientists would have expected, beginning about 110 million years ago, Alfaro and his colleagues calculated. The group includes primates and carnivores, as well as bats and rodents. Pouched mammals, such as kangaroos, are not as richly varied as other mammals, Alfaro said.

Modern birds have diversified about nine times faster than expected, starting about 103 million years ago, and the group of fish that live on coral reefs has diversified about eight times faster than expected, he said.

Who are the evolutionary losers?

Crocodiles and alligators are nearly 250 million years old yet have diversified into only 23 species, Alfaro said. They are diversifying a staggering 1,000 times slower than would have been expected. "Their species richness is so low, given how old they are," he said.

The tuatara, which lives in New Zealand and resembles lizards — although it is actually a distant cousin — has only two species. "In the same period of time that produced more than 8,000 species of snakes and lizards, there were only two species of tuatara," Alfaro said.

Why are there not thousands of species of tuataras?

"That is one of the big mysteries about biodiversity," Alfaro said. "Why these evolutionary losers are still around is a very hard thing to explain. They have been drawing inside straights for hundreds of millions of years. It's a real mystery to biologists how there can be any tuataras, given their low rate of speciation. They must have something working for them that has allowed them to persist. In species richness, these are losers, but in another sense, this highlights how unique they are. There are incredibly disparate patterns of species richness."

Tuataras were a bit more diverse in their heyday; there may have been a few dozen species of them, most of which have become extinct, Alfaro said.

In contrast, there are more than 9,000 bird species, more than 5,400 mammal species, approximately 5,500 frog species, some 3,000 snake species and 5,200 lizard species, Alfaro said.

The number of frog species, although it sounds high, is about what Alfaro would expect, given how old they are — approximately 250 million years old.

"Our analysis suggests we should not be surprised to see a group with that many species in that amount of time," Alfaro said.

There are almost 60,000 species of jawed vertebrates. Alfaro and his colleagues report evidence for exceptional diversification rates in nine taxonomic groups of jawed vertebrates. Interestingly, their findings do not coincide with traditional scientific explanations for why there are so many mammals, birds and fish.

"The timing of the rate increases does not correspond to the appearance of key characteristics that have been invoked to explain the evolutionary success of these groups, such as hair on mammals or mammals' well-coordinated chewing ability or feathers on birds," Alfaro said.

"Our results suggest that something more recent is the cause of the biodiversity. It may be that something more subtle explains the evolutionary success of mammals, birds and fish. We need to look for new explanations."

Co-authors on the PNAS paper are Luke Harmon, a professor of biological sciences at the University of Idaho; Francesco Santini, a UCLA postdoctoral scholar in Alfaro's laboratory; Chad Brock, a graduate student of biology at Washington State University; Hugo Alamillo, a graduate student of biology at Washington State University; Alex Dornburg, a former undergraduate in Alfaro's laboratory, now a graduate student at Yale University; Daniel Rabosky, a graduate student of biology at Cornell University; and Giorgio Carnevale, a postdoctoral scholar at Italy's University of Pisa.

The research is funded by the National Science Foundation.

Alfaro's laboratory also studies why some groups of animals have great diversity in their shapes and others do not, even if there are many species. He and his colleagues use DNA sequencing to tease apart evolutionary relationships, analyze the fossil record and conduct sophisticated statistical analysis.

"We are interested in understanding the causes of biodiversity," Alfaro said. "We are trying to understand what explains the staggering diversity of reef fishes and other vertebrates."

"Our analysis can highlight how much higher extinction rates are in the present, compared with the historical rates," he said.

Transcriptomic tests have uncovered the protein composition of venom from the Scorpiops jendeki scorpion. Researchers have carried out the first ever venom analysis in this arachnid, and discovered nine novel poison molecules, never before seen in any scorpion species.

Yibao Ma worked with a team of researchers from Wuhan University, China, to study the sting of S. jendeki, a member of the family Euscorpiidae, which covers Europe, Asia, Africa, and America. He said, "Our work greatly expands the current knowledge of scorpion venoms. We found ten known types and nine novel venom peptides and proteins. These molecules provide a rich, hitherto-unexplored resource for drug development as well as clues into the evolution of the scorpion venom arsenal".

To humans, the sting of scorpions from the Euscorpiidae family tend to be quite mild – about as painful as a mosquito bite. S. jendeki venom has never been studied before. The researchers found that it contains ten known poisons, with markedly diverse modes of action and nine new types of venom peptide, whose biological effects are yet to be determined. The scorpion itself, however, is considered harmless – probably because it cannot deliver enough of the poison to cause any damage to a healthy human. Interestingly, neurotoxins, which are major poisons in the venom of another scorpion species that can kill humans, were not found in the S. jendeki venom.

Ma concludes, "Many types of venom peptides and proteins have been obtained from diverse scorpion species. Some are widely distributed among scorpions from different families, while others, like some of those discovered in our study, appear to be restricted to particular scorpion lineages. The presence of these common and uncommon venom molecules among different lineages reflects the dynamic evolutionary process of the scorpion venom arsenal".

WASHINGTON – An influential geneticist who wears his faith on his sleeve says that as the new director of the National Institutes of Health he won't inject his religious convictions into medical research while pushing cutting-edge science into better bedside care.

"The NIH director needs to focus on science," Dr. Francis Collins told The Associated Press on Monday. "I have no religious agenda for the NIH."

In taking the reins of the NIH, Collins — best known for unraveling the human genetic code — said he wants a practical focus for the nation's premier research agency, that new discoveries may even help save precious health care dollars.

"We should be completely bold about pushing that agenda," Collins said — not just for U.S. health, but for global health, too.

"Here we are at a circumstance where I think our country is seeking maybe to redefine our image a bit in the world, from being the soldier to the world to being perhaps the doctor to the world. I'd like to see that happen," he said, in his first interview before greeting employees of the $30 billion agency.

The Bush administration drew criticism for allowing religious ideology to guide some decision-making, such as curbs on the NIH's funding of research involving embryonic stem cells.

Collins is well-known for finding common ground between belief in God and science, without letting his evangelical Christian beliefs influence his 15 years of research at the NIH. He led the Human Genome Project that, along with a competing private company, mapped the genetic code that he famously called "the book of human life." Remarkably for Washington, Collins' team was ahead of schedule and under budget.

The folksy Collins, who explains the complexities of DNA in language the average person can understand, at the time called it "awe-inspiring to realize that we have caught the first glimpse of our own instruction book, previously known only to God."

He left NIH last year to, among other things, work with Barack Obama's presidential campaign — and to help found the BioLogos Foundation, a Web site formed by scientists who said they want to bridge gaps between the two groups. Collins, 59, said he resigned from the Web site the day before assuming his new job, but was proud of its work.

"I do think the current battle that's going on in our culture between extreme voices is not a productive one," he said. "The chance to play some kind of useful role in that conversation by pointing out the potential harmony was something that seemed to be making some inroads."

In a near-empty office Monday, nothing yet unpacked on his bare desk, an eager Collins outlined his goals for the NIH's next few years. Look for an emphasis on the new field of personalized medicine, which promises to use someone's genes to customize ways for them to stay healthy and fight disease, rather than today's one-size-fits-all advice.

It's already starting. Thousands of breast cancer survivors undergo chemotherapy they don't need in order to be sure the handful with particularly aggressive disease are treated. New genetic tests are cutting back on the unneeded chemo, and saving at least $100 million a year in health care costs, Collins said.

Also look for an emphasis on stem cell research. Under President Barack Obama's new policy on embryonic stem cells, which Collins helped develop, the agency now is deciding which of the 700 known embryonic stem cell batches, or "lines," are eligible for taxpayer-funded research. But Collins also marvels at another option, giving ordinary skin cells the same regenerative properties of embryonic stem cells.

"Clearly there's a lot we don't know, a huge amount we don't know, about the therapeutic uses" of either type, Collins said. "We ought to be thinking of every creative way to speed up the agenda for testing" that.

He is excited by a new law pushing for academic researchers, including NIH scientists, to turn discoveries about rare or neglected diseases into potentially usable drugs by performing the risky, early-stage development that can deter drug company investment.

And new technologies — high-capacity computing, nanotechnology — make it a powerful time to finally broadly study what makes different diseases arise.

"This really does seem like a synthetic moment," he joked.

Collins' vision is to knock down a bit of the NIH's ivory-tower reputation in a bid for more openness with scientists and the public. So the gene hunter who last spring posed in cool shades as part of GQ magazine's campaign to bring celebrity to science already is looking forward to his invitation to appear on the satirical television show "The Colbert Report."

After a standing ovation from a community that he dubbed "the NIH tribe," he told employees, "It's great to be home again."

A South Korean biotechnology firm will early next year open a centre capable eventually of producing up to 1,000 cloned dogs annually, a company executive said Friday.

"We need this new facility to turn dog cloning services into a full-fledged business," Cho Seong-Ryul, director of RNL Bio, told AFP.

The centre in Yongin city south of Seoul will cost some five million dollars and focus on cloning pets, working dogs and endangered species including wolves.

RNL Bio is one of the world's few companies operating dog cloning as a business. Another is San Francisco-based BioArts, which is involved in a patents dispute with the Korean firm.

RNL Bio says it successfully cloned puppies of a retriever trained to sniff out cancer cells in humans. Four puppies are currently being trained in South Korea and Japan.

Last year it arranged to re-create a pitbull terrier for a US woman in what it claimed was the world's first commercial cloning.

ZhangTS1038940 wrote:Hwang made some big mistakes, but I dont think this should be the reason that get him involved in endless attacks.
I never doubt Hwang's ability and he can contribute to the field. Why not give him a chance?
It seems that some South Korean are still believe in Hwang and fund him. That's really good.

MichaelTS863182 wrote:
Should parents/mothers be allowed to have abortions if their child is positive for certain disorders?

Which disorders? Under what socio-economic circumstances?

Why would abortions be okay?

ScottICN000308650 wrote:Are you a Cardinals or Steelers fan? Will you be feeling good come Monday? It could depend directly on the outcome of your team's performance in the Super Bowl this Sunday.If your team wins the Super Bowl you could experience a testosterone boost from vicariously participating in the your team's Super Bowl victory.This effect has been known about for quite some time -- a 1998 paper by University of Utah researchers Berhardt et al. demonstrated that beyond its effects on mood and self esteem, watching your team win not only boosts your testosterone level, but also decreases the levels of circulating testosterone in the fans of the losing team. Because testosterone, long linked to violence, now appears to have much more to do with social dominance it's hardly surprising that these changes in hormone levels can affect not only a fan's post game euphoria (or depression) but also their future behavior. Indeed, competitors who lose a contest and subsequently experience a drop in their testosterone levels are less likely to challenge their foe again, according to a paper in the December 2006 issue of Hormones and Behavior, by Robert Josephs and Pranjal Mehta.