Tuesday, January 15, 2008

Making Science More Better For You on 01/15/08

Headlines of the day
Court Won't Accept Chimp As Person (breitbart)

Hilton suspected in 3rd disappearance (CNN/WSOC)
No. Not that one. However, it is a fine example of how a name can sell a story.

Frat gets in trouble for hiring midget wrestling company (The obscure Store)

Precocious little devils. We wonder what prom night was like.
Dinosaurs 'grew fast, bred young'
By Helen Briggs
Science reporter, BBC News

Dinosaurs bred as early as age eight, long before they reached adult size, fossil evidence suggests.

Although they were descended from reptiles, and evolved into birds, dinosaurs grew fast and bred young, much like the mammals of today.

Researchers at the University of California found hallmark "egg-making" tissue in two juvenile females.

They say early sexual maturity was needed for survival, so females could lay eggs before becoming prey.

Calcium-rich medullary bone, which, in birds, is used to produce egg shells, was found inside the fossilised shin-bones of two specimens: the meat-eating Allosaurus and the plant-eater Tenontosaurus.


Sarah Werning and Andrew Lee of the University of California (UC), Berkeley, deduced from growth rings inside the bone that the two females were aged eight and 10, very young for dinosaurs, which lived to about 30.

Medullary bone has previously been found in a female Tyrannosaurus rex, and the scientists confirmed this finding, putting her age at 18.

"We were lucky to find these female fossils," said Sarah Werning. "Medullary bone is only around for three to four weeks in females who are reproductively mature, so you'd have to cut up a lot of dinosaur bones to have a good chance of finding this."

Growth clues

Studies of the tell-tale growth rings in dinosaur bones have revealed much about the way they grew.

Dinosaurs grew faster than present-day reptiles and had only a limited lifespan as adults before they fell victim to predator attack.

Like many groups, Tenontosaurus, which lived in North America during the Early Cretaceous period, 125 to 105 million years ago, would have had to reproduce young to ensure survival of the species.


Egg-laying tissue and growth rings were found in bone

More details
"These were prey dinosaurs, so they were probably taken out when really young and small, or when old," Sarah Werning explained. "So, if you don't reproduce early, you lose your chance."

The discovery adds weight to the idea that dinosaurs were more like birds than reptiles. It also suggests that the reproductive strategy of modern birds is an ancient one, dating back some 200 million years, to when dinosaurs first evolved.

"This shows us beyond any doubt how fast dinosaurs grow," said Kevin Padian, a professor at UC Berkeley's Museum of Palaeontology, who was the students' advisor.

"They're growing as fast as big birds and big mammals," he told the BBC.

"To do this you can't have the metabolism of a crocodile; you need to have the metabolism more of a bird or a mammal."


"This shows us beyond any doubt how fast dinosaurs grow," said Kevin Padian, a professor at UC Berkeley's Museum of Palaeontology, who was the students' advisor. Grow? Present tense? Is there something he’s not sharing with us? It’s like John Derek said in “Knock on Any Door,” “Grow fast, breed young and leave a nice pile of bones in a convenient location for a grad student to find.”


We think we can help you live longer. The bad news is that you are now yeast.

Life Expectancy Of Yeast Extended To 800 In Yeast Years, No Apparent Side Effects

ScienceDaily (Jan. 14, 2008) — Biologists have created baker's yeast capable of living to 800 in yeast years without apparent side effects.

The basic but important discovery, achieved through a combination of dietary and genetic changes, brings science closer to controlling the survival and health of the unit of all living systems: the cell.

"We're setting the foundation for reprogramming healthy life," said study leader Valter Longo of the University of Southern California.

The study is scheduled to appear in the Jan. 25 issue of the journal PLoS Genetics. A companion study, showing that the same genetic changes in yeast reverse the course of an accelerated aging syndrome, appears in the Jan. 14 issue of the Journal of Cell Biology.

Longo's group put baker's yeast on a calorie-restricted diet and knocked out two genes, RAS2 and SCH9, that promote aging in yeast and cancer in humans.

"We got a 10-fold life span extension that is, I think, the longest one that has ever been achieved in any organism," Longo said. In 2005, the same research group reported a five-fold life span extension in the journal Cell. Normal yeast organisms live about a week.

"I would say 10-fold is pretty significant," said Anna McCormick, chief of the genetics and cell biology branch at the National Institute on Aging and Longo's program officer.

The NIA funds such research in the hope of extending healthy life span in humans through the development of drugs that mimic the life-prolonging techniques used by Longo and others, McCormick added.

Baker's yeast is one of the most studied and best understood organisms at the molecular and genetic level. Remarkably in light of its simplicity, yeast has led to the discovery of some of the most important genes and pathways regulating aging and disease in mice and other mammals.

A study recently published in Cell (Issue 130, pages 247-258, 2007) reported that a mouse with a gene mutation first identified by Longo's group lived 30 percent longer than normal and also was protected against heart and bone diseases without apparent side effects.

Longo's group next plans to further investigate life span extension in mice, and also is studying a human population in Ecuador with mutations analogous to those described in yeast.

"People with two copies of the mutations have very small stature and other defects," he said. "We are now identifying the relatives with only one copy of the mutation, who are apparently normal. We hope that they will show a reduced incidence of diseases and an extended life span."

Longo cautioned that, as in the Ecuador case, longevity mutations tend to come with severe growth deficits and other health problems. Finding drugs to extend the human life span without side effects will not be easy, he said.

An easier goal, Longo added, would be to use the knowledge gained about life span "in a fairly limited way, to reprogram disease prevention."

In the study appearing in the Jan. 14 Journal of Cell Biology, Longo's group developed a yeast model for human Werner/Bloom syndromes, incurable diseases that prematurely age, increase cancer incidence and eventually kill their victims.

The same mutations that play a central role in the 10-fold life span extension reversed the premature aging process, the researchers found.

Longo suggested that although a very simple system was used in his studies, existing drugs targeting analogous anti-aging pathways in humans -- specifically the pathway involving Insulin Growth Factor, or IGF-1 -- should be considered for testing on Werner/Bloom patients.

"Maybe it will do nothing, but having nothing else, I think it's certainly a good thing to try," Longo said.

In the PLOS Genetics study, Longo's group identified a major overlap between the genes previously implicated in life span regulation for yeast and mammals and those involved in life span extension under calorie restriction.

"We identified three transcription factors ... that are very important for the effect of calorie restriction, but at the same time, we also showed that it's not enough because even without these transcription factors, calorie restriction can still extend life span a little bit," Longo said.

"So that means that we've identified a lot of the key players in the calorie restriction effect but not all of them."

Calorie restriction -- in practice, controlled starvation -- has long been shown to reduce disease and extend life span in species from yeast to mice.

Scientists believe that a nutrient shortage kicks organisms into a maintenance mode, enabling them to re-direct energy from growth and reproduction into anti-aging systems until the time they can feed and breed again.

Calorie restriction is now being tested by other researchers on primates and even humans, Longo said.

Longo has been studying aging at the cellular level for 15 years and has published articles in the nation's leading scientific journals. His laboratory developed a simple and inexpensive method for measuring the true chronological life span of yeast. Previously, scientists used the number of a yeast cell's offspring as a proxy for its age.

The so-called replicative life span technique remains in use, and the NIA's McCormick said that Longo's method was controversial at first. However, she said, the scientific community now appears to accept its usefulness. She said Longo's "stationary phase" method is particularly applicable to studies of cells that do not divide for most of their life, such as those in the brain or in muscle.

"Stationary phase I think of as normal cell survival," McCormick said. She added that NIA funds both stationary phase and replicative life span research.

The studies were funded by NIA (part of the National Institutes on Health) and the American Federation for Aging Research.

Yeast years? Does this have anything to do with the Mayan calender?


Does Vincent Price know about this?

Beating Heart Created In Laboratory: Method May Revolutionize How Organ Tissues Are Developed

ScienceDaily (Jan. 14, 2008) — University of Minnesota researchers have created a beating heart in the laboratory.

By using a process called whole organ decellularization, scientists from the University of Minnesota Center for Cardiovascular Repair grew functioning heart tissue by taking dead rat and pig hearts and reseeding them with a mixture of live cells.

"The idea would be to develop transplantable blood vessels or whole organs that are made from your own cells," said Doris Taylor, Ph.D., director of the Center for Cardiovascular Repair, Medtronic Bakken professor of medicine and physiology, and principal investigator of the research.

Nearly 5 million people live with heart failure, and about 550,000 new cases are diagnosed each year in the United States. Approximately 50,000 United States patients die annually waiting for a donor heart.

While there have been advances in generating heart tissue in the lab, creating an entire 3-dimensional scaffold that mimics the complex cardiac architecture and intricacies, has always been a mystery, Taylor said.

It seems decellularization may be a solution -- essentially using nature's platform to create a bioartifical heart, she said.

Decellularization is the process of removing all of the cells from an organ -- in this case an animal cadaver heart -- leaving only the extracellular matrix, the framework between the cells, intact.

After successfully removing all of the cells from both rat and pig hearts, researchers injected them with a mixture of progenitor cells that came from neonatal or newborn rat hearts and placed the structure in a sterile setting in the lab to grow.

The results were very promising, Taylor said. Four days after seeding the decellularized heart scaffolds with the heart cells, contractions were observed. Eight days later, the hearts were pumping.

"Take a section of this 'new heart' and slice it, and cells are back in there," Taylor said. "The cells have many of the markers we associate with the heart and seem to know how to behave like heart tissue."

"We just took nature's own building blocks to build a new organ," said Harald C. Ott, M.D., co-investigator of the study and a former research associate in the center for cardiovascular repair, who now works at Massachusetts General Hospital. "When we saw the first contractions we were speechless."

Researchers are optimistic this discovery could help increase the donor organ pool.

In general, the supply of donor organs is limited and once a heart is transplanted, individuals face life-long immunosuppression, often trading heart failure for high blood pressure, diabetes, and kidney failure, Taylor said.

Researchers hope that the decellularization process could be used to make new donor organs. Because a new heart could be filled with the recipient's cells, researchers hypothesize it's much less likely to be rejected by the body. And once placed in the recipient, in theory the heart would be nourished, regulated, and regenerated similar to the heart that it replaced.

"We used immature heart cells in this version, as a proof of concept. We pretty much figured heart cells in a heart matrix had to work," Taylor said. "Going forward, our goal is to use a patient's stem cells to build a new heart."

Although heart repair was the first goal during research, decellularization shows promising potential to change how scientists think about engineering organs, Taylor said. "It opens a door to this notion that you can make any organ: kidney, liver, lung, pancreas -- you name it and we hope we can make it," she said.

Researchers of the Center for Cardiovascular Repair team were assisted in their study by researchers from the University of Minnesota Department of Biomedical Engineering, who helped analyze data.

The research will be published online in the January 13 issue of Nature Medicine. The study was funded by the Medtronic Foundation Endowment and a faculty research development grant from the University of Minnesota Academic Health Center.


We know when we’ve had enough. It’s when there’s nothing left.

Overweight People May Not Know When They've Had Enough

ScienceDaily (Jan. 14, 2008) — Researchers at the U.S. Department of Energy's Brookhaven National Laboratory have found new clues to why some people overeat and gain weight while others don't. Examining how the human brain responds to "satiety" messages delivered when the stomach is in various stages of fullness, the scientists have identified brain circuits that motivate the desire to overeat. Treatments that target these circuits may prove useful in controlling chronic overeating, according to the authors.

"By simulating feelings of fullness with an expandable balloon we saw the activation of different areas of the brain in normal weight and overweight people," said lead author Gene-Jack Wang of Brookhaven Lab's Center for Translational Neuroimaging. The overweight subjects had less activation in parts of the brain that signal satiety in normal weight subjects. The overweight subjects were also less likely than normal weight subjects to report satiety when their stomachs were moderately full. "These findings provide new evidence for why some people will continue to eat despite having eaten a moderate-size meal," said Wang.

Wang and colleagues studied the brain metabolism of 18 individuals with body mass indices (BMI) ranging from 20 (low/normal weight) to 29 (extremely overweight/borderline obese). Each study participant swallowed a balloon, which was then filled with water, emptied, and refilled again at volumes that varied between 50 and 70 percent. During this process, the researchers used functional magnetic resonance imaging (fMRI) to scan the subjects' brains. Subjects were also asked throughout the study to describe their feelings of fullness. The higher their BMI, the lower their likelihood of saying they felt "full" when the balloon was inflated 70 percent.

One notable region of the brain - the left posterior amygdala - was activated less in the high-BMI subjects, while it was activated more in their thinner counterparts. This activation was turned "on" when study subjects reported feeling full. Subjects who had the highest scores on self-reports of hunger had the least activation in the left posterior amygdala.

"This study provides the first evidence of the connection of the left amygdala and feelings of hunger during stomach fullness, demonstrating that activation of this brain region suppresses hunger," said Wang. "Our findings indicate a potential direction for treatment strategies - be they behavioral, medical or surgical -- targeting this brain region."

The scientists also looked at a range of hormones that regulate the digestive system, to see whether they played a role in responding to feelings of fullness. Ghrelin, a hormone known to stimulate the appetite and cause short-term satiety, showed the most relevance. Researchers found that individuals who had greater increases in ghrelin levels after their stomachs were moderately full also had greater activation of the left amygdala. "This indicates that ghrelin may control the reaction of the amygdala to satiety signals sent by the stomach," said Wang.

The study is published online and will appear in the February 15, 2008 issue of NeuroImage.


Replaced by the younger, thinner one. Sound familiar?

Older Arctic Sea Ice Replaced By Young, Thin Ice

ScienceDaily (Jan. 13, 2008) — A new study by University of Colorado at Boulder researchers indicates older, multi-year sea ice in the Arctic is giving way to younger, thinner ice, making it more susceptible to record summer sea-ice lows like the one that occurred in 2007.

The team used satellite data going back to 1982 to reconstruct past Arctic sea ice conditions, concluding there has been a nearly complete loss of the oldest, thickest ice and that 58 percent of the remaining perennial ice is thin and only 2-to-3 years old, said the lead study author, Research Professor James Maslanik of CU-Boulder's Colorado Center for Astrodynamics Research. In the mid-1980s, only 35 percent of the sea ice was that young and that thin according to the study, the first to quantify the magnitude of the Arctic sea ice retreat using data on the age of the ice and its thickness, he said.

"This thinner, younger ice makes the Arctic much more susceptible to rapid melt," Maslanik said. "Our concern is that if the Arctic continues to get kicked hard enough toward one physical state, it becomes increasingly difficult to reestablish the sea ice conditions of 20 or 30 years ago."

A September 2007 study by CU-Boulder's National Snow and Ice Data Center indicated last year's average sea ice extent minimum was the lowest on record, shattering the previous September 2005 record by 23 percent. The minimum extent was lower than the previous record by about 1 million square miles -- an area about the size of Alaska and Texas combined.

The new study by Maslanik and his colleagues appears in the Jan. 10 issue of Geophysical Research Letters. Co-authors include CCAR's Charles Fowler, Sheldon Drobot and William Emery, as well as Julienne Stroeve from CU-Boulder's Cooperative Institute for Research in Environmental Sciences and Jay Zwally and Donghui Yi from NASA's Goddard Space Flight Center in Greenbelt, Md.

The portion of ice more than five years old within the multi-year Arctic icepack decreased from 31 percent in 1988 to 10 percent in 2007, according to the study. Ice 7 years or older, which made up 21 percent of the multi-year Arctic ice cover in 1988, made up only 5 percent in 2007, the research team reported.

The researchers used passive microwave, visible infrared radar and laser altimeter satellite data from the National Oceanic and Atmospheric Administration, NASA and the U.S. Department of Defense, as well as ocean buoys to measure and track sections of sea ice.

The team developed "signatures" of individual ice sections roughly 15 miles square using their thickness, roughness, snow depth and ridge characteristics, tracking them over the seasons and years as they moved around the Arctic via winds and currents, Emery said. "We followed the ice in sequential images and track it back to where it had been previously, which allowed us to infer the relative ages of the ice sections."

The replacement of older, thicker Arctic ice by younger, thinner ice, combined with the effects of warming, unusual atmospheric circulation patterns and increased melting from solar radiation absorbed by open waters in 2007 all have contributed to the phenomenon, said Drobot. "These conditions are setting the Arctic up for additional, significant melting because of the positive feedback loop that plays back on itself."

"Taken together, these changes suggest that the Arctic Ocean is approaching a point where a return to pre-1990s ice conditions becomes increasingly difficult and where large, abrupt changes in summer ice cover as in 2007 may become the norm," the research team wrote in Geophysical Research Letters.

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