A new study finds that following minor spinal cord injury, rats that had to use impaired limbs showed full recovery due to increased growth of healthy nerve fibers and the formation of new nerve cell connections. Published in the September 17 issue of The Journal of Neuroscience, these findings help explain how physical therapy advances recovery, and support the use of rehabilitation therapies that specifically target impaired limbs in people with brain and spinal cord injuries.

“After brain and spinal cord injuries, exercise-based physical therapy is the primary rehabilitative strategy in use today,” said Stephen Strittmatter, MD, PhD, at Yale University School of Medicine, an expert unaffiliated with the study. “These therapies are so beneficial to patients, but the anatomical and molecular bases of improvement have not been clear,” Strittmatter said.

The researchers, led by Irin Maier and senior researcher Martin Schwab, PhD at the University of Zurich and the Swiss Federal Institute of Technology, tested rats with minor surgical injuries to the spinal cord that impaired the use of one forelimb. Slings were placed on the rats that restricted the use of either the injured or uninjured limb. After three weeks, researchers removed the slings and tested the rats on an elevated horizontal ladder.

Rats that relied on their impaired limb because use of their unimpaired limb was restricted showed complete functional recovery: they negotiated the ladder as well as rats that had not been injured. In contrast, rats that had not worn slings and those that wore slings restricting the use of the injured limb performed poorly, showing difficulty grasping and negotiating the horizontal rungs of the ladder.

In all of the rats, healthy nerve fibers, or axons, grew into injured regions of the spinal cord. However, rats that relied on their injured limb showed the most extensive nerve growth. “The study shows that when the axons that remain after a spinal cord injury are more active — because the animal is forced to use them — they grow more. This seems to help the animal recover more control of their movements,” said John Martin, PhD, at Columbia University, an expert unaffiliated with the study.

These nerve fibers formed more connections, or synapses, in rats relying on their injured limb compared with those relying on their uninjured limb. This finding suggests that forced limb use encourages healthy nerve cells to form new synapses with cells affected by spinal cord injury, perhaps rerouting and rewiring damaged spinal cord circuits that are important for movement.

Using gene chip technology, the researchers found that forced limb use turned on or turned off genes known to be involved in nerve fiber growth and synapse formation in the spinal cord. Knowing which genes are involved in recovery from spinal cord injury may help researchers develop new drug treatments.

“This study shows that a behavioral approach is remarkably effective in promoting both axon growth and recovery after injury,” said Martin. “We know that physical therapy is effective after brain and spinal injuries. But these new results suggest that a more aggressive therapy, in which the unimpaired limb is prevented from use and the impaired limb is forced to be used, might lead to new neural connections,” he said.

Higher levels of urinary Bisphenol A (BPA), a chemical compound commonly used in plastic packaging for food and beverages, is associated with cardiovascular disease, type 2 diabetes and liver-enzyme abnormalities, according to a study in the September 17 issue of JAMA. This study is being released early to coincide with a Food and Drug Administration (FDA) hearing on BPA.

BPA is one of the world’s highest production–volume chemicals, with more than two million metric tons produced worldwide in 2003 and annual increase in demand of 6 percent to 10 percent annually, according to background information in the article. It is used in plastics in many consumer products. “Widespread and continuous exposure to BPA, primarily through food but also through drinking water, dental sealants, dermal exposure, and inhalation of household dusts, is evident from the presence of detectable levels of BPA in more than 90 percent of the U.S. population,” the authors write. Evidence of adverse effects in animals has created concern over low-level chronic exposures in humans, but there is little data of sufficient statistical power to detect low-dose effects. This is the first study of associations with BPA levels in a large population, and it explores “normal” levels of BPA exposure.

David Melzer, M.B., Ph.D., of Peninsula Medical School, Exeter, U.K., and colleagues examined associations between urinary BPA concentrations and the health status of adults, using data from the National Health and Nutrition Examination Survey (NHANES) 2003-2004. The survey included 1,455 adults, age 18 through 74 years, with measured urinary BPA concentrations.

The researchers found that average BPA concentrations, adjusted for age and sex, appeared higher in those who reported diagnoses of cardiovascular diseases and diabetes. A 1-Standard Deviation (SD) increase in BPA concentration was associated with a 39 percent increased odds of cardiovascular disease (angina, coronary heart disease, or heart attack combined) and diabetes.

When dividing BPA concentrations into quartiles, participants in the highest BPA concentration quartile had nearly three times the odds of cardiovascular disease compared with those in the lowest quartile. Similarly, those in the highest BPA concentration quartile had 2.4 times the odds of diabetes compared with those in the lowest quartile.

In addition, higher BPA concentrations were associated with clinically abnormal concentrations for three liver enzymes. No associations with other diagnoses were observed.

“Using data representative of the adult U.S. population, we found that higher urinary concentrations of BPA were associated with an increased prevalence of cardiovascular disease, diabetes, and liver-enzyme abnormalities. These findings add to the evidence suggesting adverse effects of low-dose BPA in animals. Independent replication and follow-up studies are needed to confirm these findings and to provide evidence on whether the associations are causal,” the authors conclude. “Given the substantial negative effects on adult health that may be associated with increased BPA concentrations and also given the potential for reducing human exposure, our findings deserve scientific follow-up.”

Hypoglycemic seizures occur in several diseases, particularly diabetes. In rats (and humans) seizures are induced by excess insulin, which stimulates glucose uptake throughout the body, reducing the amount available to neurons. The substantia nigra pars reticulata (SNR) has been implicated in seizure control: hyperpolarization of SNR neurons is anticonvulsant, whereas increased firing in SNR is proconvulsant. To further investigate the mechanism of hypoglycemic seizures, Velíšek et al. injected insulin into rats that had fasted overnight. Fasting doubled the probability that insulin would induce a seizure and decreased the latency to seizure. But differences in blood glucose levels did not explain the difference. Instead, the proconvulsant effect of fasting was associated with decreased expression of K_ATP channels specifically in the SNR. These channels normally open (causing hyperpolarization) only when ATP levels are low (e.g., during hypoglycemia). Decreased K_ATP expression prevents hyperpolarization of SNR neurons during hypoglycemia, and thus is proconvulsant.

In the nucleus, DNA wraps around histone proteins, which pack the DNA and makes it less accessible for transcription. Many transcriptional activators promote histone acetylation, which opens the chromatin structure and helps recruit transcription machinery to the newly accessible genes. Conversely, some gene repressors promote deacetylation of histones. Because drug dependence is mediated partly by changes in gene expression, inhibitors of histone acetylation and deacetylation might prevent the development of drug dependence. Romieuet al. support this hypothesis by showing that administering histone deacetylase inhibitors shortly before giving rats access to cocaine reduced cocaine self-administration and decreased the number of times a rat poked its nose in a hole to receive a dose of cocaine. When rats receive cocaine daily, their response to a dose increases over time. This increased responsiveness, called sensitization, is thought to promote dependence. Cocaine sensitization is prevented by histone deacetylase inhibitors, suggesting inhibitors may effectively reduce dependence.

In contrast to Barrette et al., Horn al. report that macrophages may hinder regeneration in the spinal cord of rats by promoting axonal retraction. Central nervous system axons normally retract from a site of injury. To examine the role of macrophages in this process, Horn et al. specifically targeted phagocytic cells with toxin enclosed in liposomes. Depleting macrophages after a spinal cord crush did not affect the initial retraction of injured axons, but prevented later retraction that normally occurs after macrophages invade the spinal cord. In vitro studies on dorsal root ganglion neurons revealed that when an activated macrophage contacts a dystrophic axon, the macrophage adheres to and tugs on the axon, pulling it from the substrate and causing retraction. Together, these two studies suggest that whether myeloid cells help or hinder axon regeneration may depend on what type of myeloid cells are present (i.e., what subtypes of macrophages and granulocytes) and where and how macrophages are activated (e.g., by peripheral or CNS cues). Many macrophages (green) but few astrocytes (blue) were present at a lesion site 7 d after nerve crush (left). Treatment with toxic liposomes greatly reduced the number of macrophages, but astrocytes remained.

The role of macrophages in recovery from nerve injury is controversial. Some studies show that macrophages improve regeneration, but others show the opposite effect. This week, each side of the controversy gains support. After crushing a peripheral nerve in mice, Barrette et al. locally depleted myeloid white blood cells (both granulocytes and macrophages) that expressed a specific protein. This reduced axonal regeneration and functional recovery. Depletion of myeloid cells in peripheral nerve grafts, which normally permit some regeneration of spinal axons, rendered the grafts unable to support such growth. Additional experiments suggested that myeloid cells normally enhance regeneration by clearing myelin debris (which is likely to contain growth-inhibiting molecules), secreting growth-promoting neurotrophic factors (likely from granulocytes, rather than macrophages), and stimulating the growth of new blood vessels, which axons often grow along as they regenerate.

In infancy, genes are the key influence on a child’s ability to deal with stress. But as early as 6 months of age, parenting plays an important role in changing the impact of genes that may put infants at risk for responding poorly to stress.That’s the message from a new study by researchers at the University of North Carolina-Chapel Hill, Pennsylvania State University, the University of North Carolina-Greensboro, and North Carolina State University. It appears in the September/October 2008 issue of the journal Child Development.

The researchers looked at 142 infants who had been placed in a stressful situation—being separated from their mothers—when they were 3, 6, and 12 months old. They measured infants’ heart rates while they were exposed to the stressor, isolating a cardiac response called vagal tone. Vagal tone acts like a brake on the heart when the body is in a calm state, but during a challenging situation, this brake is withdrawn, allowing heart rate to increase so the body can actively deal with the challenge.

They also collected DNA to determine which form of a dopamine receptor gene the infants carried; specific forms of this gene are related to problems in adolescence and adulthood including aggression, substance abuse, and other risky behaviors. To assess the mothers’ behavior as high or low in sensitivity, they also videotaped the mothers and their infants playing together for 10 minutes when the babies were 6 months old.

Both genes and parenting were found to be important to the infants’ development of the way in which the brain helps regulate cardiac responses to stress. At 3 and 6 months old, those infants with the form of the dopamine gene associated with later risky behaviors did not display an effective cardiac response to the stressor (a decrease in vagal tone which takes the brake off the heart so it can respond appropriately), while those infants with the non-risk version of the gene did. At these early ages, the researchers found, it didn’t appear to matter whether mothers were sensitive or not.

However, by the time the infants were 12 months old, the pattern changed. Infants with the risk form of the gene who also had mothers who were highly sensitive now showed the expected cardiac response while they were exposed to the stressful situation. Those infants with the risk form of the gene who had insensitive mothers continued to show the ineffective cardiac response to the stressor. These findings suggest that although genes play a role in the development of physiological responses to stress, environmental experience (such as mothers’ sensitive care-giving behavior) can have a strong influence, enough to change the effect that genes have on physiology very early in life. The researchers suggest this may be because of the cumulative effect on infants of exposure to their mothers’ behavior.

“Our findings provide further support for the notion that the development of complex behavioral and physiological responses is not the result of nature or nurture, but rather a combination of the two,” says Cathi Propper, research scientist at the University of North Carolina-Chapel Hill and the study’s lead author. “They also illustrate the importance of parenting not just for the development of children’s behavior, but for the underlying physiological mechanisms that support this behavior.

“Lastly, infancy is an important time for developing behavioral and biological processes. Although these processes will continue to change over time, parenting can have important positive effects even when children have inherited a genetic vulnerability to problematic behaviors.”

Scientists have discovered a compound that could lead to new treatments for heart attacks as well as methods to protect hearts during open heart surgery and other situations in which blood flow to the heart is interrupted.In the process, the researchers uncovered cellular mechanisms that help explain how alcohol can protect against heart attack damage. In addition, they have uncovered a possible key to reducing chest pain and the heart attack damage among millions of people of East Asian descent who are genetically unable to respond to nitroglycerin and other cardiovascular treatments.

A research team of scientists at Stanford and Indiana universities schools of medicine reports in the Sept. 12 issue of the journal Science that by jump-starting a particular enzyme they were able to significantly reduce the amount of cell death caused by lack of blood flow to the heart.

The group, led by Daria Mochly-Rosen, Ph.D., professor of chemical and systems biology at Stanford, found that administering a compound called Alda-1 activated the enzyme, reducing heart muscle damage in experiments involving rats.

First, however, the researchers studied various mechanisms known to provide cardioprotection to heart muscle cells, including the use of ethanol, to better understand how those mechanisms worked. That work revealed a cellular signaling system that activated a particular enzyme called ALDH2.

“The idea was to find a small molecule that could bypass the signaling process and activate the enzyme directly,” said Thomas D. Hurley, Ph.D., professor of biochemistry and molecular biology and director of the Center for Structural Biology at the IU School of Medicine. Hurley’s research has included years of study of the ALDH2 enzyme.

Although the Alda-1 molecule reduced heart tissue damage in laboratory tests, years of work will be necessary to refine the compound into a version that would be potentially effective and safe for human use, Dr. Hurley said. That benefit could extend to about 40 percent of people of East Asian descent who carry a mutated form of the ALDH2 enzyme, which puts them at increased risk of cardiovascular damage.

Oliver Söhnlein and colleagues, at the Karolinska Institutet, Sweden, have identified a new function for a number of proteins secreted by human immune cells known as neutrophils or PMNs: they enhance the uptake of bacteria by other immune cells (known as macrophages) that are capable of destroying the microbes.

In the study, proteins secreted by human PMNs, specifically HBP and HNP1-3, were found to enhance the in vitro ability of human and mouse macrophages to take up bacteria coated in the immune molecule IgG. Mechanistically, HBP and HNP1-3 activated the macrophages to secrete soluble factors that, in turn, induced the macrophages to express proteins to which IgG can bind (CD32 and CD64). The authors therefore suggest that HBP and HNP1–3 secreted by PMNs have a role in clearing bacterial infections.

Individuals with a number of clinical conditions, including pneumonia, and those treated by mechanical ventilation for a prolonged period of time are at risk of acute lung injury, a life-threatening disorder for which there is no treatment. It is hoped that understanding the natural processes by which acute lung injury spontaneously resolves in some individuals might provide new therapeutic targets. Thus, Holger Eltzschig and colleagues, at the University of Colorado Health Sciences Center, Denver, suggest that their observation in mice with ventilator-induced lung injury (VILI) implicate the protein A2BAR as a potential therapeutic target for acute lung injury.

In the study, mice lacking A2BAR were found to have reduced survival time and more severe VILI, when compared with normal mice. Consistent with this, normal mice treated with an A2BAR antagonist exhibited more severe lung damage than untreated mice, whereas an A2BAR agonist attenuated the severity of VILI. Further analysis revealed that one way in which the A2BAR agonists helped was by enhancing the clearance of fluid in the lungs (i.e., they helped dry out the lungs). These data indicate that agonists of A2BAR are likely to be part of the natural mechanism by which acute lung injury spontaneously resolves and might make good therapeutics.

T. rex and Triceratops: In the popular imagination, dinosaurs are extraordinary reptiles that ruled the world for over 160 million years. But Steve Brusatte, a doctoral student at Columbia University who is an affiliate of the American Museum of Natural History, and colleagues are challenging this idea with new fossil data and math. By comparing early dinosaurs to their competitors, the crurotarsan ancestors to crocodiles, they have found that dinosaurs were not “superior,” as has long been thought. Rather, crurotarsans were the more successful group during the 30 million years they overlapped until the devastating mass extinction 200 million years ago, an event that dinosaurs weathered successfully.

“For a long time it was thought that there was something special about dinosaurs that helped them become more successful during the Triassic, the first 30 million years of their history, but this isn’t true,” says Brusatte. “If any of us were standing by during the Triassic and asked which group would rule the world for the next 130 million years, we would have identified the crurotarsans, not dinosaurs.”

Both dinosaurs and crurotarsans evolved and filled some of the same niches after a massive extinction event that occurred at the end of the Permian (250 million years ago). Of the crurotarsan group, crocodilians are the only living members. But in the Triassic, crurotarsans were amazingly diverse—from giant carnivorous rauisuchians to long–snouted, flesh eating phytosaurs to herbivorous armored aetosaurs—and they have often been mistaken for dinosaurs in the fossil record, the animals that they probably competed with for the same resources. Both groups survived an extinction event 228 million years ago, but only a few crurotarsans—the crocodiles—squeaked through a period of rapid global warming at the end of the Triassic 200 million years ago. Dinosaurs faired better during the latter extinction: most types of dinosaurs survived until an asteroid ended their dominance 65 million years ago. It is because of this stroke of luck that dinosaurs were assumed to be the better competitors.

Brusatte and colleagues tested this assumption by measuring the evolution in both competing groups. Based on a database of 437 features of the skeletons of 64 species of dinosaurs and crurotarsans, as well as a new phylogenetic tree of these groups, they performed two calculations to look at the evolutionary pattern. The first measurement is of the disparity, or the known range of different body plans, of the two groups. Disparity is a reliable indicator of the different lifestyles, diets, and habitats of a group of animals. Remarkably, Brusatte and colleagues found that crurotarsans had twice the disparity of dinosaurs: They were exploring twice the range of body plans as early dinosaurs. “With this information, it’s difficult to argue that dinosaurs were ’superior’ during the Triassic. They just lucked out when the crurotarsans were hit hard at the end Triassic extinction,” says Brusatte.

The team also measured the rate of evolution in both dinosaurs and crurotarsans to see if dinosaurs were diversifying into new species at higher rates, as may be expected if they had special abilities or were outcompeting their rivals. But the comparison showed that the two groups were evolving at the same rate over the 30 million years that they overlapped.

“Many people like to think that evolution is progressive: mammals are better than dinosaurs because they came later. This is like progressive improvements in car technology—a Ford Taurus is demonstrably better than a Model T,” says coauthor Michael Benton, a paleontologist at the University of Bristol in the United Kingdom. “So it may be hard for us to accept that dinosaurs achieved their dominant position on earth largely by chance, just as mammals did when the dinosaurs were later wiped out by a meteorite strike.”

When the world’s land was congealed in one supercontinent 240 million years ago, Antarctica wasn’t the forbiddingly icy place it is now. But paleontologists have found a previously unknown amphibious predator species that probably still made it less than hospitable.

The species, named Kryostega collinsoni, is a temnospondyl, a prehistoric amphibian distantly related to modern salamanders and frogs. K. collinsoni resembled a modern crocodile, and probably was about 15 feet in length with a long and wide skull even flatter than a crocodile’s.

In addition to large upper and lower teeth at the edge of the mouth, temnospondyls often had tiny teeth on the roof of the palate. However, fossil evidence shows the teeth on the roof of the mouth of the newly found species were probably as large as those at the edge of the mouth.

“Its teeth, compared to other amphibians, were just enormous. It leads us to believe this animal was a predator taking down large prey,” said Christian Sidor, a University of Washington associate professor of biology and curator of vertebrate paleontology at the Burke Museum of Natural History and Culture at the UW.

Sidor is lead author of a paper describing the new species published in the September issue of the Journal of Vertebrate Paleontology. Co-authors are Ross Damiani of Staatliches Museum für Naturkunde Stuttgart in Germany and William Hammer of Augustana College in Rock Island, Ill. The work was funded in part by the National Science Foundation and the Alexander von Humboldt Foundation.

The scientists worked from a fossilized piece of the snout of K. collinsoni, analyzing structures present in more complete skulls for other temnospondyl species that had similar size characteristics.

“The anatomy of the snout tells us what major group of amphibian this fossil belonged to,” Sidor said.

Teeth at the edge of the mouth, as well as on the palate roof, were clearly visible, and the presence of structures similar to those that allow fish and amphibians to sense changes in water pressure led the researchers to conclude that the species was aquatic.

The fossilized piece of snout also contains a nostril, which aided the scientists in judging proportions of the head when comparing it to other fossils. They estimated the skull was about 2.75 feet long and perhaps 2 feet across at its widest point.

“Kryostega was the largest animal in Antarctica during the Triassic,” Sidor said.

The term “Kryostega” translates to ‘frozen’ and ‘roof,’ which refer to the top of the skull. The scientists named the species for James Collinson, a professor emeritus of Earth sciences at Ohio State University who made important contributions to the study of Antarctic geology.

Hammer collected the fossil in 1986 from an Antarctic geological layer called the Fremouw Formation. He has studied a number of other Antarctic fossils, including dinosaurs, collected at about the same time, and so the temnospondyl fossil was not closely examined until the last couple of years.

At the time K. collinsoni was living, all the world’s land was massed into a giant continent called Pangea. The area of Antarctica where the fossil was found was near what is now the Karoo Basin of South Africa, one of the richest fossil depositories on Earth.

Sidor noted that in the early Triassic period, from about 245 million to 251 million years ago, just before the period that produced the K. collinsoni fossil, it appears that Antarctica and South Africa were populated by largely the same species. While Antarctica was still colder than much of the world, it was substantially warmer than it is today, though it still spent significant periods in complete darkness.

By the middle of the Triassic period perhaps only half the species were the same, he said, and in the early Jurassic period, around 190 million years ago, unique early dinosaur species were appearing in Antarctica.

“It could be that these animals were adjusting to their local environment by then, and we are seeing the results of speciation occurring at high latitude,” Sidor said. “Here we have really good evidence that Antarctic climate wasn’t always the way it is today. During the Triassic, it was warmer than it is today – it was warmer globally, not just in Antarctica.”

Marauding molecules cause the tissue damage that underlies heart attacks, sunburn, Alzheimer’s and hangovers.  But scientists at the Stanford University School of Medicine say they may have found ways to combat the carnage after discovering an important cog in the body’s molecular detoxification machinery.

The culprit molecules are oxygen byproducts called free radicals.  These highly unstable molecules start chain reactions of cellular damage an escalating storm that ravages healthy tissue.

“We’ve found a totally new pathway for reducing the damage caused by free radicals, such as the damage that happens during a heart attack,” said Daria Mochly-Rosen, PhD, professor of chemical and systems biology and the senior author of a study reporting the new findings.  The research will appear in the Sept. 12 issue of Science.

Before the study, scientists knew that heart muscle could be preconditioned to resist heart attack damage for instance, moderate drinkers tend to have smaller, less severe heart attacks than teetotalers.  But scientists didn’t understand how pre-conditioning worked.

To figure out how alcohol protects heart muscle from free-radical damage, Mochly-Rosen’s team tested alcohol pretreatment in a rat heart-attack model.  They compared the enzymes activated during the attacks to those switched on with no alcohol.  Enzymes are the “doers” of the cellular machinery, catalyzing all of the biochemical reactions that form the basis of life.

Surprisingly, the treatment activated aldehyde dehydrogenase 2 (ALDH2), an obscure alcohol-processing enzyme.  Alcohol pretreatment increased the enzyme’s activity during heart attack by 20 percent, leading to a 27 percent drop in the associated damage.

“Although this enzyme was discovered a long time ago, my research group knew nothing about the enzyme except that it helps remove alcohol when people drink,” said Mochly-Rosen, who is also the senior associate dean for research in the School of Medicine and the George D. Smith Professor in Translational Medicine.

ALDH2 wasn’t one of the well-studied antioxidant players that the scientists expected to find fighting free-radical damage.  The enzyme neutralizes an aldehyde molecule, a toxic byproduct of the ethanol in alcoholic beverages.  But aldehydes are also formed in the body when free radicals react with fat molecules.

The body’s cells contain a lot of fat, Mochly-Rosen noted.  “It’s very easy for free radicals to find fat and oxidize it to aldehydes.”

Inside cells, the accumulating aldehydes permanently bind and damage cellular machinery and DNA.  Such damage occurs in many diseases, from heart attack and Parkinson’s to sun-induced aging of the skin.

After learning of ALDH2’s novel role in reducing the damage, the researchers searched for a molecule that could make the enzyme function even better.  They enlisted the Stanford High Throughput Bioscience Center, directed by David Solow-Cordero, PhD, to find a molecule that heightened the enzyme’s activity.

The winner of this contest was a tiny molecule that reduced heart attack damage by 60 percent in the rat model.  The molecule, Alda-1, has a surprising mode of action: it protects ALDH2 itself from aldehyde attack.  The enzyme, it turns out, was being hobbled by the very chemical it removes.

Because Alda-1 is small, it should be easy to adapt for pharmacological use, Mochly-Rosen said.  She expects the new molecule to have many possible drug applications.

“It has a huge potential use,” she said.  So far, Alda-1 has been tested only in the rat model, but Mochly-Rosen’s lab is investigating other possible applications, such as fighting neurodegenerative disease and sun damage on the skin.  The team also hopes to interest drug companies in human trials.

In addition to its lofty medical applications, Alda-1 could also have a much lowlier use: fighting hangovers.  Many nasty hangover symptoms are due to aldehyde buildup.

The tiny molecule may also improve alcohol tolerance and reduce susceptibility to free-radical diseases in people with a common ALDH2 mutation.  The mutation affects 40 percent of people of Asian descent and causes an intolerance for alcohol.

A carefully framed combination of moderate exercise and nutritional supplements could help older people maintain an active lifestyle for longer.

A Manchester Metropolitan University study has found that taking carbohydrate and protein supplements just before and just after low-resistance exercise could boost muscle performance and slow muscle wastage in people over retirement age.

Moreover, this combination appears to deliver greater fitness benefits than undertaking heavy-resistance training with or without changing one’s nutritional habits.

This was the first-ever study of the combination of structured exercise and nutritional supplements to focus wholly on older people.  Undertaken as part of the SPARC (Strategic Promotion of Ageing Research Capacity) initiative, the findings will be discussed at this year’s BA Festival of Science in Liverpool on Thursday 11th September.  SPARC is supported by the Engineering and Physical Sciences Research Council (EPSRC) and the Biotechnology and Biological Sciences Research Council (BBSRC).

This groundbreaking study involved a carefully selected sample of around 60 healthy, independent-living adults aged 65 and over.

The volunteers were randomly divided into groups who underwent different 12 week programmes of physical exercise and nutritional supplementation.  Everyone was then re-assessed at the end of the programme.

Some groups undertook low-resistance exercise once a week; others undertook high-resistance exercise twice a week.  Within each group, some of the volunteers took protein and carbohydrate supplements while others did not.

When all the participants were re-assessed at the end of the 12 week programme, it was observed that muscle size and strength had increased in all groups.

However, the results suggested that older people would derive the most benefits if they took appropriate supplements coupled with low-intensity exercise.

“Maintaining muscle performance and arresting muscle wastage can offer older people real improvements in their quality of life,” says Dr Gladys Pearson, who led the research.  “Though we still need to assess precisely what level of exercise gives the best results, we believe we’ve shown that regular low-resistance exercise complemented by the right nutritional supplements could boost the well-being of the UK’s ageing population.”

Dr Pearson and her team now aim to look at the effectiveness of novel combinations of strength training and nutritional supplementation as a way of speeding recovery and improving mobility for old and young orthopaedic surgery patients.

In a paper published today in Science, Steve Brusatte and Professor Mike Benton challenge the general consensus among scientists that there must have been something special about dinosaurs that helped them rise to prominence.

Dinosaurs epitomize both success and failure.  Failure because they went extinct suddenly 65 million years ago; success because they dominated terrestrial ecosystems for well over 100 million years evolving into a wide array of species that reached tremendous sizes.

But why were the dinosaurs able to become so successful, so diverse, so large?  Many scientists argue that they must have had some feature or characteristic that helped them out-compete other vertebrate groups, including crocodiles and close crocodile cousins.

Mr Brusatte and Professor Benton are the first to look at the overall picture of the evolution of dinosaurs and their closest competitors during the Triassic period (251 to 199 million years ago).  First, they identified the most likely ‘competitors’ to early dinosaurs: the crurotarsan archosaurs, a large group of animals that are closely related to crocodiles, which form one half of the group Archosauria, the other half being dinosaurs (and their descendants, the birds).

Unlike today’s crocodiles, Triassic crurotarsans were amazingly diverse.  There were enormous quadrupedal predators, slender bipedal predators, swift bipedal omnivores, fish-eaters, root-grubbers, and low-to-mid-browsing herbivores.  Many of these crurotarsans look nothing like crocodiles, but instead are eerily similar to dinosaurs and, in fact, have been mistaken for dinosaur ancestors, or even true dinosaurs, in the past.

Crurotarsans and dinosaurs clearly shared many niches in the Late Triassic, looked very similar, and were thus very likely to be competing for similar resources.

The researchers examined the evolutionary pattern of dinosaurs and crurotarsans in the Late Triassic.  Using a very large dataset of anatomical characters – nearly 500 features of the skeleton – and a new family tree of the entire archosaur group, they measured evolutionary rates and morphological disparity (a measurement of the range of different body plans and lifestyles that a group has).

They found no difference in the rates at which dinosaurs and crurotarsans were evolving.  This was surprising as, if dinosaurs were truly ’superior’ or ‘out-competing’ crurotarsans in the Triassic, they should be expected to evolve faster.  Instead, crurotarsans were keeping pace.

The results for the second measure, morphological disparity, were even more remarkable.  Crurotarsans had a much higher disparity than dinosaurs in the Triassic.  In other words, crurotarsans were exploring a larger range of body types, diets, and lifestyles.  This greatly contrasts with the classic image of dinosaur superiority since their greatest competitors, the crurotarsans, were doing so much more.

To these surprising results can be added two other, previously known, findings: crurotarsans were more abundant (more individuals, more fossils, more species) than dinosaurs in many Triassic ecosystems, and crurotarsans were in some cases more diverse (greater number of species).  Putting all this together, it is very difficult to argue that dinosaurs were ’superior’ to crurotarsans, or that they were out-competing crurotarsans.

Steve Brusatte, who conducted the research while an Msc student in Bristol University’s Department of Earth Sciences, said: “If we were standing in the Late Triassic, 210 million years ago or so, and had to bet on which group would eventually dominate ecosystems, all reasonable gamblers would go with the crurotarsans.  There was no sign that dinosaurs were eventually going to succeed so why did they?  The answer is two mass extinction events: the dinosaurs not only got lucky, but they got lucky twice.

“They first weathered the storm during the Carnian-Norian event 228 million years ago, but so did the crurotarsans.  In contrast, many other potential competitor groups went extinct.  Then dinosaurs weathered a second, much bigger, storm 200 million years ago.  This was the end Triassic extinction event, which was a sudden and catastrophic extinction caused by rapid climate change, possibly facilitated by an asteroid impact.  Strangely, and suddenly, all crurotarsans except for a few lineages of crocodiles went extinct.  On the other hand, the dinosaurs did not.  They survived and then radiated in the Early Jurassic, and very quickly established themselves as the dominant vertebrate group on land across the world.

“Why did crurotarsans go extinct and not dinosaurs?  We don’t know the answer to that, but we suspect that it was nothing more than luck, plain and simple.”