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April 24, 2006, 7:24 PM CT

Anthrax Inhibitor Counteracts Toxin

Anthrax Inhibitor Counteracts Toxin A model of the anthrax toxin molecular structure displays the enzyme-binding surface in red. (University of Toronto/Jeremy Mogridge)
Scientists from Rensselaer Polytechnic Institute and the University of Toronto have designed a nanoscale assembly of molecules that successfully counteracts and inhibits anthrax toxin in animal and laboratory experiments. The novel approach used to neutralize anthrax toxin could be applied in designing potent therapeutics for a variety of pathogens and toxins, as per the researchers.

Anthrax toxin, secreted by the anthrax bacterium, is made of proteins and toxic enzymes that bind together to inflict damage on a host organism. The inhibitor, which is described by the Rensselaer-Toronto team in the April 23 online edition of the journal Nature Biotechnology, works by preventing the assembly of toxic enzyme components, thereby blocking the formation of fully assembled anthrax toxin and neutralizing its activity.

The inhibitor protected rats from anthrax toxin in the study.

"Our eventual goal is to use the inhibitor as a human therapeutic for anthrax exposure, one that can stop the toxin from functioning inside the body," says Ravi Kane, the Merck Associate Professor of Chemical and Biological Engineering at Rensselaer and a principal investigator of the project. "Combining the inhibitor with antibiotic treatment may increase the likelihood of survival for an infected person".........

Posted by: Mark      Permalink         Source

April 24, 2006, 6:50 PM CT

Nanotechnology May Find Disease Before It Starts

Nanotechnology May Find Disease Before It Starts Thomas J. Rosol
Nanotechnology may one day help physicians detect the very earliest stages of serious diseases like cancer, a new study suggests.

It would do so by improving the quality of images produced by one of the most common diagnostic tools used in doctors' offices - the ultrasound machine.

In laboratory experiments on mice, researchers found that nano-sized particles injected into the animals improved the resulting images. This study is one of the first reports showing that ultrasound can detect these tiny particles when they are inside the body, said Thomas Rosol, a co-author of study and dean of the college of veterinary medicine at Ohio State University.

"Given their tiny size, nobody thought it would be possible for ultrasound to detect nanoparticles," he said.

It turns out that not only can ultrasound waves sense nanoparticles, but the particles can brighten the resulting image. One day, those bright spots may indicate that a few cells in the area may be on the verge of mutating and growing out of control.

"The long-term goal is to use this technology to improve our ability to identify very early cancers and other diseases," said Jun Liu, a co-author of study and an assistant professor of biomedical engineering at Ohio State University. "We ultimately want to identify disease at its cellular level, at its very earliest stage".........

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April 24, 2006, 6:35 PM CT

Reproductive Success In Early Life Leads To Faster Ageing

Reproductive Success In Early Life Leads To Faster Ageing
Why do we stop reproducing after a certain age, and how is this age determined? A study by Oxford University scientists has shed light on this question by studying data from Dorset swans.

A theory which says that reproductive success in early life will lead to faster ageing later has been supported by the study of mute swans (Cygnus olor) which shows that those swans which reproduce early in life also stopped breeding early, and vice versa. Which pattern a swan adopts appears to be genetically inherited.

The team, from the Edward Grey Institute in Oxford's Department of Zoology, investigated data on swans that bred as youngsters and those that started to reproduce at a much later age. They discovered the age at which swans started to reproduce varied considerably - from two to twelve years old - and the age at which swans stopped breeding also showed huge variation - from two to twenty years old. The main finding, however, was that the birds that started breeding at an early age stopped reproducing earlier than the late-starters.

The study, would be reported in the science journal PNAS this week, supports the 'antagonistic pleiotropy' theory for the evolution of ageing, that says that you 'pay' in later life for your success in reproducing when young. It is thought the study is the first to show this pattern in a wild animal population.........

Posted by: Scott      Permalink         Source

April 22, 2006, 6:08 PM CT

Protein That Kills Anthrax Bacteria

Protein That Kills Anthrax Bacteria A bacterium's final gasp. A bacillus bacterium, a close relative of anthrax, begins to explode after being treated with PlyPH. The PlyPH protein, discovered by Rockefeller scientists, offers several advantages over existing anthrax treatments.
Not all biological weapons are created equal. They are separated into categories A through C, category A biological agents being the scariest: They are easy to spread, kill effectively and call for special actions by the pubic health system. One of these worrisome organisms is anthrax, which has already received its fair share of media attention. But work in Vince Fischetti's laboratory at Rockefeller University suggests that a newly discovered protein could be used to fight anthrax infections and even decontaminate areas in which anthrax spores have been released.

"Anthrax is the most efficient biowarfare agent. Its spores are stable and easy to produce, and once someone inhales them, there is only a 48-hour window when antibiotics can be used," says Fischetti. "We've found a new protein that could both potentially expand that therapy window and be used as a large-scale decontaminant of anthrax spores." Because anthrax spores are resistant to most of the chemicals that emergency workers rely on to sterilize contaminated areas, a solution based on the protein would be a powerful tool for cleaning up after an anthrax attack.

All bacteria, anthrax included, have natural predators called bacteriophage. Just as viruses infect people, bacteriophage infect bacteria, reproduce, and then kill their host cell by bursting out to find their next target. The bacteriophage use special proteins, called lysins, to bore holes in the bacteria, causing them to literally explode. Fischetti and his colleagues identified one of these lysins, called PlyG, in 2004, and showed that it could be used to help treat animals and humans infected by anthrax. Now, they have identified a second lysin, which they have named PlyPH, with special properties that make it not only a good therapeutic agent, but also useful for large-scale decontamination of areas like buildings and military equipment.........

Posted by: Mark      Permalink         Source

April 20, 2006, 9:37 PM CT

Insights Into Lazy Eye Theory

Insights Into Lazy Eye Theory
In a study that challenges conventional thinking about the condition known as lazy eye, scientists at MIT's Picower Institute for Learning and Memory show that it's the quality, not the quantity, of images and light striking the retina that causes one eye to lose function.

The study will appear in the recent issue of the Journal of Neurophysiology.

Amblyopia, or lazy eye, is a developmental disorder characterized by poor or blurry vision in an eye that is structurally normal. The problem is caused by either no transmission or poor transmission of visual images to the brain for a sustained period during early childhood. Amblyopia has been estimated to affect 1 percent to 5 percent of the population.

"It's been known for a long time that if you are born with cataracts in one eye, you will go blind in that eye," said co-author of study Mark Bear, Picower Professor of Neuroscience. "Depriving one eye of crisp images rapidly causes cortical neurons to lose responsiveness to the deprived eye".

While it was thought that inactivity caused the neurons associated with the deprived eye to wither -- a case of "use it or lose it" -- Bear and his colleagues at Brown University report that a blurry image is worse than no image at all.

The conventional therapy for lazy eye is to wear a patch over the good eye in the hope that the weaker eye will get stronger. "It's a zero-sum game," Bear said, "because as the weak eye gets stronger, the strong eye gets weaker. The challenge is to promote recovery of the weak eye without impairing the other eye".........

Posted by: Mike      Permalink         Source

April 20, 2006, 9:16 PM CT

Bringing New Life To Kidney Treatment

Bringing New Life To Kidney Treatment
Finding how two proteins conspire to get kidney cells to self-destruct when oxygen supplies are low may one day improve dismal mortality rates for ischemic renal failure, scientists say.

Dehydration, low blood pressure, septic shock, trauma or removing a kidney for transplantation can temporarily halt or reduce blood and oxygen supplies, says Dr. Zheng Dong, cell biologist at the Medical College of Georgia.

Ischemia leads to cell suicide or apoptosis, especially in the energy-consuming tubular cells of the kidneys, he says. Fifty percent mortality rates from resulting ischemic renal failure haven't changed in nearly as a number of years, Dr. Dong says.

Tubular cells - which have the daunting daily task of reabsorbing nearly 50 gallons of usuable fluid volume, including salt and glucose the kidneys filter from the blood every 24 hours - are especially vulnerable to apoptosis and injury, Dr. Dong says.

"They are highly energy-dependent," he says. "That is why when you shut off the blood supply, these cells are quickly, irreversibly damaged and they die." Tubular cell injury and death is why kidneys are so vulnerable, for example in critically ill patients.

It's in this oxygen-deprived environment that two proteins, Bid and Bax - each a known killer in its own right - are activated and may partner to induce cell death. The killing proteins are pervasive, especially in the kidneys, says Dr. Dong, who recently received a $1 million grant from the National Institute of Diabetes & Digestive & Kidney Diseases, to better understand their role in cell death during ischemic renal failure.........

Posted by: Mark      Permalink         Source

April 20, 2006, 8:42 PM CT

Clues To Eating Disorders

Clues To Eating Disorders Dr. Leon Avery (left), professor of molecular biology, led a team that included Dr. Young-jai You, postdoctoral researcher in molecular biology and pharmacology, and discovered a series of biochemical reactions that control how simple worms feed, opening the way for further research into the complicated nature of hunger.
In research that may have implications for studying eating disorders in humans, a worm the size of a pinhead is helping scientists at UT Southwestern Medical Center unravel the mechanisms of hunger.

The scientists have found a series of biochemical reactions that control how the simple worm feeds, opening the way for further research into the complicated nature of hunger. Central to the research is a worm called Caenorhabditis elegans, which eats bacteria by contracting and relaxing a large muscle called the pharynx to suck in its prey. When it can't find food, C. elegans reacts by pumping the pharynx harder.

"Despite the prevalence of eating disorders from obesity to anorexia, the identity and mechanism of action of starvation signals are largely unknown," the scientists wrote in the paper, which will appear in the recent issue of Cell Metabolism.

The study of the signaling pathways in feeding muscles suggests that feeding disorders may result from inappropriate behavioral responses to starvation signals, they wrote.

"Instead of being vague about what hunger is, we can be specific, at least in these cells in these particular animals," said Dr. Leon Avery, professor of molecular biology and senior author of the study. "There's been a lot of work on hunger and behavior, but hunger has not been well-defined at the molecular level".........

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April 17, 2006, 10:20 PM CT

A Gene For Excessive Drinking

A Gene For Excessive Drinking
Scientists supported by the National Institute on Alcohol Abuse and Alcoholism (NIAAA), part of the National Institutes of Health (NIH), have identified new genes that may contribute to excessive alcohol consumption. The new study, conducted with strains of animals that have either a high or low innate preference for alcohol, provides clues about the molecular mechanisms that underlie the tendency to drink heavily. A report of the findings appears in the April 18, 2006 issue of Proceedings of the National Academy of Sciences.

"These findings provide a wealth of new insights into the molecular determinants of excessive drinking, which could lead to a better understanding of alcoholism," notes NIAAA Director Ting-Kai Li, M.D. "They also underscore the value that animal models bring to the investigation of complex human disorders such as alcohol dependence."

Mice that have been selectively bred to have either a high or low preference for alcohol have been a mainstay of alcohol research for a number of years, allowing researchers to study diverse behavioral and physiological characteristics of alcohol dependence. In the current study, NIAAA grantee Susan E. Bergeson, Ph.D., of the University of Texas (UT) at Austin, and a multi-site team of researchers participating in NIAAA's Integrative Neuroscience Initiative on Alcoholism (INIA) used microarray techniques to study gene expression in the brains of these animals. Microarrays are powerful tools that researchers use for comprehensive analyses of gene activity.........

Posted by: JoAnn      Permalink         Source

April 16, 2006, 8:16 PM CT

Protein Facilitates "Hard-Wiring" of Brain

Protein Facilitates
A mechanism underlying the molecular switch that turns young, adaptable brains into older, less malleable brains has been discovered by an international team of scientists led by a Duke University Medical Center neurobiologist.

The scientists discovered how neurons switch between neurotransmitter receptors during early brain development. This molecular switch signals the end of a critical period of brain "plasticity" in which simple sensory experiences, such as a mother's touch on the skin, are mandatory to "wire" the brain appropriately. The scientists describe a key role for a neurotransmitter receptor called NR3A that is abundant in the brain for only a few weeks following birth.

As per the researchers, their findings could lead to a better understanding of disorders of early brain development. NR3A levels have been reported to be elevated in patients with schizophrenia, which is believed to be caused by subtle alterations of brain circuitry during development, said the scientists.

The team's results appeared this week in the advance online edition of Nature Neuroscience and will be published in an upcoming print issue of the journal. The work was supported by the National Institutes of Health, the American Heart Association, the Raymond and Beverley Sackler Foundation and the Ruth K. Broad Foundation.........

Posted by: Daniel      Permalink         Source

April 15, 2006, 2:30 PM CT

Gene Decreases Retinal Degeneration In Fruit Flies

Gene Decreases Retinal Degeneration In Fruit Flies
Johns Hopkins scientists have discovered a gene in fruit flies that helps certain specialized neurons respond more quickly to bright light. The study, reported in the April 4 issue of Current Biology, also has implications for understanding sensory perception in mammals.

In teasing apart the molecular interactions and physiology underlying light perception, the scientists studied a gene they dubbed "Lazaro" that is expressed 15 times higher in the fly eye than the rest of the fly head. They found that this gene is mandatory for a second biochemical pathway that controls the activity of a protein called the TRP channel. TRP channels are found in fruit fly neurons responsible for sensing light. The fly TRP channel is the founding member of a family of related proteins in mammals that are essential for guiding certain nerves during development and for responding to stimuli including heat, taste and sound.

By shining bright light onto and recording electrical changes in single nerve cells in the fly eye, scientists found that neurons carrying a mutation in this gene cannot respond as well to light as compared to neurons carrying normal copies of this gene. In fact, the mutant neurons turn off their response to light four times faster than normal neurons. Because Lazaro helps fly TRP channels work at their maximum, it is possible that a Lazaro-like gene in mammals might also play a role in how well mammalian TRP channels work.........

Posted by: Mike      Permalink         Source

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Did you know?
Scientists at Yale have brought to light a mechanism that regulates the way an internal organelle, the Golgi apparatus, duplicates as cells prepare to divide, according to a report in Science Express.Graham Warren, professor of cell biology, and colleagues at Yale study Trypanosoma brucei, the parasite that causes Sleeping Sickness. Like a number of parasites, it is exceptionally streamlined and has only one of each internal organelle, making it ideal for studying processes of more complex organisms that have a number of copies in each cell. Archives of research news blog

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