Following the ban of all food animal growth-promoting antibiotics by Sweden in 1986, the European Union banned avoparcin in 1997 and bacitracin, spiramycin, tylosin and virginiamycin in 1999. Three years later, the only attributable effect in humans has been a diminution in acquired resistance in enterococci isolated from human faecal carriers. There has been an increase in human infection from vancomycin-resistant enterococci in Europe, probably related to the increased in usage of vancomycin for the treatment of methicillin-resistant staphylococci. The ban of growth promoters has, however, revealed that these agents had important prophylactic activity and their withdrawal is now associated with a deterioration in animal health, including increased diarrhoea, weight loss and mortality due to Escherichia coli and Lawsonia intracellularis in early post-weaning pigs, and clostridial necrotic enteritis in broilers. A directly attributable effect of these infections is the increase in usage of therapeutic antibiotics in food animals, including that of tetracycline, aminoglycosides, trimethoprim/sulphonamide, macrolides and lincosamides, all of which are of direct importance in human medicine. The theoretical and political benefit of the widespread ban of growth promoters needs to be more carefully weighed against the increasingly apparent adverse consequences.
Human Biology 1010 Blog
Wednesday, November 30, 2011
The European ban on growth-promoting antibiotics and emerging consequences for human and animal health
Following the ban of all food animal growth-promoting antibiotics by Sweden in 1986, the European Union banned avoparcin in 1997 and bacitracin, spiramycin, tylosin and virginiamycin in 1999. Three years later, the only attributable effect in humans has been a diminution in acquired resistance in enterococci isolated from human faecal carriers. There has been an increase in human infection from vancomycin-resistant enterococci in Europe, probably related to the increased in usage of vancomycin for the treatment of methicillin-resistant staphylococci. The ban of growth promoters has, however, revealed that these agents had important prophylactic activity and their withdrawal is now associated with a deterioration in animal health, including increased diarrhoea, weight loss and mortality due to Escherichia coli and Lawsonia intracellularis in early post-weaning pigs, and clostridial necrotic enteritis in broilers. A directly attributable effect of these infections is the increase in usage of therapeutic antibiotics in food animals, including that of tetracycline, aminoglycosides, trimethoprim/sulphonamide, macrolides and lincosamides, all of which are of direct importance in human medicine. The theoretical and political benefit of the widespread ban of growth promoters needs to be more carefully weighed against the increasingly apparent adverse consequences.
Who Consumes Organic Foods?
A study on who buys organic food and why they buy organic: what makes the extra cost of organic food worth the money to some people but not others. Consumers of organics are diverse in both demographics and in reasons to support organic farming. This article synthesizes the findings of several other research studies and looks for a defining pattern in organic consumers.
E. Coli Bacteria Engineered to Eat Switchgrass and Make Transportation Fuels
Researchers with the U.S. Department of Energy (DOE)'s Joint BioEnergy Institute (JBEI) have successfully engineered a strain of E.coli that is able to survive on switchgrass and synthesize gasoline, diesel, and jet fuel. This is the first time that a microbe has been found to create jet fuel and it is an amazing step forward in a number of ways. E.coli do not normally grow on switchgrass, and this new strains ability brings together all kinds of possibilities since switchgrass is widely regarded as the future of bio fuels. At the same time, these bacteria are able to create the fuel without the help of additive enzymes, which made the process much more expensive. The new process can cut cost of production almost in half.
Smartphone Touchscreens Could Analyze Biological Smears to Diagnose Illness
Technology is continuing to expand to places never before imagined. A few researchers at the Korea Advanced Institute for Science and Technology think we could simplify the process of diagnosing simple illnesses right on our smart phones. They believe that the technology that senses our fingers on the screen is sensitive enough to read the capacitance ( value of electrical impulse) of a blood, or saliva sample and be able to diagnose illness. So far no results have been collected but they have shown the ability to use the technology to differentiate between different samples of bacteria genetic material.
Celebrities Jump on the Vegan Bandwagon
The way that celebrities are becoming vegan might make you think that it is just a passing fad. Celebrities from all corners are becoming vegan or have been vegan for a long time. Some of the top names are Mike Tyson, Bill Clinton, Katie Holmes, Tom Brady, Ozzy Osbourne and Ellen DeGeneres. Many of these celebrities praised Pure Food and Wine vegan and raw food restaurant in Manhattan. Pure Food and Wine has no animal products and no oven. Is vegan-ism just a passing fad?
Eating Disorders for Men Are More Common Than Expected
According to Harvard's national study of 3000 adults with eating disorders, more men are suffering from eating disorders than was thought. The study that men make up 25% of anorexics and bulimics and 40% of binge eaters. It was thought that men made up about 10% of anorexics and bulimics. Harvard's study shows that men suffer from eating disorders for the same reason that women do: fitness and size. Men are also less likely to seek help with their eating disorders.
France Tries to Bans Websites Supporting Anorexia and Bulimia
In 2008, French lawmakers proposed a law banning websites supporting or aiding in anorexia or bulimia. The punishments include 3 years of prison and/or up to €45,000 equivalent to 71,000 USD. Several other European governments are looking for ways to fight back against the promotion of eating disorders as a pathway to beauty.
Genetic code of first arachnid cracked
An international team of scientists - including Ghent VIB scientists - has succeeded in deciphering the genome of the spider mite. This is also the first known genome of an arachnid. This premiere not only brings along new insights into the evolution of arthropods, but also offers new opportunities to develop means of crop protection against the spider mite.
Spider mites belong to the group of the Acari (among arachnids) and are related to dust mites and other parasitic mites such as ticks that transmit serious diseases to humans and animals. (http://www.acari.be/)
Enormous damage to many crops
Spider mites are colonial, invasive mites that feed on plant juices. The spider mite Tetranychus urticae likes over 1100 different plant species and is a real plague in ornamental gardens and in greenhouse cultivation in our regions, among which, tomatoes, peppers, cucumbers, strawberries, or complete corn and soybean fields.
Spider mites pierce plant cells of the leaves and suck them dry. On most plants, spider mite damage can be recognized as small yellow spots on leaves. Spider mite pests lead to reduced harvests for farmers and are a threat to food production. In severe attacks, the leaves, or even entire plants, wither and die. Spider mites got their name from their ability to make silk threads which they wrap around plants.
The annual cost of pesticides against spider mites amounts to 0.5 to 1 billion dollars and scientists predict that due to global warming, spider mite plagues will increase. Furthermore, the spider mites are known to show resistance to different kinds of pesticides and the current study of the genome will shed light on the mechanisms present in the mite to develop fast adaptation and resistance.
Genome reveals unique characteristics
Stephane Rombauts, Pierre Rouze and other colleagues from the research team of Yves Van de Peer were part of the international team that mapped the genome of T. urticae. This genome contains unique genes that have not been identified in other arthropods. These new genes play an important role in the development of spider mites during evolution. The researchers identified numerous genes - involved in detoxification and digestion - which help to explain the unsurpassed resistance of spider mites to pesticides and his polyphagy. New genes were also identified that are responsible for the production of silk threads by the spider mite. With this knowledge, scientists can try to reproduce this nanomaterial and possibly this new material may then be used in medical biotechnology. The unique combination of properties that can be found in silk threads - including particularly strong, not too elastic elastic and shock resistant - can hardly be found in any other type of material.
Spider mites belong to the group of the Acari (among arachnids) and are related to dust mites and other parasitic mites such as ticks that transmit serious diseases to humans and animals. (http://www.acari.be/)
Enormous damage to many crops
Spider mites are colonial, invasive mites that feed on plant juices. The spider mite Tetranychus urticae likes over 1100 different plant species and is a real plague in ornamental gardens and in greenhouse cultivation in our regions, among which, tomatoes, peppers, cucumbers, strawberries, or complete corn and soybean fields.
Spider mites pierce plant cells of the leaves and suck them dry. On most plants, spider mite damage can be recognized as small yellow spots on leaves. Spider mite pests lead to reduced harvests for farmers and are a threat to food production. In severe attacks, the leaves, or even entire plants, wither and die. Spider mites got their name from their ability to make silk threads which they wrap around plants.
The annual cost of pesticides against spider mites amounts to 0.5 to 1 billion dollars and scientists predict that due to global warming, spider mite plagues will increase. Furthermore, the spider mites are known to show resistance to different kinds of pesticides and the current study of the genome will shed light on the mechanisms present in the mite to develop fast adaptation and resistance.
Genome reveals unique characteristics
Stephane Rombauts, Pierre Rouze and other colleagues from the research team of Yves Van de Peer were part of the international team that mapped the genome of T. urticae. This genome contains unique genes that have not been identified in other arthropods. These new genes play an important role in the development of spider mites during evolution. The researchers identified numerous genes - involved in detoxification and digestion - which help to explain the unsurpassed resistance of spider mites to pesticides and his polyphagy. New genes were also identified that are responsible for the production of silk threads by the spider mite. With this knowledge, scientists can try to reproduce this nanomaterial and possibly this new material may then be used in medical biotechnology. The unique combination of properties that can be found in silk threads - including particularly strong, not too elastic elastic and shock resistant - can hardly be found in any other type of material.
A better way to count molecules discovered
Researchers at the Swedish medical university Karolinska Institutet have developed a new method for counting molecules. Quantifying the amounts of different kinds of RNA and DNA molecules is a fundamental task in molecular biology as these molecules store and transfer the genetic information in cells. Thus, improved measurement techniques are crucial for understanding both normal and cancer cells.
In an article published by the scientific journal Nature Methods the researchers present a method in which the molecules are first artificially made different in such a way that the copies made from different original molecules can be later distinguished. Then the molecules can be efficiently counted using the new high-throughput sequencers that can read millions of short DNA stretches in parallel. The idea behind the method is astonishingly simple, yet it enables counting the absolute number of molecules in a cell sample whereas many current methods can only measure relative differences between samples.
Professor Jussi Taipale's group applied the new method to simultaneously count thousands of different types of messenger RNA molecules present in cells. The new method proved to be more accurate than the one that has been commonly used for this task. Efficient and reliable counting of messenger RNA molecules is important because their abundances reveal which genes are active in the cells of interest. Professor Taipale's group studies regulation of cell growth and thus wants to understand not only which genes are active in normal cells but also genes that are aberrantly activated in cancer cells.
The new molecule counting method was developed as collaboration between Jussi Taipale's and Sten Linnarsson's groups at Karolinska Institutet, The method has turned out to be especially suitable for counting molecules from a small number of cells. Thus, Sten Linnarsson plans to apply it to counting molecules from a single cell – a very exciting and challenging task. The principle of the new method can also be used to improve other important measurement techniques, and to develop technologies that allow more accurate sequencing of genomes of cancer cells and various organisms.
Teemu Kivioja and Anna Vähärautio, the first two authors, are affiliated with both University of Helsinki and Karolinska Institutet.
In an article published by the scientific journal Nature Methods the researchers present a method in which the molecules are first artificially made different in such a way that the copies made from different original molecules can be later distinguished. Then the molecules can be efficiently counted using the new high-throughput sequencers that can read millions of short DNA stretches in parallel. The idea behind the method is astonishingly simple, yet it enables counting the absolute number of molecules in a cell sample whereas many current methods can only measure relative differences between samples.
Professor Jussi Taipale's group applied the new method to simultaneously count thousands of different types of messenger RNA molecules present in cells. The new method proved to be more accurate than the one that has been commonly used for this task. Efficient and reliable counting of messenger RNA molecules is important because their abundances reveal which genes are active in the cells of interest. Professor Taipale's group studies regulation of cell growth and thus wants to understand not only which genes are active in normal cells but also genes that are aberrantly activated in cancer cells.
The new molecule counting method was developed as collaboration between Jussi Taipale's and Sten Linnarsson's groups at Karolinska Institutet, The method has turned out to be especially suitable for counting molecules from a small number of cells. Thus, Sten Linnarsson plans to apply it to counting molecules from a single cell – a very exciting and challenging task. The principle of the new method can also be used to improve other important measurement techniques, and to develop technologies that allow more accurate sequencing of genomes of cancer cells and various organisms.
Teemu Kivioja and Anna Vähärautio, the first two authors, are affiliated with both University of Helsinki and Karolinska Institutet.
Tweaking a gene makes muscles twice as strong
An international team of scientists has created super-strong, high-endurance mice and worms by suppressing a natural muscle-growth inhibitor, suggesting treatments for age-related or genetics-related muscle degeneration are within reach.
The scientists found that a tiny inhibitor may be responsible for determining the strength of our muscles. By acting on a genome regulator (NCoR1), they were able to modulate the activity of certain genes, creating a strain of mighty mice whose muscles were twice a strong as those of normal mice.
"There are now ways to develop drugs for people who are unable to exercise due to obesity or other health complications, such as diabetes, immobility and frailty," says Ronald M. Evans, a professor in Salk's Gene Expression Laboratory, who led the Salk team. "We can now engineer specific gene networks in muscle to give the benefits of exercise to sedentary mice."
Johan Auwerx, the lead author from EPFL, says molecules such as NCoR1 are molecular brakes that decrease the activity of genes. Releasing the brake by mutation or with chemicals can reactivate gene circuits to provide more energy to muscle and enhance its activity.
In an article appearing last week in the journal Cell, the Salk researchers and their collaborators reported on the results of experiments done in parallel on mice and nematodes. By genetically manipulating the offspring of these species, the researchers were able to suppress NCoR1, which normally acts to inhibit the buildup of muscle tissues.
In the absence of the inhibitor, the muscle tissue developed much more effectively. The mice with the mutation became true marathoners, capable of running faster and longer before showing any signs of fatigue. In fact, they were able to cover almost twice the distance run by mice that hadn't received the treatment. They also exhibited better cold tolerance.
Unlike previous experiments that focused on "genetic accelerators" this work shows that suppressing an inhibitor is a new way to build muscle. Examination under a microscope confirmed that the muscle fibers of the modified mice are denser, the muscles are more massive, and the cells in the tissue contain higher numbers of mitochondria ---- cellular organelles that deliver energy to the muscles.
Similar results were also observed in nematode worms, allowing the scientists to conclude that their results could be applicable to a large range of living creatures.
The scientists have not yet detected any harmful side effects associated with eliminating the NCoR1 receptor from muscle and fat tissues. Although the experiments involved genetic manipulations, the researchers are already investigating potential drug molecules that could be used to reduce the receptor's effectiveness.
The researchers say their results are a milestone in our understanding of certain fundamental mechanisms of living organisms, in particular the little-studied role of corepressors ---molecules that inhibit the expression of genes. In addition, they give a glimpse at possible long-term therapeutic applications.
"This could be used to combat muscle weakness in the elderly, which leads to falls and contributes to hospitalizations," Auwerx says. "In addition, we think that this could be used as a basis for developing a treatment for genetic muscular dystrophy."
He added that if these results are confirmed in humans, there's no question they will attract interest from athletes as well as medical experts.
The project was a collaboration between researchers at the Salk Institute for Biological Studies, and two Swiss institutions, Ecole Polytechnique Federale de Lausanne (EPFL) and the University of Lausanne.
The scientists found that a tiny inhibitor may be responsible for determining the strength of our muscles. By acting on a genome regulator (NCoR1), they were able to modulate the activity of certain genes, creating a strain of mighty mice whose muscles were twice a strong as those of normal mice.
"There are now ways to develop drugs for people who are unable to exercise due to obesity or other health complications, such as diabetes, immobility and frailty," says Ronald M. Evans, a professor in Salk's Gene Expression Laboratory, who led the Salk team. "We can now engineer specific gene networks in muscle to give the benefits of exercise to sedentary mice."
Johan Auwerx, the lead author from EPFL, says molecules such as NCoR1 are molecular brakes that decrease the activity of genes. Releasing the brake by mutation or with chemicals can reactivate gene circuits to provide more energy to muscle and enhance its activity.
In an article appearing last week in the journal Cell, the Salk researchers and their collaborators reported on the results of experiments done in parallel on mice and nematodes. By genetically manipulating the offspring of these species, the researchers were able to suppress NCoR1, which normally acts to inhibit the buildup of muscle tissues.
In the absence of the inhibitor, the muscle tissue developed much more effectively. The mice with the mutation became true marathoners, capable of running faster and longer before showing any signs of fatigue. In fact, they were able to cover almost twice the distance run by mice that hadn't received the treatment. They also exhibited better cold tolerance.
Unlike previous experiments that focused on "genetic accelerators" this work shows that suppressing an inhibitor is a new way to build muscle. Examination under a microscope confirmed that the muscle fibers of the modified mice are denser, the muscles are more massive, and the cells in the tissue contain higher numbers of mitochondria ---- cellular organelles that deliver energy to the muscles.
Similar results were also observed in nematode worms, allowing the scientists to conclude that their results could be applicable to a large range of living creatures.
The scientists have not yet detected any harmful side effects associated with eliminating the NCoR1 receptor from muscle and fat tissues. Although the experiments involved genetic manipulations, the researchers are already investigating potential drug molecules that could be used to reduce the receptor's effectiveness.
The researchers say their results are a milestone in our understanding of certain fundamental mechanisms of living organisms, in particular the little-studied role of corepressors ---molecules that inhibit the expression of genes. In addition, they give a glimpse at possible long-term therapeutic applications.
"This could be used to combat muscle weakness in the elderly, which leads to falls and contributes to hospitalizations," Auwerx says. "In addition, we think that this could be used as a basis for developing a treatment for genetic muscular dystrophy."
He added that if these results are confirmed in humans, there's no question they will attract interest from athletes as well as medical experts.
The scientists found that a tiny inhibitor may be responsible for determining the strength of our muscles. By acting on a genome regulator (NCoR1), they were able to modulate the activity of certain genes, creating a strain of mighty mice whose muscles were twice a strong as those of normal mice.
"There are now ways to develop drugs for people who are unable to exercise due to obesity or other health complications, such as diabetes, immobility and frailty," says Ronald M. Evans, a professor in Salk's Gene Expression Laboratory, who led the Salk team. "We can now engineer specific gene networks in muscle to give the benefits of exercise to sedentary mice."
Johan Auwerx, the lead author from EPFL, says molecules such as NCoR1 are molecular brakes that decrease the activity of genes. Releasing the brake by mutation or with chemicals can reactivate gene circuits to provide more energy to muscle and enhance its activity.
In an article appearing last week in the journal Cell, the Salk researchers and their collaborators reported on the results of experiments done in parallel on mice and nematodes. By genetically manipulating the offspring of these species, the researchers were able to suppress NCoR1, which normally acts to inhibit the buildup of muscle tissues.
In the absence of the inhibitor, the muscle tissue developed much more effectively. The mice with the mutation became true marathoners, capable of running faster and longer before showing any signs of fatigue. In fact, they were able to cover almost twice the distance run by mice that hadn't received the treatment. They also exhibited better cold tolerance.
Unlike previous experiments that focused on "genetic accelerators" this work shows that suppressing an inhibitor is a new way to build muscle. Examination under a microscope confirmed that the muscle fibers of the modified mice are denser, the muscles are more massive, and the cells in the tissue contain higher numbers of mitochondria ---- cellular organelles that deliver energy to the muscles.
Similar results were also observed in nematode worms, allowing the scientists to conclude that their results could be applicable to a large range of living creatures.
The scientists have not yet detected any harmful side effects associated with eliminating the NCoR1 receptor from muscle and fat tissues. Although the experiments involved genetic manipulations, the researchers are already investigating potential drug molecules that could be used to reduce the receptor's effectiveness.
The researchers say their results are a milestone in our understanding of certain fundamental mechanisms of living organisms, in particular the little-studied role of corepressors ---molecules that inhibit the expression of genes. In addition, they give a glimpse at possible long-term therapeutic applications.
"This could be used to combat muscle weakness in the elderly, which leads to falls and contributes to hospitalizations," Auwerx says. "In addition, we think that this could be used as a basis for developing a treatment for genetic muscular dystrophy."
He added that if these results are confirmed in humans, there's no question they will attract interest from athletes as well as medical experts.
The project was a collaboration between researchers at the Salk Institute for Biological Studies, and two Swiss institutions, Ecole Polytechnique Federale de Lausanne (EPFL) and the University of Lausanne.
The scientists found that a tiny inhibitor may be responsible for determining the strength of our muscles. By acting on a genome regulator (NCoR1), they were able to modulate the activity of certain genes, creating a strain of mighty mice whose muscles were twice a strong as those of normal mice.
"There are now ways to develop drugs for people who are unable to exercise due to obesity or other health complications, such as diabetes, immobility and frailty," says Ronald M. Evans, a professor in Salk's Gene Expression Laboratory, who led the Salk team. "We can now engineer specific gene networks in muscle to give the benefits of exercise to sedentary mice."
Johan Auwerx, the lead author from EPFL, says molecules such as NCoR1 are molecular brakes that decrease the activity of genes. Releasing the brake by mutation or with chemicals can reactivate gene circuits to provide more energy to muscle and enhance its activity.
In an article appearing last week in the journal Cell, the Salk researchers and their collaborators reported on the results of experiments done in parallel on mice and nematodes. By genetically manipulating the offspring of these species, the researchers were able to suppress NCoR1, which normally acts to inhibit the buildup of muscle tissues.
In the absence of the inhibitor, the muscle tissue developed much more effectively. The mice with the mutation became true marathoners, capable of running faster and longer before showing any signs of fatigue. In fact, they were able to cover almost twice the distance run by mice that hadn't received the treatment. They also exhibited better cold tolerance.
Unlike previous experiments that focused on "genetic accelerators" this work shows that suppressing an inhibitor is a new way to build muscle. Examination under a microscope confirmed that the muscle fibers of the modified mice are denser, the muscles are more massive, and the cells in the tissue contain higher numbers of mitochondria ---- cellular organelles that deliver energy to the muscles.
Similar results were also observed in nematode worms, allowing the scientists to conclude that their results could be applicable to a large range of living creatures.
The scientists have not yet detected any harmful side effects associated with eliminating the NCoR1 receptor from muscle and fat tissues. Although the experiments involved genetic manipulations, the researchers are already investigating potential drug molecules that could be used to reduce the receptor's effectiveness.
The researchers say their results are a milestone in our understanding of certain fundamental mechanisms of living organisms, in particular the little-studied role of corepressors ---molecules that inhibit the expression of genes. In addition, they give a glimpse at possible long-term therapeutic applications.
"This could be used to combat muscle weakness in the elderly, which leads to falls and contributes to hospitalizations," Auwerx says. "In addition, we think that this could be used as a basis for developing a treatment for genetic muscular dystrophy."
He added that if these results are confirmed in humans, there's no question they will attract interest from athletes as well as medical experts.
A first -- lab creates cells used by brain to control muscle cells
University of Central Florida researchers, for the first time, have used stem cells to grow neuromuscular junctions between human muscle cells and human spinal cord cells, the key connectors used by the brain to communicate and control muscles in the body.
"These types of systems have to be developed if you ever want to get to a human-on-a-chip that recreates human function," said James Hickman, a UCF bioengineer who led the breakthrough research. "It's taken many trials over a number of years to get this to occur using human derived stem cells."
Hickman's work, funded through the National Institute of Neurological Disorders and Stroke (NINDS) at the National Institutes of Health, is described in the December issue of Biomaterials. (http://www.sciencedirect.com/science/article/pii/S0142961211010556)
Hickman is excited about the future of his research because several federal agencies recently launched an ambitious plan to jump-start research in "human-on-a-chip" models by making available at least $140 million in grant funding.
The National Institutes of Health (NIH), the Defense Advanced Research Projects Agency (DARPA), and the Federal Drug Administration (FDA) are leading the research push.
The goal of the call for action is to produce systems that include various miniature organs connected in realistic ways to simulate human body function. This would make it possible, for instance, to test drugs on human cells well before they could safely and ethically be tested on living humans. The technique could potentially be more effective than testing in mice and other animals currently used to screen promising drug candidates and to develop other medical treatments.
Such conventional animal testing is not only slow and expensive, but often leads to failures that might be overcome with better testing options. The limitations of conventional testing options have dramatically slowed the emergence of new drugs, Hickman said.
The successful UCF technique began with a collaborator, Brown University Professor Emeritus Herman Vandenburgh, who collected muscle stem cells via biopsy from adult volunteers. Stem cells are cells that can, under the right conditions, grow into specific forms. They can be found among normal cells in adults, as well as in developing fetuses.
Nadine Guo, a UCF research professor, conducted a series of experiments and found that numerous conditions had to come together just right to make the muscle and spinal cord cells "happy" enough to join and form working junctions. This meant exploring different concentrations of cells and various timescales, among other parameters, before hitting on the right conditions.
"Right now we rely a lot on animal systems for medical research but this is a pure human system," Guo said. "This work proved that, biologically, this is workable."
Besides being a key requirement for any complete human-on-a-chip model, such nerve-muscle junctions might themselves prove important research tools. These junctions play key roles in Amyotrophic lateral sclerosis, commonly known as Lou Gehrig's disease, in spinal cord injury, and in other debilitating or life threatening conditions. With further development, the team's techniques could be used to test new drugs or other treatments for these conditions even before more expansive chip-based models are developed.
"These types of systems have to be developed if you ever want to get to a human-on-a-chip that recreates human function," said James Hickman, a UCF bioengineer who led the breakthrough research. "It's taken many trials over a number of years to get this to occur using human derived stem cells."
Hickman's work, funded through the National Institute of Neurological Disorders and Stroke (NINDS) at the National Institutes of Health, is described in the December issue of Biomaterials. (http://www.sciencedirect.com/science/article/pii/S0142961211010556)
Hickman is excited about the future of his research because several federal agencies recently launched an ambitious plan to jump-start research in "human-on-a-chip" models by making available at least $140 million in grant funding.
The National Institutes of Health (NIH), the Defense Advanced Research Projects Agency (DARPA), and the Federal Drug Administration (FDA) are leading the research push.
The goal of the call for action is to produce systems that include various miniature organs connected in realistic ways to simulate human body function. This would make it possible, for instance, to test drugs on human cells well before they could safely and ethically be tested on living humans. The technique could potentially be more effective than testing in mice and other animals currently used to screen promising drug candidates and to develop other medical treatments.
Such conventional animal testing is not only slow and expensive, but often leads to failures that might be overcome with better testing options. The limitations of conventional testing options have dramatically slowed the emergence of new drugs, Hickman said.
The successful UCF technique began with a collaborator, Brown University Professor Emeritus Herman Vandenburgh, who collected muscle stem cells via biopsy from adult volunteers. Stem cells are cells that can, under the right conditions, grow into specific forms. They can be found among normal cells in adults, as well as in developing fetuses.
Nadine Guo, a UCF research professor, conducted a series of experiments and found that numerous conditions had to come together just right to make the muscle and spinal cord cells "happy" enough to join and form working junctions. This meant exploring different concentrations of cells and various timescales, among other parameters, before hitting on the right conditions.
"Right now we rely a lot on animal systems for medical research but this is a pure human system," Guo said. "This work proved that, biologically, this is workable."
Besides being a key requirement for any complete human-on-a-chip model, such nerve-muscle junctions might themselves prove important research tools. These junctions play key roles in Amyotrophic lateral sclerosis, commonly known as Lou Gehrig's disease, in spinal cord injury, and in other debilitating or life threatening conditions. With further development, the team's techniques could be used to test new drugs or other treatments for these conditions even before more expansive chip-based models are developed.
Metabolic defects in mice corrected with transplanted embryonic neurons
A new study has revealed that immature neurons taken from healthy mouse embryos can repair damaged brain circuitry and partially normalize metabolism when transplanted into adult mice that have grown morbidly obese due to a genetic deficiency. This proof-of-principle discovery represents one step down a long road toward neuronal replacement therapy, which researchers hope might one day be used to repair brains that have been injured by trauma or disease.
Their study appears in the 25 November 2011 issue of the journal Science, which is published by AAAS, the nonprofit science society.
"We chose this problem not because, even for a moment, we would pursue the idea of neuron transplantation for the treatment of obesity," explained Jeffrey Macklis from Harvard University, a corresponding author of the report. "What we did was take this very complicated circuitry in the hypothalamus that has a very clear, measurable outcome—not only obesity in the mice, but changes in their serum glucose (like diabetic human beings have), changes in their insulin levels and changes in their fat vs. lean body weights—and we used that complex circuitry as a test case for whether precisely selected and controlled neuron transplants could really rewire the brain."
The transplanted neurons did apparently restore leptin signaling in the brains of the obese mice because the rodents slimmed down and their metabolism began returning to normal levels, according to Czupryn and his colleagues.
"What we found is that these neurons not only turned into the right kinds of cells, but that they sent signals to the recipients' brain and received signals from the recipients' brain," said Macklis.
Although the researchers say that neuronal replacement is certainly not a practical approach to treating obesity, their study nonetheless provides evidence that the transplantation of donor neurons at the appropriate stage of development can promote functional recovery of a brain region that controls a complex phenotype.
Source : American Association for the Advancement of Science
Their study appears in the 25 November 2011 issue of the journal Science, which is published by AAAS, the nonprofit science society.
"We chose this problem not because, even for a moment, we would pursue the idea of neuron transplantation for the treatment of obesity," explained Jeffrey Macklis from Harvard University, a corresponding author of the report. "What we did was take this very complicated circuitry in the hypothalamus that has a very clear, measurable outcome—not only obesity in the mice, but changes in their serum glucose (like diabetic human beings have), changes in their insulin levels and changes in their fat vs. lean body weights—and we used that complex circuitry as a test case for whether precisely selected and controlled neuron transplants could really rewire the brain."
The transplanted neurons did apparently restore leptin signaling in the brains of the obese mice because the rodents slimmed down and their metabolism began returning to normal levels, according to Czupryn and his colleagues.
"What we found is that these neurons not only turned into the right kinds of cells, but that they sent signals to the recipients' brain and received signals from the recipients' brain," said Macklis.
Although the researchers say that neuronal replacement is certainly not a practical approach to treating obesity, their study nonetheless provides evidence that the transplantation of donor neurons at the appropriate stage of development can promote functional recovery of a brain region that controls a complex phenotype.
Source : American Association for the Advancement of Science
Scientists determine how antibody recognizes key sugars on HIV surface
WHAT: HIV is coated in sugars that usually hide the virus from the immune system. Newly published research reveals how one broadly neutralizing HIV antibody actually uses part of the sugary cloak to help bind to the virus. The antibody binding site, called the V1/V2 region, represents a suitable HIV vaccine target, according to the scientists who conducted the study. In addition, their research reveals the detailed structure of the V1/V2 region, the last part of the virus surface to be visualized at the atomic level.
Some people who have been infected with HIV for several years begin to make antibodies that can neutralize a wide range of virus strains. These broadly neutralizing antibodies bind to one of four sites on the virus. One site involves a sugar at a spot called amino acid residue 160. (Amino acids are the building blocks of proteins.) The sugar is located on the protein-based spikes that jut out of the surface of HIV.
The new study demonstrates how a broadly neutralizing HIV antibody called PG9 disarms the virus by grabbing hold of the sugar at residue 160, along with part of a second sugar and a short string of amino acid residues in the V1/V2 region of an HIV spike.
Similarly, a separate, recently published report* from the IAVI Neutralizing Antibody Center at The Scripps Research Institute showed how a different broadly neutralizing HIV antibody also binds to the virus via two sugars and a string of amino acid residues. Taken together, these two studies indicate that in some cases, the combination of viral sugars and amino acids can form the binding site for broadly neutralizing HIV antibodies.
The new study may also help scientists who are examining data from the clinical trial of the first HIV vaccine to demonstrate effectiveness in people (http://www.niaid.nih.gov/news/newsreleases/2009/Pages/ThaiVaxStudy.aspx). Recent analyses of blood samples from that trial showed that study participants who were vaccinated and then developed antibodies to the V1/V2 region were less likely to become infected. Although the role of those antibodies in protection against HIV is unknown, this finding underscores how understanding antibody-V1/V2 binding could aid the design of a more effective HIV vaccine.
Source : NIH/National Institute of Allergy and Infectious Diseases
Some people who have been infected with HIV for several years begin to make antibodies that can neutralize a wide range of virus strains. These broadly neutralizing antibodies bind to one of four sites on the virus. One site involves a sugar at a spot called amino acid residue 160. (Amino acids are the building blocks of proteins.) The sugar is located on the protein-based spikes that jut out of the surface of HIV.
The new study demonstrates how a broadly neutralizing HIV antibody called PG9 disarms the virus by grabbing hold of the sugar at residue 160, along with part of a second sugar and a short string of amino acid residues in the V1/V2 region of an HIV spike.
Similarly, a separate, recently published report* from the IAVI Neutralizing Antibody Center at The Scripps Research Institute showed how a different broadly neutralizing HIV antibody also binds to the virus via two sugars and a string of amino acid residues. Taken together, these two studies indicate that in some cases, the combination of viral sugars and amino acids can form the binding site for broadly neutralizing HIV antibodies.
The new study may also help scientists who are examining data from the clinical trial of the first HIV vaccine to demonstrate effectiveness in people (http://www.niaid.nih.gov/news/newsreleases/2009/Pages/ThaiVaxStudy.aspx). Recent analyses of blood samples from that trial showed that study participants who were vaccinated and then developed antibodies to the V1/V2 region were less likely to become infected. Although the role of those antibodies in protection against HIV is unknown, this finding underscores how understanding antibody-V1/V2 binding could aid the design of a more effective HIV vaccine.
Source : NIH/National Institute of Allergy and Infectious Diseases
Blood Type Diet
Here is a new diet and exercise plan that is tailored to individuals' needs according to their blood type. The creator of this new diet plan, Dr. Peter J. D'Adamo N.D., maintains that dieting according to hereditary traits alone is too broad to be as effective as his approach, which focuses on the individual's specific biochemistry. According to Dr. D'Adamo, knowing our blood type can help up make informed choices regarding which foods to eat, which ones to avoid, and how to balance diet with exercise.
What's your blood type?
Follow the link to find out what you should be eating!
The ABCC9 of sleep: A genetic factor regulates how long we sleep
A new study reveals that there is a gene found in the genetic code that regulates how we sleep. While other things are still a factor (ie age, and sex) the gene helps regulate how long each individual sleeps.
Bioterror fears could block crucial flu research
There is new research on H5N1 flu strains that is not being published yet due to fear of bioterror effect because within the paper lies a theoretical mutation that could make H5N1 a lethal human pandemic. H5N1 already kills those that it infects, but it cannot be passed from person to person. Reprts say that this study could show a way that the infection could jump hosts from human to human which could be disastrous. The article was submitted to Science magazine, but it was passed on to National Science Advisory Board for Biosecurity.
It Could Be Old Age, or It Could Be Low B12
New research in the field of Alzheimer’s research is finding that along with sodium receptors in your brain, low levels of the vitamin B12 could be contributing to memory loss. Low B12 usually leads to anemia, low blood pressure, and cognitive problems, such as memory loss. People most at risk are vegetarians or vegans because plant material has very little B12. Scientists suggest taking B12 vitamin supplements to improve memory and cognitive functions.
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