Whether different odors can be quickly distinguished depends on certain synapses in the brain that inhibit nerve stimulation. The researchers in Professor Dr. Thomas Kuner's team at the Institute of Anatomy and Cell Biology at Heidelberg University Medical School and Dr. Andreas Schäfer at the Max Planck Institute for Medical Research have shown that mice in which a certain receptor in the olfactory center is missing can distinguish similar smells more quickly than mice without genetic manipulation. This behavior was directly attributed to inhibitor loops between adjacent nerve cells.
The discovery of the activation principle of "lateral inhibition" in the eye 43 years ago by Haldan K. Hartline, George Wald, and Ragnar Granit was honored with a Nobel Prize. The Heidelberg researchers have for the first time succeeded in confirming the same mechanism for the olfactory system, from the molecular level to behavior. The results of the studies were published in the prestigious journal "Neuron".
Odors attach to receptors of olfactory cells in nasal mucosa, where they trigger nerve signals. These signals are processed in what is known as the olfactory bulb, a part of the brain. In the neuronal network, the incoming signal is converted to a specific electrical pattern that is transmitted to the cerebral cortex and other areas of the brain and is recognized there. Local inhibitor loops make recognizing smells more preciseM I B S I T B T
Wednesday, November 9, 2011
Fluorescent compounds make tumors glow....New research reveals.
A series of novel imaging agents could light up tumors as they begin to form – before they turn deadly – and signal their transition to aggressive cancers. The compounds – fluorescent inhibitors of the enzyme cyclooxygenase-2 (COX-2) – could have broad applications for detecting tumors earlier, monitoring a tumor's transition from pre-malignancy to more aggressive growth, and defining tumor margins during surgical removal.
"We're very excited about these new agents and are moving forward to develop them for human clinical trials," said Lawrence Marnett, Ph.D., the leader of the Vanderbilt University team that developed the compounds, which are described in the May 1 issue of Cancer Research. COX-2 is an attractive target for molecular imaging. It's not found in most normal tissues, and then it is "turned on" in inflammatory lesions and tumors, Marnett explained.
"COX-2 is expressed at the earliest stages of pre-malignancy – in pre-malignant lesions, but not in surrounding normal tissue – and as a tumor grows and becomes increasingly malignant, COX-2 levels go up," Marnett said. Compounds that bind selectively to COX-2 – and carry a fluorescent marker – should act as "beacons" for tumor cells and for inflammation.
Marnett and his colleagues previously demonstrated that fluorescent COX-2 inhibitors – which they have now dubbed "fluorocoxibs" – were useful probes for protein binding, but their early molecules were not appropriate for cellular or in vivo imaging. "It was a real challenge to make a compound that is COX-2 selective (doesn't bind to the related COX-1 enzyme), has desirable fluorescence properties, and gets to the tissue in vivo," Marnett said.
To develop such compounds, Jashim Uddin, Ph.D., research assistant professor of Biochemistry, started with the "core" chemical structure of the anti-inflammatory medicines indomethacin and celecoxib. He then tethered various fluorescent parts to the core structure, ultimately synthesizing more than 200 compounds. The group tested each compound for its interaction with purified COX-2 and COX-1 proteins and then assessed promising compounds for COX-2 selectivity and fluorescence in cultured cells and in animals. Two compounds made the cut.M I B S I T B T
"We're very excited about these new agents and are moving forward to develop them for human clinical trials," said Lawrence Marnett, Ph.D., the leader of the Vanderbilt University team that developed the compounds, which are described in the May 1 issue of Cancer Research. COX-2 is an attractive target for molecular imaging. It's not found in most normal tissues, and then it is "turned on" in inflammatory lesions and tumors, Marnett explained.
"COX-2 is expressed at the earliest stages of pre-malignancy – in pre-malignant lesions, but not in surrounding normal tissue – and as a tumor grows and becomes increasingly malignant, COX-2 levels go up," Marnett said. Compounds that bind selectively to COX-2 – and carry a fluorescent marker – should act as "beacons" for tumor cells and for inflammation.
Marnett and his colleagues previously demonstrated that fluorescent COX-2 inhibitors – which they have now dubbed "fluorocoxibs" – were useful probes for protein binding, but their early molecules were not appropriate for cellular or in vivo imaging. "It was a real challenge to make a compound that is COX-2 selective (doesn't bind to the related COX-1 enzyme), has desirable fluorescence properties, and gets to the tissue in vivo," Marnett said.
To develop such compounds, Jashim Uddin, Ph.D., research assistant professor of Biochemistry, started with the "core" chemical structure of the anti-inflammatory medicines indomethacin and celecoxib. He then tethered various fluorescent parts to the core structure, ultimately synthesizing more than 200 compounds. The group tested each compound for its interaction with purified COX-2 and COX-1 proteins and then assessed promising compounds for COX-2 selectivity and fluorescence in cultured cells and in animals. Two compounds made the cut.M I B S I T B T
Did You know ? 1 in 25 people have gene that causes heart failure in India
One in 25 people from India and other south Asian countries carries a mutated gene that causes heart failure.
Studying this gene, and the protein it encodes, could lead to new treatments for heart failure, Loyola University Health System researcher Sakthivel Sadayappan, PhD, wrote in a recent review article in the Journal of Molecular and Cellular Cardiology. Sadayappan has studied the gene and protein for 15 years. Investigating the protein could provide "a better understanding of the mechanics of heart function during health and disease," Sadayappan and first author David Barefield wrote. Barefield is a graduate student and Sadayappan is an assistant professor in the Department of Cell and Molecular Physiology at Loyola University Chicago Stritch School of Medicine.
Previous studies by Sadayappan and other researchers found that about 4 percent of people who live in India, Pakistan, Sri Lanka, Indonesia and Malaysia carry the mutation. Carriers have about a 90 percent chance of developing heart failure after age 45. About 60 million people worldwide, including about 40 million Indians, carry the mutation. (Sadayappan, who is from India, is not a carrier.) Sadayappan said the mutation likely arose in a single person roughly 33,000 years ago, and spread throughout south Asia.
The gene encodes for a protein, called cardiac myosin binding protein-C (cMyBP-C), that is critical for the normal functioning of the heart. In the mutated gene, 25 base pairs (DNA letters) are missing. As a result, the tail end of the protein is altered. Due to this modification, the protein is not properly incorporated into the functioning unit of cardiac muscle called sarcomere. Consequently, the heart does not contract properly. In younger carriers, the heart can compensate for this defect. But as the person ages, his or her heart is no longer able to compensate. Heart muscle becomes inflamed and does not work well, a condition called cardiomyopathy. The most common manifestation of cardiomyopathy is heart failure -- the heart can't pump enough blood to the rest of the body.M I B S I T B T
Studying this gene, and the protein it encodes, could lead to new treatments for heart failure, Loyola University Health System researcher Sakthivel Sadayappan, PhD, wrote in a recent review article in the Journal of Molecular and Cellular Cardiology. Sadayappan has studied the gene and protein for 15 years. Investigating the protein could provide "a better understanding of the mechanics of heart function during health and disease," Sadayappan and first author David Barefield wrote. Barefield is a graduate student and Sadayappan is an assistant professor in the Department of Cell and Molecular Physiology at Loyola University Chicago Stritch School of Medicine.
Previous studies by Sadayappan and other researchers found that about 4 percent of people who live in India, Pakistan, Sri Lanka, Indonesia and Malaysia carry the mutation. Carriers have about a 90 percent chance of developing heart failure after age 45. About 60 million people worldwide, including about 40 million Indians, carry the mutation. (Sadayappan, who is from India, is not a carrier.) Sadayappan said the mutation likely arose in a single person roughly 33,000 years ago, and spread throughout south Asia.
The gene encodes for a protein, called cardiac myosin binding protein-C (cMyBP-C), that is critical for the normal functioning of the heart. In the mutated gene, 25 base pairs (DNA letters) are missing. As a result, the tail end of the protein is altered. Due to this modification, the protein is not properly incorporated into the functioning unit of cardiac muscle called sarcomere. Consequently, the heart does not contract properly. In younger carriers, the heart can compensate for this defect. But as the person ages, his or her heart is no longer able to compensate. Heart muscle becomes inflamed and does not work well, a condition called cardiomyopathy. The most common manifestation of cardiomyopathy is heart failure -- the heart can't pump enough blood to the rest of the body.M I B S I T B T
Fond of Dark Chocolates...!!! Then good news it lowers blood pressure
For people with hypertension, eating dark chocolate can significantly reduce blood pressure. Researchers writing in the open access journal BMC Medicine combined the results of 15 studies into the effects of flavanols, the compounds in chocolate which cause dilation of blood vessels, on blood pressure.
Dr Karin Ried worked with a team of researchers from the University of Adelaide, Australia, to conduct the analysis. She said, "Flavanols have been shown to increase the formation of endothelial nitric oxide, which promotes vasodilation and consequently may lower blood pressure. There have, however, been conflicting results as to the real-life effects of eating chocolate. We've found that consumption can significantly, albeit modestly, reduce blood pressure for people with high blood pressure but not for people with normal blood pressure".
The pressure reduction seen in the combined results for people with hypertension, 5mm Hg systolic, may be clinically relevant – it is comparable to the known effects of 30 daily minutes of physical activity (4-9mm Hg) and could theoretically reduce the risk of a cardiovascular event by about 20% over five years. The researchers are cautious, however, "The practicability of chocolate or cocoa drinks as long-term treatment is questionable", said Dr Ried.
Source : BioMed CentralM I B S I T B T
Dr Karin Ried worked with a team of researchers from the University of Adelaide, Australia, to conduct the analysis. She said, "Flavanols have been shown to increase the formation of endothelial nitric oxide, which promotes vasodilation and consequently may lower blood pressure. There have, however, been conflicting results as to the real-life effects of eating chocolate. We've found that consumption can significantly, albeit modestly, reduce blood pressure for people with high blood pressure but not for people with normal blood pressure".
The pressure reduction seen in the combined results for people with hypertension, 5mm Hg systolic, may be clinically relevant – it is comparable to the known effects of 30 daily minutes of physical activity (4-9mm Hg) and could theoretically reduce the risk of a cardiovascular event by about 20% over five years. The researchers are cautious, however, "The practicability of chocolate or cocoa drinks as long-term treatment is questionable", said Dr Ried.
Source : BioMed CentralM I B S I T B T
Brief Illustration Of Transgenic Method For Creating Transgenic Mice
Genetically engineered animals have been used from decades. These genetically engineered or modified animals play a vital role in the unearthing, development and improvement of new methods and techniques of the treatment of many diseases that had been a threat to the survival and healthy way of life of the mankind. Their different techniques (such as the use of transgenic mice, knockout mice and others) help the genetic engineers and researchers to differentiate new strings of human genome. Due to their graceful work, pharmaceutical industry has grown extensively and helped mankind in the treatment of various deadly diseases and still on the road of development. Because of the development of biomedical research, the use of transgenic animals has been considerably increased. According to the government rules and regulations and other renowned pharmaceutical companies’ inflexible reviews, authorize the use of transgenic animals when there is no alternative left. In the twentieth century, all biomedical and pharmaceutical breakthroughs are the upshot of research on animals.
There are two major techniques for commencing transgenic method in mice, which are pronuclear injection and embryonic stem cells. Pronuclear injection means that peculiar DNA is injected in the pronucleus of a fertilized egg of a mouse which is then integrated in the genome at unsystematic location mostly after two cell divisions. It means that the mouse will be partial transgenic in nature because that peculiar DNA is not a part in each and every cell of the body. The sperms or eggs of these partial transgenic mice are then manipulated to produce entirely Transgenic mice in the next generation. Another method of creating transgenic mice, embryonic stem cells, is inducing DNA in the stem cells of embryo which is randomly integrated in the genome. However, if it has a structure alike to the existing fraction of genome then it goes through the homologous recombination and a sole copy is incorporated at a particular location in the genome. These peculiar cells are then injected into the host embryo, allowing them to grow and be a part of it. Chimera is a terminology that is used for a mouse that is grown from the host embryo, which is created from embryonic cells of two separate mice. Several sperms generated by chimera would be transgenic in nature and as soon as they fertilize a regular egg, the result would be fully transgenic mice comprising that peculiar DNA in every cell.
Guest Post by Sophie Alexander from http://www.transposagenbio.com/
Transposagen Biopharmaceuticals, Inc.
145 Graham Avenue, A217
Lexington, KY 40506
M I B S I T B T
There are two major techniques for commencing transgenic method in mice, which are pronuclear injection and embryonic stem cells. Pronuclear injection means that peculiar DNA is injected in the pronucleus of a fertilized egg of a mouse which is then integrated in the genome at unsystematic location mostly after two cell divisions. It means that the mouse will be partial transgenic in nature because that peculiar DNA is not a part in each and every cell of the body. The sperms or eggs of these partial transgenic mice are then manipulated to produce entirely Transgenic mice in the next generation. Another method of creating transgenic mice, embryonic stem cells, is inducing DNA in the stem cells of embryo which is randomly integrated in the genome. However, if it has a structure alike to the existing fraction of genome then it goes through the homologous recombination and a sole copy is incorporated at a particular location in the genome. These peculiar cells are then injected into the host embryo, allowing them to grow and be a part of it. Chimera is a terminology that is used for a mouse that is grown from the host embryo, which is created from embryonic cells of two separate mice. Several sperms generated by chimera would be transgenic in nature and as soon as they fertilize a regular egg, the result would be fully transgenic mice comprising that peculiar DNA in every cell.
Guest Post by Sophie Alexander from http://www.transposagenbio.com/
Transposagen Biopharmaceuticals, Inc.
145 Graham Avenue, A217
Lexington, KY 40506
M I B S I T B T
Why fish don't freeze in the Arctic Ocean
Temperatures of minus 1.8 ° C should really be enough to freeze any fish: the freezing point of fish blood is about minus 0.9 ° C. How Antarctic fish are able to keep moving at these temperatures has interested researchers for a long time. As long as 50 years ago, special frost protection proteins were found in the blood of these fish. These so-called anti-freeze proteins work better than any household antifreeze. How they work, however, was still unclear. The Bochum researchers used a special technique, terahertz spectroscopy, to unravel the underlying mechanism. With the aid of terahertz radiation, the collective motion of water molecules and proteins can be recorded. Thus, the working group has already been able to show that water molecules, which usually perform a permanent dance in liquid water, and constantly enter new bonds, dance a more ordered dance in the presence of proteins – "the disco dance becomes a minuet" says Prof. Havenith.
Souvenir from an Antarctic expedition
The subject of the current investigations was the anti-freeze glycoproteins of the Antarctic toothfish Dissostichus mawsoni, which one of the American partners, Arthur L. Devries, had fished himself on an Antarctic expedition. "We could see that the protein has an especially long-range effect on the water molecules around it. We speak of an extended dynamical hydration shell", says co-author Konrad Meister. "This effect, which prevents ice crystallization, is even more pronounced at low temperatures than at room temperature", adds Prof. Havenith. Nevertheless, to freeze the water, lower temperatures would be necessary. Complexation of the AFP by borate strongly reduces the antifreeze activity. In this case, the researchers also found no change in the terahertz dance. The researchers' results provide evidence for a new model of how AFGPs prevent water from freezing: Antifreeze activity is not achieved by a single molecular binding between the protein and the water, but instead AFP perturbs the aqueous solvent over long distances. The investigation demonstrated for the first time a direct link between the function of a protein and its signature in the terahertz range. The studies were funded by the Volkswagen Foundation.
Source : Ruhr-University BochumM I B S I T B T
Souvenir from an Antarctic expedition
The subject of the current investigations was the anti-freeze glycoproteins of the Antarctic toothfish Dissostichus mawsoni, which one of the American partners, Arthur L. Devries, had fished himself on an Antarctic expedition. "We could see that the protein has an especially long-range effect on the water molecules around it. We speak of an extended dynamical hydration shell", says co-author Konrad Meister. "This effect, which prevents ice crystallization, is even more pronounced at low temperatures than at room temperature", adds Prof. Havenith. Nevertheless, to freeze the water, lower temperatures would be necessary. Complexation of the AFP by borate strongly reduces the antifreeze activity. In this case, the researchers also found no change in the terahertz dance. The researchers' results provide evidence for a new model of how AFGPs prevent water from freezing: Antifreeze activity is not achieved by a single molecular binding between the protein and the water, but instead AFP perturbs the aqueous solvent over long distances. The investigation demonstrated for the first time a direct link between the function of a protein and its signature in the terahertz range. The studies were funded by the Volkswagen Foundation.
Source : Ruhr-University BochumM I B S I T B T
Mosquitoes use several different kinds of odor sensors to track human prey...Quite intelligent..!!!
It now appears that the malaria mosquito needs more than one family of odor sensors to sniff out its human prey. The experiments described in the paper provide striking new evidence that Anopheles gambiae – the species of mosquito that spreads malaria that infects some 250 million and kills 900,000 people annually – has a second set of olfactory sensors that are fundamentally different from the set of sensors that scientists have known about and have been studying for the last 10 years.
The discovery may help explain a puzzling question that has been plaguing scientists trying to develop new and more effective forms of mosquito lures and repellents: "The ORs [odorant receptors] that were identified in the lab before don't respond to a lot of human odors," says Vanderbilt graduate student Chao Liu, who is the lead author on the paper. "Now that we have a new set of receptors, we may be able to fill in the picture."
There is a good chance that this new set of receptors may be specifically tuned to detect a number of the odorants given off by humans, adds co-author R. Jason Pitts, a senior research specialist and graduate student at Vanderbilt. "If this is the case then it is quite likely that it will play a critical role in attempts to develop improved lures and repellents to control the spread of malaria." According to Pitts, they also have preliminary evidence that the mosquito's olfactory system may include additional families of sensors as well.
Vanderbilt Professor of Biological Sciences and Pharmacology Laurence Zwiebel, who was the principal investigator on the study, heads a major interdisciplinary research project to develop new ways to control by spread of malaria based on mosquito olfaction supported by the Grand Challenges in Global Health Initiative funded by the Foundation for NIH through a grant from the Bill & Melinda Gates Foundation.
"It's not at all surprising that the mosquito's olfactory system is more sophisticated than we thought," says Zwiebel. "Olfaction is absolutely essential to the mosquito. If the female cannot find a host for a blood meal she cannot reproduce. As a result, mosquitoes have developed an uncanny ability to detect odors. This is true of all species of mosquitoes, not just Anopheles. So it is highly likely that the mosquitoes that spread West Nile, dengue fever, yellow fever and encephalitis also have similar sets of odor sensors."
About ten years ago, when the mosquito genome was first sequenced, scientists at Vanderbilt and Yale identified the genes and the structure of one set of Anopheles sensors, called odorant receptors (AgORs). At first, they thought that these receptors had the same basic design as the sensors found in the nose of humans and other mammals. But recent studies have found that the mosquito receptors, along with those of several other insects, have a distinctly different structure.
Researchers have identified about 75 different AgORs that respond to a variety of volatile compounds. These receptors are expressed on the surface of nerves located in tiny hollow spikes, called sensilla, located on the mosquito's antennae. When a target molecule wafts into the interior of one of these sensilla and comes into contact with the AgOR designed to detect it, the receptor causes the nerve to fire, signaling the compound's presence. Earlier this year the Vanderbilt researchers and their colleagues at Yale succeeded in pairing more than 40 of the AgORs with the specific odorants that trigger them. In the process, the researchers discovered that these receptors are broadly tuned. That is, each receptor responds to a number of different compounds. They also overlap. More than one AgOR responds to individual odorants.
As a result, last year when scientists at Rockefeller University announced they had discovered a second set of olfactory receptors in the fruit fly Drosophila melanogaster, an animal model for basic genetics, "it was like a light switched on," says Pitts. Because of the many parallels between the olfactory systems of the fruit fly and mosquito, the Vanderbilt researchers knew it was extremely likely that the mosquito had a second set of receptors as well. So they began searching for them.The search was successful and the researchers identified genes that code for about 50 versions of the new type receptor. The new receptors appear to have a slightly different structure from that of AgORs: They are called "ionotropic receptors" (AgIRs) and they closely resemble the type of receptor found in the brain that responds to the common neurotransmitter, glutamate.
At this point, the researchers can only speculate about what effect this structural difference has on the way that the AgIRs function as odor detectors. However, they have managed to associate an AgIR with butylamine, a human odorant that AgORs do not appear to identify. Butylamine sensitivity is located in grooved peg sensilla, a type of sensory hair on the mosquito antennae. The correlation of AgIR to butylamine could indicate that AgIRs are responsible for grooved peg sensilla sensitivities to other human odors such as ammonia and lactic acid, an idea that the Zwiebel Lab has begun exploring.
The basic problem facing the mosquito searching for human prey – and the humans who are trying to figure out how it does it – is that none of the hundreds of odors given off by humans are necessarily unique. They are actually produced by the bacteria that live on human skin. But these bacteria live on other animals as well. So the current theory is that mosquitoes must identify a blend of different odorants that provide a unique signature for humans. Determining the way that the AgIRs work may be the key to identifying such a signature and that, in turn, could be the key to developing non-toxic, ecologically benign methods for combating malaria and other mosquito-borne illnesses.
Source : Vanderbilt University
The discovery may help explain a puzzling question that has been plaguing scientists trying to develop new and more effective forms of mosquito lures and repellents: "The ORs [odorant receptors] that were identified in the lab before don't respond to a lot of human odors," says Vanderbilt graduate student Chao Liu, who is the lead author on the paper. "Now that we have a new set of receptors, we may be able to fill in the picture."
There is a good chance that this new set of receptors may be specifically tuned to detect a number of the odorants given off by humans, adds co-author R. Jason Pitts, a senior research specialist and graduate student at Vanderbilt. "If this is the case then it is quite likely that it will play a critical role in attempts to develop improved lures and repellents to control the spread of malaria." According to Pitts, they also have preliminary evidence that the mosquito's olfactory system may include additional families of sensors as well.
Vanderbilt Professor of Biological Sciences and Pharmacology Laurence Zwiebel, who was the principal investigator on the study, heads a major interdisciplinary research project to develop new ways to control by spread of malaria based on mosquito olfaction supported by the Grand Challenges in Global Health Initiative funded by the Foundation for NIH through a grant from the Bill & Melinda Gates Foundation.
"It's not at all surprising that the mosquito's olfactory system is more sophisticated than we thought," says Zwiebel. "Olfaction is absolutely essential to the mosquito. If the female cannot find a host for a blood meal she cannot reproduce. As a result, mosquitoes have developed an uncanny ability to detect odors. This is true of all species of mosquitoes, not just Anopheles. So it is highly likely that the mosquitoes that spread West Nile, dengue fever, yellow fever and encephalitis also have similar sets of odor sensors."
About ten years ago, when the mosquito genome was first sequenced, scientists at Vanderbilt and Yale identified the genes and the structure of one set of Anopheles sensors, called odorant receptors (AgORs). At first, they thought that these receptors had the same basic design as the sensors found in the nose of humans and other mammals. But recent studies have found that the mosquito receptors, along with those of several other insects, have a distinctly different structure.
Researchers have identified about 75 different AgORs that respond to a variety of volatile compounds. These receptors are expressed on the surface of nerves located in tiny hollow spikes, called sensilla, located on the mosquito's antennae. When a target molecule wafts into the interior of one of these sensilla and comes into contact with the AgOR designed to detect it, the receptor causes the nerve to fire, signaling the compound's presence. Earlier this year the Vanderbilt researchers and their colleagues at Yale succeeded in pairing more than 40 of the AgORs with the specific odorants that trigger them. In the process, the researchers discovered that these receptors are broadly tuned. That is, each receptor responds to a number of different compounds. They also overlap. More than one AgOR responds to individual odorants.
As a result, last year when scientists at Rockefeller University announced they had discovered a second set of olfactory receptors in the fruit fly Drosophila melanogaster, an animal model for basic genetics, "it was like a light switched on," says Pitts. Because of the many parallels between the olfactory systems of the fruit fly and mosquito, the Vanderbilt researchers knew it was extremely likely that the mosquito had a second set of receptors as well. So they began searching for them.The search was successful and the researchers identified genes that code for about 50 versions of the new type receptor. The new receptors appear to have a slightly different structure from that of AgORs: They are called "ionotropic receptors" (AgIRs) and they closely resemble the type of receptor found in the brain that responds to the common neurotransmitter, glutamate.
At this point, the researchers can only speculate about what effect this structural difference has on the way that the AgIRs function as odor detectors. However, they have managed to associate an AgIR with butylamine, a human odorant that AgORs do not appear to identify. Butylamine sensitivity is located in grooved peg sensilla, a type of sensory hair on the mosquito antennae. The correlation of AgIR to butylamine could indicate that AgIRs are responsible for grooved peg sensilla sensitivities to other human odors such as ammonia and lactic acid, an idea that the Zwiebel Lab has begun exploring.
The basic problem facing the mosquito searching for human prey – and the humans who are trying to figure out how it does it – is that none of the hundreds of odors given off by humans are necessarily unique. They are actually produced by the bacteria that live on human skin. But these bacteria live on other animals as well. So the current theory is that mosquitoes must identify a blend of different odorants that provide a unique signature for humans. Determining the way that the AgIRs work may be the key to identifying such a signature and that, in turn, could be the key to developing non-toxic, ecologically benign methods for combating malaria and other mosquito-borne illnesses.
Source : Vanderbilt University
Wednesday, October 12, 2011
Tuesday, September 13, 2011
Are sharks color blind?
Sharks are unable to distinguish colors, even though their close relatives rays and chimaeras have some color vision, according to new research by Dr. Nathan Scott Hart and colleagues from the University of Western Australia and the University of Queensland in Australia. Their study shows that although the eyes of sharks function over a wide range of light levels, they only have a single long-wavelength-sensitive cone* type in the retina and therefore are potentially totally color blind. Hart and team's findings are published online in Springer's journal Naturwissenschaften – The Science of Nature.
"This new research on how sharks see may help to prevent attacks on humans and assist in the development of fishing gear that may reduce shark bycatch in long-line fisheries. Our study shows that contrast against the background, rather than colour per se, may be more important for object detection by sharks. This may help us to design long-line fishing lures that are less attractive to sharks as well as to design swimming attire and surf craft that have a lower visual contrast to sharks and, therefore, are less 'attractive' to them," said Prof. Hart.
Sharks are efficient predators and their evolutionary success is thought to be due in part to an impressive range of sensory systems, including vision. To date, it is unclear whether sharks have color vision, despite well-developed eyes and a large sensory brain area dedicated to the processing of visual information. In an attempt to demonstrate whether or not sharks have color vision, Hart and colleagues used a different technique - microspectrophotometry - to identify cone visual pigments in shark retinas and measure their spectral absorbance.
They looked at the retinas of 17 shark species caught in a variety of waters in both Queensland and Western Australia. Rod cells were the most common type of photoreceptor in all species. In ten of the 17 species, no cone cells were observed. However, cones were found in the retinae of 7 species of shark from three different families and in each case only a single type of long-wavelength-sensitive cone photoreceptor was present. Hart and team's results provide strong evidence that sharks possess only a single cone type, suggesting that sharks may be cone monochromats, and therefore potentially totally color blind.
The authors conclude : "While cone monochromacy on land is rare, it may be a common strategy in the marine environment. Many aquatic mammals − whales, dolphins and seals − also possess only a single, green-sensitive cone type. It appears that both sharks and marine mammals may have arrived at the same visual design by convergent evolution, in other words, they acquired the same biological trait in unrelated lineages."
Source : Springer
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New TB vaccine enters proof-of-concept trial in people living with HIV
Aeras and the Oxford-Emergent Tuberculosis Consortium (OETC) announce today the start of a Phase IIb proof-of-concept efficacy trial of a new investigational tuberculosis (TB) vaccine that involves people living with the human immunodeficiency virus (HIV). The trial will be conducted at research sites in Senegal and South Africa with primary funding support from the European and Developing Countries Clinical Trials Partnership (EDCTP). TB is a leading cause of death for people infected with HIV and the second leading infectious disease killer in the world. This is the first proof-of-concept efficacy trial in people infected with HIV using MVA85A, which is being developed by OETC (a joint venture between the University of Oxford and Emergent BioSolutions) and Aeras. It is expected that the trial will generate important safety, immunogenicity and efficacy data about this vaccine.
The trial will test the vaccine candidate in approximately 1,400 adults ages 18-50 who are infected with HIV. The study will be led by the UK Medical Research Council in The Gambia, Aeras, and the University of Oxford, and conducted at two sites by the University of Cape Town (UCT) Institute of Infectious Disease and Molecular Medicine in Khayelitsha, South Africa and Laboratoire de Bacteriologie-Virologie du Centre Hospitalier Universitaire Aristide Le Dantec in Dakar, Senegal. This follows the first proof-of-concept clinical trial of the same candidate TB vaccine, which recently reached full enrollment with almost 3,000 infant participants in South Africa. "Clinical trials of new vaccines against tuberculosis must be an urgent priority on our agenda, as too many lives are lost to TB, especially among people living with HIV," said Member of the European Parliament Michael Cashman. "I recently visited a clinical trial site of this vaccine candidate in infants in South Africa, and I was impressed with the progress. I am anxious to see a new TB vaccine licensed, and I am proud that European Union Member States are investing in this critically-important work."
Professor Charles Mgone, Executive Director of EDCTP, said, "The TB and HIV co-epidemic is devastating, requiring a concerted global response. EDCTP in partnership with Aeras, Oxford-Emergent Tuberculosis Consortium and others is committed to accelerate research and development of this promising vaccine against tuberculosis by co-financing the clinical trial as an essential part in its evaluation."
Tuberculosis kills 1.7 million people per year, and more than two billion people worldwide are infected with TB Рapproximately one out of every three people on the planet. People infected with HIV living in countries with high TB prevalence are 20 times more likely to develop TB than those who are HIV-negative. In 2008, there were an estimated 1.4 million new cases of TB among persons with HIV infection, and TB accounted for 23 percent of AIDS-related deaths, according to the World Health Organization (WHO). The Bacille Calmette-Gu̩rin (BCG) vaccine, the only currently-licensed vaccine against TB, is not effective in preventing adult pulmonary TB, the most common form of the disease. "A new, more effective TB vaccine would be game-changing in international efforts to eliminate TB globally by 2050," said Jim Connolly, President and Chief Executive Officer of Aeras. "Studies have already shown that this promising vaccine has an acceptable safety profile and stimulates strong immune responses in HIV-infected individuals."
Aeras is the trial sponsor, and significant funding is provided by EDCTP, a pan-European body that supports multicenter projects which combine clinical trials, capacity building and networking. This study has been approved by the Medicines Control Council of South Africa, the South African Department of Health, and the Comité National d'Ethique pour la Recherche en Santé (CNERS) in Senegal. The Scientific Institute of Public Health (WIV-ISP) in Belgium, which first identified the antigen 85A for possible use in a vaccine candidate, is providing in-kind laboratory services for the study. "Together with our partners, Emergent BioSolutions is proud to be leading the development of a new vaccine to defeat TB, one of the world's deadliest infectious diseases. This trial is particularly critical because of its focus on adults living with HIV. If we are successful, MVA85A will help make the dream of a world free from TB a reality," said Fuad El-Hibri, Chairman and Chief Executive Officer of Emergent BioSolutions.
"It is great to see the vaccine candidate we initially developed at Oxford University reach this stage of clinical trials," said Dr. Helen McShane, a Wellcome Trust Senior Clinical Research Fellow at the University of Oxford. "In the next few years we should begin to get results on how effective the vaccine is in protecting those who are most at risk of TB. It's our hope that this vaccine will turn out to be a powerful new weapon to combat TB in the parts of the world that need it most."
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