Showing posts with label Science and Technology. Show all posts
Showing posts with label Science and Technology. Show all posts

Autistic Children More Likely To Have Handwriting Problems
Wednesday, November 11, 2009

A new study reveals that Autistic children are more likely to have problems in handwriting than those without autism. The study was conducted by researchers at the Kennedy Krieger Institute. Handwriting samples, motor skills, and visuospatial abilities of children were compared with autism spectrum disorders to typically developing children. The researchers found that handwriting of children with ASD was worse than that of typically developing children. Particularly, children with ASD had trouble forming letters. In other categories like size, alignment, and spacing, their handwriting was comparable to that of typically developing children. Parents of children with ASD are often the first ones to examine their children’s poor handwriting quality. This finding recognises fine motor control as a core source of the problem and reveals that children with ASD may not have difficulties across all domains. By identifying handwriting as a valid impairment, parents, teachers and therapists will now be able to follow techniques that will improve children’s handwriting. "The ability to keep up in classes and convey ideas through handwriting is fundamental to life," said Christina Fuentes, lead study author and researcher at the Kennedy Krieger Institute. "Knowing the causes of impairment allows us to strategically identify techniques that will help children with ASD improve their handwriting”. “Our study suggests that teaching children how to form letters, in combination with general training of fine motor control through techniques that include stabilizing the arm and the use of proper writing utensils, may be the best direction for improving handwriting performance," Fuentes added. The study has been published in the journal, Neurology.

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Gonorrhea Medication Might Help Fight Cancer
Sunday, November 8, 2009

Drugs sometimes have beneficial side effects. A glaucoma treatment causes luscious eyelashes. A blood pressure drug also aids those with a rare genetic disease. The newest surprise discovered by researchers at the Johns Hopkins University School of Medicine is a gonorrhea medication that might help battle cancer. "Often times we are surprised that a drug known to do something else has another hidden property," says Jun Liu, Ph.D., a professor of pharmacology and molecular sciences at Johns Hopkins and author on the study published Oct. 1 in the Proceedings of the National Academy of Sciences. In this case, the surprise is a big one. The drug, acriflavine, used in the 1930s for treating gonorrhea, has turned out to have the previously unknown ability to halt the growth of new blood vessels. Preliminary tests showed that mice engineered to develop cancer had no tumor growth if treated with daily injections of acriflavine. Acriflavine stops blood vessel growth by inhibiting the function of the protein hypoxia-inducible factor (HIF)-1, which was discovered by Semenza's team in 1992. When HIF-1 senses that the surrounding environment is low in oxygen, it turns on genes necessary for building new vessels. Though essential for normal tissue growth and wound healing, HIF-1 is also turned on by cancers to obtain the oxygen they need to survive. Most importantly, in order for HIF-1 to work, two subunits must bind together like puzzle pieces. Most drugs are unable to prevent protein binding because the drug molecules can be much smaller than the proteins they interact with. A medicine must hit just the right spot, a critical domain or pocket on the surface of one protein to stop it from binding to another protein. Even though drugs that stop binding are uncommon, they are such an effective means to stop protein function that Semenza decided to look for one that might block HIF-1. To do that, he turned to the Johns Hopkins Drug Library, a collection of FDA- and internationally approved compounds in that was assembled by Liu. To visualize protein binding, scientists engineered a cell line so that when the HIF-1 subunits came together, they would cause the cell to light up like a firefly. They then tested each of the more than 3,000 drugs in the drug library in hopes of finding one that would turn out the light. Acriflavine did, andfurther studies confirmed that it was binding directly to HIF-1. Liu hopes that acriflavine can one day be incorporated into chemotherapy cocktails, one drug among many that help fight cancer. Hopkins is seeking even more new uses for old drugs. So far, drugs in the library have been screened for use against malaria, uberculosis, HIV and the Ebola virus. In the future, Liu expects even more researchers to take advantage of the library, which is continuing to grow as more drugs are added to the collection. "In the public domain, Hopkins has the largest drug library," says Liu. "The more drugs you have, the more possibilities, the higher the chance you rediscover something that will help." This study was funded by the Johns Hopkins Institute for Cell Engineering and the Foundation for Advanced Research in the Medical Sciences. So keep visiting.

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Bad Driving : Genetic Basis
Friday, October 30, 2009

Now, bad drivers may in part have their genes to blame, suggests a new study by UC Irvine neuroscientists. People with a particular gene variant performed more than 20 percent worse on a driving test than people without it -- and a follow-up test a few days later yielded similar results. About 30 percent of Americans have the variant. "These people make more errors from the get-go, and they forget more of what they learned after time away," said Dr. Steven Cramer, neurology associate professor and senior author of the study published recently in the journal Cerebral Cortex. This gene variant limits the availability of a protein called brain-derived neurotrophic factor during activity. BDNF keeps memory strong by supporting communication among brain cells and keeping them functioning optimally. When a person is engaged in a particular task, BDNF is secreted in the brain area connected with that activity to help the body respond. Previous studies have shown that in people with the variant, a smaller portion of the brain is stimulated when doing a task than in those with a normal BDNF gene. People with the variant also don't recover as well after a stroke. Given these differences, the UCI scientists wondered: Could the variant affect an activity such as driving? "We wanted to study motor behavior, something more complex than finger-tapping," said Stephanie McHughen, graduate student and lead author of the study. "Driving seemed like a good choice because it has a learning curve and it's something most people know how to do." The driving test was taken by 29 people -- 22 without the gene variant and seven with it. They were asked to drive 15 laps on a simulator that required them to learn the nuances of a track programmed to have difficult curves and turns. Researchers recorded how well they stayed on the course over time. Four days later, the test was repeated. Results showed that people with the variant did worse on both tests than the other participants, and they remembered less the second time. "Behavior derives from dozens and dozens of neurophysiologic events, so it's somewhat surprising this exercise bore fruit," Cramer said. The gene variant isn't always bad, though. Studies have found that people with it maintain their usual mental sharpness longer than those without it when neurodegenerative diseases such as Parkinson's, Huntington's and multiple sclerosis are present. "It's as if nature is trying to determine the best approach," Cramer said. "If you want to learn a new skill or have had a stroke and need to regenerate brain cells, there's evidence that having the variant is not good. But if you've got a disease that affects cognitive function, there's evidence it can act in your favor. The variant brings a different balance between flexibility and stability." A test to determine whether someone has the gene variant is not commercially available. Letz wait and watch, what the researchers do further in this field.

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More on DNA Replication
Monday, October 26, 2009

Now a study from the University of North Carolina at Chapel Hill has identified a key player in a molecular process essential for DNA replication within cells. The new findings highlight a protein called FLASH, already shown to play a role in initiating apoptosis, or programmed cell death. Apoptosis is a normal biochemical response that occurs when a cell is damaged beyond repair after viral infection or accumulation of mutations that could lead to uncontrolled cellular proliferation, or cancer. Apoptosis is also crucial to the developing embryo through selective cell death, which allows proper differentiation of physical structures, such as fingers and toes. According to senior study author Zbigniew Dominski, Ph.D., associate professor of biochemistry and biophysics at UNC, the new study demonstrates that FLASH is also required for the proper synthesis of histone messenger RNA, which gives rise to histone proteins. Histones are the chief protein components of chromatin and act as a scaffold allowing packaging of DNA into a condensed form that fits inside the nucleus of a cell. As the DNA interacts with histones and with metabolic signals from within the cell, these proteins help regulate gene expression."Our study suggests for the first time that a potential link exists between the processes of histone messenger RNA formation and apoptosis," Dominski said. "FLASH is crucial for the production of histone messenger RNA, without which the cell can't make the histone proteins around which DNA is packaged."The research is described in the October 23rd issue of the journal Molecular Cell.For the study, Dominski adapted a laboratory system that reproduces in the test tube what normally occurs in the cell when FLASH participates in the biochemical cleavage event that results in mature histone messenger RNA. This enabled his team to explore what might occur when FLASH was added or removed."We could then figure out exactly what portion of FLASH would restore the protein's function in generating histone mRNAs and remarkably, only the first 100 or so amino acids are required. The remaining 2,000 amino acids of this large protein likely control other processes in the cell, including apoptosis and DNA replication" he explained.Co-author William F. Marzluff, Ph.D., is Distinguished Professor of biochemistry & biophysics and executive associate dean for basic research. He noted that FLASH is the first component found in this protein complex "that integrates or initiates many cellular functions -- DNA replication, apoptosis, histone production. Having this small piece of the puzzle makes it a lot easier to identify others."Other UNC coauthors include Xiao-cui Yang, laboratory technician, and Yan Yan, undergraduate student, both of the dept of biochemistry & biophysics and the UNC Program in Molecular Biology and Biotechnology and Brandon D. Burch, graduate student in the Curriculum in Genetics and Molecular Biology.

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Scientists Develop Brain-To-Brain Communication
Sunday, October 18, 2009

A group of scientists at the University of Southampton have developed brain to brain communication, which makes it possible to send messages from one person to other living far apart. In this process, the signal of a person’s brain is carried over the internet to another person staying at a long distance apart. This is called brain-computer interfacing, which allows computers to analyse brain signals and send messages through an internet connection. According to the scientist, Christopher James, this is an initial step to achieve an advanced technology by which people will be able to send own thoughts, images and images directly into the minds of other people. “This could be useful for those people who are locked into their bodies, who can’t speak, can’t even blink,” James also said. As part of the experiment, two people were connected to electrodes that measure activity in specific parts of the brain. Then the first person generated a series of zeros and ones through the movement of arms. It was sent via internet after the first person’s PC converted the signals to the PC of the second person. The scientists saw flashes for one and zero. James clarified, “It’s not telepathy.” He also said, “There’s no conscious thought forming in one person’s head and another conscious thought appearing in another person’s mind.The next experiments are to get that second person to be aware of the information that is being sent to them. For that, I need to get my thinking cap on, so to speak.”

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Nasalsprayformemoryimprovemenmt
Sunday, October 4, 2009

Good news for procrastinating students: a nasal spray developed by a team of German scientists promises to give late night cram sessions a major boost, if a good night's sleep follows. In a research report featured as the cover story of the October 2009 print issue of The FASEB Journal, these scientists show that a molecule from the body's immune system administered through the nose helps the brain retain emotional and procedural memories during REM sleep."Sleep to remember, a dream or reality?" said Lisa Marshall, co-author of the study, from the Department of Neuroendocrinology at the University of Lubeck in Germany. "Here, we provide the first evidence that the immunoregulatory signal interleukin-6 plays a beneficial role in sleep-dependent formation of long-term memory in humans. "To make this discovery, Marshall and colleagues had 17 healthy young men spend two nights in the laboratory. On each night after reading either an emotional or neutral short story, they sprayed a fluid into their nostrils which contained either interleukin-6 or a placebo fluid. The subsequent sleep and brain electric activity was monitored throughout the night. The next morning subjects wrote down as many words as they could remember from each of the two stories. Those who received the dose of IL-6 could remember more words. "If a nasal spray can improve memory, perhaps we're on our way to giving some folks a whiff of common sense, such as accepting the realities of olution," said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal. "This is exciting piece of interdisciplinary science, since IL-6 had previously been considered a by-product of inflammation, not an agent that affects cognition."

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New Genetic discovery in the field of wine
Thursday, September 24, 2009

One of the best known episodes in the 8000-year history of grapevine cultivation led to iological changes that have not been well understood – until now. Through biomolecular detective work, German researchers have uncovered new details about the heredity of Vitis varieties in ltivation today. In the process, they have opened the way to more meaningful classification, accelerated breeding, and more accurate evaluation of the results, potentially breaking a bottleneck in the progress of the wine industry. Their discovery removes a major obstacle to a development already under way – that is, a shift toward grapevine breeding guided by highly specific genetic markers. It may even point the way toward production of European-tasting wines from North American cultivars, free of the "musty" or "foxy" flavors associated with New World grapevines. In response to the "great European wine blight" of the mid-1800s, growers aimed at preserving the most desirable qualities of European grapes while breeding in the hardiness of North American varieties. These were naturally resistant to native pests that had found their way – by steamship, most likely – across the Atlantic to Europe. Beginning around 1860, the introduction of two North American pests – an aphid and a fungus – nearly destroyed the wine industry, particularly in France. A century ago, many hybrids were in use, but the wine they produced was judged to be so inferior in flavor that winemakers were prohibited from blending them with higher-quality traditional wines. Today, breeders as well as growers have many reasons to want to know the heritage of grapevines, and readily observed traits are seldom sufficient. To distinguish among the countless grapevine cultivars, even experts need more than meets the eye. Much of a plant's history can be read on the molecular level, from its DNA and biochemistry, and modern scientific tools have been developed to discern the "fingerprints" of Old World, New World, and hybrid grapevines. New research shows, however, that one of the best established fingerprinting tools is not completely reliable, because it assumes a simpler genetic history than the biomolecular evidence records. The investigation was a collaboration between the Technische Universität München in Bavaria and the JKI Institute for Grapevine Breeding, along the famous Weinstrasse or "wine route" in the Pfalz region. Clues led the researchers to suspect that a difference in a particular phytochemical marker that has long been used to distinguish grape varieties stemmed not from a single gene mutation, but from a double mutation. Furthermore, they revealed, the chromosome bearing the double-mutated gene is one that may also carry a gene responsible for the poor, "musty" aroma of the North American varieties. A complex series of experiments and analyses confirmed this, and ruled out other possible explanations. A detailed description of the methods and results has been published in the Journal of Agricultural and Food Chemistry. The biochemical process at the crux of the investigation is the production of anthocyanin pigments. Red European Vitis vinifera cultivars produce only pigment compounds such as the one called oenin whereas most other Vitis species and hybrids can produce pigment compounds like malvin as well. This subtle difference, which has been used to classify wines according to their varietal origin, had been attributed to a particular gene mutation inherited by the European plants. If that was the whole story, however, certain breeding programs might have been expected to turn on malvin production in European varieties, and this had never been observed.

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Sony To Launch 3-D Television
Thursday, September 3, 2009

Sony Corp, which is one of the world's largest electronic company has decided to launch a liquid-crystal-display television which will be capable of playing 3-D programming. According to sources, the company will launch the liquid-crystal-display television by the end of next year. The Sony is to announce its plans for the new TV next week at the IFA consumer electronics show in Berlin. South Korea's Samsung Electronics Co, LG Electronics Inc and Japan's Panasonic Corp, who are Sony's rivals have also said that they are planning to introduce 3-D products as well because 3-D video for the home is a big money maker. The 3-D plan has come up after Sony Corp incurred losses in its television sector for five years in a row and is undertaking cost cutting measures.

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World's Smallest Semiconductor Laser
Monday, August 31, 2009

Now researchers at the University of California, Berkeley, have reached a new milestone in laser physics by creating the world's smallest semiconductor laser, capable of generating visible light in a space smaller than a single protein molecule. This breakthrough, described in an advanced online publication of the journal Nature on Aug. 30, breaks new ground in the field of optics. The UC Berkeley team not only successfully squeezed light into such a tight space, but found a novel way to keep that light energy from dissipating as it moved along, thereby achieving laser action. "This work shatters traditional notions of laser limits, and makes a major advance toward applications in the biomedical, communications and computing fields," said Xiang Zhang, professor of mechanical engineering and director of UC Berkeley's Nanoscale Science and Engineering Center, which is funded by the National Science Foundation, and head of the research team behind this work. The achievement helps enable the development of such innovations as nanolasers that can probe, manipulate and characterize DNA molecules; optics-based telecommunications many times faster than current technology; and optical computing in which light replaces electronic circuitry with a corresponding leap in speed and processing power. While it is traditionally accepted that an electromagnetic wave - including laser light - cannot be focused beyond the size of half its wavelength, research teams around the world have found a way to compress light down to dozens of nanometers by binding it to the electrons that oscillate collectively at the surface of metals. This interaction between light and oscillating electrons is known as surface plasmons. Scientists have been racing to construct surface plasmon lasers that can sustain and utilize these tiny optical excitations. However, the resistance inherent in metals causes these surface plasmons to dissipate almost immediately after being generated, posing a critical challenge to achieving the buildup of the electromagnetic field necessary for lasing. Zhang and his research team took a novel approach to stem the loss of light energy by pairing a cadmium sulfide nanowire - 1,000 times thinner than a human hair - with a silver surface separated by an insulating gap of only 5 nanometers, the size of a single protein molecule. In this structure, the gap region stores light within an area 20 times smaller than its wavelength. Because light energy is largely stored in this tiny non-metallic gap, loss is significantly diminished. With the loss finally under control through this unique "hybrid" design, the researchers could then work on amplifying the light. "When you are working at such small scales, you do not have much space to play around with," said Rupert Oulton, the research associate in Zhang's lab who first theorized this approach last year and the study's co-lead author. "In our design, the nanowire acts as both a confinement mechanism and an amplifier. It's pulling double duty." Trapping and sustaining light in radically tight quarters creates such extreme conditions that the very interaction of light and matter is strongly altered, the study authors explained. An increase in the spontaneous emission rate of light is a telltale sign of this altered interaction; in this study, the researchers measured a six-fold increase in the spontaneous emission rate of light in a gap size of 5 nanometers. Recently, researchers from Norfolk State University reported lasing action of gold spheres in a dye-filled, glasslike shell immersed in a solution. The dye coupled to the gold spheres could generate surface plasmons when exposed to light. The UC Berkeley researchers used semiconductor materials and fabrication technologies that are commonly employed in modern electronics manufacturing. By engineering hybrid surface plasmons in the tiny gap between semiconductors and metals, they were able to sustain the strongly confined light long enough that its oscillations stabilized into the coherent state that is a key characteristic of a laser. "What is particularly exciting about the plasmonic lasers we demonstrated here is that they are solid state and fully compatible with semiconductor manufacturing, so they can be electrically pumped and fully integrated at chip-scale," said Volker Sorger, a Ph.D. student in Zhang's lab and study co-lead author. "Plasmon lasers represent an exciting class of coherent light sources capable of extremely small confinement," said Zhang. "This work can bridge the worlds of electronics and optics at truly molecular length scales." Scientists hope to eventually shrink light down to the size of an electron's wavelength, which is about a nanometer, or one-billionth of a meter, so that the two can work together on equal footing. "The advantages of optics over electronics are multifold," added Thomas Zentgraf, a post-doctoral fellow in Zhang's lab and another co-lead author of the Nature paper. "For example, devices will be more power efficient at the same time they offer increased speed or bandwidth." In addition to the three co-lead authors, other co-authors of the paper are Renmin Ma and Lun Dai from Peking University, and Christopher Gladden and Guy Bartal from Zhang's research group.

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Transmissible Prion Disease is caused by Gene Mutation
Thursday, August 27, 2009

For the first time, Whitehead Institute researchers have shown definitively that mutations associated with prion diseases are sufficient to cause a transmissible neurodegenerative disease. Until now, two theories about the role mutations play in prion diseases have been at odds. According to one theory, mutations make carriers more susceptible to prions in the environment. Alternatively, mutations themselves might cause the disease and the spontaneous generation of transmissible prions. Prions cause several diseases, including Creutzfeldt-Jakob disease (CJD) in humans, bovine spongiform encephalitis (BSE, or "mad cow disease") in cows, and scrapie in sheep. Some prion diseases, like BSE, can be transmitted from feed animals to humans. Deciphering the origins of prion diseases could help farmers and policy-makers determine how best to control a prion disease outbreak in livestock and to prevent prion transmission to humans. Prions are misfolded versions of a protein called PrP. In its normal form, PrP is expressed in the brain and other neural tissues. But specific events, such as exposure to prions from the environment, can cause PrP to change from its normal shape to that of a prion. Once in the prion shape, the protein can convert other normal PrP proteins to the abnormal shape. As PrP proteins convert to prions, they form long chains that damage brain and nerve cells, causing the neurodegenerative and behavioral symptoms characteristic of prion diseases. To determine if a mutation in the PrP gene can cause a transmissible prion disease, Walker Jackson, first author of the Neuron article and a postdoctoral researcher in the lab of Whitehead Member Susan Lindquist, engineered a knock-in mouse expressing a PrP gene carrying the mutation associated with the human prion disease fatal familial insomnia. In knock-in experiments, the researcher removes a gene of interest, makes specific changes to it in a test tube, and then places it back in its original place in the genome. In this case, Jackson replaced the mouse PrP gene with an altered version carrying the FFI mutation. This version also carried a sequence from human PrP that prevented the mice from acquiring normal mouse prions that could potentially be in the environment.
"It's more difficult to create a knock-in mouse, instead of randomly integrating the mutated gene into the mouse's genome," says Jackson. "But creating a knock-in like this makes sure the gene is expressed when and where it normally would be. That's the number one reason we think this disease model worked so well, compared to others' experiments." As adults, the mice exhibited many of the same traits as human FFI patients: reduced activity levels and sleep abnormalities. When Jackson examined the mice's brains, they resembled those of human FFI patients, with prominent damage to the thalamic region of the brain. After establishing that the mice have the behavioral and pathological characteristics of FFI, Jackson injected diseased brain tissue from the FFI mice into healthy mice. The healthy mice also carried the same human derived barrier as the FFI mice, preventing their infection by normal mouse prions and ensuring that the only prion they could acquire was the one engineered by Jackson. After injection with the affected tissue, the healthy mice exhibited similar symptoms and neuropathology as the mice with the FFI mutation. The mutated gene engineered by Jackson had created a transmissible prion disease that could not be attributed to any prions in the environment. "One of the major tenets of the prion hypothesis is that a single amino acid change in PrP, associated with human disease, is sufficient to cause the spontaneous production of infectious material," says Lindquist, who is also a professor of biology at MIT and a Howard Hughes Medical Institute investigator. "Many people have tried and come close. But this is the first time it has been nailed."

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Use Of Genes in Evolutionarily Preserved Mechanism
Sunday, August 23, 2009

Researchers at Uppsala University have found that the protein coding parts of a gene are packed in special nucleosomes. The same type of packaging is found in the roundworm C elegans, which is a primeval relative of humans. The mechanism can thereby be traced back a billion years in time, according to the study presented in the journal Genome Research. Human genes are packed in nucleosomes, which contain epigenetic signals directing how the genes are to be used. The cell nucleus contains DNA, which is wound around proteins to form units called nucleosomes, not unlike pearls on a string. Genes on average contain ten protein coding units called exons. Previously there was no known correlation between nucleosomes and exons . New results show that nucleosomes are placed over exons. This means that the area containing the protein code is packed in discrete units. These results are presented by a research team at Uppsala University, led by Professor Claes Wadelius at the Department of Genetics and Pathology and Professor Jan Komorowski at the Linnaeus Centre for Bioinformatics as well as University of Warsaw. Epigenetics is a cellular memory which identifies a cell's identity and way to respond to the environment. Epigenetic signals control genes in a flexible manner. Each genetic package, or pearl on the string, has an epigenetic signal indicating how active it is. In the present study it was shown that there is a previously undiscovered epigenetic mark on protein coding parts of the gene. "A gene can be read in several ways and create different proteins. We have now demonstrated that there is an epigenetic control that determines which parts of the gene that are read," says Claes Wadelius. The study is based on extremely large amounts of data published by other scientists, but not previously analyzed in such detail. "Our findings show the value of sophisticated bioinformatic analyses and the need to delve deeper into the gigantic amounts of data from modern biological research," says Jan Komorowski. The scientists also show that the same type of genetic packaging exists in the tiny roundworm C elegans. Humans are related to this worm through a common ancestor that lived a billion years ago. This means that the mechanism has been evolutionarily preserved during nearly one fourth of the time the earth has existed eller one fourth of earth's existence. In humans, the genetic code has been divided into smaller parts that fit into the individual packages or pearls.

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Anti-aging Gene and High Blood Pressure
Thursday, August 20, 2009

Now researchers at the University of Oklahoma Health Sciences Center have shown the first link between a newly discovered anti-aging gene and high blood pressure. The results, which appear this month in the journal Hypertension, offer new clues on how we age and how we might live longer. Persistent hypertension, or high blood pressure, is a risk factor for stroke, heart attack, heart failure, arterial aneurysm and is the leading cause of chronic kidney failure. Even a modest elevation of arterial blood pressure leads to shortened life expectancy. Researchers, led by principal investigator Zhongjie Sun, tested the effect of an anti-aging gene called klotho on reducing hypertension. They found that by increasing the expression of the gene in laboratory models, they not only stopped blood pressure from continuing to rise, but succeeded in lowering it. Perhaps most impressive was the complete reversal of kidney damage, which is associated with prolonged high blood pressure and often leads to kidney failure. “One single injection of the klotho gene can reduce hypertension for at least 12 weeks and possibly longer. Klotho is also available as a protein and, conceivably, we could ingest it as a powder much like we do with protein drinks,” said Sun, M.D., Ph.D., a cardiovascular expert at the OU College of Medicine.Scientists have been working with the klotho gene and its link to aging since 1997 when it was discovered by Japanese scientists. This is the first study showing that a decline in klotho protein level may be involved in the progression of hypertension and kidney damage, Sun said. With age, the klotho level decreases while the prevalence of hypertension increases. Researchers used one injection of the klotho gene in hypertensive research models and were able to markedly reduce blood pressure by the second week. It continued to decline steadily for the length of the project – 12 weeks. The klotho gene was delivered with a safe viral vector that is currently used for gene therapy. The virus is already approved by the U.S. Food and Drug Administration for use in humans. Researchers are studying the gene’s effect for longer periods to test its ability to return blood pressure levels to normal. They also are looking at whether klotho can prevent hypertension.

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A Way To Treat Ischemic Pathologies
Tuesday, August 18, 2009

Now a team of researchers from CIC bioGUNE from the Cellular Biology and Stem Cell Unit, alongside a team from Paris’ Cardiovascular Research Centre have developed a new area of research which looks extremely promising regarding the development of new therapeutic responses to ischemic pathologies and cardiovascular diseases in general. he results of this research project, which was initiated in 2005 and is supported by Bizkaia:Xede and the Basque Government’s Etortek programme, were published in the journal Circulation. By activating a protein called HIF, the strategy is to stimulate revascularisation and the repair of the damaged organ following ischemia caused by the obstruction of a blood vessel preventing normal blood flow. These obstructions occur, for example, in the event of thrombosis in a limb, myocardial infarction or a stroke. In this sense, it is important to highlight the fact that cardiovascular diseases are the principal cause of death throughout the world.In general, cells tend to respond to the lack of oxygen caused by poor blood flow by activating HIF. However, in the case of an ischemic pathology, HIF is not sufficiently activated. Dr Berra, Cellular Biology and Stem Cell Unit’s leader, stated that they decided to over-produce HIF following ischemia as an attractive therapeutic alternative. For their research purposes, they used an ischemic model provoked in a mouse leg through ligation of the femoral artery. In other words, they closed off the femoral artery and stopped the blood flow to the limb. When this happens, the leg develops necrosis and after a time, the mouse dies. The aim was to artificially help stimulate the production of HIF after the femoral artery had been closed off. And they saw that when they did this, the mouse’s leg revascularised and no longer entered into a degenerative process. How is this high level of HIF production achieved? HIF is a protein which, when not required, degrades constitutively and this degradation is regulated by enzymes called PHDs.

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Metastatic Cancer And Macrophages
Monday, August 17, 2009

The deadliest part of the cancer process, metastasis, appears to rely on help from macrophages, potent immune system cells that usually defend vigorously against disease, researchers at Albert Einstein College of Medicine of Yeshiva University report. n a new study published online in PLoS ONE, Einstein cancer research specialist Jeffrey W. Pollard, Ph.D., and seven colleagues analyzed the movement of breast cancer cells in mice to show that a distinct population of macrophages helps malignant cells set up shop at distant sites. This process, known as metastasis, is the main reason cancer patients die. Dr. Pollard and his colleagues propose that their discovery offers a potentially useful new target for anti-cancer therapy. What they've found is a vulnerable step in the cancer process that might be blocked by drug treatments. In three different ways, the scientists showed that metastatic tumor growth is inhibited if these unusual macrophages are killed. They also showed that even after breast cancer cells have lodged in the animals' lungs and started aggressive growth, erasing the special macrophages dramatically slowed growth of the metastasized tumors. "This suggests that anti-macrophage therapy will have an impact in patients even with metastatic disease," Dr. Pollard said. Based on this new work, he added, "macrophages themselves, or their unique signaling pathways, represent new therapeutic targets that may be efficacious in reducing cancer mortality." Ordinarily, macrophages are vital for maintaining health as an integral arm of the immune system, one of the body's main lines of defense. Their assigned tasks include cleaning up debris in the wake of disease or injury, alerting other immune system cells when an infection begins, and helping identify viruses and bacteria that need to be killed. The findings of this study build on earlier cancer research by Dr. Pollard and his team that shows macrophages can act at the primary tumor site to enhance tumor progression and malignancy. Thus, they've now shown that macrophages can become traitors, enhancing the worst aspect of the disease – metastatic tumor growth. "This new study is important because it definitively shows the effects of macrophages at distant sites, as well as the identity of the macrophage population," Dr. Pollard explained. "This is the first proof that they have impact at this location, at the site of metastatic tumor growth." Dr. Pollard noted that "metastatic disease is the major cause of cancer mortality," in part because the distant tumors tend to resist chemotherapy and radiation treatments. Unfortunately, "the biological mechanisms that underlie metastatic disease are poorly understood," so continuing research is needed. And if metastasis can somehow be blocked -- particularly through influencing cells of the metastatic microenvironment -- the impact on cancer mortality would be enormous. The paper, "A Distinct Macrophage Population Mediates Metastatic Breast Cancer Cell Extravasation, Establishment and Growth," was published August 10 in PLoS ONE, a journal of the Public Library of Science. The lead author is post-doctoral fellow Binzhi Qian, Ph.D., Einstein. Other co-authors are Yan Deng and Yiyu Zou, Einstein; Jae Hong Im and Ruth J. Muschel, University of Oxford Churchill Hospital in England; and Richard A. Lang, Children's Hospital Research Foundation, in Cincinnati, Ohio. Dr. Pollard is the director of the Center for the Study of Reproductive Biology and Women's Health, deputy director of the Albert Einstein Cancer Center, professor of developmental and molecular biology, and of obstetrics & gynecology and women's health.

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New Way To Extract Diluted And Contaminated DNA
Saturday, August 15, 2009

University of British Columbia researchers have developed a new way to extract DNA and RNA from small or heavily contaminated samples that could help forensic investigators and molecular biologists get to "the truth." "By exploiting the physical traits of DNA – electric charge, length and flexibility – we've been able to extract DNA from samples that would otherwise not produce enough clean DNA for analysis," says UBC Biophysics Prof. Andre Marziali.
The technique is being commercialized through Boreal Genomics, a UBC spin-off company, and is expected to have broad applications from basic life-science research to forensic sample analysis, bio-defence and pathogen detection for food safety and clinical diagnostics. The research team, which includes scientists from UBC and BC Cancer Agency's Genome Science Centre, details the technique in this week's Proceedings of the National Academy of Science. Extracting DNA by conventional methods – which rely on the molecules' chemical properties – has proven challenging when there are only trace amounts of DNA or when the source sample has contaminants with similar chemical traits. "We've found that DNA and RNA respond to electric fields in a way that is very different from other molecules," says Marziali. "By exploiting this unique property, we were able to extract high quality DNA from a highly contaminated sample from the Athabasca oil sands." The team also successfully tested the technique on samples provided by the RCMP.

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Exercise Is Healthy During Pregnancy
Thursday, August 13, 2009

Now Physicians recommend low to moderate levels of exercise to their pregnant patients, even if they have not exercised prior to pregnancy, states a report published in the August 2009 issue of the Journal of the American Academy of Orthopaedic Surgeons (JAAOS). According to this review article, exercise can strengthen and improve overall musculoskeletal and physiologic health as well as pregnancy related symptoms. Exercise such as aerobics, impact and nonimpact activities, resistance training and swimming: -
1.eases back and other musculoskeletal pain;
2.lowers maternal blood pressure;
3.reduces swelling; and
4.improves post-partum mood, including sadness.
According to study author Capt. Marlene DeMaio, M.D., M.C ., U.S.N., Research Director, Naval Medical Center, Portsmouth, Virginia, data shows that the pregnant woman’s body can compensate for the changes with no harm to the fetus during low to moderate intensity exercise.
“It is important to remember that pregnancy is a temporary condition, not a disease, and that the musculoskeletal and physiologic changes that happen are normal in the majority of patients,” she said.
Capt. DeMaio’s findings contradict what some physicians recommended in the past. As recently as the 1990s, there was concern that exercise could be detrimental to a pregnant woman and her fetus. These past concerns included a focus on normal changes related to musculoskeletal health that occur during pregnancy, such as increased ligament laxity, weight gain and change in the center of gravity. Today, some physicians continue to advise their pregnant patients to ease back on exercise or refrain from it altogether if they have not already made it a part of their lifestyle.
DeMaio, who collaborated with Capt. Everett Magann, M.D., M.C. U.S.N., Chairman in the Department of Obstetrics and Gynecology, also at the Naval Medical Center in Portsmouth, not only reports that exercise is important during pregnancy, but also believes that starting an exercise program when pregnant, is a perfect way to begin – and stick with – a fitness program.
“When a woman becomes pregnant, she often re-evaluates her lifestyle,” said Dr. DeMaio. “She is motivated in a new way to deliver a healthy baby, and be healthy herself.” Physicians may recommend exercise for pregnant patients in the following categories:-
1.Prenatal: Patients should begin or continue low to moderate exercise. The goal is to maintain fitness and adapt exercise as needed as pregnancy progresses. (For example, runners might switch to running in a swimming pool later in their pregnancy.)
2.Postnatal: Continue exercising at low to moderate levels. Lactation is not negatively affected by exercise. There are fewer reports of mothers having post-partum depression or mood changes when they are exercising.
3.Older: Exercise is even more important if the patient is older, according to Dr. DeMaio. The risk for high blood pressure and increased glucose goes up the older a patient is, but exercise can help reduce these levels.
4.Obese: Physicians should discuss pregnancy as an opportunity to improve overall health and suggest the patient start exercise for life-long health and as an example to the child when the child is older.
5.Infertile: Even if a woman is under treatment for infertility, she can exercise under the supervision of her obstetrician.
6.Athlete: For a pregnant woman wanting more strenuous exercise, or who wants to increase training from moderate to high intensity, a qualified doctor should direct her exercise programs.

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Geneticists Unearth The Roots Of Human Genetic Variation
Thursday, August 6, 2009

A new study at the University of Leicester is using advanced single molecule methods to explore processes that lie at the very core of DNA variation in humans. The study by researcher Shriparna Sarbajna focuses on the process of ‘recombination’, which re-shuffles our genetic content at the time of egg and sperm production. This ‘re-shuffling’ creates new combinations that are passed on to future generations. Ultimately, these new combinations accumulate over many years to generate the patterns of genetic variations seen in contemporary human populations.
Doctoral research by Sarbajna uses techniques pioneered by world-renowned geneticist Professor Sir Alec Jeffreys, to analyse human sperm DNA molecules. These techniques are ultimately used to directly understand the nature, location and frequency of changes occurring in our DNA. Sarbajna said: “These studies are enabling us to explore the very basis of human genetic variation and aiding our understanding of how errors in the process produce pathological changes like those associated with conditions such as alpha thalassaemia and Down syndrome.” “Our research has far reaching consequences, ranging from assisting in genetic counselling through identifying factors contributing to infertility and chromosomal abnormalities, to understanding pathogenic rearrangements frequently seen in cancers and some inherited disorders.”
“Interestingly, understanding how recombination influences patterns of diversity can also shed valuable light into the history and origins of various human populations. Studying recombination is thus, not only of basic scientific importance, but also allows valuable insights into issues ranging from medicine to history and ancestry.” “At the heart of the problem is the fact that although vast catalogues of human genetic variation now exist, little is known about the processes that give rise to these in the first place.” This research is funded by The Royal Society, the U.K. Medical Research Council and the Louis-Jeantet Foundation.

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How To Diagnose, Fight Flu
Wednesday, August 5, 2009

Researchers at Emory University are using a new and faster method of rapidly producing highly targeted monoclonal antibodies for use in diagnostic tests as well as a temporary therapy to stave off infectious diseases such as the H1N1 (swine flu) virus. Rafi Ahmed, PhD, director of the Emory Vaccine Center and a Georgia Research Alliance Eminent Scholar, and his collaborators generated high-affinity monoclonal antibodies against a strain of the influenza virus only a month after vaccinating human volunteers.
This new, timely technique allows researchers to quickly generate human antibodies against a pandemic flu strain as a stopgap therapy or to protect people from infection.
The antibodies, which can be isolated from a small amount of blood of humans infected with the virus, could be targeted against H1N1 and rapidly reproduced to detect or attack the virus. The monoclonal antibody technology was described last year in the journal Nature and is being developed in collaboration with scientists at the University of Chicago. Not only is the new method quicker and less cumbersome, the researchers' new technique could be applied to almost any infectious disease, says Ahmed.

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Implantable Bone Material
Sunday, August 2, 2009

Now scientists are very closer to understanding how to grow replacement bones with stem cell technology, thanks to research published in the journal Nature Materials. Many scientists are currently trying to create bone-like materials, derived from stem cells, to implant into patients who have damaged or fractured bones, or who have had parts of diseased bones removed. The idea is that, ultimately, these bone-like materials could be inserted into cavities so that real bone could meld with it and repair the bone. So far, scientists have found they can grow small 'nodules' of what appeared to be bone-like material in the laboratory from different types of bone cells and stem cells. All of these cell types are attracting considerable interest as promising candidates for future implants in people with clinical trials already underway. However, scientists still need to thoroughly explore and understand the in-depth chemical properties and structure of the bone-like materials they are growing.
Now, scientists from Imperial College London have compared the 'bone-like' material grown from three different commonly used clinically relevant cell types and have discovered significant differences between the quality of bone-like material that these can form. For example, the researchers have discovered that the 'bone-like' materials that were grown from bone cells from mouse skull and mouse bone marrow stem cells successfully mimicked many of the hallmarks of real bone, which include stiffness. However, they found that the 'bone-like' material grown from mouse embryonic stem cells was much less stiff and less complex in its mineral composition when compared to the other materials. The researchers suggest that further research is now needed to explore the implications of these results for different stem cell therapies.
Professor Molly Stevens, from the Department of Materials and the Institute of Biomedical Engineering at Imperial College London, says: "Many patients who have had bone removed because of tumours or accidents live in real pain. By repairing bone defect sites in the body with bone-like material that best mimics the properties of their real bone we could improve their lives immeasurably. Our study provides an important insight into how different cell sources can really influence the quality of bone that we can produce. It brings us one step closer to developing materials that will have the highest chance of success when implanted into patients." To carry out their analysis, researchers used laser-based raman spectroscopy to understand the detailed chemical make-up of live cells as they grew and multivariate statistical analysis techniques, which enabled them to compare and analyse data about the growth of different cell populations. They also used a nano-indenter and high resolution electron microscopy, which allowed the researchers to probe the samples so that they could understand how stiff the bone-like materials were and what their structure was at a microscopic level. So stay in touch to know further.

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Teen Pregnancy
Wednesday, July 29, 2009

“Psychological distress does not appear to be caused by teen childbearing, nor does it cause teen childbearing, except apparently among girls from poor households,” said Stefanie Mollborn, Ph.D., an assistant professor of sociology at the Institute of Behavioral Science of the University of Colorado at Boulder. The study, published in the September issue of the Journal of Health and Social Behavior, used data from two large long-term U.S. surveys that followed thousands of teen girls and women. Participants responded to items on symptoms associated with depression, such as how often they found things that did not usually bother them to be bothersome, how easily they could shake off feeling blue or whether they had trouble concentrating. The researchers did not use the term “depression,” which is a clinical diagnosis. Only the combination of poverty and existing distress was a good predictor of teen pregnancy.
Previous studies had shown high levels of depression among teen mothers, but nationally representative studies had not examined if distress was present before the pregnancy and stresses of young motherhood. “Psychologically distressed girls are at risk for teen childbearing and vice versa, even if the two things usually do not cause each other,” Mollborn said. “This could help educators and clinicians identify at-risk adolescents.”
Looking for symptoms of depression or distress should be part of normal health screening for all teenagers, said Diane Merritt, M.D., director of Pediatric and Adolescent Gynecology at the Washington University School of Medicine in St. Louis. “Talking to teenagers about their sexuality and responsible behavior is key,” she said. Responsible behavior would include the use of birth control if the teenager were sexually active. One of the best ways to prevent teen pregnancy is for teens to have long-term goals and good self-esteem, Merritt added. High levels of depression have long-term negative consequences for both mothers and children, Mollborn said. The higher levels of psychological distress in women who had teenage pregnancies continued well into adulthood, she added.

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