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Friday, 9 August 2013

Exercise May be the Best Medicine for Alzheimer's

New research out of the University of Maryland School of Public Health shows that exercise may improve cognitive function in those at risk for Alzheimer’s by improving the efficiency of brain activity associated with memory. Memory loss leading to Alzheimer’s disease is one of the greatest fears among older Americans. While some memory loss is normal and to be expected as we age, a diagnosis of mild cognitive impairment, or MCI, signals more substantial memory loss and a greater risk for Alzheimer’s, for which there currently is no cure. 
The study, led by Dr. J. Carson Smith, assistant professor in the Department of Kinesiology, provides new hope for those diagnosed with MCI. It is the first to show that an exercise intervention with older adults with mild cognitive impairment (average age 78) improved not only memory recall, but also brain function, as measured by functional neuroimaging (via fMRI).The study, led by Dr. J. Carson Smith, assistant professor in theDepartment of Kinesiology, provides new hope for those diagnosed with MCI. It is the first to show that an exercise intervention with older adults with mild cognitive impairment (average age 78) improved not only memory recall, but also brain function, as measured by functional neuroimaging (via fMRI). The findings are published in theJournal of Alzheimer’s Disease.“We found that after 12 weeks of being on a moderate exercise program, study participants improved their neural efficiency – basically they were using fewer neural resources to perform the same memory task,” says Dr. Smith. “No study has shown that a drug can do what we showed is possible with exercise.”Recommended Daily Activity: Good for the Body, Good for the BrainTwo groups of physically inactive older adults (ranging from 60-88 years old) were put on a 12-week exercise program that focused on regular treadmill walking and was guided by a personal trainer.  Both groups – one which included adults with MCI and the other with healthy brain function – improved their cardiovascular fitness by about ten percent at the end of the intervention. More notably, both groups also improved their memory performance and showed enhanced neural efficiency while engaged in memory retrieval tasks.The good news is that these results were achieved with a dose of exercise consistent with the physical activity recommendations for older adults. These guidelines urge moderate intensity exercise (activity that increases your heart rate and makes you sweat, but isn’t so strenuous that you can’t hold a conversation while doing it) on most days for a weekly total of 150 minutes.Measuring Exercise’s Impact on Brain Health and MemoryOne of the first observable symptoms of Alzheimer’s disease is the inability to remember familiar names. Smith and colleagues had study participants identify famous names and measured their brain activation while engaged in correctly recognizing a name – e.g., Frank Sinatra, or other celebrities well known to adults born in the 1930s and 40s. “The task gives us the ability to see what is going on in the brain when there is a correct memory performance,” Smith explains.Tests and imaging were performed both before and after the 12-week exercise intervention. Brain scans taken after the exercise intervention showed a significant decrease in the intensity of brain activation in eleven brain regions while participants correctly identified famous names. The brain regions with improved efficiency corresponded to those involved in the pathology of Alzheimer’s disease, including the precuneus region, the temporal lobe, and the parahippocampal gyrus.The exercise intervention was also effective in improving word recall via a “list learning task,” i.e., when people were read a list of 15 words and asked to remember and repeat as many words as possible on five consecutive attempts, and again after a distraction of being given another list of words.“People with MCI are on a very sharp decline in their memory function, so being able to improve their recall is a very big step in the right direction,” Smith states.The results of Smith’s study suggest that exercise may reduce the need for over-activation of the brain to correctly remember something.  That is encouraging news for those who are looking for something they can do to help preserve brain function.Dr. Smith has plans for a larger study that would include more participants, including those who are healthy but have a genetic risk for Alzheimer’s, and follow them for a longer time period with exercise in comparison to other types of treatments. He and his team hope to learn more about the impact of exercise on brain function and whether it could delay the onset or progression of Alzheimer’s disease.
Source:University of Maryland

Prolactin reduces arthritis inflammation

inflammatory joint diseases such as rheumatoid arthritis are the result of cartilage damage and loss. Chondrocytes are the only cells that are found in cartilage and their death is linked to decreased cartilage health. In this issue of the Journal of Clinical Investigation, Carmen Clapp and colleagues at the National University of Mexico identify prolactin as a potential treatment for inflammatory joint disease. Prolactin treatment prevented chondrocyte death and associated cartilage degradation. In a rat model of inflammatory arthritis, prolactin treatment reduced inflammation, bone erosion, joint swelling, and pain. This study indicates that prolactin therapy has the potential to relieve many symptoms associated with rheumatoid arthritis and other inflammatory-related diseases.
Source:Journal of Clinical Investigation

Chemists Design ‘Smart’ Nanoparticles to Improve Drug Delivery, DNA Self-Assembly

Associate Professor Mathew M. Maye supervises graduate students Colleen Alexander, left, and Kristen Hamner  in his chemistry lab.A team of chemists in SU's College of Arts and Scientists has used a temperature-sensitive polymer to regulate DNA interactions in both a DNA-mediated assembly system and a DNA-encoded drug-delivery system.Their findings, led by Associate Professor Mathew M. Maye and graduate students Kristen Hamner and Colleen Alexander, may improve how nanomaterials self-assemble into functional devices and how anticancer drugs, includingdoxorubicin, are delivered into the body. More information is available in a July 30 article in ACS Nano, published by the American Chemical Society.One area of nanoscience that connects a range of fields—including optics, chemical sensing and drug delivery and treatment—is the self-assembly of nanoparticles. During self-assembly, the chemistry attached to the nanoparticle interface drives a reaction. As a result, particles come together to form a solid, a chai or a small molecule-like cluster.Maye and others have recently figured out how to use DNA linkages to create an array of structures. The reactions are fast and stable, he says, but can also be problematic.“For example, we want to know how to turn a reaction on and off, without tedious changes to the procedure,” says Maye. “We’ve been addressing this problem by providing a thermal trigger in the form of a smart polymer, which changes its structure at the nano level.”A smart polymer is a large molecule, made up of many atomic units, that changes structure when exposed to external stimuli, such as light, acidity or temperature.Maye and his colleagues have synthesized a designer polymer that not only reacts to temperature, but also may be assembled to a gold nanoparticle. The novelty of this approach, he says, is that the nanoparticle possesses short segments of single-stranded DNA.“This multipurpose functionality and added 'smart' component are indicative of where nanoscience is going,” says Maye. “We want nanomaterials to perform many tasks at once, and we want to be able to turn their interactions on and off remotely.”Maye’s team, therefore, has designed a system in which a high temperature (e.g., 50 degrees Celsius) causes polymer strands to shrink, thereby exposing and making them operational, and a low temperature causes them to extend, blocking their DNA recognition properties.Maye says that, in one test, self-assembly between complementary DNA nanoparticles occurred at only a high temperature. In a second study, his team found that heat triggered the release of doxorubicin at the DNA shell of the encoded nanocarrier.Recently invented by Maye and his SU colleagues, the nanocarrier boasts a six-fold increase in toxicity, compared to ones used in previous studies.“What’s novel about this approach is that interparticle linkages are dynamic and reconfigurable,” Maye says. “Such reconfiguration may lead to smart solids and metamaterials that react to environmental stimuli, much the same way smart polymers react in bulk.”Maye and his team have also employed a number of advanced techniques to better understand the mechanisms of their system, including dynamic light scattering and small-angle X-ray scattering.“Being able to control nanoparticle assembly with temperature allows us to fine-tune their reactions and form more predictable structures. It also gives us a more improved system in which to scale assembly,” he says.Maye goes on to explain that for DNA-encoded nanoparticles, such classes of particles are an excellent platform for drug delivery: “When combined with thermosensitive polymers such as the ones in our system, they could become very lucrative.”In addition to Maye, Hamner and Alexander, the article was co-authored by students from two National Science Foundation (NSF) Research Experiences for Undergraduates programs—one in SU’s chemistry department and the other in the Syracuse Biomaterials Institute—both of which are sponsored by the NSF.Maye’s work is supported by the Air Force Office of Scientific Research, as part of his Presidential Early Career Award for Scientists and Engineers. Additional support is provided by SBI and by SU’s Forensic and National Security Sciences Institute. Maye’s work has also made use of X-ray scattering equipment in the Cornell High Energy Synchrotron Source lab at Cornell University.

Why You Should Eat Breakfast Like a King ?

A recent research found that the timing of your meals is crucial to maintain weight as well as offset many lifestyle diseases like hypertension, diabetes and cardiovascular disease.Researchers said that a good breakfast helped in giving the body the right amount of nutrients, improving mood and keeping disease at bay. Since metabolism is influenced by the circadian rhythm, it is important to follow meal timings strictly. So, it is not just what we eat that matters but also when we eat food that matters in aiding a healthy metabolism. 
In a recent study, researchers found that those who consume their hugest daily meal during breakfast have a greater chance of losing weight and having a healthy waistline as compared to those who consume a huge dinner. Such people also had markedly reduced levels of insulin, glucose, and triglycerides throughout the day, translating into reduced risk of hypertension, diabetes and cardiovascular disease. 
So, "eat breakfast like a king, lunch like a prince, and dinner like a pauper", to live a healthy life.
Source: Medindia



Researchers: Protein Involved in Nerve-cell Migration Implicated in Spread of Brain Cancer

The same protein molecule that neurons need to migrate into position as they differentiate and mature, is required for the invasion of brain-tumor cells into surrounding tissue, according to new research from the University of Illinois at Chicago College of Medicine and published August 7 in the online journal PLOS ONE.The researchers investigated similarities between the transition of neural stem cells into neurons and the process whereby cancer cells invade surrounding tissues. 
"Both processes involve the mobilization of cells," says Anjen Chenn, director of clinical pathology and molecular diagnostics at UIC. "During embryonic development, stem cells that go on to become neurons must migrate long distances to other parts of the brain before they mature into adult neurons. We thought that this type of cell migration might have similarities with cancer cells that spread from tumors." 
Chenn and colleagues analyzed the proteins expressed by embryonic mouse neural stem cells as they began their migration. 
They found that one protein, cadherin11, was found in especially high concentrations in these transitioning cells. 
Chenn said the protein "regulates how the cells stick to each other and is also important in helping cells pull themselves along certain pathways as they travel to their final destinations." 
When the researchers caused the protein to be overexpressed in embryonic mice, the neural stem cells began their migration prematurely. 
"This confirmed that cadherin11 was involved in the initiation of migration," said Chen. 
To determine whether the protein was involved in the invasion of cancer cells into healthy tissues, the researchers looked at its function in glioblastoma, the most common and aggressive type of adult brain cancer. They examined survival data from patients with glioblastoma and noticed that patients whose tumors expressed elevated levels of the cadherin11 gene had the worst survival rates. 
"We also saw that in our tissue samples, the tumor cells with high expression of cadherin11 tended to be located near blood vessels, suggesting that the protein could be involved in encouraging blood vessels to enervate tumors," Chenn said. 
When Chenn and his colleagues mixed cells from blood vessel walls with human glioblastoma cells, the glioblastoma cells increased their expression of cadherin11. 
"We have long known that tumors recruit their own blood supply, but this finding was particularly interesting because it suggests that blood vessels might actually be stimulating tumor cells to come to them," Chenn said. "Our results together indicate that cadherin11 is critical in inducing cell migration in cancer, and could be an important therapeutic target for preventing its spread." 

Source: journal PLOS ONE

Intelligent Women Less Likely to Have Kids, Says Study

A new study finds that the more intelligent the woman, the less likely she is to become a mother. 
Satoshi Kanazawa, a researcher from the London School of Economics, found that maternal urges drop 25 percent for every 15 extra IQ points.The study, which is discussed in his book 'The Intelligence Paradox,' cites data from UK's National Child Development Study with added economic and education information. 
According to Kanazawa, "if any value is truly unnatural, if there is one thing that humans (and all other species in nature) are decisively not designed for, it is voluntary childlessness," the New York Daily News reported 
In the book, he goes on to say in a chapter called "Why Intelligent People Are the Ultimate Losers in Life" that all living organisms are "evolutionarily designed to reproduce" and that "reproductive success is the ultimate end of all biological existence." 
According to the Guardian, Kanazawa doesn't give a reason why this is a case, and it's not clear why some of these "loser" women elect to do something as "unnatural" as not having children. 
However, it is becoming more common, at least in the United States. According to a Pew Research report from 2010, one in five American women did not have children when her biological clock stopped ticking, compared to one in 10 in the 1970s.




Thursday, 8 August 2013

Scientists use genome sequencing to prove herbal remedy causes upper urinary tract cancers

DNA mutation 'signature' identified in cancers linked to birthwort herb

Genomic sequencing experts at Johns Hopkins partnered with pharmacologists at Stony Brook University to reveal a striking mutational signature of upper urinary tract cancers caused by aristolochic acid, a plant compound contained in herbal remedies used for thousands of years to treat a variety of ailments such as arthritis, gout and inflammation. Their discovery is described in the Aug. 7 issue of Science Translational Medicine.
Aristolochic [pronounced a-ris-to-lo-kik] acid is found in the plant family "Aristolochia," a vine known widely as birthwort, and while the U.S. Food and Drug Administration first warned of its cancer-causing potential in 2001, botanical products and herbal remedies containing it can still be purchased online. Moreover, the vine has been found to be an environmental carcinogen through the contamination of food supplies of farming villages in the Balkans, where Aristolochia grows wildly in the local wheat fields. For years, scientists have known of some mutations in upper urinary tract cancer patients exposed to the plant toxin. But the genome-wide spectrum of mutations associated with aristolochic acid exposure remained largely unknown.
For the current study, the Johns Hopkins and Stony Brook team used whole-exome sequencing on 19 Taiwanese upper urinary tract cancer patients exposed to aristolochic acid, and seven patients with no suspected exposure to the toxin. The technique scours the exome, part of the human genome that contains codes for functional proteins and can reveal particular mutations, in this case, those associated with cancer.
"Genome-wide sequencing has allowed us to tie aristolochic acid exposure directly to an individual getting cancer," Kenneth Kinzler, Ph.D., professor of oncology in the Johns Hopkins Kimmel Cancer Center's Ludwig Center for Cancer Genetics and Therapeutics. "The technology gives us the recognizable mutational signature to say with certainty that a specific toxin is responsible for causing a specific cancer. Our hope is that using the more targeted whole-exome-sequencing process will provide the necessary data to guide public health decisions related to cancer prevention."
Specifically, Kinzler says they found an average of 753 mutations in each tumor from the toxin-exposed group compared with 91 in tumors from the non-exposed group. This level of mutation is more than that found in melanomas caused by ultraviolet radiation and lung cancer caused by smoking.
The toxin-exposed group had a large number of a particular, rare type of mistake (a mutational signature) in the ATCG chemical code of their DNA. The predominant mutation type in the toxin-exposed tumors (72 percent) was an A substituted with a T. In one instance, the scientists used the mutational signature to uncover an artistolochic-related tumor in a patient who was unaware of prior exposure.
This study illustrates how genomic sequencing could also be used to pinpoint a culprit carcinogen in some cancer clusters, says Margaret L. Hoang, Ph.D., lead author of the study. Cancer clusters are defined as an unusually large number of similar cancers occurring within a specific group of people, geographic area or period of time.
Source:Science Translational Medicine

Muscle health depends on sugar superstructure

Study identifies 3 enzymes required for building sugar superstructure involved in muscular dystrophies

For many inherited diseases, such as cystic fibrosis or Huntington disease, the disease-causing genetic mutation damages or removes a protein that has an essential role in the body. This protein defect is the root cause of the disease symptoms.
However, for a group of muscular dystrophies known collectively as congenital muscular dystrophies (CMDs), the sequence of the protein that is central to normal function is typically unaffected. Instead, the defects lie in processing proteins—ones that are responsible for modifying the central protein by adding sugar chains (glycans). Either loss of the glycans or disruption of their structure is sufficient to cause muscle disease.
In a new study, published online Aug. 8 in the journal Science, a University of Iowa team led by Kevin Campbell, Ph.D., has pinpointed not just one, but three proteins that are required for constructing a key, early section of a critical sugar chain. Mutations affecting any one of these three proteins can cause CMD disease in humans.
The central protein in CMDs is dystroglycan (DG). "It looks like at least 10 to 15 genes encode proteins that contribute to the glycan superstructure that makes DG effective," says Campbell, professor and head of molecular physiology and biophysics at the UI Carver College of Medicine, and a Howard Hughes Medical Institute investigator. "Our goal is to figure out the whole pathway by which the glycan structure is built, since defects in any of the proteins can potentially lead to disease. Knowing which genes are involved is expected to help us develop clinical tests for these dystrophies, and also ways to screen for potential therapeutic agents."
Normally, DG is modified with a unique sugar chain that acts like glue, allowing DG to attach to other proteins and, by doing so, to reinforce cell membranes in many tissues—including muscle and brain. DG does not function properly without this sugar modification, and glitches in the construction of the glycan cause the progressive muscle dysfunction and the brain abnormalities that characterize many forms of muscular dystrophy.
Almost a dozen genetic mutations are now known to cause DG-related CMDs, which include Fukuyama Congenital Muscular Dystrophy, Walker-Warburg Syndrome, Muscle-Eye-Brain disease, and certain types of limb-girdle muscular dystrophy. All of these mutations affect proteins (enzymes) that are responsible for building DG's unique sugar chain.
The new study assigns a role to three of these causative mutations, showing that the three affected enzymes act sequentially to build an early section of DG's critical glycan. When any of these proteins are mutated, the sugar chain is not constructed correctly and the DG protein loses its function. The first author of the study was Takako Yoshida-Moriguchi, Ph.D., a UI research assistant professor in Campbell's lab
The three enzymes connect a series of sugars together to form the glycan; like stringing beads together to make a necklace. The starting point of the chain is a mannose sugar, which is attached to the backbone of the DG protein. The first enzyme analyzed in the study, called GTDC2, links a glucosamine (GlcNAc) sugar to this starting mannose. The second enzyme, B3GALNT2, then adds a galactosamine sugar to the GlcNAc. Only when this disaccharide is complete can a third enzyme—an unusual type of kinase called SGK196—add a phosphate group to the mannose at the beginning of the chain.
Earlier work from Campbell's lab has shown that this phosphate link is required for other enzymes to build the final section of the sugar chain—the part that actually allows dystroglycan to do its job.
"What I find really exciting is that even with the whole genome having been described, we are still finding novel enzymes that carry out functions we didn't know about even two or three years ago," Campbell says.
Identifying these enzymes and understanding their functions may eventually provide leads for developing therapies to treat CMD and other muscle diseases, Campbell adds.

Atomic insights into plant growth

Researchers from Tubingen resolve how a plant steroid hormone makes plants grow

This news release is available in German.
If one wants to better understand how plants grow, one must analyse the chemistry of life in its molecular detail. Michael Hothorn from the Friedrich-Miescher-Laboratory of the Max Planck Society in Tübingen and his team are doing just that. Their latest work now reveals that a plant membrane receptor requires a helper protein to sense a growth-promoting steroid hormone and to transduce this signal across the cell membrane.
Every cell is surrounded by a greasy cell membrane. Signals from other cells and from the environment must be sensed at the cell surface, transduced across this membrane and translated into a specific response inside the cell. All organisms have evolved membrane receptor proteins to get these complex tasks done, but plant membrane receptors look drastically different from the well-studied players in animals and bacteria. The plant steroid receptor BRI1, which can sense a small steroid hormone promoting plant growth, belongs to the family of leucine-rich repeat (LRR) receptor kinases, which are responsible for most membrane signalling events in plants. It was previously shown that BRI1 directly binds the small steroid hormone with its LRR-domain at the cell surface.
Julia Santiago, a postdoctoral fellow in the Hothorn lab, could now demonstrate that BRI1 requires a helper protein to correctly sense the hormone and transduce the signal across the membrane. The helper SERK1 is a known player in the brassinosteroid signalling pathway, but it came as a surprise to see how early on it is required. By hitting protein crystals containing the ternary BRI1 – steroid hormone – SERK1 complex with intense X-rays, Santiago could see that SERK1 contributes directly to the formation of the hormone binding pocket, with both proteins interacting with the hormone. The steroid thus acts as a molecular glue which promotes association of the BRI1 and SERK1 LRR domains at the cell surface. This then causes interaction of the cytoplasmic kinases domains in the cell interior, which in turn activates a well characterized signalling pathway triggering the growth response.
The interesting feature of SERK1 is that it can help activate several seemingly unrelated plant receptor kinases, which bind vastly different ligands and trigger different responses. The new structures provide a first glimpse on how SERK1 might be able to do that. Instead of shaking hands with BRI1, it only uses a few 'finger tips' to contact the receptor. Other, strictly conserved surface patches remain available for the interaction with other plant receptor kinases and, potentially their ligands. "There must be some advantage to having all this different functions combined into a single helper protein", Hothorn speculates. Notably, the use of a shared helper protein could allow different signalling pathway to communicate with each other.
The atomic models offer other novel insights too: "Looking at our models, we can now predict pretty well, which mutation in the receptor or helper protein should have an effect on the down-stream signalling pathway. We also know what parts of the hormone are really important to make it bind to the receptor or to the helper protein". Such detailed insights may promote the rational design of synthetic plant steroid hormones and receptor antagonist with applications in basic research, and perhaps someday in the field.

News Video:Robot uses steerable needles to treat brain clots

Surgery to relieve the damaging pressure caused by hemorrhaging in the brain is a perfect job for a robot.That is the basic premise of a new image-guided surgical system under development at Vanderbilt University. It employs steerable needles about the size of those used for biopsies to penetrate the brain with minimal damage and suction away the blood clot that has formed.The system is described in an article accepted for publication in the journal IEEE Transactions on Biomedical Engineering. It is the product of an ongoing collaboration between a team of engineers and physicians headed by Assistant Professor Robert J. Webster III and Assistant Professor of Neurological Surgery Kyle Weaver.

Brain clots are leading cause of death, disability

The odds of a person getting an intracerebral hemorrhage are one in 50 over his or her lifetime. When it does occur, 40 percent of the individuals die within a month. Many of the survivors have serious brain damage.“When I was in college, my dad had a brain hemorrhage,” said Webster. “Fortunately, he was one of the lucky few who survived and recovered fully. I’m glad I didn’t know how high his odds of death or severe brain damage were at the time, or else I would have been even more scared than I already was.”

Steerable needle could prevent “collateral damage” during surgery

Operations to “debulk” intracerebral hemorrhages are not popular among neurosurgeons: They know their efforts are not likely to make a difference, except when the clots are small and lie on the brain’s surface where they are easy to reach. Surgeons generally agree that there is a clinical benefit from removing 25-50 percent of a clot but that benefit can be offset by the damage that is done to the surrounding tissue when the clot is removed. Therefore, when a serious clot is detected in the brain, doctors take a “watchful waiting” approach – administering drugs that decrease the swelling around the clot in hopes that this will be enough to make the patient improve without surgery.For the last four years, Webster’s team has been developing a steerable needle system for “transnasal” surgery: operations to remove tumors in the pituitary gland and at the skull base that traditionally involve cutting large openings in a patient’s skull and/or face. Studies have shown that using an endoscope to go through the nasal cavity is less traumatic, but the procedure is so difficult that only a handful of surgeons have mastered it.Last summer, Webster attended a conference in Italy where one of the speakers, Marc Simard, a neurosurgeon at the University of Maryland School of Medicine, ran through his wish list of useful imaginary neurosurgical devices, hoping that some engineer in the audience might one day be able to build one of them. When he described his wish to have a needle-sized robot arm to reach deep into the brain to remove clots, Webster couldn’t help smiling because the steerable needle system he had been developing was perfect for the job.Webster’s design, which he calls an active cannula, consists of a series of thin, nested tubes. Each tube has a different intrinsic curvature. By precisely rotating, extending and retracting these tubes, an operator can steer the tip in different directions, allowing it to follow a curving path through the body. The single needle system required for removing brain clots was actually much simpler than the multi-needle transnasal system.

Active cannula removed 92 percent of clots in simulations

The brain-clot system only needs two tubes: a straight outer tube and a curved inner tube. Both are less than one twentieth of an inch in diameter. When a CT scan has determined the location of the blood clot, the surgeon determines the best point on the skull and the proper insertion angle for the probe. The angle is dialed into a fixture, called a trajectory stem, which is attached to the skull immediately above a small hole that has been drilled to enable the needle to pass into the patient’s brain.The surgeon positions the robot so it can insert the straight outer tube through the trajectory stem and into the brain. He also selects the small inner tube with the curvature that best matches the size and shape of the clot, attaches a suction pump to its external end and places it in the outer tube.Guided by the CT scan, the robot inserts the outer tube into the brain until it reaches the outer surface of the clot. Then it extends the curved, inner tube into the clot’s interior. The pump is turned on and the tube begins acting like a tiny vacuum cleaner, sucking out the material. The robot moves the tip around the interior of the clot, controlling its motion by rotating, extending and retracting the tubes. According to the feasibility studies the researchers have performed, the robot can remove up to 92 percent of simulated blood clots.“The trickiest part of the operation comes after you have removed a substantial amount of the clot. External pressure can cause the edges of the clot to partially collapse making it difficult to keep track of the clot’s boundaries,” said Webster.The goal of a future project is to add ultrasound imaging combined with a computer model of how brain tissue deforms to ensure that all of the desired clot material can be removed safely and effectively.Other members of the research team are Jessica Burgner, formerly a postdoctoral fellow at Vanderbilt and now executive director of the Hannover University Center for Mechatronics in Germany, and Ray Lathrop, a graduate student at Vanderbilt.The research was supported by National Science Foundation CAREER Award IIS-1054331 and Graduate Research Fellowship as well as a grant from the German Academic Exchange Service.

Simple Tips to Have a Healthy Lifestyle

Experts have shared simple, easy tips to have a healthy lifestyle. shares easy tips to have a healthy lifestyle:
1. Indulge more in physical activities. When you get out of the bed in the morning, before heading to the shower, try doing 15 knee bends, 15 lunges and 15 crunches. 

2. Add some peanuts or peanut butter to your breakfast. This can help control cravings for up to 12 hours. 

3. Go for morning walk. But double your walking speed. It helps burn a lot of calories and keeps you fit and healthy. It's great for those who take their dogs out for walks or mothers who take their babies out in strollers. 

4. You can workout even while sitting on a chair in office. Raise your thighs slightly by clenching your muscles and then take them back down to two inches above the floor. You have to lean back slightly. It helps tone legs. 

5. Try not to use lifts or escalators; instead, take the stairs. Start with one such substitution a day, and build up slowly. If your office is on the 20th floor. Take the lift till the 18th floor and walk up from there. 

6. Park your car a little away from the office or shopping centre and rather walk. It will not only help you stay fit but it will also decrease stress. 

7. You can download fitness applications in your smartphones as it will help you keep a check on your diet plans and fitness regimes. Check out the fitness applications available for your phones.




Frozen Broccoli's 'Lost' Cancer-fighting Powers Restored

University of Illinois scientists have restored the frozen broccoli's ability to form sulforaphane, the cancer-fighting phytochemical present in fresh broccoli.The research conducted by University of Illinois broccoli also demonstrated how the food industry can act to restore the frozen vegetable's health benefits. 
Elizabeth Jeffery, a U of I professor of nutrition said that as little as three to five servings of broccoli a week provides a cancer-protective benefit, but that isn't true for bags of broccoli that you pluck out of your grocery's freezer. 
The problem begins when soon-to-be-frozen broccoli is blanched, or heated to high temperatures, to inactivate enzymes that can cause off-colors, tastes, and aromas during the product's 18-month shelf life, she explained. 
The extreme heat destroys the enzyme myrosinase, which is necessary to form sulforaphane, the powerful cancer-preventive compound in broccoli, she said. 
In the second study, the researchers experimented with blanching broccoli at slightly lower temperatures instead of at 86 degree C. When they used a temperature of 76 degree C, 82 percent of the enzyme myrosinase was preserved without compromising food safety and quality. 
The researchers first thought that thawing frozen broccoli in the refrigerator might rupture the plant's cells and kick-start the enzyme-substrate interaction. It didn't work. 
The researchers decided to expose frozen broccoli to myrosinase from a related cruciferous vegetable. 
When they sprinkled 0.25 percent of daikon radish-an amount that's invisible to the eye and undetectable to our taste buds-on the frozen broccoli, the two compounds worked together to form sulforaphane, said Edward B. Dosz, a graduate student in Jeffery's laboratory. 
The researchers found that the radish enzyme was heat stable enough to preserve broccoli's health benefits even when it was cooked for 10 minutes at 120 degree F. So you can cook frozen broccoli in the microwave and it will retain its cancer-fighting capabilities.

India Denies Revoking Breast Cancer Drug Patent

 India Denies Revoking Breast Cancer Drug PatentIndia denied revoking additional patents related to Roche Holding's breast cancer drug Herceptin, saying the applications lapsed because the Swiss giant failed to follow legal procedures.
India granted Herceptin a patent in April 2007 but said the company failed to protect its intellectual property rights for three other patents related to the best-selling drug. 

The Kolkata Patent Office said Roche, which still holds an Indian patent on its main Herceptin invention, failed to turn up for hearings for the additional patents and filed incorrect paperwork. 
"Before the patent controllers issued their decisions, the applicants (Roche) were given due opportunity of being heard but the applicants have chosen not to attend," the office said in a statement. 
The Kolkata Patent Office objected to Roche's patent problems, reported at the weekend, being portrayed by foreign media as the latest in a string of intellectual property setbacks for multinational pharmaceutical firms in India's $13-billion drug market. 
The patent office said in the case of Roche, it was following "due course of the principle of natural justice, gave the applicant the opportunity of being heard and then only finally disposed of the matter". 
The Herceptin additional patents had "not been revoked" but the request for them was treated as "withdrawn" due to failure to follow prescribed steps, the patent office said. 
The government does not normally comment at such length on patent issues but it has been under fire from the international drug industry and the United States over its series of rejections of patents accepted in other nations. 
The country has been smarting from accusations it fails to uphold intellectual property rights -- charges it strongly denies. 
India's patent laws are, however, tougher than those in many other countries as part of its attempt to make medicines more affordable for its vast poor population. 
It insists drugs must stand the "test of innovation" to be granted patents and refuses to allow so-called "evergreening" -- the awarding of a patent for a small improvement to an existing medicine to extend the patent's shelf life. 
Once drugs go off patent, they can be sold much more cheaply. 
India, known as the "pharmacy to the world", has a huge generics industry that turns out cheaper copycat versions of life-saving branded drugs for poor patients in developing nations. 
Roche spokesman Daniel Grotzky told AFP that the company could "confirm that the Assistant Controller of Patents at the Kolkata Patent Office has refused" Herceptin the additional patents. 
"We are now considering the further course of action," he said in an email, adding he could not immediately comment on the Indian account of events. 
Roche's drug, Herceptin, has become one of its most successful medicines, blocking the action of a protein that spurs tumour growth. 
"The applicant may explore further legal possibilities, as they so desire," the Kolkata Patent Office said in its statement late Monday, without elaborating. 
The Roche controversy comes after the Intellectual Property Appellate Board in India last week revoked a local patent granted to Britain's GlaxoSmithKline for breast cancer drug Tykerb, calling it an incremental improvement on an earlier drug. 
The Roche patents were rejected for procedural problems rather than for intellectual property reasons. 
Western drug-makers are seeking to win a larger part of India's rapidly expanding drugs market to compensate for slowing sales in advanced markets. 
India earlier did not grant drug patents but changed the law in 2005 to allow them as part of a World Trade Organization agreement.


Monday, 5 August 2013

News Video: More effective treatments for chronic pain

Source:Fox News

First Successful Laboratory Model for Studying Hepatitis C Developed

 First Successful Laboratory Model for Studying Hepatitis C DevelopedFor the first time Icahn School of Medicine researchers have identified that the hepatitis C virus can replicate in monkeys. The new findings may lead to the first new animal model and provide new avenues for developing treatments and vaccines for this disease, which impacts more than three million people in the United States.Scientists have tried for decades to develop animal models to study HCV, but the virus was incapable of infecting any species except for humans and chimpanzees. With a recent National Institutes of Health-imposed moratorium restricting chimpanzee research, the Mount Sinai research team turned to a close relative of chimpanzees and humans—macaques. Led by Matthew Evans, PhD, and Valerie Gouon-Evans, PhD, of Mount Sinai, the research team sought to find out why previous attempts to infect macaques with HCV failed. Dr. Gouon-Evans, who is Assistant Professor of in the Department of Developmental and Regenerative Biology at Mount Sinai, worked with a team at the Fred Hutchison Cancer Research Center in Seattle to differentiate macaque stem cells into liver cells. Dr. Evans, who is an Assistant Professor in the Department of Microbiology, and his team then attempted to infect these cells with HCV in a petri dish. They found that these differentiated cells were able to support HCV infection and replication, although not as effectively as in human liver cells. "Now that we know that HCV infection in macaque cells is possible, we wanted to find out why it only worked in liver cells that were derived from stem cells," said Dr. Gouon-Evans. "By identifying where in the viral life cycle the infection is dysfunctional, we can develop an effective animal model of HCV." Dr. Evans and his team found that HCV was less efficient at entering macaque cells to initiate infection compared to human cells because changes in the macaque form of a certain cell surface receptor rendered it less functional than the human version. This cell entry block could be overcome by expressing the human version of this receptor in macaque cells. Furthermore, HCV infection of normal macaque cells was greatly enhanced by changes to the virus that loosened its requirements for that receptor. "Our discovery shows that by manipulating either host or viral genetics we can efficiently infect macaque cells," said Dr. Evans. "These findings may open doors for the field of HCV research, lead to new animal models, and hopefully vaccines and therapies." Next, Dr. Evans plans to take these experiments out of petri dishes by attempting to infect macaques in vivo with the mutant HCV that can use the receptors this animal naturally expresses. If successful, this work would provide a new, much-needed animal model for HCV studies and vaccine development. 


Sugar Metabolism Plays Key Role in Formation of Cancer-Stimulating Blood Vessels

Glycolysis, or sugar metabolism, plays a key role in the formation of new blood vessels that stimulate the growth of cancer and other diseases, a new study published in the journal Cell and led by Peter Carmeliet from VIB-KU Leuven reveals.These totally revolutionary insights open up many new therapeutic opportunities for the treatment of cancer and diseases as a result of excessive blood vessel formation. Every growing cell in our body is provided with oxygen and nutrients via our blood vessels. Blood vessels are formed by endothelial cells which line the inside wall of the vessel. These cells require energy to be able to form new blood vessels. However, it was not known how these cells produced the required energy and it was never considered to inhibit the energy production process in order to block angiogenesis. Under the guidance of Peter Carmeliet, a team consisting of Katrien De Bock, Maria Georgiadou and Sandra Schoors discovered that glycolysis is the most important mechanism for endothelial cells to supply energy for blood vessel formation. Peter Carmeliet and his team demonstrated that endothelial cells can be paralyzed by blocking glycolysis and consequently stop to form blood vessels. This is the first evidence that starvation of endothelial cells could offer new therapeutic opportunities for the treatment of excessive angiogenesis in diseases (like cancer). Peter Carmeliet: "Our discovery opens up a whole new domain for inhibition of angiogenesis in various diseases such as cancer. Endothelial cells need nutrients and energy for growth and if you take away their energy, you can prevent them from forming new blood vessels". 

Lettuce - The Phallic Symbol and a Favorite of the Egyptian God of Fertility

You may add it to your salads and burgers, but this simple green veggie had a much more important use in ancient Egypt.An Egyptologist from the American University of Cairo claims that lettuce was actually a phallic symbol in the ancient Egypt, and was the favorite food of the Egyptian god of fertility. Turns out, it was this simple veggie that earned him a reputation as an irresistible lover. Salima Ikram, the Egyptologist, claims that lettuces can be seen drawn on the walls of ancient Egyptian tombs dating back to as long as 2,000 BC. What's more, apparently, Min, the Egyptian god of fertility, was known to have lettuce as his favorite food. Min, often described in ancient paintings with an erect penis, may have used lettuce as an aphrodisiac, Ikram claims. "One of the reasons why [the Egyptians] associated the lettuce with Min was because it grows straight and tall—an obvious phallic symbol," Ikram explains. Even today, modern Egyptians use lettuce as a home remedy to accelerate hair growth. The Greeks and the Romans too, made use of this vegetable to help induce sleep in people. Thanks to this new revelation, the aphrodisiac properties of lettuce may now be used in different medicines, or may prove to be an effective home remedy for many reproductive problems.


Genetics Behind Debilitating Inflammatory Disease Takayasu Arthritis Uncovered By Study

 Genetics Behind Debilitating Inflammatory Disease Takayasu Arthritis Uncovered By StudyThe genetics behind what makes some people susceptible to Takayasu arteritis, a debilitating disease that can lead to poor circulation, easy tiredness in the legs and arms, organ damage and stroke was uncovered by researchers.A study led by the University of Michigan has identified five genes tied to Takayasu arthritis, an inflammation that damages the aorta and can lead to narrowed arteries, aneurysms, high blood pressure, and heart failure. The findings appear in the August issue of The American Journal of Human Genetics. "Discovering the genetic makeup of Takayasu arteritis is a pivotal step that will lead to fundamental understanding of the disease mechanisms and developing therapies to more effectively treat it," says senior author Amr Sawalha, M.D., associate professor of internal medicine in the division of rheumatology at the U-M Medical School. "This disease can be devastating but is understudied and poorly understood." Takayasu arthritis mainly causes inflammation in the aorta - the large artery that carries blood from the heart to body- and other major blood vessels. This inflammation can also affect the heart valves, reduce blood flow to the legs and arms, and cause a stroke. Other symptoms include weight loss, fever, night sweats, fatigue and joint and muscle pain. The disease is most common among women and typically occurs between the ages 20 and 40. The new findings increase the number of genes linked to susceptibility to the disease to five risk areas both in the HLA (an inherited group of genes known as human leukocyte antigen) and outside the HLA. In addition to the previously established genetic association in HLA-B for Takayasu arteritis, researchers discovered and carefully localized novel genetic risk areas in HLA-DQB1/HLA-DRB1, FCGR2A/FCGR3A, and PSMG1. "We have established and localized the genetic association with IL12B, which encodes the P40 subunit of the interleukin-12 (IL-12) and IL-23," says Güher Saruhan-Direskeneli, M.D., professor of physiology at Istanbul University and co-author of the study. "Therapies to inhibit the IL12/IL23 pathway have been successful in other inflammatory diseases, and these recent findings support investigating this pathway closer in Takayasu arteritis as a potential therapeutic target," Sawalha adds. 
Source:American Journal of Human Genetics.

Green Tea Extract can Kill Childhood Cancers, Finds Study

Catechin - a green tea extract could help kill deadly childhood cancers that are resistant to chemotherapy, finds study.
Cancer researcher Orazio Vittorio said that a modified antioxidant called catechin can kill 50 per cent of the cells from neuroblastoma cancers within three days in laboratory studies. On Friday night he was awarded the Kid's Cancer Project Award in the NSW Premier's Awards for Outstanding Cancer Research, which will give him 25,000 dollars to put towards developing potentially life-saving treatment from his research, the Sydney Morning Herald reported. Neuroblastoma is the most common cancer to strike infants, and has the lowest survival rate of all childhood cancers. Catechin, extracted from green tea, is thought to be a promising cancer treatment, but its instability when it enters the body limits its effectiveness. Dr Vittorio worked with a team of chemists to modify the catechin into a more stable form. Dr Vittorio, from the Children's Cancer Institute Australia and the Lowy cancer research centre at UNSW said that the modified form of catechin is effective at destroying neuroblastoma cells that are highly resistant to conventional chemotherapy, yet has minimal effects on normal cells.

Second Ayurveda cluster in state costing Rs.16 cr to come up at Pune soon

The second Ayurveda industry cluster namely Maharashtra Ayurved Centre Pvt Ltd. (MAC) under the Centre's Ayush scheme will come at Kolewadi of Pune district shortly. The work on the first Ayurveda cluster in the state known as Konkan Cluster at Sangmeshwar Taluka is almost completed and is scheduled to be operational anytime now.

Scheduled to open by the second week of October 2013, Pune cluster will house a Ayurvedic cafe for the development of Ayurveda cuisine, a dedicated raw material processing centre for supply of standardized, graded, certified and processed raw materials in bulk to the ayurvedic manufacturers.The procurement of the raw materials will be done by the cluster from the farmers growing herbal and medicinal plants across the country by setting up backward linkages. The project is costing Rs.15.82 crores of which Rs.9.49 crore has been sanctioned as Ayush grant from the Central Government and remaining Rs.6.33 crore as contribution from the shareholders who are part of the cluster.Spanning an area of 45,000 square feet built up facility, the cluster will have a common facility centre on 120,000 square feet land at Kolewadi with its corporate office at Pune. The project is also estimated to give employment to 108 people directly and 1000 people indirectly."The cluster has given us an opportunity to develop a 360 degree horizontal model to propagate concepts and principles of Ayurveda to the farmers, traders, doctors, researchers, pharmacists and other stakeholders through interventions like exhibition, new drug and process design for mass production, contract manufacturing, raw material processing and sale, quality control lab and entrepreneurship development centre.“MAC Pune will be launching two certificate courses of one year duration one of which would be on raw material identification, grading and standardisation and the other on Ayurveda production techniques respectively approved by Maharashtra University of Health Sciences, Nashik at MAC Pune from July 2014 to bridge the gap between industry and education sector for generating skilled work force,” Dr Sunita Belgamwar, chairperson of MAC explained.The project would bring about quality improvement of raw material and finished goods, reduction in the individual capital investment through contract manufacturing, reduction in the pre manufacturing time (40 per cent time saving) by virtue of bulk raw material supply, reduction in the packaging and labeling costs through a common facility centre, reduction in marketing costs by common marketing and branding (40 per cent cost saving), development of new drugs, process design and validation to compete globally, IPR protection and assistance in R&D and global exposure through common exhibitions.It is also envisaged to establish EU/ USA FDA approved manufacturing facilities in three years, setting up advanced teaching institutes, create exclusive exports division in five years, establish 15 exclusive herbal and Ayurveda products distribution centres (Ayurways stores) by 2015 across Maharashtra.

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