#Drug for parasitic worms fights diabetes in mice Rutgers rightoriginal Studyposted by Rob Forman-Rutgers on October 7 2014a modified form of a drug commonly used to eliminate intestinal parasites may hold the key to battling type
2 diabetes at its source. The Centers for Disease Control and Prevention projects that 40 percent of all Americans now alive will develop type 2 diabetes.
Type 2 is the form of diabetes once known as##adult onset##in which the body produces insulin that ordinarily would keep blood sugar under control
but either it does not produce enough insulin or the body s ability to use that insulin is degraded.
Researchers say it s important to find a suitable medication to correct the cause of the disease as quickly as possible
because the only way now known to##cure##the condition involves major gastric bypass surgery.##
##The surgery can only be performed on highly obese people##says Victor Shengkan Jin associate professor of pharmacology at Rutgers Robert Wood Johnson Medical school
and lead author of a new study published in the journal Nature Medicine ##and carries significant risks that include death
so it is not a realistic solution for most patients.####A major cause of insulin resistance is the accumulation of excess fat in the cells of the liver as well as in muscle tissue.
The fat disrupts the process where ordinarily insulin would cause body tissues to correctly absorb glucoseâ##blood sugarâ##and use it as a fuel.
With nowhere else to go much of the excess glucose remains in the bloodstream where in high concentrations it can damage tissues throughout the bodyâ##potentially leading to blindness kidney damage cardiovascular diseases and other severe health problems.##
##Our goal in this study was to find a safe and practical way of diminishing fat content in the liver.
We used mice to perform proof-of-principle experiments in our laboratory##Jin says.####We succeeded in removing fat
and that in turn improved the animalsâ##ability to use insulin correctly and reduce blood sugar.####The modified medicationâ##niclosamide ethanolamine salt (NEN) or simply niclosamideâ##burns the excess fat in liver cells through a process known as mitochondrial uncoupling.
Mitochondria are the microscopic energy source for each cell in the body and ordinarilyâ##like a well-tuned car engineâ##they burn fuels including fats
and sugars in modest quantities to keep the cells functioning.####The cell is like a car
and the mitochondria are the engine##Jin explains.####What we re doing inside cells is like putting the car s transmission into neutral by uncoupling it from the transmission.
Then you step on the gas so the engine runs full throttle but the car doesn t move.##
##If too much of the fuel in the cell is fat you keep burning it until the fuel gauge reaches empty.
and ultimately reverse the diabetes entirely. That outcome is far from certain but Jin says the positive changes he saw in the mice are encouraging.
people of normal weight can develop fatty livers and type 2 diabetes. This kind of medication if shown to be effective could safely treat patients of all weights.
#These ignored cells might prevent osteoporosis Johns hopkins university rightoriginal Studyposted by Catherine Kolf-Johns Hopkins on October 7 2014a type of cell overlooked by scientists appears to play a critical role in preventing osteoporosis a condition that affects an estimated
It also explains the success of an experimental osteoporosis drug that has had promising results in clinical trials.
A summary of the new research conducted using mice with a bone condition similar to osteoporosis has been published in the journal Nature Medicine.##
##We didn t know that the drug affects preosteoclasts nor did we understand how important preosteoclasts are in maintaining healthy bones##says study leader Xu Cao professor of orthopedic surgery at the Johns hopkins university School of medicine.##
##Now drug companies hoping to reverse osteoporosis can look for even more drugs that make use of and target these interesting cells.##
##The bones of mice people and all land animals are not only necessary for strength and structure but also as warehouses for calcium.
and dissolve the calcium and other stored minerals. Specialized blood vessels nearby pick up the calcium and send it throughout the body.
But in women who have entered menopause decreases in estrogen can cause bone resorption to outpace bone rebuilding leading to osteoporosis and frequent bone breaks.##
##Most osteoporosis drugs on the market slow down bone resorption but do nothing to encourage bone rebuilding##Cao says.
Previous data including that from early clinical trials in humans indicated that the drug odanacatib decreases bone resorption by hobbling CTSK one of the enzymes used to resorb bone.
##Before a new building is constructed the roads have to be in place so that the materials and equipment can be brought in##says Cao.##
and PDGF-BB are to bone building which is information we can use in designing future studies.##
##The National Institute of Diabetes and Digestive and Kidney Disorders the National Institute of Arthritis and Musculoskeletal and Skin diseases China s National Science Fund for Distinguished Young Scientists and Merck
#Stop cancer from spreading without chemo Stanford university rightoriginal Studyposted by Tom Abate-Stanford on October 6 2014 Researchers are testing a protein therapy that stops breast
and ovarian cancer from metastasizing in mice. The majority of patients who succumb to cancer fall prey to metastatic forms of the disease says Jennifer Cochran an associate professor of bioengineering at Stanford university.
Today doctors try to use chemotherapy to slow or stop cancer from spreading from the original tumor site to other parts of the body
but these treatments are unfortunately not very effective and have severe side effects. The new therapy doesn't have side effects.
It works by preventing two proteins Axl and Gas6 rom interacting to initiate the spread of cancer.
Axl proteins stand like bristles on the surface of cancer cells poised to receive biochemical signals from Gas6 proteins.
When two Gas6 proteins link with two Axls the signals that are generated enable cancer cells to leave the original tumor site migrate to other parts of the body and form new cancer nodules.
To stop this process Cochran used protein engineering to create a harmless version of Axl that acts like a decoy.
This decoy Axl latches on to Gas6 proteins in the bloodstream and prevents them from linking with
and activating the Axls present on cancer cells. In collaboration with Amato Giaccia professor of radiation oncology the researchers gave intravenous treatments of this bioengineered decoy protein to mice with aggressive breast and ovarian cancers.
Mice in the breast cancer treatment group had 78 percent fewer metastatic nodules than untreated mice.
Mice with ovarian cancer had a 90 percent reduction in metastatic nodules when treated with the engineered decoy protein.
A paper published in the journal Nature Chemical Biology details the results. This is a very promising therapy that appears to be effective and nontoxic in preclinical experiments Giaccia says.
It could open up a new approach to cancer treatment. Giaccia and Cochran are scientific advisors to Ruga Corp. a biotech startup in Palo alto that has licensed this technology from Stanford.
Further preclinical and animal tests must be done before determining whether this therapy is safe and effective in humans.
Source: Stanford Universityyou are free to share this article under the Creative Commons Attribution-Noderivs 3. 0 Unported license e
#Why a deadly drug didn t hurt lab rat livers Scientists believe they ve solved the mystery of why a diabetes drug introduced in 1997 caused fatal liver failure in 63 patients.
Their discovery makes it likely that similar drug-related deaths can be prevented in the future. In 1997 troglitazone was approved for use in the United states as one of the first drugs designed to treat type 2 diabetes.
It was withdrawn from the market in 2000 after 63 people died from liver failure after taking it.
No one at the time really understood what happened. In preclinical studies using rats there was no sign of danger to the liver.
During human trials adverse effects from the drug were characterized as rare and relatively mild. There were some hints at the potential for liver damage
and the human trials weren t large enough for the true risk of liver injury to become apparent says Paul Watkins coauthor of the study and professor of medicine and pharmacy at University of North carolina.
The research team at the UNC Eshelman School of Pharmacy used DILISYM a computer program designed to predict how drugs will affect the liver.
The team combined information about troglitazone with data specific to the human liver generated in the lab of senior author Kim Brouwer a professor at the pharmacy school.
In a simulated population the model successfully predicted that rare patients would develop life-threatening liver injury
The team s findings are published online in Clinical Pharmacology and Therapeutics. The simulation we used was able to predict the effects that were seen in patients who actually took troglitazone
The researchers cite the accumulation of bile acids substances produced by the liver that promote digestion and aid in the absorption of fats as the most likely suspect in the deaths.
The study shows that a computer model could accurately forecast the occurrence of troglitazone-induced liver injury.
Before DILISYM no one had been able to completely explain troglitazone liver injury or suggest improved approaches
It turns out that animals do a poor job predicting human drug-induced liver injury.
but one important reason is that bile acids are different in each species. Recent data suggest that the use of humanized systems has greater predictive power for adverse events like DILI.
Drug-induced liver injury is the most common reason drug-development programs are terminated. It is also the leading cause of regulatory actions that lead to failed
Rare liver toxicity is now the major safety concern with new drugs and can often be detected only after many thousands of patients have received treatment Watkins says.
and reducing the costs of new medicines. The DILISYM software is the result of the DILI-sim Initiative a partnership between the Hamner-UNC Institute for Drug Safety Sciences
and fourteen major drug companies that shared data to develop a tool that can predict a drug s risk of injuring the liver.
Kyunghee Yang is currently a postdoctoral fellow at the Hamner Institutes. Paul Watkins is chairman of the DILI-sim Scientific Advisory board.
Kim Brouwer is chair of the Division of Pharmacotherapy and Experimental Therapeutics at the UNC Eshelman School of Pharmacy.
Funding for the study came from the National Institute of General Medical sciences. Source: UNC-Chapel Hil l
#Autism diagnosis catches up for kids in Tanzania Brown University rightoriginal Studyposted by David Orenstein-Brown on October 2 2014to diagnose autism in Tanzania researchers adapted several techniques
used in the United states so they were culturally relevant and familiar to children and their parents.
There is no autism diagnostic measure validated for use in Swahili a major language of the region.##
##Historically in Tanzania parents that have sought autism diagnoses had to go to other countries to receive those diagnoses##says Ashley Johnson Harrison a former postdoctoral fellow at Brown University who is now an assistant professor at University of Georgia. Researchers used the new
Using the diagnostic panel researchers were able to make diagnoses that consistently distinguished kids with autism spectrum disorder from those with other similar disorders.
because distinguishing between autism spectrum disorders and other conditions can ensure that children receive proper education
##Initially we only identified the most severe cases of autism##says Johnson Harrison who works under the mentorship of Eric Morrow in the department of psychiatry and human behavior at Brown.##
and Developmental Disabilities and was presented at a meeting of the International Meeting for Autism Research.
or adaptable and piloted the approach with the help of Tanzanian clinicians including Karim Manji of Muhimbili University of Health and Allied Sciences in Dar es salaam and Brenda Shuma and Anthony Ephraim at the Gabriella Centre in Moshi.
They used the Childhood Autism Rating Scale-Second Edition (CARS-2) to help rate child behavior because of the instrument s flexible usage guidelines.
Another advantage of the CARS-2 as well as subtests of the Kaufman Assessment Battery for Children selected for cognitive assessment is that the behavioral observations
or guardians information about autism and guidance on using behavioral strategies to improve child skills.
Of the children she tested 30 were diagnosed as having autism spectrum disorders and 11 as having other##global delay##conditions such as suspected intellectual disabilities Down syndrome or other disorders.
After returning to the United states Johnson Harrison tallied precise quantifications of the CARS-2 score
and DSM-5 checklist symptoms to see if her diagnostic assessment had produced reliable statistically significant differences between the autism and non-autism groups.
It did. The average CARS-2 score for the autism group was 28 percent higher (at 37.75) than the average for the global delays group (at 27.15) a statistically significant difference.
In addition Tanzanian children diagnosed with autism scored in similar ranges on the CARS-2 as compared to children with autism in the United states. The autism group also had significantly more DSM-V autism symptoms than the global delays group suggesting that the assessment measures
were helpful in reliably eliciting the information needed to assess autism spectrum disorders. Johnson Harrison says she hopes that the assessment protocol
if supported by further testing could become a standard approach for clinicians in the country at least
The National institutes of health and Brown University funded the study. Source: Brown Universityyou are free to share this article under the Creative Commons Attribution-Noderivs 3. 0 Unported license i
#DNA VIRUSES shift from solid to liquid to infect Carnegie mellon University University of Pittsburgh right Original Studyposted by Jocelyn Duffy-Carnegie mellon on October 1 2014 Many double-stranded DNA VIRUSES
infect cells by ejecting their genetic information into a host cell. But how does the usually rigid DNA packaged inside a virus shell flow from the virus to the cell?
In two separate studies Carnegie mellon University biophysicist Alex Evilevitch has shown that in viruses that infect both bacteria
and humans a phase transition at the temperature of infection allows the DNA to change from a rigid crystalline structure into a fluid-like structure that facilitates infection.
The findings published in Nature Chemical Biology and the Proceedings of the National Academy of Sciences (PNAS) provide a promising new target for antiviral therapies.
Most antiviral drugs work by deactivating viral proteins but viruses often evolve and become drug resistant.
Evilevitch believes that researchers now have a possible new way to prevent infectionâ blocking the phase transition.
Such a therapy could be generalizable across all types of Herpes viruses and wouldn't be prone to developing resistance The exciting part of this is that the physical properties of packaged DNA play a very important role in the spread of a viral infection
and those properties are universal says Evilevitch an associate professor in Carnegie mellon s physics department. This could lead to a therapy that isn't linked to the virus gene sequence or protein structure
which would make developing resistance to the therapy highly unlikely. Most viruses whether they infect bacteria plants
or animals have fairly similar structures. They consist of an outer shell called a capsid that contains the viral genomeâ either DNA or RNA.
In many DNA VIRUSES the long strands of nucleic acid are tightly wound in a crystalline structure.
The repulsive forces formed by the layered strands of genetic material exert a large amount of pressure on the capsid
In the HSV-1 study which was published in Nature Chemical Biology Evilevitch set out to see what physical conditions lead to successful viral infection.
and mobility of the DNA inside a virus. The VIRAL DNA was much more fluid at temperatures close to that of infection (37 degrees Celsius)
They found that at the temperature of infection the phage s DNA underwent a solid-to-fluid-like disordering
which resulted in increased DNA mobility and subsequent cell infection. The Swedish Research Council the National Science Foundation the National institutes of health and the Mcwilliams Fellowship at Carnegie mellon supported the research published in Nature Chemical Biology.
Coauthors include Udom Sae-Ueng and Dong Li at Carnegie mellon; Xiaobing Zuo at Argonne National Laboratory;
Jamie B. Huffman and Fred L. Homa at the University of Pittsburgh; and Donald Rau at the National institutes of health.
Bengt JÃ nsson at Lund University; and Donald Rau at the National institutes of health. Source: Carnegie Mellonyou are free to share this article under the Creative Commons Attribution-Noderivs 3. 0 Unported license c
#Dengue virus pumps out RNA to evade attack Duke university National University of Singapore right Original Study Posted by Karen Loh-NUS on September 29 2014 A newly discovered pathway lets the dengue virus
The findings which appear in PLOS Pathogens provide knowledge that could help researchers treat the disease more effectively.
For years the conventional approach to target the dengue virus was through control of the vectorâ the mosquito that carries the disease from one host to another.
The elusive mechanics of the virus have hampered the development of effective treatments and vaccines. Typically when a virus enters the body
In examining the dengue virus-2 strain a team at Duke-NUS Graduate Medical school Singapore observed that
In 30 years of dengue-related research this new mechanism was discovered never according to senior author Professor Mariano Garcia-Blanco of the Program in Emerging Infectious diseases.
We not only found a new way in which the pathogen (dengue virus) interferes with the host response (human immune system) we also uncovered the first mechanistic insight into how this non-coding RNA works says Garcia-Blanco.
He believes that the latest discovery opens the door to exploring therapeutics through this channel.
and for dengue how the virus has managed to evade these defenses. The work also highlights the differences between the four dengue strains
and how more research is necessary to understand this highly complex virus. Source: National University of Singaporeyou are free to share this article under the Creative Commons Attribution-Noderivs 3. 0 Unported license n
#3, 600 crystals in wearable skin monitor health 24/7 A new wearable medical device that uses up to 3600 liquid crystals can quickly let you know
if you re having heart trouble or if it s simply time to slather on some moisturizer.
and comfortable much like skin itself says Yonggang Huang professor of civil and environmental engineering and mechanical engineering at Northwestern University.
The technology and its relevance to basic medicine have been demonstrated in the study but additional testing is needed before it can be put to use.
The device is very practical says Yihui Zhang co-first author and research assistant professor of civil and environmental engineering.
When skin is dehydrated the thermal conductivity property changes. The device is an array of up to 3600 liquid crystals each half a millimeter square laid out on a thin soft and stretchable substrate.
An algorithm translates the temperature data into an accurate health report all in less than 30 seconds.
These results provide the first examples of epidermal photonic sensors says John A. Rogers the paper s corresponding author
and professor of materials science and engineering at the University of Illinois. This technology significantly expands the range of functionality in skin-mounted devices beyond that possible with electronics alone.
With its 3600 liquid crystals the photonic device has 3600 temperature points providing sub-millimeter spatial resolution that is comparable to the infrared technology currently used in hospitals.
#DNA test could diagnose TB without the wait University of Warwick right Original Studyposted by Kelly Parkes-Harrison-Warwick on September 24 2014 A new approach quickly diagnoses tuberculosis by relying on direct sequencing of DNA
Laboratory diagnosis of TB using conventional approaches is a long drawn-out process which takes weeks
or months says Mark Pallen professor of microbial genomics at University of Warwick Medical school. Plus relying on laboratory culture means using techniques that date back to the 1880s.
and some smart bioinformatics allows us to detect and characterize the bacteria that cause TB in a matter of a day
while also giving us key insights into their genome sequences and the lineages that they belong to.
It is exciting to be involved in the development of new diagnostic approaches for this deadly disease says Martin Antonio head of the TB diagnostics laboratory at the Medical Research Council Unit in The gambia.
The researches have used shotgun metagenomics before to detect bacterial pathogens in contemporary and historical human material.
Last year they used metagenomics to obtain an outbreak strain genome from stool samples from an E coli outbreak
and to recover TB genomes from Hungarian mummies approximately 200 years-old. Earlier this year they recovered the genome of Brucella melitensis
which causes an infection called brucellosis in livestock and humans from a 700-year-old skeleton from Sardinia Italy.
The researchers aim to test the metagenomics technique on a wide range of samplesâ and hope it will help detect mixed infections caused by more than one kind of bacterium.
But metagenomics is still some way from routine diagnostic use Pallen says. We have provided proof-of-principle here
University of Warwickyou are free to share this article under the Creative Commons Attribution-Noderivs 3. 0 Unported license s
But they can##feel##the physical environment around them according to new research. Platelets respond to surfaces with greater stiffness by increasing their stickiness the degree to
##Platelets are smarter than we give them credit for in that they are able to sense the physical characteristics of their environment
and respond in a graduated way##says Wilbur Lam assistant professor in the pediatrics department at Emory University School of medicine and a physician in the Aflac Cancer and Blood disorders Center at Children s Healthcare of Atlanta.
The researchers findings could influence the design of medical devices because when platelets grab onto the surfaces of catheters
and medical implants they tend to form clots a major problem for patient care. Modifying the stiffness of materials used in these devices could reduce clot formation the authors suggest.
The results could also guide the refinement of blood-thinning drugs which are prescribed to millions to reduce the risk of heart attack or stroke.
The team was able to separate physical and biochemical effects on platelet behavior by forming polymer gels with different degrees of stiffness
and then overlaying them each with the same coating of fibrinogen a sticky protein critical for blood clotting.
First author Yongzhi Qiu and colleagues were also able to dissect platelet biochemistry by allowing the platelets to adhere
and then spread on the various gels under the influence of drugs that interfere with different biochemical steps.
because different biochemical pathways are involved in each step##Lam says.####Our data show that mechanosensing can occur
and plays important roles even when the cellular structural building blocks are fairly basic even when the nucleus is absent.##
##The results are published in the Proceedings of the National Academy of Sciences. Lam is affiliated also with the Wallace H. Coulter Department of Biomedical engineering at Georgia Tech and Emory University.
The National Science Foundation the American Heart Association the National Heart Lung & Blood Institute and the National Eye Institute provided financial support for the work.
Source: Emory Universit i
#At home test diagnoses anemia in 60 seconds A device that uses a single drop of blood can quickly diagnose anemia
and allow inexpensive at home monitoring. The basic test produces results in about 60 seconds and requires no electrical power.
A companion smartphone application can automatically correlate the visual results to specific blood hemoglobin levels.
The disposable self-testing device uses a chemical reagent that produces visible color changes corresponding to different levels of anemia.
By allowing rapid diagnosis and more convenient monitoring of patients with chronic anemia the device could help patients receive treatment before the disease becomes severe potentially heading off emergency room visits and hospitalizations.
Anemia which affects two billion people worldwide is diagnosed now and monitored using blood tests done with costly test equipment maintained in hospitals clinics or commercial laboratories.
Because of its simplicity and ability to deliver results without electricity the device could also be used in resource-poor nations.
Our goal is to get this device into patients'hands so they can diagnose and monitor anemia themselves says Wilbur Lam a physician in the Aflac Cancer and Blood disorders Center at Children's Healthcare of Atlanta and the department of pediatrics at Emory University School of medicine.
Patients could use this device in a way that's very similar to how diabetics use glucose-monitoring devices
but this will be even simpler because this is a visual-based test that doesn't require an additional electrical device to analyze the results adds Lam who is senior author of a paper published in the Journal of Clinical Investigation.
T he test device was developed in a collaboration of Emory University Children's Healthcare of Atlanta and Georgia Institute of technology.
It grew out of a 2011 undergraduate senior design project at Georgia Tech and Emory University.
Using a two-piece prototype device the test works this way: A patient sticks a finger with a lance similar to those used by diabetics to produce a droplet of blood.
The device's cap a small vial is touched then to the droplet drawing in a precise amount of blood using capillary action.
The cap containing the blood sample is placed then onto the body of the clear plastic test kit
which contains the chemical reagent. After the cap is closed the device is shaken briefly to mix the blood and reagent.
When the capillary is filled we have a very precise volume of blood about five microliters
which is less than a droplet much less than what is required by other anemia tests says Erika Tyburski the paper's first author
and leader of the undergraduate team that developed the device. Blood hemoglobin then serves as a catalyst for a reduction-oxidation reaction that takes place in the device.
After about 45 seconds the reaction is complete and the patient sees a color ranging from green-blue to red indicating the degree of anemia.
Tyburski and Lam have teamed up with two other partners and worked with Emory's Office of Technology Transfer to launch a startup company Sanguina to commercialize the test
The team also plans to study how the test may be applied to specific diseases such as sickle cell anemia.
The FDA-funded Atlantic Pediatric Device Consortium the Georgia Research Alliance Children's Healthcare of Atlanta the Georgia Center of Innovation for Manufacturing and the Global Center for Medical Innovation
Overtext Web Module V3.0 Alpha
Copyright Semantic-Knowledge, 1994-2011