#Nanomaterial rivals hardness of diamond An article by Scientific American. It s only a matter of time before a movie villain pulling off the crime of the century needs a cutting tool that is harder than anything else On earth.
Perhaps it s a burglary that involves cutting into a case made of diamond#which,
which precursors of neural support cells grown from human ES cells were injected into people with spinal-cord injuries.
these are showing early evidence that a product made from human ES cells can help to rebuild the layer of cells that support photoreceptors in the eyes of people with certain types of blindness.
But the live viruses in the Sabin vaccine can revert to disease-causing forms especially in populations where immunity is not widespread.
which holds the promise of treatments for a variety of diseases, but which depends on the destruction of days-old human embryos.
saying that work on embryonic-stem-cell lines could lead to therapies for Parkinson s disease, diabetes and other ailments."
Researchers stumbled on the grisly cataloguing technique while studying a form of anthrax that kills chimpanzees in C# te d'Ivoire.
whether the insects could harbour the anthrax bacterium after feasting on infected bodies, but soon realized"that detecting mammal DNA from flies could also be an extremely cool tool for assessing biodiversity,
from creating organic computers to uniting different parts of the same brain that have been cut off by damage or disease.
Mir-7 targets have been linked to cancer and Parkinson s disease. Hansen s team found that expression of the circular RNA blocked the blockers.
while shifting focus to prevention in patients at risk of a heart attack.""We can t just assume that modifying the risk factor is modifying risk,
ATP III reflected a growing consensus among physicians that sharply lowering cholesterol would lessen the likelihood of heart attacks
Clinical trials have shown repeatedly that statins reduce the risk of heart attack and stroke, but lowering LDL with other medications does not work as well.
including fighting inflammation, another risk factor for heart disease. Krumholz s scepticism is rooted in experience. In 2008 and 2010, the Action to Control Cardiovascular Risk in Diabetes (ACCORD) clinical trial challenged dogma
when it reported that lowering blood pressure or blood sugar to prespecified targets did not reduce the risk of heart attack or stroke.
In the case of blood sugar, the risks were worsened. The trial demonstrated the folly of assuming that risk factors must have a causal role in disease,
says Robert Vogel, a cardiologist at the University of Colorado, Denver.""Short people have a higher risk of heart disease,
he says.""But wearing high heels does not lower your risk. Jay Cohn, a cardiologist at the University of Minnesota Medical school in Minneapolis, also worries that the focus on LDL levels offers up the wrong patients for statin therapy.
Most of those who have a heart attack do not have high LDL, he notes. Cohn advocates treating patients with statins based on the state of health of their arteries,
but has not yet been shown to reduce heart attacks or strokes. Francis expects the new guidelines to relax the targets.
System gives hope to those blinded by a rare genetic eye condition called advanced retinitis pigmentosa, which damages the light-sensitive cells that line the retina.
Retinitis pigmentosa#which affects about one in 4, 000 people in the US and about 1. 5 million people worldwide#kills the retina s photoreceptors,
Second sight plans to adapt its technology to someday assist people afflicted with age-related macular degeneration, a similar but more common disease.
When influenza hit early and hard in the United states this year, it quietly claimed an unacknowledged victim:
"It is hard to think today that one can provide disease surveillance without existing systems, says Alain-Jacques Valleron, an epidemiologist at the Pierre and Marie Curie University in Paris,
It is also causing more serious illness and deaths than usual, particularly among the elderly,
Traditional flu monitoring depends in part on national networks of physicians who report cases of patients with influenza-like illness (ILI)##a diffuse set of symptoms
including high fever, that is used as a proxy for flu. That estimate is refined then by testing a subset of people with these symptoms to determine how many have flu and not some other infection.
With its creation of the Sentinelles network in 1984, France was the first country to computerize its surveillance.
overseen by the Centers for Disease Control and Prevention (CDC) in Atlanta, Georgia, includes some 2,
and has been extended to include surveillance for a second disease, dengue. Sources: Google Flu Trends (www. google. org/flutrends;
Its estimate for the Christmas national peak of flu is almost double the CDC s (see Fever peaks),
In 2009, Flu Trends had to tweak its algorithms after its models badly underestimated ILI in the United states at the start of the H1n1 (swine flu) pandemic###a glitch attributed to changes in people s search behaviour as a result of the exceptional nature of the pandemic (S. Cook et al.
SLIDESHOW France's Sentinelles'network of doctors reporting cases of influenza-like illness has produced a clear picture of how the 2012-13#flu season has evolved.
#Small-molecule drug drives cancer cells to suicide Cancer researchers have pinned down a molecule that can kick-start the body s own tumour-destroying systems,
which has long been a target for cancer researchers looking for drugs that would avoid the debilitating effects of conventional therapies."
Mice with glioblastomas that were treated with TIC10 in combination with bevacizumab#a drug used against diseases including brain tumours
This is by no means the only mechanism thought to trigger cell death in cancer. In particular, cancer researchers have been developing a number of drugs,
including TRAIL-based therapeutics, that work by activating the cellular messenger tumour protein 53 (p53).
so in order to develop new therapeutics for cancer, one needs them to be effective in tumours with mutated p53,
The potential for TRAIL to usher in a new age in cancer therapy was identified first in the mid-1990s3.
they were not very successful at treating cancer, says Andrew Thorburn, an oncologist at the University of Colorado Denver,
whose work at the Scripps Research Institute Molecular Screening Center in La jolla, California, led to a compound now in clinical trials for multiple sclerosis.
The vaccine could prevent future outbreaks of the disease, and potentially lead to new treatments for polio and other human diseases.
Bryan Charleston, head of the Livestock Viral Diseases Programme at the Pirbright Institute in Woking, UK,
and his colleagues used computer simulations to create a model of the protein shell of the virus that causes the disease,
then reconstructed it from synthetic protein components. The synthetic shell contains no genetic material and so it cannot infect the animals.
it could also be used to create vaccines for human diseases that are caused by viruses of the same family, such as hand, foot and mouth disease,
because we are so close to ending this disease. JEFF J MITCHELL/REUTERSA 2001 outbreak of foot and mouth disease led to the slaughter of huge numbers of sheep and cows.
and Charleston that the new vaccine is unable to cause an infection or outbreak. Marvin Grubman, an animal-disease researcher at the US Department of agriculture in Orient Point, New york, says that the new vaccine"is a good piece of work,
The discovery suggests new approaches to combat antibiotic resistance and boost the power of cancer therapies,
Geoffrey Chang, a structural biologist at the University of California, San diego, says that the findings are very similar to those for the MATE protein from Vibrio cholerae, the bacterium that causes cholera.
says Michel Sadelain, a researcher at the Memorial Sloan-Kettering Cancer Center in New york and an author of the study.
whether it could take on the faster-growing acute lymphoblastic leukaemia, a tenacious disease that kills more than 60%of those afflicted.#
#Carl June, an immunologist at the University of Pennsylvania in Philadelphia and a pioneer in engineering T cells to fight cancer, says that he is surprised that the method worked so well against such a swift-growing cancer.
is to move the technique out of the boutique academic cancer centres that developed it and into multicentre clinical trials."
and cancer biologists that this new kind of immunotherapy can work, he says. Oncologist Renier Brentjens, also at Memorial Sloan-Kettering Cancer Center, remembers the day that he had to tell one of the patients in the trial that the weeks of high-dose chemotherapy the 58-year-old man had endured had worked not after all."
"It was painful to have that conversation, says Brentjens.""He tells me now it was the worst news he has heard ever in his life.
The treatment had driven his cancer into remission#as it did for the other four patients in the trial
and faces an untested path to regulatory approval, says Steven Rosenberg, head of the tumour immunology section at the National Cancer Institute in Bethesda, Maryland.
And Sadelein says that he is an investigator on a trial with the Dana-Farber Cancer Institute in Boston
#Gene-analysis firms reach for the cloud For Chaim Jalas at the Center for Rare Jewish Genetic disorders in New york,
and identify mutations that might be causing the undiagnosed diseases that afflict his clients families.
and finds those most likely to cause disease. Personalis, down the road in Menlo Park, offers sequencing services and interpretation for clinicians and pharmaceutical and biotechnology companies.
to explore the variants roles in disease. The company will outsource the sequencing to Illumina,
diseases and scavengers#but acknowledge that it might have been caused by behavioural changes, such as the birds learning to avoid cars.
#Distinctive virus behind mystery horse disease For almost 100 years, veterinarians have puzzled over the cause of Theiler's disease,
a mysterious type of equine hepatitis that is linked to blood products and causes liver failure in up to 90%of afflicted animals.
A team of US scientists has discovered now that the disease is caused by a virus that shares just 35%of its amino acid sequences with its closest-known relative.
The team named it Theiler's disease-associated virus (TDAV), and published the discovery in the Proceedings of the National Academy of Sciences1.
Led by Amy Kistler at the Novartis Institutes for Biomedical Research in Emeryville California, the team responded to an outbreak of Theiler's disease at a farm in
which eight horses had developed suddenly hepatitis after being injected with an antitoxin to prevent them from developing botulism.
The researchers used next-generation sequencing to analyse RNA samples from the antitoxin and from two of the horses,
and one later showed rising levels of liver enzymes that suggested liver disease. Although the researchers did not purify the virus before injecting it into the horses, Pablo Murcia, a virologist from the University of Glasgow,
It is also possible that there is another unknown virus behind Theiler's disease. After all, human hepatitis can be caused by at least five viruses. TDAV belongs to the family Flaviviridae,
which includes the viruses behind yellow fever, dengue fever and hepatitis C. It is associated most closely with a genus of newly discovered viruses called Pegivirus,
and is the first of these to be linked convincingly to disease.""The challenges in culturing pegiviruses mean that we re only now getting an understanding of how widely distributed and significant they are,
says James wood, who studies animal infections at the University of Cambridge, UK. He hints that some studies on new pegiviruses may be published in the future u
#Obama to announce $2 billion plan to get US cars off gasoline An article by Scientific American.
This afternoon, President Barack Obama will ask Congress to direct our cars, trucks and buses to a realm that doesn t include gas stations.
to have an implant with electrodes paired with drug delivery pumps that could sense an oncoming epileptic seizure
simulate lesion dynamics or implement network analysis functions from a library of graph theoretic measures. Within the immersive mixed/virtual reality space of Brainx3 users can explore and analysis dynamical activity patterns of brain networks
Knowledge of brain activity in these various states is clinically relevant for assessing levels of consciousness in patients with severe brain injury y
and study diseases in functioning human muscle outside of the human body. The study was led by Nenad Bursac, associate professor of biomedical engineering at Duke university
Bursac group is also trying to grow contracting human muscles using induced pluripotent stem cells instead of biopsied cells. here are a some diseases, like Duchenne Muscular dystrophy for example,
The research was supported by NIH Grants R01ar055226 and R01ar065873 from the National Institute of Arthritis and Musculoskeletal and Skin disease and UH2TR000505 from the NIH Common Fund for the Microphysiological Systems Initiative.
myobundles undergo dose-dependent hypertrophy or toxic myopathy similar to clinical outcomes. Human myobundles provide an enabling platform for predictive drug
#Researchers Identify Important Control Mechanisms for Walking Even after complete spinal paralysis, the human spinal cord is able to trigger activity in the leg muscles using electrical pulses from an implanted stimulator.
even if the neural pathways from the brain are interrupted physically as the result of a spinal cord injury.
This is the first time throughout the world that the spinal-cord activation patterns for walking have been decoded Paraplegics still have neural connections (so-called locomotion centers) below the site of the injury
New possibilities for rehabilitation following spinal paralysis These new findings relating to the basic patterns for triggering
and the resulting paralysis by stimulating them electrically. This opens the way to new therapeutic options for helping paraplegics to at least partially regain lost rhythmic movements.
Exactly how the neural networks need to be stimulated depends upon the patient individual injury profile and is the subject of further studies.
To help with this, the scientists at Meduni Vienna have developed a unique, noninvasive method for stimulating the spinal cord,
which involves attaching electrodes to the surface of the skin. his method allows easy access to the neural connections in the spinal cord below a spinal injury
#Genetic Brain disorders Converge at the Synapse Several genetic disorders cause intellectual disability and autism. Historically, these genetic brain diseases were viewed as untreatable.
However, in recent years neuroscientists have shown in animal models that it is possible to reverse the debilitating effects of these gene mutations.
a treatment developed for one genetic cause of autism and intellectual disability might be useful for many others.
In a paper published today in the online edition of Nature Neuroscience, a research team led by Mark Bear,
the Picower Professor of Neuroscience in MIT Picower Institute for Learning and Memory, showed that two very different genetic causes of autism
and intellectual disability disrupt protein synthesis at synapses, and that a treatment developed for one disease produced a cognitive benefit in the other.
The research was performed by postdoc and lead author Di Tian, graduate student Laura Stoppel, and research scientist Arnold Heynen, in collaboration with scientists at Cold Spring Harbor Laboratory and Roche pharmaceuticals.
Researching the role of fragile X syndrome One heritable cause of intellectual disability and autism is fragile X syndrome,
which arises when a single gene on the X chromosome, called FMR1, is turned off during brain development.
Different genes, same consequences Another cause of autism and intellectual disability is the loss of a series of genes on human chromosome 16,
Some of the 27 affected genes play a role in protein synthesis regulation, leading Bear and colleagues to wonder if 16p11.2 microdeletion syndrome and fragile X syndrome affect synapses in the same way.
similar to fragile X. Restoring brain function after disease onset These findings encouraged the MIT researchers to attempt to improve memory function in the 16p11.2 mice with the same approach that has worked in fragile X mice.
The implication, according to Bear, is that ome cognitive aspects of this disease, previously believed to be an intractable consequence of altered early brain development,
Current research indicates that well over 100 distinct gene mutations can manifest as intellectual disability and autism.
Studies at other institutions have identified mutations in the gene for Syngap associated with autism and intellectual disability.
All three of the disability-associated mutations showed similar effects: Compared to normal neurons, there was less Syngap in synapses
Biomedical Research, the UCSF Diabetes Center Obesity Pilot program, and the National institutes of health b
#New ALS Gene and Signaling Pathways Identified Using advanced DNA sequencing methods, researchers have identified a new gene that is associated with sporadic amyotrophic lateral sclerosis (ALS),
or Lou Gehrig disease. ALS is a devastating neurodegenerative disorder that results in the loss of all voluntary movement
inflammation (a reaction to injury or infection) and autophagy (a cellular process involved in the removal of damaged cellular components.
especially since the inflammatory and autophagy pathways have been implicated previously in the disease, said Lucie Bruijn, Phd,
Chief Scientist for The ALS Association. he fact that TBK1 accounts for one percent of ALS adds significantly to our growing understanding of the genetic underpinnings of the disease.
LS is an incredibly diverse disease, caused by dozens of different genetic mutations, which wee only beginning to discover.
the better we can deciphernd influencehe pathways that lead to disease. The other co-leaders of the study are Richard M. Myers, Phd, president and scientific director of Hudsonalpha,
and Tim Harris, Phd, DSC, Senior vice president, Technology and Translational Sciences, Biogen idec. hese findings demonstrate the power of exome sequencing in the search for rare variants that predispose individuals to disease and in identifying potential
focused collaborations with the best academic scientists to advance our understanding of the molecular pathology of disease.
The combination of those groups with a large number of the clinical collaborators who have been seeing patients with this disease for many years and providing clinical information
TBK1 mutations appeared in about 1 percent of the ALS patients large proportion in the context of a complex disease with multiple genetic components, according to Dr. Goldstein.
may actually be a major player in the disease. emarkably, the TBK1 protein and optineurin, which is encoded by the OPTN gene,
and mouse models with mutations in TBK1 or OPTN to study ALS disease mechanisms and to screen for drug candidates.
Several compounds that affect TBK1 signaling have already been developed for use in cancer, where the gene is thought to play a role in tumor-cell survival. his is a great example of the potential of precision medicine,
said Tom Maniatis, Phd, the Isidore S. Edelman Professor, chair of biochemistry and molecular biophysics,
and director of Columbia university-wide precision medicine initiative. t now seems clear that future ALS treatments will not be equally effective for all patients because of the disease genetic diversity.
protect against infection and supply nerve cells with nutrients. With the help of this detailed map, the scientists were able to identify hitherto unknown cell types,
The new knowledge the project has generated can shed more light on diseases that affect the myelin
such as multiple sclerosis (MS). e could also confirm previous findings, such as that the pyramidal cells of the cerebral cortex are organised functionally in layers,
This gives science a new tool for studying these cell types in disease models and helps us to understand better how brain cell respond to disease and injury.
There are estimated to be 100 million cells in a mouse brain and 65 billion in a human brain.
It also involved researchers from Karolinska Institutet Department of Oncology-Pathology, and Uppsala University. The study was financed with grants from several bodies,
including the European Research Council, the Swedish Research Council, the Swedish Cancer Society, the EU Seventh Framework Programme, the Swedish Society of Medicine, the Swedish Brain Fund, Karolinska Institutet strategic programme for neuroscience (Stratneuro), the Human Frontier Science Program
#Molecular Inhibitor Breaks Cycle That Leads to Alzheimer's A molecular chaperone has been found to inhibit a key stage in the development of Alzheimer disease and break the toxic chain reaction that leads to the death of brain cells, a new study shows.
A molecule that can block the progress of Alzheimer disease at a crucial stage in its development has been identified by researchers in a new study,
breaking the cycle of events that scientists believe leads to the disease. Specifically, the molecule, called Brichos, sticks to threads made up of malfunctioning proteins, called amyloid fibrils,
which are the hallmark of the disease. By doing so, it stops these threads from coming into contact with other proteins,
scientists have moved closer to identifying a substance that could eventually be used to treat the disease.
great deal of work in this field has gone into understanding which microscopic processes are important in the development of Alzheimer disease;
Alzheimer disease is one of a number of conditions caused by naturally occurring protein molecules folding into the wrong shape
however a second critical step in the disease development. After amyloid fibrils first form from misfolded proteins, they help other proteins
and are thought now to be responsible for the devastating effects of Alzheimer disease. This second stage, known as secondary nucleation, sets off a chain reaction which creates many more toxic oligomers
what happens during the progression of Alzheimer disease, but also what might happen if one stage in the process was switched somehow off. e had reached a stage where we knew what the data should look like
The research team then carried out further tests in which living mouse brain tissue was exposed to amyloid-beta, the specific protein that forms the amyloid fibrils in Alzheimer disease.
confirming that the molecule had suppressed the chain reaction from secondary nucleation that feeds the catastrophic production of oligomers leading to Alzheimer disease.
#Tau Associated MAPT Gene Increases Risk for Alzheimer's disease A international team of scientists, led by researchers at the University of California,
San diego School of medicine, has identified the microtubule associated-protein protein tau (MAPT) gene as increasing the risk for developing Alzheimer disease (AD).
including Parkinson disease (PD) and AD. These findings provide novel insight into Alzheimer neurodegeneration, possibly opening the door for improved clinical diagnosis and treatment.
Alzheimer disease, which afflicts an estimated 5 million Americans, is characterized typically by progressive decline in cognitive skills, such as memory and language and behavioral changes.
such as PD. hough a tremendous amount of work has been conducted showing the involvement of the tau protein in Alzheimer disease,
Microscopic image depicting plaques and tangles characteristic of Alzheimer disease. Image credit: Tom Deerinck, NCMIR, UC San diego. In the new Molecular Psychiatry paper, conducted with collaborators across the country and world,
and more likely to experience increased brain atrophy than non-carriers. his study demonstrates that tau deposits in the brains of Alzheimer disease subjects are not just a consequence of the disease,
and progression of the disease, said Gerard Schellenberg, Phd, professor of pathology and laboratory medicine at the University of Pennsylvania,
principal investigator of the Alzheimer Disease Genetics Consortium and a study co-author. n important aspect was the collaborative nature of this work.
Thanks to our collaborators from the Consortium, the International Parkinson Disease Genetics Consortium, the Genetic and Environmental Risk in Alzheimer Disease, the Cohorts for Heart and Aging research in Genomic Epidemiology, decode Genetics and the Demgene cohort,
since Alois Alzheimer time that both plaques (with amyloid) and tangles (of tau) are key features of Alzheimer pathology,
or slow down clinical disease progression have focused on the amyloid pathway. Until this year no one had shown convincingly that the MAPT (tau) gene altered the risk of AD and this,
#What Autism Can Teach Us About Brain Cancer Both disorders involve faults in the same protein.
Applying lessons learned from autism to brain cancer, researchers at The Johns hopkins university have discovered why elevated levels of the protein NHE9 add to the lethality of the most common and aggressive form of brain cancer, glioblastoma.
Their discovery suggests that drugs designed to target NHE9 could help to successfully fight the deadly disease.
A summary of their work in human tumor cells and mice will be published on Feb 9 in the journal Nature Communications. y laboratory research on cargo transport inside the cells of patients with autism has led to a new strategy
for treating a deadly brain cancer says Rajini Rao, Ph d, . a professor of physiology at the Johns hopkins university School of medicine. his is a great example of the unexpected good that can come from going wherever the science takes us.
All animal and human cells contain many argo packagessurrounded by membranes. These so-called endosomes carry newly minted proteins to specific destinations throughout the cell
Rao research group previously showed that autism-associated defects in the protein NHE9 are harmful
the researchers examined NHE9 in tumor cells from several patients. Cells with low levels of NHE9 grew the slowest, the team found,
. And this was confirmed when the tumor cells, which were manipulated to have high or low NHE9, were transplanted into the brains of mice.
Based on their autism research, the team suspected that the boost NHE9 gave to glioblastomas was explained by abnormal endosome acidity.
Further studies revealed that, in contrast to autism, NHE9 is overactive in brain cancer, causing endosomes to leak too many protons
and become too alkaline. This slows down the hipping rateof cancer-promoting cargo and leaves them on the cell surface for too long.
Research from other laboratories suggested that one such cargo protein is EGFR, which maintains cancer-promoting signals at the cell surface
and helps tumors become more robust so they grow and move faster. It is also found at elevated levels in more than one-half of patients with glioblastomas.
Drugs targeting EGFR in these patients are sometimes effective. As they suspected, the team found that alkaline endosomes slow down the removal of EGFR from cell surfaces.
Lab-grown tumor cells were killed more readily when treated with both a drug countering NHE proteins
so that hopefully we can make this disease less aggressive and less devastating. About this genetics research Other authors of the report include Kalyan Kondapalli, Jose Llongueras, Vivian Capilla-Gonzalez, Hari Prasad, Anniesha Hack, Christopher Smith and Hugo Guerrero
This work was supported by grants from the National Institute of Neurological disorders and Stroke (NS070024), the National Institute of Diabetes and Digestive and Kidney diseases (DK054214
Overtext Web Module V3.0 Alpha
Copyright Semantic-Knowledge, 1994-2011