to provide disease resistance, or even to introduce novel traits that are not found in humans.'
But it continues to attract controversy as critics fear DNA alterations could create unforeseen health problems that would be passed down from generation to generation of the population.
It could also help doctors understand how infections spread. But in the short-term, the thought that we are enveloped each in millions of bugs is likely to terrify hygiene obsessives.
or is caused under stress by road rage or similar. It then responds by offering a suitable massage and blowing air through its ventilation system.
and we derive stress and energy level from that,'Olaf Biedermann, director of innovation at Faurecia said.'
and whether someone is having a heart attack. The idea is that if higher than usual heart activity is detected,
Research has shown that drivers suffering from cardiovascular disease are 23 per cent more likely to be involved in a road accident
rising to 52 per cent for drivers suffering from angina-chest pains caused by the heart.
Ford's car seat may in some cases detect increased heart activity before the driver notices they are having a heart attack,
'What happens when a member of the team comes down with cellulitis or pneumonia? We have got to use telemedicine to tele-mentor them on the diagnosis and treatment.
#HIV breakthrough could lead to a CURE as markers on immune cells identified The way a patient's immune system responds to HIV infection could offer clues as to
'Normally, if someone is being treated for HIV infection and they stop their medication, the virus can be detected back in the blood stream within days.'
and ultimately a cure for HIV infection.''He added:''Our work has identified that there are certain markers on the immune cells of patients
'Interestingly, some of these markers have also been shown to be good targets for therapy in some cancers.'
The infection persists in latent cells,'hidden'reservoirs, from where they can re-emerge. Destroying these reservoirs remains one of the'Holy grails'of HIV research.
Dr Frater and his team analysed the data from a study of patients with primary HIV infection involved in the SPARTAC trial.
Immune cells with the PD1 biomarker have already been identified as a target for drugs to treat stage-four melanoma
or end stage cancer. Researchers are now considering how to manipulate immune cells with the PD1 marker in their HIV research.
Scientists discovered for the first time that people left in agony by arthritis develop more receptors in the brain that respond to opiate pain relief.
They found that arthritis patients who had suffered more recent severe pain had more opiate receptors.
a patient who suffers chronic pain from osteoarthritis, said she was xtremely interestedin the research. feel
the brain is still susceptible to injuries from impacts. The 6d helmet contains a foam liner inside
which can cause the brain to spin inside the skull and lead to brain injuries. Bob Weber, cofounder of 6d helmets, said the combination of the suspension system
and thus curb infectious disease. Plant and animal breeders may find it useful, too, for creating new strains of crops and livestock.
Viral infection is a serious threat to these microbes, and the natural job of both CRISPR-Cas9 and CRISPR-Cpf1 is to recognise viral genes
#A drug used to rid people of worms is a new weapon against malaria IVERMECTIN,
a drug employed for the treatment of worm infections, has a side effect. It has been known since the 1980s that it kills arthropods (lice, mites,
which transmit malaria. Preliminary studies suggested so. Mosquitoes do, indeed, get poisoned when they bite people who have taken the drug.
And, since ivermectin is deployed routinely en masse to deal with lymphatic filariasis (a nasty disease that can lead to extreme swelling of limbs and genitalia), river blindness and so on,
Dr Foy and his colleagues ran a small clinical trial in Burkina faso that is the first to measure the effect of the drug on rates of malaria.
People in a comparison group of villages got just the first dosehich is the routine annual mass-treatment for worm diseases.
Dr Kobylinski and his colleagues fed mosquitoes malaria-infected human blood mixed with the drug.
In Thailand, a country well on its way to eliminating the scourge of malaria, one line of attack is mass-treatment with drugs that can clear the parasite from its human hosts.
since this is already a familiar treatment for common problems like scabies. The discoverers of ivermectin predecessor, avermectin, were among the winners of this year Nobel prize for medicine.
it will increase the chance that the disease can be knocked on the head once and for all r
The target Soundhawk customer doesn have severe hearing loss but rather a situational needhe inability to hear during a lecture or in a noisy restaurant,
Regarding customers with even minimal hearing loss, Kisch explains, ou want to motivate people to be able to do something about it very quickly.
potentially impacting the hundreds of millions of people experiencing hearing loss globally who do not qualify for existing solutions.
What is more, the energy from the laser causes the blood to coagulate on the wound, which prevents bleeding.
the result is a potentially fatal arrhythmia. Now, a team of researchers from Oxford and Stony Brook universities has found a way to precisely control these waves-using light.
'When there is scar tissue in the heart or fibrosis, this can cause part of the wave to slow down.
and disease, appear today in the Proceedings of the National Academy of Sciences (PNAS).""This is a fundamental advance that is broadly applicable
and turnover,"said senior author Jamey Marth, Ph d.,professor in SBP's NCI-designated Cancer Center."
and thereby maintain health as well as contribute to various diseases.""This newly discovered mechanism encompasses multiple factors,
which we increasingly note is occurring at the interface of health and disease, "Marth explained."
"In retrospect from published literature and from studies in progress, we can now see how sepsis,
diabetes and inflammatory bowel disorders can arise by the targeted acceleration or deceleration of secreted protein aging and turnover."
"The discovery of this mechanism provides a unique window into disease origins and progression,"Marth added."
"It has been known that circulating glycosidase enzyme levels are altered in diseases such as sepsis, diabetes, cancer and various inflammatory conditions.
We are beginning to see previously unknown molecular pathways and connections in the onset and progression of disease
and Genistein, the compound found in soybean which has been suggested to play a role in prevention of steroid-hormone related cancers, particularly breast cancer.
and works on the synthesis of substances that can inhibit tumor cell growth. The US research group under Professor Anthony J. Arduengo III is interested particularly in developing industrially applicable methods for using materials derived from wood biomass for the sustainable manufacture of a broad array of basic chemicals such as, for example,
In children with one of those conditions, autoimmune lymphoproliferative syndrome (ALPS), all the patients showed a durable, complete response, with normal blood cell counts and rapid improvements,
""Patients with ALPS and similar autoimmune disorders have had few long-term treatment options for managing their disease,
ALPS is one of the autoimmune cytopenias, a group of diseases in which the immune system inappropriately destroys blood cells.
Patients may suffer anemia, uncontrolled bleeding and vulnerability to infections. Parents often see their children struggle with swollen lymph nodes, painful enlarged spleens, fatigue and anxiety.
Because autoimmune cytopenias are relatively rare, families often experience a"diagnostic odyssey"--years of testing,
Moreover, over the long term, corticosteroids increase the risk of osteoporosis and vulnerability to infection. The current study builds on preliminary results published by Teachey
and 12 others had caused secondary cytopenias by other underlying autoimmune diseases. All were intolerant of or resistant to corticosteroids.
Patients also had improvements in spleen and lymph node abnormalities. All 12 patients were able to discontinue steroids
#UT Southwestern researchers identify an enzyme as a major culprit of autoimmune diseases Activating an enzyme that sounds an alarm for the body's innate immune system causes two lethal autoimmune diseases in mice,
could someday lead to new therapies for autoimmune diseases.""These results suggest that inhibition of the enzyme cgas may be an effective therapy for autoimmune diseases such as Aicardi-Goutieres Syndrome (AGS) and systemic lupus erythematosus (SLE),
which are linked to the same inflammatory pathway, "said senior author Dr. Zhijian"James"Chen, Professor of Molecular biology and a Howard Hughes Medical Institute (HHMI) investigator at UT Southwestern.
In autoimmune diseases, the immune system turns against the body instead of protecting it. AGS is a rare genetic disorder that mainly affects the brain,
while SLE can affect the skin, joints, kidneys, brain, and other organs. Neither disease has a cure
only treatments to control symptoms. Dr. Chen said cgas is likely amenable to inhibition by small-molecule drugs
The same elegant system can trigger autoimmune disease when self-DNA is inappropriately present in the cytoplasm,
"Even deletion of just one of the two genes for cgas largely rescued the mice from the autoimmune disease,
#New finding offers clues for blocking cancer gene A new study suggests a potential new way to block one of the most common cancer-causing genes, without causing severe side effects.
The Notch gene plays a role in many types of cancer. It's the most common cancer-causing gene in T-cell acute lymphoblastic leukemia.
About 60 percent of children and adults with T-cell leukemia harbor a Notch mutation. But drugs designed to block Notch have caused serious side effects such as severe diarrhea or skin cancers.
Now a team from the University of Michigan Comprehensive Cancer Center offers a potential new target to block Notch without the toxic effects.
Researchers found that a protein called Zmiz1 sticks to Notch triggering the gene to turn on its cancer function.
But Zmiz1 does not impact normal healthy Notch functions.""Notch controls the genes that cause cancer,
but it's also important for normal health. The challenge is to knock out the cancer function of Notch
but preserve its normal function,"says Mark Chiang, M d.,Ph d.,assistant professor of internal medicine at the University of Michigan Medical school."
"If you unstick Zmiz1 from Notch, the cancer cells die. And Zmiz1 seems to be selective in turning on the cancer functions of Notch,
"Chiang adds. The researchers found mice lived longer when Zmiz1 was deleted. The mice had normal body weight and no severe side effects from blocking Zmiz1.
We think this would block the Notch cancer pathway without causing toxic side effects, like we see with current Notch inhibitors,
While the majority of kids with T-cell leukemia are cured, about 20 percent will relapse. Those kids face a grim prognosis.
"We need to develop therapies against Notch to help kids with relapsed cancer and to cure kids with fewer toxicities or long-term effects,
the brushes also could someday deliver cancer therapeutics s
#Researchers want to turn acid-loving microbes into safe drug-carriers Usually the microbe S. islandicus is found in hot and acidic volcanic springs,
Many diabetics need to daily inject insulin directly into their body, and they would benefit greatly by taking insulin in a tablet instead.
they chose the most complex one known, Down syndrome cell adhesion molecule 1 (Dscam1), which controls the wiring of the brain in fruit flies.
#Researcher develops vaccine for fatal disease Over 200 million people in 74 countries suffer from schistosomiasis
and four times that many are at risk for the disease since they do not have access to clean water.
A recent discovery in the Texas Tech University Health Sciences Center (TTUHSC) research laboratory may make it possible to reduce the number of infections from this disease.
Siddiqui, a Grover E. Murray Distinguished Professor at the TTUHSC School of medicine, received a patent from the U s. Patent and Trademark Office for his schistosomiasis vaccine.
An effective schistosomiasis vaccine has the potential to impact one billion people.""Praziquantel, a drug developed over 40 years ago,
is the only effective treatment available for schistosomiasis. However, re-infection frequently occurs following drug treatment.
An effective vaccine is critical toward providing long-term treatment. This schistosomiasis vaccine offers unique opportunities for organizations to market it as a method for completely eliminating this disease.
The vaccine's advantages make it easy to sell because it eliminates the instances of re-infection common with the current chemotherapeutic drug,
is easier and less expensive to distribute and can be administered with current chemotherapy regimen. Long-term vaccine efficacy will effectively reduce the transmission of schistosomiasis in endemic areas.
According to the World health organization there are no commercially available vaccines against schistosomiasis, which afflicts people in countries primarily in Asia, Africa and South america.
Symptomatic schistosomiasis can result in increased susceptibility to sexually transmitted infections including HIV, which is prevalent in many countries plagued by schistosomiasis.
A person gets a schistosoma infection through contact with contaminated water. The parasite swims freely in open bodies of water.
Once contact is made with humans, the parasite burrows into the skin, matures into another stage,
and then migrates to the lungs and liver, where it matures into the adult form.
Siddiqui said detection of calcified schistosome eggs in Egyptian mummies from the 20th dynasty (1250 to1000 BC) tells us that schistosomiasis is an ancient disease."
"Major pathology of schistosomiasis is due to immunological reactions to schistosome eggs trapped in tissues, "Siddiqui said."
"Continuing infection causes enlargement of the liver and blood in urine. We see pictures of children from Africa with bulging bellies because of this disease."
"Despite mass treatment with drugs, infection rates continue to rise. An additional 800 million people are at risk of contracting schistosomiasis.
Durable and sustained reduction in the disease spectrum and transmission can only be obtained by long-term protection through vaccination.
Siddiqui has studied schistosomiasis for over 20 years working to develop this vaccine n
#Three-minute test detects common form of dementia that's hard to diagnose Although Lewy Body disease (LBD) is the second-most-common degenerative disease after Alzheimer's disease,
it's not exactly a household name. It affects more than 1. 3 million Americans, is recognized poorly,
and diagnosis is delayed often significantly. Patients with LBD simultaneously experience losses in cognitive function, mobility and behavior.
The late Robin williams had this form of dementia as did legendary NHL coach Alger Joseph"Radar"Arbour,
which also can cause visual hallucinations and make depression worse. Until now, there has been no way to assess or operationalize many of the cognitive and behavioral symptoms of LBD in clinical practice.
A leading neuroscientist at Florida Atlantic University has developed the"Lewy Body Composite Risk Score"(LBCRS) to quickly
and effectively diagnose LBD and Parkinson's disease dementia (PDD) in about three minutes. The LBCRS is a brief rating scale that can be completed by a clinician to assess clinical signs
and symptoms highly associated with the pathology of this disease. With this important tool, a clinician can assess
whether the patient has bradykinesia, rigidity, postural instability, or rest tremor without having to grade each extremity.
but are much less commonly found in other forms of dementia. The LBCRS study,"Improving the Clinical Detection of Lewy Body Dementia with the Lewy Body Composite Risk Score,
"recently published in Alzheimer's & Dementia, the journal of the Alzheimer's Association, involved 256 patients who were compared with the clinical dementia rating
and gold standard measures of cognition, motor symptoms, function and behavior. The test was administered in a"real-world"clinic setting with patients who were referred from the community rather than in a research sample.
The clinic sample had a mixture of gender education, comorbidities, behavioral, affective, motor symptoms, and diagnoses.
The LBCRS was able to discriminate between Alzheimer's disease and LBD with 96.8 percent accuracy, and provided sensitivity of 90 percent and specificity of 87 percent.
"Most patients never receive an evaluation by a neurologist skilled in the diagnosis of Lewy body dementia,
and significant delays and misdiagnoses occur in most patients with this disease, "said James E. Galvin, M d.,M p h,
"Early detection of Lewy body dementias will be important to enable future interventions at the earliest stages
and differentiate LBD from healthy aging and other neurodegenerative diseases. Galvin has led efforts to develop a number of dementia screening tools,
including the Quick Dementia Rating system (QDRS), AD8, a brief informant interview to translate research findings to community settings.
He has done cross-cultural validation of dementia screening methods in comparison with Gold standard clinical evaluations and biomarker assays.
His team also has developed sophisticated statistical models to explore transition points in clinical cognitive, functional, behavioral and biological markers of disease in healthy aging, mild cognitive impairment, Alzheimer disease,
and Parkinson's disease e
#A molecular switch to stop inflammation Our immune system is vital to us and can sometimes overreact causing chronic illnesses,
such as for instance rheumatism and allergy. Now, researchers from Umeå University and University of Gothenburg have identified a molecular switch-MYSM1-that can suppress such an overreaction
and avoid inflammation. The study is published in the prestigious journal Immunity.""The discovery of MYSM1 is a major milestone in our understanding of how our immune system works,
in order to prevent inflammatory diseases such as sepsis, "says Nelson O. Gekara, research leader at MIMS, Molecular Infection Medicine Sweden at Umeå University.
Our innate immune system is activated when our body needs to protect itself against pathogens, for instance bacteria and viruses,
as well as for tissue healing. In some people, the immune system overreacts which can cause chronic inflammatory diseases and result in tumour development.
The innate immune system is activated by receptors that recognise certain molecular patterns found on microbes or dead cells.
Together with Professor Jonas A Nilsson at Sahlgrenska Cancer Center at the University of Gothenburg
For the first time, the researchers are now able to show that during infection or inflammation MYSM1 accumulates outside of the nucleus,
Therefore lack of MYSM1 in animal results in unrestrained activation of the innate immune system, leading to inflammatory diseases"says Nelson O. Gekara.
The hope is to find new therapeutics against infections and other inflammatory diseases e
#Study charts'genomic biography'of form of leukemia A new study by scientists at Dana-Farber Cancer Institute and the Broad Institute of MIT and Harvard offers a glimpse of the wealth of information
that can be gleaned by combing the genome of a large collection of leukemia tissue samples. By analyzing genetic material in chronic lymphocytic leukemia (CLL) and normal tissue from more than 500 patients,
researchers identified dozens of genetic abnormalities that may drive the disease, including two that had never before been linked to human cancer.
They began to trace how some of these abnormalities affect the course of the disease and its susceptibility to treatment.
And they started tracking the evolutionary path of CLL as its ever-churning genome spawns new groups and subgroups of tumor cells in a single patient.
This type of information is critical as the treatment of CLL is geared increasingly to the unique genetic features of each patient's tumor.
Traditional chemotherapy regimens are now being supplemented by drugs that target the specific set of delinquent genes within cancer cells."
"Sequencing the DNA of CLL has taught us a great deal about the genetic basis of the disease,
"said Catherine Wu, MD, of Dana-Farber, the Broad Institute of MIT and Harvard, and Brigham and Women's Hospital, a senior author of the study, which is being published today by the journal Nature."
however, were limited by the relatively small number of tumor tissue samples analyzed, and by the fact that those samples were taken at different stages of the treatment process,
similarly-treated group of patients provides the statistical power necessary to study the disease in all its genetic diversity-to draw connections between certain mutations and the aggressiveness of the disease,
and their role in helping the disease advance, "she continued.""Our results demonstrate the range of insights to be gained by this approach.""
"The growing sample size allows us to start engaging deeply with the complex interplay between different mutations found in any individual tumor,
which these mutations are acquired to allow the malignancy to thrive and overcome therapy.""Wu and her team collected tumor and normal tissue samples from 538 patients with CLL, 278 of
whom had participated in a German clinical trial that helped determine the standard treatment for the disease.
They performed whole-exome sequencing (WES) on each sample, reading the genetic code letter by letter in sections of DNA that hold the code for making proteins.
and analyze large cohorts of tumor tissue samples with defined clinical status, "remarked Gad Getz, Phd, of the Broad Institute and Massachusetts General Hospital, co-senior author of the paper."
"Our work has enabled us to discover novel cancer genes, begin to chart the evolutionary path of CLL,
These discoveries will form the basis for precision medicine of CLL and other tumor types
BRAF-mutant melanoma A team of Massachusetts General Hospital (MGH) investigators has discovered a new combination of drugs that may be effective against one of the deadliest cancers, malignant melanoma.
whether very-large-scale screening across a diverse collection of cancer cell lines and a large number of drugs could yield new combinations for patients with cancer,
"says Adam Friedman, MD, Phd, of the CBRC and the MGH Cancer Center, who led the study."
"By conducting such a screen, we found one specific combination of agents that are already being used clinically that potentially could be used for a specific group of patients-those with BRAF-mutant cancers."
even with the increasing number of drugs targeting specific molecular abnormalities that drive tumor growth,
often because their tumors have become resistant, and some tumors never respond to the targeted drugs.
While combining anticancer drugs appears a promising strategy, the sheer volume of drugs currently in use or in development-more than 500,
This study utilized 36 well-characterized melanoma cell lines assembled by the MGH Center for Molecular Therapeutics to test all possible combinations of more than 100 oncology drugs,
looking for effects on the number and viability of tumor cells. While several combinations showed synergistic effects-with some drugs sensitizing the cells against several other drugs-most combinations increased the response of only one or two cell lines
implying that the vulnerability of an individual patient's tumor to these combinations depends on its unique genetic signature.
and found significant synergistic effects against both tumor models.""We need to confirm this synergistic activity of vemurafenib
and cediranib across a broader range of melanoma models, investigate why the particular combination is effective,
and find biomarkers that predict which patients with BRAF-mutant melanoma should receive this combination,
and identify patients whose tumors might respond.""He adds, "This study was actually a pilot project for a much larger effort within the Center for Molecular Therapeutics to map responses against drug combinations across hundreds of cancer cell lines, not just melanoma,
and look for novel combinations that will benefit subsets of patients regardless of the particular type of tumor they have.
Since our collection of cell lines is annotated completely genetically -which means that mutations and expression changes in each line's genes have been documented-we should be able to identify in advance patients who will benefit from specific combinations.
'In recent years, Héctor Peinado, Head of the Microenvironment and Metastasis Group at the Spanish National Cancer Research Centre (CNIO), David Lyden from Weill Cornell Medical College,
and Jaqueline Bromberg from the Memorial Sloan Kettering Cancer Center, have developed a theory that supports Paget's'seed
and pancreas cancer to the liver--metastasis is reduced in these organs. LAYING THE GROUNDWORK The researchers have discovered also the molecular signals that intercede in the reaction of the recipient tissue
inflammation is associated a process with cancer. These results represent the identification of potential new pharmacological targets,
as well as plasma from cancer patients. The latter served for the preliminary study of the predictive power of the integrins identified, that is,
and pancreas cancer seems to predict the organ where the metastasis will occur, "says Peinado."
and quickly develop tumors. The new work, published the week of November 2, 2015 in PNAS, suggests that Epha2 could be a new target for a subset of lung cancer,
and is the leading cause of cancer-related deaths worldwide.""Sometimes there are hundreds of mutations in the genes of a patient's tumors,
but you don't know whether they are drivers of the disease or byproducts,"says senior author Inder Verma, professor of genetics and holder of Salk's Irwin and Joan Jacobs Chair in Exemplary Life science."
"We found a new way by which to identify cancer suppressor genes and understand how they could be targeted for therapies."
"Two gene mutations in particular are known to spur the growth of human tumors: KRAS and p53. Though both genes have been studied heavily,
they are difficult to therapeutically target, so the Salk team decided to look at genes that might police KRAS and p53 instead.
and efficiently test the effect of these thousands of genes on tumor development. In animal models, the Salk team found that 16 of these cell-signaling genes produced molecules that had a significant effect on KRAS-and p53-related tumors.
Of these 16 molecules one especially stood out: the Epha2 enzyme, originally discovered in the lab of another Salk scientist, Tony Hunter.
but the team discovered that its absence let KRAS-associated tumors grow much more aggressively."
"With a mutation in KRAS, a tumor forms in 300 days. But without Epha2, the KRAS mutation leads to tumors in half the time, 120 to 150 days,"says Verma,
who is also an American Cancer Society Professor of Molecular biology.""This molecule Epha2 is having a huge effect on restraining cancer growth
when KRAS is mutated.""Mutated KRAS is a common culprit in approximately 10 to 20 percent of all cancers, particularly colon cancer and human lung cancer."
"Since activating Epha2 led to the suppression of both cell signaling and cell proliferation, we believe that the enzyme might serve as a potential drug target in KRAS-dependent lung adenocarcinoma,
"says Narayana Yeddula, a Salk research associate and first author of the paper. A 10-year national project called the Cancer Genome Atlas mapped the genomes of hundreds of patients for over 20 different cancers
and uncovered a number of related genetic mutations, though the role of these mutations has not been understood well in lung cancer (especially adenocarcinoma,
which makes up almost a quarter of all lung cancers). From the Cancer Genome Atlas data, the Salk team found that genetic alterations of Epha2 were detected in 54 out of 230 patients with adenocarcinoma.
The team also found, surprisingly, that the loss of Epha2 activated a pathway commonly associated with cancer (dubbed Hedgehog) that promotes tumor growth."
"Oddly, among human lung cancer patients with Epha2 mutations, around 8 percent of patients actually have high Epha2 expression.
So, in some instances, Epha2 is not suppressing tumors and may be context-dependent. Therefore, we need to carefully evaluate the molecule's function
when designing new therapeutics,"adds Yifeng Xia, a Salk staff researcher involved in the work k
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