Bacteria frequently implicated in respiratory and urinary infections in hospitals may soon develop complete resistance to antibiotics, even those used as a last resort, experts warn.
A new study shows that two genes that confer resistance against a particularly strong class of antibiotics can be shared easily among a family of bacteria responsible for a significant portion of hospital-associated infections.
Drug-resistant germs in the same family of bacteria recently infected several patients at two Los Angeles hospitals. Those infections are linked to medical scopes believed to have been contaminated with bacteria that can resist carbapenems, potent antibiotics that are supposed to be used only in gravely ill patients or those infected by resistant bacteria.
“Carbapenems are one of our last resorts for treating bacterial infections, what we use when nothing else works,” says senior author Gautam Dantas, associate professor of pathology and immunologyat Washington University in St. Louis.
Scientists have developed a blood test using human stem cells that predicts whether new drugs will cause severe side effects. The test, which only requires blood from a single donor, could help prevent catastrophic inflammatory reactions known as a cytokine storm in people participating in drug trials.
"As biological therapies become more mainstream, it’s more likely that drugs being tested on humans for the first time will have unexpected and potentially catastrophic effects," says Professor Jane Mitchell from the National Heart and Lung Institute at Imperial College London, who led the study. "We’ve used adult stem cell technology to develop a laboratory test that could prevent another disaster like the TGN1412 trial."
In 2006 six healthy young men were hospitalized with multiple organ failure after experiencing a cytokine storm as a result of taking part in the first tests in humans of the drug TGN1412.
Tests on human cells are essential because biological therapies, or "biologics" (such as the cancer drugs Herceptin and Avastin), use antibodies which are specific to humans. They can cause severe reactions, such as a cytokine storm, that don’t occur in animal studies.
Let me give you an example that I'm thinking about a lot today, concerning the future of humankind in the field of medicine. At least to the best of my understanding, we're in the middle of a revolution in medicine. After medicine in the 20th century focused on healing the sick, now it is more and more focused on upgrading the healthy, which is a completely different project. And it's a fundamentally different project in social and political terms, because whereas healing the sick is an egalitarian project ... you assume there is a norm of health, anybody that falls below the norm, you try to give them a push to come back to the norm, upgrading is by definition an elitist project. There is no norm that can be applicable to everybody.
And this opens the possibility of creating huge gaps between the rich and the poor, bigger than ever existed before in history. And many people say no, it will not happen, because we have the experience of the 20th century, that we had many medical advances, beginning with the rich or with the most advanced countries, and gradually they trickled down to everybody, and now everybody enjoys antibiotics or vaccinations or whatever, so this will happen again.
The user presses the bulb of the smartphone dongle, designed to fit in one hand, to initiate the fluid flow (credit: Tassaneewan Laksanasopin, Columbia-
A low-cost smartphone accessory that can detect three infectious disease markers from a finger prick of blood in just 15 minutes, performing all mechanical, optical, and electronic functions of a lab-based blood test.
That’s what team of researchers led by Samuel K. Sia, associate professor of biomedical engineering at Columbia Engineering, has developed.
It performs an enzyme-linked immunosorbent assay (ELISA) triplexed immunoassay not currently available in a single test format: HIV antibody, treponemal-specific antibody for syphilis, and non-treponemal antibody for active syphilis infection.
Sia’s innovative accessory (dongle), a small device that easily connects to a smartphone or computer, was recently piloted by health care workers in Rwanda. They tested whole blood obtained via a finger prick from 96 patients who were enrolling into prevention-of-mother-to-child-transmission clinics or voluntary counseling and testing centers.
A compound found in green tea can kill oral cancer cells without damaging healthy cells, and now scientists think they've figured out how it works.
Earlier studies showed the compound called epigallocatechin-3-gallate (EGCG) killed oral cancer cells, but researchers didn’t how it worked, says Joshua Lambert, associate professor of food science at Penn State University.
“EGCG is doing something to damage the mitochondria and that mitochondrial damage sets up a cycle causing more damage and it spirals out, until the cell undergoes programmed cell death.
“It looks like EGCG causes the formation of reactive oxygen species in cancer cells, which damages the mitochondria, and the mitochondria responds by making more reactive oxygen species.”
As this mitochondrial demise continues, the cancer cell also reduces the expression of antioxidant genes, further lowering its defenses.
“So, it’s turning off its mechanism of protection at the same time that EGCG is causing this oxidative stress,” Lambert says.
The compound did not cause the same reaction in normal cells—in fact it appeared to increase the protective capabilities of the cell, according to the study published online in the journal Molecular Nutrition and Food
Gladstone Institutes researchers have uncovered a new memory regulator in the brain that may offer a potential treatment to improve memory in Alzheimer’s disease using a drug that targets those receptors.
They found in their research* that decreasing the number of A2A adenosine receptors in astrocyte brain cells improved memory in healthy mice. It also prevented memory impairments in a mouse model of Alzheimer’s disease.
The findings were published Monday (Jan. 26) in Nature Neuroscience.
In the largest collaborative study of the brain to date, about 300 researchers in a global consortium of 190 institutions identified eight common genetic mutations that appear to age the brain an average of three years.
The discovery could lead to targeted therapies and interventions for Alzheimer’s disease, autism, and other neurological conditions.
Led by the Keck School of Medicine of the University of Southern California (USC), an international team known as the Enhancing Neuro Imaging Genetics through Meta Analysis (ENIGMA) Network, pooled brain scans and genetic data worldwide to pinpoint genes that enhance or break down key brain regions in people from 33 countries.
This is the first high-profile study since the National Institutes of Health (NIH) launched its Big Data to Knowledge (BD2K) centers of excellence in 2014. The research was published Wednesday, Jan. 21, in the peer-reviewed journal Nature.
“Our global team discovered eight genes that may erode or boost brain tissue in people worldwide,” said Paul Thompson, Ph.D., Keck School of Medicine of USC professor and principal investigator of ENIGMA. ” Any change in those genes appears to alter your mental bank account or brain reserve by 2 or 3 percent. The discovery will guide research into more personalized medical treatments for Alzheimer’s, autism, depression and other disorders.”
Physicians assistants are highly paid medical professionals who provide a lot of the same healthcare services that doctors do. They take patient histories and perform physical exams, diagnose illnesses and develop treatment plans, prescribe medications and counsel patients. And in surgical settings, they suture wounds and assist with the procedures. PAs, as they’re known in the industry, typically earn master’s degrees in medical science before practicing. These programs usually last three academic years and include classroom instruction in topics ranging from anatomy to pharmacology. Students also participate in more than 2,000 hours of clinical rotations. This training entails a lot of rigorous coursework—education that would, in theory, be hard to deliver outside the brick-and-mortar walls of the 175 or so higher-education institutions with accredited PA master’s programs.
Or maybe not. Soon, an aspiring PA might be able to complete nearly all this coursework online—and through an Ivy League to boot: Yale.
Yale announced earlier this month that it’s partnering with 2U, Inc.—a firm that helps selective nonprofit universities develop virtual degree programs—to launch its online PA initiative. The project is still pending approval by the accrediting commission for PA schools and from various state licensing agencies. But if it gets the green light, it would likely be the country’s first fully online PA degree. (Some programs are considered "hybrid" and entail a combination of on-campus and online coursework.) It would also become Yale’s first fully online master’s program and join the university’s existing on-campus PA program, which was launched in the early 1970s. The online program would cost the same as the on-campus one, whose sticker price is $35,654 annually for the first two years, excluding other fees.
Researchers at the University of Cambridge have grown functional "mini-lungs" using stems cells derived from the skin cells of patients with a debilitating lung disease. Not only can the development help them in coming up with effective treatments for specific lung diseases like cystic fibrosis, but the process has the potential to be scaled up to screen thousands of new compounds to identify potential new drugs.
Creating miniature organoids has been the focus of many a research group, as it allows scientists to better understand the processes that take place inside an organ, figure out how specific diseases occur and develop or even work towards creating bioengineered lungs.
The research team from the Wellcome Trust-Medical Research Council Cambridge Stem Cell Institute studied a lung disease called cystic fibrosis, which is caused by genetic mutation and shortens a patient's average lifespan. Patients have great difficulty breathing as the lungs are overwhelmed by thickened mucus.
To create working mini-lungs, the researchers took skin cells from patients with the most common form of cystic fibrosis and reprogrammed them to an induced pluripotent state (iPS), which allows the cells to grow into a different type of cell inside the body.
A research team from The Scripps Research Institute (TSRI), Mayo Clinic and other institutions has identified a new class of drugs that in animal models dramatically slows the aging process, alleviating symptoms of frailty, improving cardiac function, and extending a healthy lifespan.
They found two drugs — the cancer drug dasatinib (sold under the trade name Sprycel) and quercetin, a natural compound found in many fruits, vegetables, leaves and grains and also sold as a supplement that acts as an antihistamine and anti-inflammatory — can kill senescent cells. These are cells that have stopped dividing and accumulate with age, accelerating the aging process.
The scientists coined the term “senolytics” for this new class of drugs.
“We view this study as a big first step toward developing treatments that can be given safely to patients to extend healthspan or to treat age-related diseases and disorders,” said TSRI Professor Paul Robbins, PhD, who with Associate Professor Laura Niedernhofer, MD, PhD, led the research efforts for the paper at Scripps Florida. “When senolytic agents, like the combination we identified, are used clinically, the results could be transformative.”
“The prototypes of these senolytic agents have more than proven their ability to alleviate multiple characteristics associated with aging,” said Mayo Clinic Professor James Kirkland, MD, PhD, senior author of the new study. “It may eventually become feasible to delay, prevent, alleviate or even reverse multiple chronic diseases and disabilities as a group, instead of just one at a time.”
In its latest attempt to kick-start lady libidos with a pill, Sprout Pharmaceuticals announced this week that it will resubmit its female sex drug, flibanserin, for FDA approval. If it gets the okay, the drug would be the first prescription of its kind for women in the United States: a treatment for female hypoactive sexual disorder, or a low sex drive. More…
SuperAgers, aged 80 and above — but with memories that are as sharp as those of healthy persons decades younger — have distinctly different looking brains than those of normal older people, according to new Northwestern Medicine research.
Understanding Superagers’ unique “brain signature” may enable scientists to decipher the genetic or molecular source and develop strategies to protect the memories of normal aging persons, as well as treat dementia.
Published Jan. 28 in the Journal of Neuroscience, the study is the first to quantify brain differences of SuperAgers and normal older people.
Cognitive SuperAgers were first identified in 2007 by scientists at Northwestern’s Cognitive Neurology and Alzheimer’s Disease Center at Northwestern University Feinberg School of Medicine.
Discovery gives scientists hope of developing a therapy that could slowdown the progression of Alzheimer’s disease and other forms of dementia
People who carry a mutated gene linked to longer lifespan have extra tissue in part of the brain that seems to protect them against mental decline in old age.
The finding has shed light on a biological pathway that researchers now hope to turn into a therapy that slows the progression of Alzheimer’s disease and other forms of dementia.
Brain scans of more than 400 healthy men and women aged 53 and over found that those who carried a single copy of a particular gene variant had a larger brain region that deals with planning and decision making.
Further tests on the group found that those with an enlarged right dorsolateral prefrontal cortex (rDLPFC), as the brain region is known, fared better on a series of mental tasks.
About one in five people inherits a single copy of the gene variant, or allele, known as KL-VS, which improves heart and kidney function, and on average adds about three years to human lifespan, according to Dena Dubal, a neurologist at University of California, San Francisco.
Her latest work suggests that the same genetic mutation has broader effects on the brain. While having a larger rDLPFC accounted for only 12% of the improvement in people’s mental test scores, Dubal suspects the gene alters the brain in other ways, perhaps by improving the connections that form between neurons.
Scientists at the Stanford University School of Medicine have developed a new procedure that uses modified messenger RNA to quickly and efficiently increase the length of human telomeres, the protective caps on the ends of chromosomes that are associated with aging and disease.
Treated cells behave as if they are much younger than untreated cells, multiplying with abandon in the laboratory dish rather than stagnating or dying. Skin cells with telomeres lengthened by the procedure were able to divide up to 40 more times than untreated cells.
The procedure will improve the ability of researchers to generate large numbers of cells for study or drug development and may lead to preventing or treating diseases of aging, the scientists say.
Telomeres are the protective caps on the ends of chromosomes, which house our genomes. In young humans, telomeres are about 8,000–10,000 nucleotides long. They shorten with each cell division, however, and when they reach a critical length, the cell stops dividing or dies. This internal “clock” makes it difficult to keep most cells growing in a laboratory for more than a few cell doublings.
‘Turning back the internal clock’
“Now we have found a way to lengthen human telomeres by as much as 1,000 nucleotides, turning back the internal clock in these cells by the equivalent of many years of human life,” said Helen Blau, PhD, professor of microbiology and immunology at Stanford and director of the university’s Baxter Laboratory for Stem Cell Biology. “This greatly increases the number of cells available for studies such as drug testing or disease modeling.”
A paper describing the research was published in the FASEB Journal. Blau, who also holds the Donald E. and Delia B. Baxter Professorship, is the senior author. Postdoctoral scholar John Ramunas, PhD, of Stanford shares lead authorship with Eduard Yakubov, PhD, of the Houston Methodist Research Institute.
Is sugar making us sick? A team of scientists at the University of California in San Francisco believes so, and they're doing something about it. They launched an initiative to bring information on food and drink and added sugar to the public by reviewing more than 8,000 scientific papers that show ...
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