While the risks of dehydration are well known, new international guidelines seek to protect athletes from the serious health risks associated with drinking too many fluids while exercising.
Overhydrating with water or sports drinks can lead to a condition called exercise-associated hyponatremia, said Dr. Mitchell Rosner, a kidney specialist at the University of Virginia School of Medicine who chaired a group of 16 experts from four countries who drafted the new guidelines. The condition occurs when the body has too much water relative to its salt level, Rosner said. When the salt level in the blood falls too low, he added, it leads to significant neurological problems and can be fatal.
Although exercise-associated hyponatremia once occurred primarily among participants in endurance sports such as marathons and triathlons, Rosner said physicians now see the condition in participants in a wider range of sports, leading to the new guidelines.
“We have documented at least 14 deaths [from exercise-associated hyponatremia] since 1981, including two deaths last summer in young athletes playing football,” he said. “The common feature in all cases is excessive water consumption during athletic events. This is driven by common misbeliefs that overhydration can improve performance and even prevent dehydration. It is worth noting that data demonstrates mild degrees of dehydration do not impair performance.”
The key to preventing overhydration, Rosner said, is to let your body tell you when you need a drink.
“We recommend using your thirst as a guide,” he said. “If you drink when thirsty, you will not become hyponatremic and you will not suffer from significant dehydration.”
Rosner said this recommendation applies whether athletes are consuming water or sports drinks. “Overdrinking a sports beverage will still lead to hyponatremia,” he said. “They contain small amounts of sodium that may lessen the risk very slightly, but they are still mostly water.”
The initial mild symptoms of exercise-associated hyponatremia can include cloudy thinking, nausea and headaches, Rosner said. In severe cases, symptoms include seizures, severe confusion and coma. If coaches or parents suspect an athlete is suffering from the condition, the most important steps are to stop them from drinking and call for medical assistance.
For athletes with mild symptoms, limiting fluids and closely monitoring their condition will help them recover within a few hours, Rosner said, but more severe symptoms such as confusion require urgent medical attention.
The new guidelines were published in the Clinical Journal of Sports Medicine.
Source: University of Virginia
Published on 9th July 2015
The more ice is melted of the Antarctic Filchner-Ronne shelf, the more ice flows into the ocean and the more the region contributes to global sea-level rise. While this might seem obvious, it is no matter of course for the huge ice masses of Antarctica: parts of the ice continent are characterized by instabilities that, once triggered, can lead to persistent ice discharge into the ocean even without a further increase of warming – resulting in unstoppable long-term sea-level rise. In the Filchner-Ronne region however, ice-loss will likely not show such behavior, scientists from the Potsdam Institute for Climate Impact Research now found. Published in Nature Climate Change, their study shows that in this area the ice flow into the ocean increases just constantly with the heat provided by the ocean over time.
“While for other parts of Antarctica unstoppable long-term ice loss might be provoked by a single warming pulse, caused by nature itself or human action, ice loss in the Filchner-Ronne region increases directly with ocean warming,” lead author Matthias Mengel explains. “This is good news, because it is in our hands to determine how much the region contributes to the global sea-level rise.” Ocean warming results from greenhouse gases in the atmosphere, produced by humankind’s unabated burning of coal, oil and gas. Importantly, however, the oceans might not respond linearly to atmospheric warming, and not in the same way in all parts of the world. This includes the risk that ocean temperatures first lag behind, and then rise rapidly.
“Good news” – yet only compared to other parts of the ice continent
The Filchner-Ronne shelf covers an area bigger than Germany; its grounded-ice tributaries store water equivalent to a total of several meters of sea-level rise. “Our calculations show that this relatively small part of the Antarctic ice sheet within just 200 years of unabated climate change could contribute up to 40 centimeters to global sea-level rise,” says Mengel. “This kind of sea-level rise alone could already be enough to bring coastal cities like Hamburg into serious difficulties.”
“At present, most Antarctic ice shelves are surrounded by cold water masses near the freezing point,” co-author Anders Levermann says. “The topography around the ice continent acts as a barrier for heat and salt exchange with the northern warmer and saltier water masses, creating a cold water wall around the continent”. Projections of the breakdown of this front in ocean simulations for the Filchner-Ronne region under atmospheric warming raised concerns that such ocean instability might lead to unstoppable future ice loss also from this part of Antarctica, as is projected to occur in the Wilkes Basin region, for instance. “We found that this is not the case for the Filchner-Ronne shelf – which luckily means that we can still very well limit the ice loss in this area by limiting greenhouse gas emissions.”
Different mechanisms in different regions
Sea-level rise poses a challenge to coastal regions worldwide. While today sea-level rise is mainly caused by thermal expansion of the warming oceans, and by the melting of mountain glaciers, the major contributors to long-term future sea-level rise are expected to be Greenland and Antarctica with their vast ice sheets. The causes of ice loss differ greatly between the two. While on Greenland ice melting at the surface plays a large role, the Antarctic ice sheet loses almost all its ice through ice flow into the ocean. The simulation of the Antarctic ice flow is complex because the flow can become unstable. Ice shelves, the floating extensions of the ice sheet, can act as a break to the ice flow and inhibit instability. Warming oceans around Antarctica that melt the ice shelves therefore increase the risk of high sea-level rise.
The Parallel Ice Sheet Model, as used by the authors, resolves unstable grounding line retreat and simulates the flow of both the ice sheet and the ice shelves. It can therefore help to answer urgent questions as to the extent of Antarctica’s sea-level risks.
“It is more difficult to determine the risk that comes with global warming in parts of Antarctica that are considered unstable, and less difficult for the Filchner-Ronne region that responds linearly to global warming,” concludes Levermann. “One thing is clear: the more warming we cause by burning coal, gas and oil, the more expensive it will be for coastal regions to adapt.”
Source: Potsdam Institute for Climate Impact Research (PIK)
Published on 8th October 2015
Researchers have identified two seemingly unrelated but strong predictors of obesity: having low self-esteem related to one’s weight and keeping food visibly available around the house, outside the kitchen.
Extreme weather events like floods, heat waves and droughts can devastate communities and populations worldwide. Recent scientific advances have enabled researchers to confidently say that the increased intensity and frequency of some, but not all, of these extreme weather events is influenced by human-induced climate change, according to an international National Academies of Science, Engineering, and Medicine report released (March 11).
A new study led by bioengineers at the University of California, San Diego defines the core set of genes and functions that a bacterial cell needs to sustain life. The research, which answers the fundamental question of what minimum set of functions bacterial cells require to survive, could lead to new cell engineering approaches for E. coli and other microorganisms, the researchers said.
An adaptive material invented at Rice University combines self-healing and reversible self-stiffening properties.
Scientists at the UCLA Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research are one step closer to engineering a tool that could one day arm the body’s immune system to fight HIV — and win. The new technique harnesses the regenerative capacity of stem cells to generate an immune response to the virus.
The findings were published today in the journal Molecular Therapy.
“We hope this approach could one day allow HIV-positive individuals to reduce or even stop their current HIV drug regimen and clear the virus from the body altogether,” said Scott Kitchen, the study’s lead author and a member of the Broad Stem Cell Research Center. “We also think this approach could possibly be extended to other diseases.” Kitchen also is a member of the UCLA AIDS Institute and an associate professor of medicine in the division of hematology and oncology at the David Geffen School of Medicine at UCLA.
Kitchen and his colleagues were the first to report the use of an engineered molecule called a chimeric antigen receptor, or CAR, in blood-forming stem cells. Blood-forming stem cells are capable of turning into any type of blood cell, including T cells, the white blood cells that are central to the immune system. In a healthy immune system, T cells can usually rid the body of viral or bacterial infection. But HIV is too strong and mutates too rapidly for T cells to fight against the virus.
The researchers inserted a gene for a CAR into blood-forming stem cells in the lab. The CAR, which is a two-part receptor that recognizes an antigen, was engineered to be carried by T cells and direct them to locate and kill HIV-infected cells. The CAR-modified blood stem cells were then transplanted into HIV-infected mice that had been genetically engineered with human immune systems. (As a result, HIV infection causes disease similar to that in humans.)
The researchers found that the CAR-carrying blood stem cells successfully turned into functional T cells that could kill HIV-infected cells in the mice. The result was a decrease in HIV levels of 80 to 95 percent.
The findings strongly suggest that stem cell-based gene therapy with a CAR may be a feasible and effective treatment for chronic HIV infection in humans.
The world’s leading infectious killer, HIV has caused approximately 40 million deaths worldwide since it was first identified in the early 1980s. Once HIV invades the body, it targets the very immune cells that are working against it, using the machinery of T cells to make copies of itself to spread through the body. This kills the T cells and weakens the immune system so much that the body can’t fight even a simple infection. Certain drugs help suppress the virus, but since the human immune system can’t clear the virus from the body, people with HIV have the virus for life.
“Despite increased scientific understanding of HIV and better prevention and treatment with available drugs, a majority of the 35 million people living with HIV, and millions more at risk of infection, do not have adequate access to prevention and treatment, and there is still no practical cure,” said Jerome Zack, professor of medicine and of microbiology, immunology and molecular genetics in the UCLA David Geffen School of Medicine and a co-author of the study. “With the CAR approach, we aim to change that.” Zack is co-director of the UCLA AIDS Institute and is affiliated with UCLA’s Jonsson Comprehensive Cancer Center and a member of the Broad Stem Cell Research Center.
Previous studies by Kitchen and Zack demonstrated similar results with other T cell receptors, although it is known that HIV could mutate away from those receptors. Another shortcoming of T cell receptors used in previous clinical studies was that they could not be universally used in patients, because they would have to be individually matched to patients — in the same way organs are matched to transplant recipients.
Kitchen said the CAR approach is more flexible and potentially more effective because it could theoretically be employed in anyone. If further testing continues to show promise, the researchers hope a treatment based on their approach could be brought to human clinical trials within five to 10 years.
The study’s first author was Anjie Zhen, a postdoctoral fellow at UCLA in the Division of Hematology/Oncology, the UCLA AIDS Institute and the Broad Stem Cell Research Center.
The work was supported by the National Institute of Allergy and Infectious Disease, the National Institutes of Health, the UCLA Center for AIDS Research, the California Institute for Regenerative Medicine, the University of California Multicampus Research Program and Initiatives, the California Center for Antiviral Drug Discovery, the California HIV/AIDS Research Program and the UCLA Broad Stem Cell Research Center.
The chimeric antigen receptor method is used in preclinical tests only and has not been tested in humans or approved by the Food and Drug Administration for use in humans.
Source: University of California, Los Angeles
Published on 2nd July 2015
Ieshea Thomas was the first adult to be cured of sickle cell disease with the chemotherapy-free procedure at UI Health. Credit: Image courtesy of University of Illinois at Chicago
Physicians at the University of Illinois Hospital & Health Sciences System have cured 12 adult patients of sickle cell disease using a unique procedure for stem cell transplantation from healthy, tissue-matched siblings. The transplants were the first to be performed outside of the National Institutes of Health campus in Maryland, where the procedure was developed. Physicians there have treated 30 patients, with an 87 percent success rate. The results of the phase I/II clinical trial at UI Health, in which 92 percent of treated patients were cured, are published online in the journal Biology of Blood & Marrow Transplantation. The new technique eliminates the need for chemotherapy to prepare the patient to receive the transplanted cells and offers the prospect of cure for tens of thousands of adults suffering from sickle cell disease.
About 90 percent of the approximately 450 patients who have received stem cell transplants for sickle cell disease have been children. Chemotherapy has been considered too risky for adult patients, who are often more weakened than children by the disease. “Adults with sickle cell disease are now living on average until about age 50 with blood transfusions and drugs to help with pain crises, but their quality of life can be very low,” says Dr. Damiano Rondelli, chief of hematology/oncology and director of the blood and marrow transplant program at UI Health, and corresponding author on the paper. “Now, with this chemotherapy-free transplant, we are curing adults with sickle cell disease, and we see that their quality of life improves vastly within just one month of the transplant,” said Rondelli, who is also the Michael Reese Professor of Hematology in the UIC College of Medicine. “They are able to go back to school, go back to work, and can experience life without pain.” Sickle cell disease is inherited. It primarily affects people of African descent, including about one in every 500 African Americans born in the U.S. The defect causes the oxygen-carrying red blood cells to be crescent shaped, like a sickle. The misshapen cells deliver less oxygen to the body’s tissues, causing severe pain and eventually stroke or organ damage. Doctors have known for some time that bone marrow transplantation from a healthy donor can cure sickle cell disease. But few adults were transplanted because high-dose chemotherapy was needed to kill off the patients’ own blood-forming cells — and their entire immune system, to prevent rejection of the transplanted cells, leaving patients open to infection. In the new procedure, patients receive immunosuppressive drugs just before the transplant, along with a very low dose of total body irradiation — a treatment much less harsh and with fewer potentially serious side effects than chemotherapy. Next, donor cells from a healthy and tissue-matched sibling are transfused into the patient. Stem cells from the donor produce healthy new blood cells in the patient, eventually in sufficient quantity to eliminate symptoms. In many cases, sickle cells can no longer be detected. Patients must continue to take immunosuppressant drugs for at least a year.
In the reported trial, the researchers transplanted 13 patients, 17 to 40 years of age, with a stem cell preparation from the blood of a tissue-matched sibling. Healthy sibling donor-candidates and patients were tested for human leukocyte antigen, a set of markers found on cells in the body. Ten of these HLA markers must match between the donor and the recipient for the transplant to have the best chance of evading rejection. In a further advance of the NIH procedure, physicians at UI Health successfully transplanted two patients with cells from siblings who matched for HLA but had a different blood type. In all 13 patients, the transplanted cells successfully took up residence in the marrow and produced healthy red blood cells. One patient who failed to follow the post-transplant therapy regimen reverted to the original sickle cell condition. None of the patients experienced graft-versus-host disease, a condition where immune cells originating from the donor attack the recipient’s body. One year after transplantation, the 12 successfully transplanted patients had normal hemoglobin concentrations in their blood and better cardiopulmonary function. They reported less pain and improved health and vitality. Four of the patients were able to stop post-transplantation immunotherapy without transplant rejection or other complications.
“Adults with sickle cell disease can be cured without chemotherapy – the main barrier that has stood in the way for them for so long,” Rondelli said. “Our data provide more support that this therapy is safe and effective and prevents patients from living shortened lives, condemned to pain and progressive complications.”
Source: University of Illinois at Chicago
Published on 21st September 2015
Remembering robots from film portrayals may help ease some of the anxiety that older adults have about using a robot, according to Penn State researchers.
A well-known class of molecules, many of which are already in use therapeutically, may be able to block the Ebola virus’s entry into cells and halt the disease in its tracks, according to researchers at the University of Illinois at Chicago.
The study is available online in advance of print in the Journal of Virology.
Ebola and the closely related Marburg virus are among the most lethal in the world, both highly contagious and deadly. There is an urgent need to develop either a vaccine or effective antiviral therapy to prevent future outbreaks.
“We know very little about the basic biology of these diseases,” said Lijun Rong, UIC professor in microbiology and immunology and principal investigator on the new study.
Rong and his colleagues found that Ebola and Marburg viruses both use gateways called G protein-coupled receptors, or GPCRs, to enter a cell after attaching to its surface. Blocking entry with a drug that ties up the receptor may prove to be an effective therapy.
“These G protein-coupled receptors are a big family of closely related molecules in humans — altogether, probably more than a thousand,” said Rong. Because GPCRs are involved in many human diseases, he said, a host of drugs have already been developed that target them.
“In the history of therapeutics, about half of our drugs were developed to target GPCRs. For example, a number of antihistamines used as allergy medications are GPCR receptor antagonists,” he said.
Rong and his coworkers screened approximately a thousand compounds using a NIH-funded high-throughput screening facility. They found 20 GPCR antagonists, or molecules that block GPCR receptors, were able to block Ebola and Marburg viruses from entering cells.
Learning how the two viruses infect cells and how they can be blocked offers the hope of finding therapeutics to combat both deadly diseases, Rong said.
“There are a lot of drugs and compounds that work through this mechanism — acting as antagonists to GPCR receptors,” he said. “This gives us a huge repertoire that can be tested against Ebola/Marburg.”
Source: University of Illinois at Chicago
Published on 13th August 2015