داروهای چند منظوره: راه حل جدید درمان گروهی از بیماری های نادر ژنتیکی

متن اصلی سایت منبع خبر

دانشمندان دانشگاه روچستر با کشف مسیرهایی که اختلالات یک دسته از بیماری های متابولیک در بدن تولیدذ سم کرده و موجب مشکلات متعدد ذهنی، حرکتی، مغزی و.. می شوند توالنسته اند دسته ای از داروها را بیابند که اکنون مصارف دیگری دارند اما می توان از آن ها در درمان این بیماری ها ا ستفاده کرد. این دسته از بیمارزی ها بیماری های اختلال ذخیره ای لیزوزوم  نامیده می شود و منجر به موارد متععدی از بیماری ها فوق آلذکر می شوند. مقاله مورد نظر در مجله PLOS Biology چاپ شده است.

متن اصلی مطلب با جزییات بیشتر به زبان انگلیسی

تحول خارق العاده در کد گزاری DNA

متن اصلی سایت منبع خبر

منبع اصلی این خبر با جزییات کامل

A team of researchers at Sinai Health System’s Lunenfeld-Tanenbaum Research Institute (LTRI) and University of Toronto’s Donnelly Centre has developed a new technology that can stitch together DNA barcodes inside a cell to simultaneously search amongst millions of protein pairs for protein interactions. The paper will be published in the journal Molecular Systems Biology.

In recent years, DNA barcoding has enabled scientists to carry out highly parallel experiments, in which many different types of cells can be tested in the same tube. This has been further enabled by next-generation DNA sequencing which can efficiently count barcodes and ‘read out’ the results. However, the number of experiments that can be combined in the same tube has been limited to the number of barcoded cell types. Allowing barcodes to fuse together inside cells means scientists can now break that barrier. The new technology results in a 10-fold increased rate of discovery for the same price.

“Using DNA barcodes for multiplex experiments has been an extremely powerful technology,” said Frederick (Fritz) Roth, senior author on the study who is cross-appointed at Lunenfeld-Tanenbaum Research Institute and Donnelly Centre, and is also a Canada Excellence Research Chair and Senior Fellow of the Canadian Institute for Advanced Research. “However it has been one-dimensional, in the sense that we only got to read one experiment per barcode. By combining barcodes inside cells, we can dramatically increase the number of experiments we can combine together in a single test tube”

In a widely-used method called Yeast Two Hybrid (Y2H), yeast cells carrying a ‘bait’ protein are mated with yeast cells carrying a ‘prey’ protein. The Y2H system is rigged so that only cells in which bait and prey proteins stick together can survive and this allows scientists to see which proteins associate with which other proteins. Dr. Roth’s team named their new technology Barcode Fusion Genetics-Yeast Two Hybrid (BFG-Y2H). In BFG-Y2H, cells carrying thousands of ‘bait’ and ‘prey’ proteins are mated together in the same culture. Says Roth, “To ensure that every protein pair is tested for interaction, the process ensures that every cell type mates with every other cell type. It’s like Spring Break in Miami.”

The authors say that the BFG-Y2H method’s novelty is that the cells are programmed to connect DNA barcodes from bait and prey cells together into a single ‘fused barcode.’ Next-generation DNA sequencing methods can then be applied to detect fused barcodes that correspond to the combinations of bait and prey proteins that stuck together and enabled their cell to survive.

Proteins, working alone or in larger assemblies, are the machinery that carries out many of the operations of a cell. The authors say that more efficient technologies for mapping protein interactions could expand researchers’ understanding of how our cells work, and reveal protein interactions that only occur under certain environmental conditions.

Nozomu Yachie of the University of Tokyo, one of the paper’s lead authors, notes that “millions of protein pairs can be tested for interaction in a single flask, so that dozens of conditions could be tested in parallel by one researcher in as little as two weeks in the lab.”

Evangelia Petsalaki of the LTRI, also a lead author, notes that “the ultimate goal is to generate a ‘3D video’ of the protein interaction network map rather than a static picture. Our BFG-Y2H method will accelerate our understanding of gene functions and human disease by efficiently generating more information-rich protein interaction maps.”

Story Source:

The above post is reprinted from materials provided by University of Toronto. Note: Materials may be edited for content and length.

چگونه سلول های بنیادی اسکلتی شکل صورت را طراحی می کنند.

متن اصلی سایت منبع خبر

منبع اصلی این خبر با جزییات کامل

Timing is everything when it comes to the development of the vertebrate face. In a new study published in PLoS Genetics, USC Stem Cell researcher Lindsey Barske from the laboratory of Gage Crump and her colleagues identify the roles of key molecular signals that control this critical timing.

Previous work from the Crump and other labs demonstrated that two types of molecular signals, called Jagged-Notch and Endothelin1 (Edn1), are critical for shaping the face. Loss of these signals results in facial deformities in both zebrafish and humans, revealing these as essential for patterning the faces of all vertebrates.

Using sophisticated genetic, genomic and imaging tools to study zebrafish, the researchers discovered that Jagged-Notch and Edn1 work in tandem to control where and when stem cells turn into facial cartilage. In the lower face, Edn1 signals accelerate cartilage formation early in development. In the upper face, Jagged-Notch signals prevent stem cells from making cartilage until later in development. The authors found that these differences in the timing of stem cells turning into cartilage play a major role in making the upper and lower regions of the face distinct from one another.

“We’ve shown that the earliest blueprint of the facial skeleton is set up by spatially intersecting signals that control when stem cells turn into cartilage or bone. Logically, therefore, small shifts in the levels of these signals throughout evolution could account for much of the diversity of shapes we see within the skulls of different animals, as well as the wonderful array of facial shapes seen in humans,” said Barske, lead author and A.P. Giannini postdoctoral research fellow.

Story Source:

The above post is reprinted from materials provided by University of Southern California – Health Sciences. The original item was written by Cristy Lytal. Note: Materials may be edited for content and length.

ماشين كپي سلولي: چگونه دحتر ها شبيه مادرانشان مي شوند؟

متن اصلی سایت منبع خبر

منبع اصلی این خبر با جزییات کامل

Tiny structures in our cells, called centrioles, control both cell division and motility. The number of these structures is highly monitored, with deviations causing infertility, microcephaly and accelerating cancer. But how do mother cells know they provide the right number of centrioles to their daughters? They do it by copying those structures only once, so that each daughter inherits one of the copies. A research team, from Instituto Gulbenkian de Ciencia (IGC; Portugal), led by Monica Bettencourt-Dias uncovered the mechanism by which the mother copies only once before it distributes it to the two daughters. This study is now published in the latest issue of the scientific journal Current Biology.

When a mother cell divides in two daughters, its structures need to duplicate, so that each daughter cell gets the right complement and looks like its mother. While much is known about the regulation of the duplication of the genetic material, it was a mystery how centrioles are copied only once. Bettencourt Dias’ team tackled this question by focusing on the key molecular trigger of centriole formation, a protein called PLK4, which they identified recently. “We found that the trigger only works just before centrioles are made. Something in the cell was inhibiting the trigger at other time points, ensuring the right copy number of centrioles was formed at the right time,” says Zitouni Sihem, co-first author of this study.

The research team, in collaboration with scientists from Germany, USA, Japan and France, set out to investigate what was inhibiting this trigger protein at other time points. “We discovered that a key protein complex that sets the cell division clock, CDK1, inhibits PLK4 activity by kidnapping its partner (STIL). In consequence, PLK4 can only start forming centrioles at a particular time of the cell cycle, when CDK1 is not there,” explains Zitouni Sihem. The centriole formation machinery is thus regulated by the cell cycle clock, ensuring daughters look like their mothers.

Mónica Bettencourt-Dias adds: “I am very proud of this paper, we knew the cell cycle clock and centriole formation had to be linked- otherwise how would cells ensure the right copy number is made? This is the first link showing how the cell cycle machinery regulates the trigger of centriole biogenesis, ensuring the right number of centrioles is formed at the right time, which is critical for homeostasis.”

Story Source:

The above post is reprinted from materials provided by Instituto Gulbenkian de Ciencia. Note: Materials may be edited for content and length.

شواهد ژنتيكي جديد در ارتباط با نزديك بيني

متن اصلی سایت منبع خبر

منبع اصلی این خبر با جزییات کامل

Myopia, also known as short-sightedness or near-sightedness, is the most common disorder affecting the eyesight and it is on the increase. The causes are both genetic and environmental. The Consortium for Refractive Error and Myopia (CREAM) has now made important progress towards understanding the mechanisms behind the development of the condition. This international group of researchers includes scientists involved in the Gutenberg Health Study of the University Medical Center of Johannes Gutenberg University Mainz (JGU). The team has uncovered nine new genetic risk factors which work together with education-related behavior as the most important environmental factor causing myopia to generate the disorder. The results of the study “Genome-wide joint meta-analyses of genetic main effects and interaction with education level identify additional loci for refractive error: The CREAM Consortium” have recently been published in the scientific journal Nature Communications.

There has been a massive rise in the prevalence of short-sightedness across the globe in recent decades and this upwards trend is continuing. It is known from previous studies of twins and families that the risk of acquiring short-sightedness is determined to a large extent by heredity. However, the myopia-causing genes that had been previously identified do not alone sufficiently explain the extent to which the condition is inherited. In addition to the genetic causes of myopia there are also environmental factors, the most significant of which are education-related behavior patterns. “We know from the Gutenberg Health Study conducted at Mainz that the number of years of education increases the risk of developing myopia,” said Professor Norbert Pfeiffer, Director of the Department of Ophthalmology at the Mainz University Medical Center.

Meta-analysis of multi-national datasets

With the aim of identifying genetic mutations relating to myopia and acquiring better insight into the development of the condition, the international research group CREAM carried out a meta-analysis of data collected from around the world. The data compiled for this analysis originated from more than 50,000 participants who were analyzed in 34 studies. The second largest group of participants was formed by the more than 4,500 subjects of the Gutenberg Health Study of the Mainz University Medical Center. “In the field of genetic research, international cooperation is of particular importance. This is also borne out by this study, to which we were able to make a valuable contribution in the form of data from our Gutenberg Health Study,” continued Professor Norbert Pfeiffer. “And in view of the fact that a survey undertaken by the European Eye Epidemiology Consortium with the help of the Gutenberg Health Study shows that about one third of the adult population of Europe is short-sighted, it is essential that we learn more about its causes in order to come up with possible approaches for future treatments.”

Aware that environmental effects and hereditary factors reinforce one another in the development of myopia, the scientists devised a novel research concept for their investigations. They used a statistical analysis technique that takes into account both the effects of the environmental and hereditary factors and does so in equal measure and simultaneously. Their efforts were crowned with success as they were able to classify nine previously unknown genetic risk factors.

Risk-associated gene involved in the development of short-sightedness

These newly discovered genetic variants are associated with proteins which perform important functions when it comes to the transmission of signals in the eye. One of these genes is of particular interest because it plays a major role in the transmission of the neurotransmitter gamma-aminobutyric acid (GABA) in the eye. Previous studies have shown that there is greater activation of the gene in question in eyes that are myopic. The results of current research substantiate this conclusion. The CREAM researchers interpret this as evidence that this newly discovered risk-related gene is actually involved in the development of short-sightedness. This represents significant initial headway towards understanding how genetic causes interact with the level of education as an environmental factor to produce the heterogeneity of myopia. Further research will be needed to clarify the details of how the mechanisms actually work and interact with one another.

The spread of short-sightedness is a worldwide phenomenon. Particularly in South East Asia the incidence of myopia in school children has increased notably over the last decades. This is likely due to an improvement in educational attainment. People who read a great deal also perform a lot of close-up work, usually in poor levels of daylight. The eye adjusts to these visual habits and the eyeball becomes more elongated than normal as a result. But if it becomes too elongated, the cornea and lens focus the image just in front of the retina instead of on it so that distant objects appear blurry. The individual in question is then short-sighted.

Story Source:

The above post is reprinted from materials provided by Johannes Gutenberg Universitaet Mainz. Note: Materials may be edited for content and length.

كشف ارتباط تستوسترون با بياري قلبي در مردان

متن اصلی سایت منبع خبر

منبع اصلی این خبر با جزییات کامل

Testosterone might be involved in explaining why men have a greater risk of heart attacks than women of similar age, according to a study funded by the British Heart Foundation (BHF) and the Biotechnology and Biological Sciences Research Council (BBSRC). The findings, published in the journal Scientific Reports, could lead to new therapies to help reduce heart attack risk.

Each year in the UK 188,000 people visit hospital whilst suffering from a heart attack, which is around one person every three minutes.

Scientists at the University of Edinburgh examined the effects of testosterone on blood vessel tissue from mice. They found that the hormone triggers cells from the blood vessels to produce bone-like deposits — a process called calcification. When the mouse cells were modified, by removing the testosterone receptor, so they could no longer respond to testosterone, they produced far less of the calcium deposits.

The team also looked at blood vessel and valve tissue from people with heart disease who had undergone surgery for their condition. They found that cells from these tissues contained bone-like deposits and also carried the testosterone receptor on their surface. This suggests that testosterone may trigger calcification in people.

Calcification causes blood vessels to harden and thicken, which means the heart has to work harder to pump blood around the body. It is strongly linked to increased risk of heart attack and stroke. Calcification can also affect the heart’s valves, meaning that the valves cannot open and shut properly and may need to be replaced.

Little is known about what triggers calcification and there are currently no treatments. The research team now hope to drill down into the exact mechanism behind this process.

Although naturally occurring, testosterone is also used to counteract low levels of natural testosterone production in a treatment known as androgen replacement therapy. Synthetic substances similar to testosterone are also sometimes misused by athletes in order to enhance athletic performance.

Dr Vicky MacRae, of the University of Edinburgh’s Roslin Institute, said: “Calcification is particularly difficult to treat, as the biological processes behind the disease are similar to those used by our body to make and repair bone. By finding this link between testosterone and calcification we may have discovered a new way of treating this disease and also reducing heart disease.”

Professor Jeremy Pearson, Associate Medical Director at the British Heart Foundation, which helped fund the research, said: “The role of male sex hormones in the control of vascular calcification is poorly understood. This study, in cells taken from mice and human tissue, provides new evidence that testosterone can increase calcification. But significantly more research is needed to understand whether the results have implications for patients with heart disease or those taking androgen replacement therapy.”

Story Source:

The above post is reprinted from materials provided by British Heart Foundation (BHF). Note: Materials may be edited for content and length.

آيا ميكروب ها به تكامل زيستي انسان سمت و سو مي دهند؟

متن اصلی سایت منبع خبر

منبع اصلی این خبر با جزییات کامل

Scientists increasingly realize the importance of gut and other microbes to our health and well-being, but one University of California, Berkeley, biologist is asking whether these microbes — our microbiota — might also have played a role in shaping who we are by steering evolution.

Biologists have gathered evidence that the interdependence between animals and their symbionts — the organisms, typically bacteria, that live in or on them — has consequences for the evolution of both. But Michael Shapira, a UC Berkeley assistant professor of integrative biology, believes that the diverse microbial communities that we harbor have a more profound effect, significantly ratcheting up evolution in an intimate collaboration for survival.

In a recent paper in the journal Trends in Ecology and Evolution, Shapira, who studies the gut microbes of the nematode C. elegans, reviews evidence that demonstrates how microbiotas affect and contribute to host evolution, either by evolving along with the host, or by stepping in at critical moments to help the host adapt to a new environmental challenge.

These examples, he says, bolster the relatively recent concept of the hologenome, a term referring to the genomes of the host and its microbes together, encompassing perhaps thousands of different types of bacteria on the skin, in the gut and even in reproductive organs. In his recent paper, Shapira elaborates on a 2008 proposal by Tel Aviv University researchers that evolution can act on the hologenome, rather than on the genomes of the host and its microbiota separately. This implies that as the host evolves to suit a changing environment, its microbiota play a critical role in directing and participating in that evolution.

“When I came across the paper by Ilana Zilber-Rosenberg and Eugene Rosenberg describing the hologenome concept, it blew my mind,” Shapira said. “The idea that animals could undergo selection not based solely on their own genome, but with the help of many more, opens the door for previously unimagined evolutionary paths.”

Shapira expands on this idea to encompass some of the newest discoveries about amazing symbiotic relationships between organisms that, because they depend on one another, are tied together for life.

Aphids and their gut bacteria

Examples of co-evolution of hosts and their symbionts are all around us, Shapira said. Aphids have been shown to rely on bacteria to provide essential amino acids the aphids cannot make themselves, and cannot readily obtain from their diet, while the bacteria — a group called Buchnera — get room and, in the form of sap-derived sugars, board.

Researchers examining the genes of different species of aphids and of their individual gut bacteria found that the emergence of new species of aphids during evolution was mirrored by speciation events in the insects’ Buchnera symbionts. This demonstrates how the linked fates of the two species lead to co-evolution. But Buchnera are not alone. Subsequent work showed that aphids also harbor other symbionts that are less important for, or dependent on, their host, but nevertheless help the insects adapt to new niches in a changing environment.

Together, Shapira suggests, these species represent a basic hologenome, with essential, co-evolving symbionts, but also with a pool of microbes useful for flexibly adapting to a changing environment. Adaptation to new niches can potentially lead to population fragmentation, isolation and, subsequently, to the evolution of a new species. This is a pivotal consequence of life with symbionts, said Shapira, who believes that microbiotas, which involve many types of symbionts, represent an expanded version of this aphid-symbiont relationship.

An experiment performed in fruit flies demonstrates this. When raised on different types of food, flies develop different gut microbiotas, presumably better at handling the available food.

The surprising outcome, however, was that “within one generation, the flies developed mate preference for their own group, ignoring the others, and that this was dependent on the microbes in the gut that helped them utilize the food,” he said. “This led to de facto reproductive isolation of two populations and could facilitate future speciation, that is, real reproductive isolation — a genetic barrier preventing members of the two groups from parenting viable or fertile progeny.”

Nematode’s upset tummies

In his own lab, he is raising nematodes on soil enriched with different types of produce — sugary versus fibrous, for example — and finds that no matter what the food source and the resulting environmental microbial diversity, worms have similar sets of bacteria in their guts. Some 32 types, in fact. The balance shifts with different food, as has been seen in humans as well. People with diets high in fat, for example, have a different microbiota than do vegans, though in humans it is far more difficult to identify a core microbiota.

Studies have shown that these gut bacteria contribute to many aspects of the host’s life, including development, fertility, metabolism, immunity and behavior. Microbe-free mice don’t develop a robust immune system, for example, while nematodes rely on some gut microbes to fight off bad bugs.

In his paper, Shapira proposes that animals and a set of core bacteria — or in general, a host with its core microbiota — evolve together, adapting as they can to changing conditions and perhaps, over time, becoming new species. The other bacteria swimming around in our guts are less tied to our essential functions, but are influenced by the changing environment, and ideally serve as a resource to help us adapt to sudden changes in diet or toxins, for example.

In thinking about these possibilities, Shapira draws from various examples of symbiosis. One recent experiment showed, for example, that an insect, the broad-headed stink bug, was able to survive pesticide exposure thanks to acquisition of one type of gut microbe that detoxified the pesticide — a boon for the bug but a service needed from the microbe only in one unique situation.

“In my mind, this is an example of the advantages of having a flexible pool of microbes. You can exchange them with the environment, you can get the strains that are better able to protect yourself,” he said. “That’s one way to achieve adaptation.”

Shapira’s proposal implies, too, that some parts of the microbiota — that is, the core microbiota — can likely be passed on to an individual’s children, but that other parts, belonging to the flexible pool, could be exchanged with the environment. Changes in either the host or the microbes change the entire hologenome.

“With the growing understanding that all animals are in fact in a symbiotic relationship with complex microbial communities, the framework to consider how symbiotic interactions shape host evolution should be expanded,” he said.

Shapira plans future experiments with C. elegans to test these ideas and clarify the mutually beneficial relationship between hosts and their microbiotas.

گيجي سلو لها عامل بيماري ژنتيكي و پيري زودرس !!

متن اصلی سایت منبع خبر

منبع اصلی این خبر با جزییات کامل

It has been disorienting to the scientific and medical community as to why different subtle changes in a protein-coding gene causes many different genetic disorders in different patients — including premature aging, nerve problems, heart problems and muscle problems. no other gene works like this. According to a new study, co-authored by Binghamton University faculty Eric Hoffman, it has to do with cell “commitment.”

From initial conception of an egg and sperm, the cells that start dividing need to start making decisions as to what type of tissue or organ they are supposed to become (often called ‘cell lineages’). This is part and parcel of ‘stem cells’ — e.g. how to get cells to make certain decisions to become nerve, heart, muscle, or something else.

The study, “Laminopathies disrupt epigenomic developmental programs and cell fate,” published on April 20 in Science Translational Medicine, provides a unifying model for this process, and how it is disrupted by subtle mutations of the LMNA gene.

“A one-letter change, a one amino acid change, in this big protein, we see in patients that have severe muscle problems. Just a couple letters away, the same amino acid change instead causes loss of fat in other patients,” said Eric Hoffman, associate dean for research at Binghamton University’s School of Pharmacy and Pharmaceutical Sciences and co-author of the study. “What we show is that’s because of subtle changes in the context of a cell trying to make a decision whether it’s going to be muscle or fat. It really needs to make sure the right areas are taken out of circulation. If you start taking the wrong areas or not enough areas or too many areas out of circulation, the cell starts getting confused; it’s not being given the right instructions.”

Different parts of the genome need to become attached to the outside of the nucleus (nuclear envelope — the key structure that separates animals with organs, from bacteria), where these attached regions are taken out of genetic circulation (called heterochromatin — never to be used again). In a way, this attachment process defines what part of the genome is no longer useful to that particular cell/organ type — and this type of discarding of the DNA keeps a cell focused on what it is supposed to be (e.g. a heart cell not suddenly confused if it should be nerve instead).

“We provide a model for how these very subtle changes in a single protein cause such dramatically different clinical problems because of this process of taking parts of the genome out of circulation during cell commitment, when a cell’s trying to make these decisions,” Hoffman added.

Story Source:

The above post is reprinted from materials provided by Binghamton University, State University of New York. Note: Materials may be edited for content and length.

چگونه ميشود از قطع پا در ديابت جلوگيري كرد؟

متن اصلی سایت منبع خبر

منبع اصلی این خبر با جزییات کامل

Scientists from Tomsk Polytechnic University and National Autonomous Mexico University develop techniques to treat diabetic foot syndrome with special insoles with silver nano-particles. The techniques help to fight ulcers appearing on feet in diabetic patients, facilitates their healing and disinfection, reducing the risk of amputation.

Silver preparations being developed by Tomsk Polytechnic University jointly with Novosibirsk and Mexican counterparts are able to reduce such risks.

“The research has shown silver’s antibacterial properties facilitate rapid healing of ulcers and suppurations in patients with diabetic foot syndrome. Together with colleagues from Mexico, where the problem is particularly acute, we are working to create special insoles for diabetic patients. The development has passed clinical tests. In patients who had used the insoles impregnated with silver nanoparticles, foot ulcers healed up, the risk of amputations significantly reduced,” says TPU Professor Alexey Pestryakov, Head of the Department of Physical and Analytical Chemistry.

Diabetic foot syndrome is one of the latest and most serious complications of diabetes. Due to the large amount of sugar in the body there are changes in peripheral nerves, blood vessels, skin and soft tissues, bones and joints of the patient. Infections, ulcers, suppurations and so on are emerging. Up to 15% of people with diabetes have the risk of developing ulcers on feet. In the advanced form diabetic foot syndrome can lead to amputation.

A team led by the scientist develops pharmaceuticals based on silver nano-particles having universal impact on viruses, bacteria and fungi. The scientists have cooperated with Mexican colleagues for more than 10 years.

“We have got a contract with the Mexican government, gained large grants for research. Built a serious team consisted of scientists and doctors. Together we work to improve the quality of our products, we carry out joint research and experiments,” says Prof Alexey Pestryakov.

Story Source:

The above post is reprinted from materials provided by Tomsk Polytechnic University (TPU). Note: Materials may be edited for content and length.

تمرين هاي مناسب قدرتي در افراد مسن به طول عمر آنها كمك ميكند.

متن اصلی سایت منبع خبر

منبع اصلی این خبر با جزییات کامل

كهنسالاني كه هفته اي دو بار تمرين ورزشي قدرتي انجام مي دهند كمتر در معرض خطر مرگ هستند. 

از گذشته منافع ورزش و تغذيه مناسب در افزايش سلامت و ماهش بيماري قلبي روشن بوده است اما اهميت مورزس هاي قدرتي تا اين اندازه بررسي نشده بود. 

اين ورزش ها خطر مرگ به هر دليل را تا نزديك ٥٠درصد و خطر مرگ از سرطان را تا نزديك بيست درصد كاهش مي دهند 

جزييات اين تحقيق در مجله طب پيشگيري چاپ شده است

 Preventive Medicine

The NHIS collects overall health, disease and disability data of the U.S. population from a nationally representative sampling of all 50 states and the District of Columbia. The 1997-2001 survey included more than 30,000 adults age 65 and older.

During the survey period, more than 9 percent of older adults reported strength training at least twice a week.

“That’s only a small fraction of the population, but it’s actually higher than we had anticipated,” Kraschnewski said.

The researchers followed the respondents for 15 years through death certificate data from the National Center for Health Statistics National Death Index. About a third of respondents had died by 2011.

Older adults who strength trained at least twice a week had 46 percent lower odds of death for any reason than those who did not. They also had 41 percent lower odds of cardiac death and 19 percent lower odds of dying from cancer.

Older adults who met strength training guidelines were, on average, slightly younger, and were more likely to be married white males with higher levels of education. They were also more likely to have normal body weight, to engage in aerobic exercise and to abstain from alcohol and tobacco.

When the researchers adjusted for demographic variables, health behaviors and health conditions, a statistically significant effect on mortality remained. Although the effects on cardiac and cancer mortality were no longer statistically significant, the data still pointed to a benefit.

Importantly, after the researchers controlled for physical activity level, people who reported strength exercises appeared to see a greater mortality benefit than those who reported physical activity alone.

The study is strong evidence that strength training in older adults is beneficial beyond improving muscle strength and physical function, the researchers said.

“We need to identify more ways that we can help get people engaged in strength training so we can increase the number from just under 10 percent to a much higher percentage of our older adults who are engaged in these activities,” Kraschnewski said.