For Insulin Sensitive Overweight Patients, One Session Of Exercise Improves Metabolic Health, New Research Suggests

Obesity-related complications are associated with an abnormal fat metabolism in the muscle.  As a result, accumulated fat by-products inside the muscle affect insulin resistance. To avoid the build up of fat by-products, fat must either be oxidized (burned, as in exercise) or stored (as benign fat) in muscle.

A team of researchers has examined the effect of exercise on fat accumulation in a new study involving five obese women. In one session the women overate and did not exercise; in a follow-on session they overate and did exercise. The researchers found that:

the body’s fat-burning oxidation rate was reduced after one day of overeating;
conversely, just one session of exercise increased the rate of fat-burning oxidation; and
exercise increased the amount of fat that would eventually be stored in the muscle. 

The findings indicate that even one bout of exercise helps to reduce the fat by-products inside the muscle, which affects the insulin sensitivity. The findings also suggest that a single session of exercise “steers” muscle fat towards oxidation, thereby avoiding the accumulation of fat by-products.

The study was conducted by Andrea Cornford, Minghua Li, Simon Schenk, Matthew Harber and Jeffrey Horowitz, Division of Kinesiology, University of Michigan, Ann Arbor. Their research is entitled "Alteration in Lipid Metabolism After One Day of Overeating Are Reversed by a Single Session of Exercise.” They will present their findings at a meeting sponsored by the American Physiological Society. The conference, The Integrative Biology of Exercise V, will be held September 24-27, 2008 in Hilton Head, SC. 

Study Summary

The aim of the study was to assess changes in fatty acid (FA) metabolism in response to acute overeating and exercise. Five obese women performed three separate two-day trials in which they consumed (1) a weight-maintaining diet [Control]; (2) a hypercaloric diet (700 calories above normal); and (3) the same hypercaloric diet, but exercised to the point where they expended the 700 excess calories.

The morning after each trial, researchers measured whole-body FA oxidation [FAO] and calculated non-oxidative FA disposal as the difference between FA uptake and FAO.

A muscle biopsy was performed to measure the presences of triglycerides that are involved in fat storage.

The morning after the trials, the researchers observed that overeating suppressed fatty acid oxidation below the control levels, while exercising increased oxidation. Non-oxidative FA disposal was the same in each trial and a direct correlation between FA uptake and muscle GPAT activity were found.

Conclusions

According to Andrea Cornford, a member of the research team, “Exercise decreases everyone’s insulin resistance and therefore reduces the chances of developing diseases such as type 2 diabetes. This study shows that even a single bout of exercise helps obese individuals increase their body’s fat-burning rate and improve their metabolic health.” 

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U Of MN Researchers Find Regular Use Of Aspirin May Lower Risk Of Adult Leukemia

Led by Julie Ross, Ph.D., associate professor of pediatrics and a member of The Cancer Center, researchers analyzed data from the Iowa Women’s Health Study to determine whether taking aspirin or other non-steroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen could protect against the leukemia. Since 1985, the Iowa Women’s Health Study has followed more than 41,000 post-menopausal women, tracking their overall health, lifestyle, behaviors, and incidence of cancer. For this particular investigation, 28,224 women from that group were included in the study.

“There’s a growing body of evidence that aspirin may be a powerful cancer-preventing agent,” said Ross. “To our knowledge, this is the first prospective study to examine the association between NSAID use and adult leukemia.”

Adult leukemia accounts for nearly 5 percent of all newly diagnosed cancers in the United States. Currently, little is known about what causes leukemia in adults or possible prevention strategies.

Through their research, Ross and her team found that women who developed leukemia took aspirin significantly less often than women who did not develop leukemia. They also found that aspirin appears to have a more potent protective effect for adult leukemia than non-aspirin NSAIDs.

Ross noted that several previous studies in this area have grouped aspirin and non-aspirin NSAIDs together. “A strength of our study was the ability to examine separately the effects of aspirin and non-aspirin NSAIDs,” she said. “While the results are preliminary, notable differences in leukemia risk between aspirin and non-aspirin NSAID use definitely call for additional research with other large populations.”

Although aspirin is generally a safe drug, it can have adverse effects for some individuals. Before people embark on an aspirin regimen, they should check with their doctor.

Co-authors of this study are Christine Kasum, M.P.H., Cindy Blair, B.S. and Aaron Folsom, M.D., M.P.H.

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Zinc Found To Be Integral Part Of Brain Communication Channels

The study, which appears in the current issue of Nature Structural Biology, may explain why zinc deficiency has been linked to cognitive impairment.

"We don't know yet what zinc is doing, but it is definitely a component in these essential structures," said Senyon Choe, an assistant professor at The Salk Institute for Biological Studies and senior author on the study. "And it was surprising–at first we tried to disregard it, thinking it must be a contaminant, but, of course as you try to disprove it, it keeps coming back."

Ion channels are important "gatekeepers" that regulate the way ions such as calcium and potassium flow into and out of cells. Their flux is necessary for important neuronal processes. Calcium streams into brain cells and helps to initiate changes that accompany learning. Abnormalities in potassium channels have been found in some epileptics and in persons with both insulin-resistance and mobility disorders.

In the current study, Choe and his colleagues used X-ray crystallography to resolve the structures of four potassium channels from the sea slug Aplysia. The channels, called Shaw, Shab, Shal and Shaker, represent the four classes of potassium channels found in all higher organisms, including humans. With the exception of Shaker, all of the channels contained four zinc atoms in analogous positions.

"Each channel resembles a funnel," said Choe, "and the zinc elements ring the end that empties into the cell's interior."

Neuroscientists have known for decades that dyes that bind to zinc stain brain cells in unique patterns, indicating that zinc should have a role in brain function and studies have shown that zinc can enhance learning in undernourished children. The nature of zinc's organization in the brain, however, had been unclear.

"Now we know that zinc is embedded within structures that are absolutely critical for nerve cell activity," said Choe. "Furthermore, the amino acids that cradle the zinc atoms are completely conserved among the three classes of channels, telling us that during evolution there has been selective pressure to keep that zinc in place."

All four kinds of Aplysia potassium channels studied by Choe and colleagues have analogs in the human nervous system, so the investigators believe that their studies of zinc's role in Aplysia channel function are directly relevant to understanding its function in the human brain.

First author of the study, titled "Zn2+-binding and molecular determinants of tetramerization in voltage-gated K+ channels," is Kathryn Bixby, currently at the University of California, San Diego. Other Salk authors include Andreas Kreusch, a postdoctoral researcher in Choe's laboratory and Max Nanao, who is also a graduate student at the University of California, San Diego. The study was done in collaboration with N. Vivienne Shen and Paul J. Pffafinger at Baylor College of Medicine and Henry Bellamy at the Stanford Synchroton Radiation Laboratory. The work was supported by the National Institutes of Health and the American Heart Association.

The Salk Institute for Biological Studies, located in La Jolla, Calif., is an independent nonprofit institution dedicated to fundamental discoveries in the life sciences, the improvement of human health and conditions, and the training of future generations of researchers. The Institute was founded in 1960 by Jonas Salk, M.D., with a gift of land from the City of San Diego and the financial support of the March of Dimes Birth Defects Foundation.

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Polycystic Ovary Syndrome: 1 In 15 Women Affected Worldwide And Burden Likely To Increase

Many body systems are affected in PCOS, resulting in several health complications, including menstrual dysfunction, infertility, hirsutism (excessive body hair growth), acne, obesity, and metabolic syndrome. Principal symptoms of PCOS are polycystic ovaries shown by ultrasonography, irregular ovulation, and excessive amounts or activity of male hormones (hyperandrogenism). Type 2 diabetes is also more common in women with PCOS. Two differing definitions of PCOS, one from 1990 and the other from 2003, lead to differing statistics and consequences for studies depending on which definition is selected.

The cause of PCOS remains unknown, although both environmental and genetic factors are implicated. Research is focussing on whether the primary cause of the syndrome is due to a defect within the ovary, the hypothalamic-pituitary axis, or is primarily due to abnormal insulin activity. Obesity is a major risk factor for PCOS, and as such realistic and achievable weight loss can be sufficient to restore regular ovulation and improve fertility in obese women with this disorder.

The authors say: “Skin and hair disorders can be substantial in women with PCOS, and are physically and psychologically very damaging.” Abnormal body hair growth and acne are usually combated with oral contraceptives, which have the advantage of both regulating the menstrual cycle and providing contraception.

The connection between PCOS and infertility is discussed in detail, as is the so called “gold standard” treatment of clomifene, which simulates follicle growth and ovulation. Complications of infertility treatment for women with PCOS include multiple pregnancy after ovulation induction, ovarian hyperstimulation syndrome (which can be life-threatening) and in-vitro fertilisation cycle cancellation. For pregnant women, PCOS can cause early pregnancy loss, gestational diabetes, pregnancy-induced high blood pressure, pre-eclampsia, and a higher risk of delivery by caesarean section.

The authors conclude that the burden of PCOS is likely to expand, saying: “Future priorities in relation to PCOS include the development of evidence-based criteria for diagnosis and treatment, and determination of the natural history, cause, long-term consequences and prevention of the disorder.”

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Childbearing Increases Chance Of Developing The Metabolic Syndrome

UAB Professor of Preventive Medicine Cora E. Lewis, M.D., M.S.P.H., and colleagues used data collected in the CARDIA (Coronary Artery Risk Development in Young Adults) study to determine the correlation between a higher incidence of the metabolic syndrome among women ages 18-30 at the start of the study who bore at least one child during the 20-year period following.

"Pregnancy can have lasting, adverse physiological effects and may result in behavioral changes," Lewis said. "Some previous studies have shown an association between childbearing and the metabolic syndrome, and some have shown that a history of gestational diabetes is a strong predictor of Type 2 diabetes.

"However, these studies lacked the preconception measurements to establish a baseline with which to measure the changes brought on by pregnancy," she said. "Many have not had control groups of women who had not had pregnancies, and thus they have rarely provided conclusive evidence linking pregnancy-related risk factor changes to disease onset. CARDIA began following participants ages 18-30 years in 1985-1986 and continues today, and we had the necessary information to track women both before and after pregnancy and to compare women with pregnancies to those without."

Of the 2,787 women in the CARDIA study, 1,451 were included in this study analysis. Of those, 706 had no births and 745 had at least one birth during the 20 years following. Of the 745, 88 had at least one birth complicated by gestational diabetes.

After controlling for preconception measurements of body mass index (BMI), all metabolic syndrome components and physical activity, Lewis and her colleagues found that women who had given birth to one child or more than one child were independently associated with a higher incidence of the metabolic syndrome (33 percent and 62 percent higher, respectively) than women who had not had children. Among women with gestational diabetes, once baseline adjustments were made, the researchers found that they were nearly two-and-a-half times more likely to develop the metabolic syndrome than those women who had not had gestational diabetes-complicated pregnancies.

"Our findings suggest that childbearing can contribute to the development of the metabolic syndrome and that part of the association may be through weight gain and lack of physical activity," Lewis said. "And, although women with gestational diabetes had the highest relative risk of developing the metabolic syndrome, those with non-gestational diabetes pregnancies made up the larger at-risk group."

Lewis and her colleagues suggested that future studies may determine whether reductions in weight retention and central obesity, and reductions through treatment of cholesterol and triglycerides, after pregnancy may prevent disease later in life. They also suggested postpartum screening of cardio-metabolic risk factors, especially among women with gestational diabetes, may offer an important opportunity for disease prevention among women of reproductive and older ages.

Until then, Lewis said, the best way for everyone to prevent disease, including women of childbearing age, is to make the necessary lifestyle changes: exercise regularly and eat a healthy diet.

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Scientists Uncover Critical Step In DNA Mutation

The process that gives rise to mutations in DNA, or mutagenesis, is a complex one involving a series of chemical reactions, which are not completely understood. A free radical, a stable neutral atom or a chemical group containing at least one unpaired electron, can scavenge an electron from DNA in a process known as oxidation, creating a hole in place of the scavenged electron. Such oxidation events can be caused by natural processes occurring in the body, or by ionizing radiation. It’s well known that the ionization hole can travel long distances of up to 20 nanometers along the base pairs that form the rungs of the DNA ladder (discussed by Landman, Schuster and their collaborators in a 2001 Science article, volume 294, page 567). It is also well known that the hole tends to settle longer at spots in the DNA where two guanines (G) are located next to each other.

It’s the next step that has eluded DNA researchers for decades – somehow the hole in the ionized DNA reacts with water. This critical step is the first in a series that brings about a change in the DNA molecule – one that evades the body’s proof reading mechanism and leaves the altered DNA coding for the wrong proteins. When the wrong proteins are produced, it can lead through a complicated chain of events to an abnormally high rate of cell division – the result is cancer.

"We set out to explore the elementary processes that lead to mutagenesis and eventually cancer,” said Uzi Landman, director of the Center for Computational Materials Science and Regents’ professor and Callaway chair of physics at Georgia Tech.

"Until now, the mechanism by which water reacts with the guanine of the ionized DNA remained a puzzle. Through our first-principles, computer-based quantum mechanical theoretical modeling, coupled with theory-driven laboratory experiments, we have gained important insights into a critical step in a reaction that can have far reaching health consequences,” he said.

Once the hole is settled on the two guanine bases, water molecules react with one of the bases at a location called the 8-th carbon site (C8). This reaction converts it into 8-oxo-7, 8-dihyrdroguanine (8-Oxo-G). But, this reaction requires more energy than seems to be available because, formally, it requires that a water molecule (H2O) split apart into a proton (H+) and a hydroxyl anion (OH-). This large energy requirement has puzzled scientists for a long time. Now the research team, led by Landman and Gary Schuster, provost-designate of Georgia Tech, professor of Chemistry and dean of the College of Sciences, has uncovered how the reaction occurs.

Here’s what they found: A sodium counter-ion (Na+) diffusing in the hydration environment of the DNA molecule wanders into the major groove of the DNA double helical ladder. When the Na+ comes close to the hole created by the missing electron, its positive charge promotes the C8 carbon atom of the guanine to bond with a water molecule. In a concerted motion, the oxygen atom of the water molecule with one of its hydrogen atoms attaches to the C8 carbon atom. At the same time, the other proton of the water molecule connects the oxygen atom to that of a neighboring water molecule. This hydrogen bond elongates, leading to the formation of a transition state complex involving the two neighboring water molecules. The complex breaks up, transferring one of its protons (a positively charged hydrogen atom) to the neighboring water molecule, making a hydronium ion H3O+. This leaves the guanine neutral, with the rest of the first water molecule attached to it and prepares it for the rest of the already-known steps to making 8-Oxo-G.

Because it is positively charged, the H3O+ binds to the adjacent negatively charged phosphate, (PO4-) that is part of the backbone of the DNA molecule, to complete this step in the reaction.

The phosphate is crucial to the reaction because it acts as a sink that holds one of the reaction products, (H3O+) together with the other product (the guanine base with an attached OH- at the C8 location). According to quantum simulations, the energy barrier leading to formation of the transition state complex, and thus the required energy for this reaction step to occur, is 0.7 electron-volts (eV) – well below the energy required for dissociation of a water molecule immersed in a water environment. Obviously, without the presence of neighboring water molecules, the above reaction mechanism involving transfer of the proton to the neighboring phosphate group through the hydronium shuttle, does not occur and no products are generated.

The simulations unveiled that the Na+ plays a key role in promoting the reaction. To test this theoretical prediction in the laboratory, the team substituted the negatively charged PO4- near the reaction site with a phosphonate (PO3CH3) group. Because phosphonate is neutral, it doesn’t attract the Na+. Without the Na+ to promote the reaction of the ionized DNA at the C8 carbon atom of the guanine base, the reaction becomes less likely. Furthermore, even if a reaction occurs and a H3O+ forms, it does not get attached to the neutral phosphonate, and consequently the reaction does not come to completion, and very little, or no 8-oxo-G is formed.

"The complexity of this reaction is an intrinsic part of the chemical process that we investigated, because it occurs only under very specific conditions requiring a complex choreography from its players, I believe that this complexity is part of nature’s control mechanism,” said Landman. “Perhaps such inherent complexity guards us from harmful mutagenetic events occurring more frequently, and it is possible that similar principles may hold in other important processes of biological relevance.”

"This type of research requires the development of new modeling strategies and significant computational power. It also needed indispensable complementary and supplementary laboratory experiments. We were very fortunate to have this combination in our research team,” he said.

The authors of the paper published in the Journal of the American Chemical Society are: Robert N. Barnett, Angelo Bongiorno, Charles L. Cleveland, Abraham Joy, Uzi Landman and Gary B. Schuster from the Schools of Physics and Chemistry and Biochemistry at the Georgia Institute of Technology.

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Stereotactic Radiotherapy Slows Pancreatic Cancer Progression for Inoperable Patients

Called stereotactic body radiotherapy (SBRT), the study found it was able to delay pancreatic cancer progression locally, on average, by almost six months.

While, on average, the patients in the study lived about 10 months, one-third lived more than a year.

Without any treatment — surgery, chemotherapy or radiation therapy — most pancreatic cancer patients only live about four to six months.

"Our research establishes stereotactic body radiotherapy as a reasonable treatment option for patients who can’t have surgery or aren’t candidates for chemotherapy," says study lead author Michael Haley, D.O., a resident in the Department of Radiation Oncology at Henry Ford Hospital.

"While it’s not a curative therapy, it does seem to allow some progression-free survival benefit with minimal side-effects for patients. Ultimately, we’re able to provide a treatment to patients who don’t have any other options other than a traditionally prolonged course of radiation, which may not be as effective, and possibly has more side effects."

Says study co-author Munther Ajlouni, M.D., senior staff physician in the Department of Radiation Oncology at Henry Ford: "SBRT allows us to effectively treat patients who are unable to tolerate prolonged, aggressive therapy within a short period of time and with minimal toxicity."

The study will be presented Nov. 2 during the poster session at the 52nd annual American Society for Radiation Oncology (ASTRO) meeting in San Diego. Results also are online in the November issue of the International Journal of Radiation Oncology.

According to the National Cancer Institute, in 2010 there will be an estimated 43,140 new cases of pancreatic cancer, and approximately 36,800 will die from the disease. Risk factors for pancreatic cancer include smoking, diabetes, obesity, family history of the disease and pancreatitis. Most people diagnosed with the disease are older than 65.

Surgery is the only known cure for resectable pancreatic cancer, where the cancer is localized to the pancreas and hasn’t spread.

It is estimated that only 20 percent of pancreatic cancer patients have their tumors present with localized disease amendable to surgical removal. A select number of those patients, however, are not candidates for surgery due to having other co-morbidities such as heart disease. This leaves only chemotherapy and radiation, or a combination of the two, available for treatment.

SBRT is a method of giving radiation that can be highly targeted to the tumor, sparing the normal tissue around it. It also provides a higher dose of radiation, meaning patients have fewer treatments. It is most commonly used for lung cancer patients, but has been used for liver and brain tumors as well.

The Henry Ford study looked to determine if SBRT was a viable option to slow cancer progression in medically inoperable patients with potentially resectable pancreatic cancer.

The study included 12 medically inoperable patients with stage I or II pancreatic cancer. The median patient age was 83. Patients received between three and seven SBRT treatments.

Among those patients whose cancer spread, SBRT was able to slow cancer progression for five to six months. Once the patients’ cancer started to progress, they lived about 2.5 months. "This may indicate that this slowing of the progression of disease accomplished by SBRT may modestly increase overall life span," notes Dr. Haley.

A few patients reported some minor side effects from treatment, including fatigue, loss of appetite and weakness. Two patients developed gastric ulcers, but both recovered.

Study funding: Henry Ford Hospital

Along with Dr. Haley and Dr. Ajlouni, Henry Ford study co-authors are Samuel Ryu, M.D.; Indrin Chetty, Ph.D.; Teamour Nurushev, Ph.D.; and Benjamin Movsas, M.D.

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Harvard Medical School Researchers Identify Four Human Genes Essential To Cell Division; Discovery Yields New Target For Cancer Therapies

Hongtao Yu, a postdoctoral fellow in the laboratory of Marc Kirschner, the Carl W. Walter professor of cell biology at Harvard Medical School, and his colleagues used frog (Xenopus) protein sequences as a guide to identify the remaining four human genes in the eight-unit anaphase-promoting complex (APC). The APC's critical role in cell division makes it a perfect target for the fight against cancer, in which cells escape regulation and divide uncontrollably. The findings are published in the February 20 Science.

APC proteins are activated as the cell progresses through mitosis, but as yet, Kirschner and Yu do not know exactly how they are regulated. However, uncertainty about APC's regulation does not diminish the potential of this multi-subunit complex for anticancer therapeutics. With its seminal role in mitosis, the APC seems to be a perfect site to halt cell division. Like the anticancer drug Taxol that also disrupts mitosis, the advantage with an APC inhibitor would be preferential delivery to rapidly dividing tumor cells. "A lot of normal cells are just not dividing at all," says Yu. These law-abiding noncancerous cells would be invisible to the APC inhibitor, avoiding dangerous side effects that plague many anticancer drugs. The APC complex provides "a whole new set of targets which don't function at all in non-dividing cells," says Kirschner.

For successful cell division — when the cytoplasmic and genetic contents of a cell are faithfully reproduced in the daughter progeny — two cycles must be synchronized. The DNA is replicated in one cycle, and the chromosomes divide during mitosis — the second cycle.

The APC is one of the mitotic ringleaders. "It is absolutely required for cell proliferation," says Yu. The protein complex drives a dividing cell from the metaphase stage of mitosis into anaphase–from the point in which the chromosomes find their partner and gather in pairs in the center of the cell, to the point in which each member of the chromosomal pair separates and migrates to the distant cellular poles. A new cell membrane forms between the chromosomal clumps, and mitosis concludes with the formation of two identical daughter cells, each containing an intact copy of the parent cell's genetic information.

An essential step in the development of any new drug is an accurate detection system that will report whether the compound being tested is having the desired effect on the target cell. If APC inhibition is detected following addition of a certain compound the chemical that sounded the alarm can be carefully investigated for its clinical suitability. The Kirschner group has filed a patent for the biochemical method that they devised for analyzing APC activity. The assay is amenable to automation, making it an attractive way to quickly screen many different chemical compounds.

"The intention is to use [the assay] to screen for small molecule inhibitors which might be very useful in anticancer and antiproliferation drugs," says Kirschner.

The study was funded by two grants from the National Institutes of Health.

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Vegetables Can Protect Unborn Child Against Diabetes

The study was performed in collaboration with Linköping University, which is conducting a population study called ABIS (All Babies in Southeast Sweden). The results have been published in the journal Pediatric Diabetes.

"This is the first study to show a link between vegetable intake during pregnancy and the risk of the child subsequently developing type 1 diabetes, but more studies of various kinds will be needed before we can say anything definitive," says researcher and clinical nutritionist Hilde Brekke from the Sahlgrenska Academy.

Blood samples from almost 6,000 five year-olds were analysed in the study. In type 1 diabetes, certain cells in the pancreas gradually get worse at producing insulin, leading to insulin deficiency. Children at risk of developing type 1 diabetes have antibodies in their blood which attack these insulin-producing cells.

Of the 6,000 children tested, three per cent had either elevated levels of these antibodies or fully developed type 1 diabetes at the age of five. These risk markers were up to twice as common in children whose mothers rarely ate vegetables during pregnancy. The risk was lowest among children whose mothers stated that they ate vegetables every day.

"We cannot say with certainty on the basis of this study that it’s the vegetables themselves that have this protective effect, but other factors related to vegetable intake, such as the mother’s standard of education, do not seem to explain the link," says Brekke. "Nor can this protection be explained by other measured dietary factors or other known risk factors."

The term "Vegetables "in this study included all vegetables except for root vegetables.

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Cancer Data Not Readily Available for Future Research

The results come from a study of patterns of research data availability conducted by Dr Heather Piwowar of the National Evolutionary Synthesis Center.

Data collected in scientific research is often useful for future studies by other investigators, but scientists have rarely made their raw research data widely available. Tools and initiatives are underway to encourage scientists to publicly archive their data. This analysis confirms there is still much room for improvement.

By querying the full text of the scientific literature through websites like Google Scholar and PubMed Central, Piwowar identified eleven thousand studies that collected a particular type of data about cellular activity, called gene expression microarray data. Only 45% of recent gene expression studies were found to have deposited their data in the public databases developed for this purpose. The rate of data publication has increased only slightly from 2007 to 2009. Data is shared least often from studies on cancer and human subjects: cancer studies make their data available for wide reuse half as often as similar studies outside cancer.

"It was disheartening to discover that studies on cancer and human subjects were least likely to make their data available. These data are surely some of the most valuable for reuse, to confirm, refute, inform and advance bench-to-bedside translational research," Piwowar said.

"We want as much scientific progress as we can get from our tax and charity dollars. This requires increased access to data resources. Data can be shared while maintaining patient privacy," Piwowar added, noting that patient re-identification is rarely an issue for gene expression microarray studies.

Most likely to share their data in public databases were investigators from Stanford University and those who published in the journal Physiological Genomics.

Scientist sometimes email each other to request datasets that aren’t available online, but these requests often go unanswered or are denied by the original investigators. Publishing data in online data repositories is considered the best way to share data for future reuse.

Recent policies by the NSF seek to increase the amount of data disseminated from federally-funded research by requiring data management and dissemination plans in all new grant applications.

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