Category: Brain and Body

You Can’t Beat the Heat

Even when the body is able to maintain core body temperature, cardiovascular performance is decreased in the heat.

      Researchers from the American College of Sports Medicine conducted research in January 2010 that shows that environmental heat stress with only modest hyperthermia has a significant impact on aerobic endurance. This research is of importance to a military operating in a desert environment in which temperatures can exceed 120˚ F in the summer.

      Subjects were asked to perform fifteen minutes of cycling in a temperate (69˚F) or hot environment (104˚F). Core and skin temperature and heart rate were constantly monitored. Performance and pacing were analyzed by kJ of work completed. Core temperature was modestly elevated in both environments, with skin temperature being higher in the hot environment. While heart rate and fatigue level were consistent between the two environments, the total amount of work done in the hot environment was 17% less than in the temperate environment. Also, while the pace was maintained in the temperate climate, it dropped significantly over time in the hot environment.

      So, although excessive hyperthermia was avoided, performance was still impacted by the hot environment. While it has been established that marked hyperthermia leads to increased fatigue during exercise, it seems that a hot environment can increase fatigue even without significant increase in core temperature. There are a few theories about how this happens. One idea is that athletes use an anticipatory control mechanism during exercise to ensure maintenance of core body temperature by making unconscious adjustments in work rate. Increased cardiovascular strain resulting from the maintenance of high skin blood flow required to maintain core temperature may also explain the observed decrease in performance. So, impact aerobic ability in the heat may come from either an early modification of work output or an inability to maintain a desired work output over time. This study supported the idea that initial pace could not be maintained, as the participants in the hot group got much slower over time.

       It seems clear that cardiovascular performance is decreased in the heat even when the body is able to maintain core temperatures. Further research may elucidate whether an early modification of pace in the heat may minimize the overall decline in performance associated with environmental heat stress. This information can help athletes who must compete in the heat to pace themselves, and may also shed light on tactics the military can use to maintain optimum performance in hot climates.

 Nicole Myers

For more information visit: http://www.dtic.mil/cgi-bin/GetTRDoc?AD=ADA513059&Location=U2&doc=GetTRDoc.pdf

Kicking it to good health

By Abby Larson
Photo from the study of women and soccer. Credit: Mikal Schlosser

In European countries, soccer is not just a sport; it’s a lifestyle. Now, soccer has joined the side of science.

Led by Professors Peter Krustrup and Jens Bangsbo at the University of Copenhagen’s Department of Exercise and Sports Sciences, over 50 researchers from 7 countries are finding out the benefits of soccer from a physical, psychological, and social perspective. Numerous articles will be published in the Scandinavian Journal of Medicine and Science in Sports on the effects of soccer on bone mass and bone density, standing postural balance, and muscle strength.   All of these can help reduce falls and bone fractures, especially in the elderly.

One of the studies had women aged 20-47 play soccer twice a week for 14 weeks. At the end of the time period, their leg bones and muscles were significantly denser and stronger. The same women, having never played soccer before, participated in a long term 16-week study showing that whole body bone mineral density was increased. The short and long-term effects found were higher than a similar study on the effects of running on bone and muscle mass. This is due to the combination of sprinting, long distance running, and high forces that act on the legs when cutting in soccer.

The benefits of soccer are not just for the young and middle aged. A study performed by the researchers showed that men in their 70s who have played recreational soccer most of their lives have much better muscle strength and balance than men of the same age who do not play soccer. They even had equal muscle strength and balance compared to untrained men in their 30s.

This cohort of studies can benefit men and women of all ages. The immediate effects of soccer may be beneficial to women going through menopause at risk for osteoporosis, since it quickly adds bone mineral density to the legs and improves balance. It can prevent falls and fractures in elderly men and women because it increases muscle mass and balance, especially in people who play soccer all their lives.

Funding for the projects comes from FIFA—Medical Assessment and Research Centre (F-MARC), The Danish Ministry of Culture, TrygFonden, United Federation of Danish Workers (3F), The Danish Football Association, Team Denmark and The Danish Sports Confederation. Future studies by Krustrup and Bangsbo include the effects of soccer on patients with diabetis and cancer, long-term effects on osteoporosis, and the cardiovascular and musculoskeletal effects on kids in youth soccer.

Discoveries in Diabetes, Depression, and Dementia

By Shelly Hwang

Diabetes, Depression, and Dementia are three of the most common medical conditions among Americans today. A recent study released on March 5 by a group of researchers at the University of Washington (UW) revealed that depression in diabetic patients doubles the risk of developing dementia, a finding that may affect the way that depression is screened and treated in order to prevent the development of other diseases.

Dementia is the gradual loss of cognitive and reasoning abilities, including memory loss, wandering, inability to do basic math, and forgetting familiar things or people.  Depression is a mental disorder marked by low mood and poor concentration. Diabetes is a medical condition in which a person has a high blood sugar level. While both diabetes and major depression have been shown to be separate risk factors for dementia, the effect of both diabetes and depression on dementia has not been studied. It turns out that adults with both conditions are twice as likely to develop dementia, compared with adults with only diabetes.

This project, led by Dr. Wayne Katon, a professor of psychiatry and behavior sciences at UW, is a part of the Pathways Epidemiological Follow-Up study, which examines adults from the Group Health Cooperative’s diabetes registry. Patients from nine clinics in western Washington State were studied for five years. 163 of 3,382 (4.8%) patients with diabetes alone developed dementia, while 36 of 455 (7.9%) of the diabetes patients with major depression were diagnosed with dementia. This presents a 2.7 fold increase of dementia in diabetic patients with depression.

Depression is common among individuals with diabetes. Previous studies found depression increases mortality rate among diabetes patients, in addition to health complications. However, the way the two diseases interact is unknown. Perhaps they interact by genetics, increasing stress levels, or resulting in unhealthy behaviors such as smoking, lack of exercise, and over-eating, which raise the risk of dementia. Diabetes is a known risk factor for dementia because it causes blood vessel problems, tissue damage, and increased blood sugar levels, which all increase odds of developing dementia. Although the link between depression, diabetes, and dementia is still not understood, it is useful for doctors to screen and treat for depression as a preventive measure against the development of cognitive deficits or dementia in diabetic patients.

Original Press Release

VA Puget Sound Health Care System Clinical Research Unit

Info on Dementia

TB or not TB?

Justin Williams ’13

Ever since doctor Robert Koch discovered the bacteria responsible for tuberculous, there has been many hours poured into researching everything about the disease. Through the years, researchers have unearthed almost everything, but one area that is notably lacking is determining any kinds or risk factors. However, on March 4, 2010, researchers at the University of Washington have discovered a gene that may be a major determining factor in susceptibility to TB.

Researchers conducted experiments on zebrafish, in which the severity of the TB could be easily identified due to their clear bodies. The scientists genetically altered the genetic makeup of the zebrafish before injecting them with the tuberculous bacteria and then observing the severity of their TB symptoms.

X-ray of a person with tuberculous.

Their experimentation and subsequent results turned out to be very interesting. They found that the lta4h gene, and it’s genotype (what two particular copies of it you have) are very important in determining how susceptible a person is to contracting TB.

For those of you who are not familiar with genetics, the majority of genes come in two differentforms. You get one copy from each of your  parents. It is possible to get both of one kind, one of each, or one of  the other kind. In this particular lta4h gene, the two different types  are inflammatory and anti-inflammatory. Researchers found that  when zebrafish have one copy of each of the genes, their response to  TB is much better than if they only have copies of one or the other  (i.e. the response of zebrafish with one inflammatory and one anti-inflammatory copy was much better than those who had two copies of the inflammatory or two copies of the anti-inflammatory).

Comic illustration of the lta4h gene.

While this research was conducted on zebrafish, the scientists did look into the structure of the gene in humans to determine its relevance. Their investigations proved fruitful and the implications of this for humans are promising.Also, their newfound knowledge that an over inflammatory response can be hurtful for the fight against TB provides some hope “that corticosteroids and other anti-inflammatory agents can be useful as adjuvants in some cases of TB where antibiotics alone are failing.” Whichever way you look at it, the results are exciting and promising for people involved with tuberculous.

Sources:

http://www.eurekalert.org/pub_releases/2010-03/uow-rdg030210.php

http://nobelprize.org/educational_games/medicine/tuberculosis/readmore.html


The Sea Squirt: An Answer to Alzheimer’s?

Ciona intestinalis

By Kelly Lohr

The newest breakthrough in Alzheimer’s research is coming from an unlikely source–a sea squirt.  Just this week (March 2, 2010) Mike Virata and Bob Zeller of San Diego State University believe that Ciona intestinalis, known commonly as the sea squirt, may be the perfect model organism for this disease.

The brains of Alzheimer’s patients are typically filled with tangles and plaques made of the protein fragment beta-amyloid.  Alzheimer’s disease affects nearly 4 million Americans and an estimated 27 million people worldwide. It is the most common form of age-related dementia and has no cure. Current drug regimens only relieve symptoms and cannot halt the progression of the disease. Research in the scientific community is currently  aimed at slowing the disease through drugs such as Aricept and Namenda which are focused on decreasing plaque accumulation.

Recently, research has shown the need for an improved model organism to aid  in understanding the pathology of the disease.  Currently, genetically modified strains of mice have been the organism of choice in the research of this disease. However, there are limitations in the use of mice including an extremely long waiting period for plaque development like those seen in Alzheimer’s brains. Also, these mice do not contain the same genetic mutations linked to hereditary risk of Alzheimer’s disease.  Mice are also more costly to purchase and maintain for research.

Sea squirts are tunicates, marine organisms with a hard outer tunic and a soft body. They live on underwater structures and are filter feeders that eat small plant material. It has been suggested that sea squirts are actually our closest invertebrate relatives.  As far as research benefits, sea squirts share nearly 80% of our genes and resemble vertebrates in their immature form.  These animals are inexpensive to house and contain all of the genes needed for the development of Alzheimer’s plaques in humans.

An immature sea squirt.

Virata and Zeller found that by giving the immature sea squirt amyloid precursor protein, a mutant protein linked to hereditary Alzheimer’s, sea squirts developed brain plaques in a single day.  Further, these plaques and the behavioral deficits seen in these animals were able to be reversed using a drug meant to remove plaques.  Such techniques have been ineffective in all other invertebrate models, including the commonly used nematode, C. elegans.  Now, investigators can be freed from genetic, time, and financial constraints.  These findings provide a resource for an entirely new take on Alzheimer’s research…all because of a sea squirt.

For more information, click here.

A Human Powered Future? Maybe.

Dan Conant
What the chip would look like

 

With all sorts of alternative energy sources vying to prove themselves the cheapest and cleanest of them all, human generated energy has recently made a big stride due to a new piece of technology from Princeton.  However, before you begin to think of something similar to the Matrix with humans being plugged into a power grid, it is important to note that humans will not generate mass quantities of energy.  This is because the energy generated is by our muscles movement, not by the small but frequent electrical impulses that trigger muscle movement. 

Princeton University engineers created a chip composed of ceramic and rubber nanoribbons.  This allows the chip to be able to flex.  The idea behind the chip is that when a muscle moves, this chip attached to it will also flex and by doing so, create a small amount of energy.  The chip is also fairly efficient in terms of energy conversion, turning mechanical energy into electrical energy at an efficiency rate of 80%. 

This chip is very important to the many fields of medicine.  There are currently a number of medical devices such as implants that require a source of energy.  Currently batteries fill this role, but when they begin to run out of energy, the patient has to undergo another surgery to have another battery put in.  With this chip implanted, repeated operations would never have to happen again unless the chip became damaged or the pacemaker was having issues.  For someone with a pacemaker, this chip would be implanted near the lungs due to its proximity to the heart as well as the constant movement of a person’s lungs due to breathing would provide a consistent a steady source of energy for the pacemaker. 

This is not the first human powered energy converter to have been conceived, but it is arguably one of the best ones.  Due to the materials in the chip, the body should also accept the chip with no issues.  Furthermore, due to the simplicity of the chip and the materials not costing too much, chips like these should become affordable soon after their debut and mass production; certainly a relief for the many people out there with heart problems and wallet problems.

Information for this article was gathered from this link.

Where can I get that gene “juice”?

By Abby Larson

Athletes are competitive by nature, and many will do whatever they can to win.  Steroid usage is heavily monitored in competitions, yet with the coming of the Winter Olympics, whispers of “gene doping” are becoming audible. There has been a craze by athletes for “gene juice” ever since a 2005 study performed by Dr. Ronald Evans, a geneticist at the Salk Institute for Biological Studies in San Diego, California, produced the “Marathon Mouse”.  Evans discovered a gene involved in muscle formation and altered it, producing a mouse that could run twice as far as normal mice.  This spurred the World Anti-Doping Agency (WADA) to list gene doping as illegal.

Evans was searching for a way to treat muscular dystrophy, characterized by muscle wasting and inability to build muscle.  His study was based on the idea of gene therapy: treating a disease caused by a mutated or malfunctioning gene by inserting copies of the normal gene into cells.  The cells essentially replace the non-functional gene with the normal one.  So, if you can use gene therapy to treat mutated genes, why can’t you use gene therapy to replace a “normal” athletic gene with a “high performance” athletic gene?

A review article by Dr. Craig Sharp that will be published in March, 2010, titled “The Human Genome and Sport, Including Epigenetics, Gene Doping, and Athleticogenomics,” discusses many athletic performance gene discoveries that may be possible targets for gene doping.   One example is a gene encoding myostatin, an inhibitor of muscle growth.  Exercise tears muscles, which results in increased expression of actin and myosin.  This increase in expression is eventually repressed by the protein myostatin, preventing excessive muscle growth.  In 2004, a boy was born with a mutated form of myostatin that disrupted some of the protein’s function.  The boy had significantly hypertrophied muscles, and was still unusually muscular at age 4.  Based on studies like this one, by injecting muscle cells with the mutated form of myostatin, Sharp believes that athletes and bodybuilders can create greater muscle mass than without the gene doping because inhibition of muscle production will be decreased following exercise.  Who knew genetic studies could lead to Schwarzenegger-sized people?

Death does not seem to scare overzealous coaches and athletes, who may bypass the risks of gene doping to achieve that extra edge.  In several gene therapy studies, some patients developed cancers or severe autoimmune responses to the product of the injected genes.  A 2008 report by Dr. E.B. Wheeldon showed that a patient went into an extreme immune response due to a reaction with a carrier virus used to transmit the gene of interest into his cells, causing death from organ failure.  This does not seem to discourage some athletes and coaches.

Have athletes started using gene doping to get ahead?  An experimental drug, Repoxygen, was developed to treat severe anemia due to a mutated gene.  As several Olympic coaches discovered, Repoxygen contained the gene for erythropoietin (EPO), which increases red blood cell production and performance.  EPO itself is a currently banned substance by WADA for performance enhancement—but how can one detect the gene for it?  There are no current established methods for gene doping detection aside from muscle biopsy, says Sharp, which is a painful and unappealing method of detecting changes in tissue development.  A rising technique commonly used in cancer genomics may be the key: DNA microarray.  A DNA microarray detects changes in gene expression in a person between two periods in time.  In order for anti-doping agencies to use this method in top competitions such as the Olympics, an athlete’s genetic file must be established as a reference.  WADA has already developed a “passport” program to keep blood and urine samples of athletes on file to use for future genomic comparisons.

Gene doping raises an ethical issue that surpasses steroid use due to its difficulty in detection, although gene doping has been banned for over 5 years for major competitions.  By the 2012 Summer Olympics in London, genetic testing could be a common procedure by anti-doping committees.  It seems that as we learn more about the way the body responds to exercise and why the world’s top athletes are so good, more daemons are unleashed from Pandora’s box.

How heart malfunctions function

By Justin Williams ’13

Calcineurin Enzyme

Heart disease is among the deadliest diseases in the world. Last year it was responsible for  631,636 deaths in the United States alone. For many years it has been known that the enzyme calcineurin plays a major role in heart function, but what exactly it did was not known until now. Just this week (February 19th), researchers at the Cincinnati Children’s Hospital Medical Center and the Howard Hughes Medical Institute published the results of their study, which shows that calcineurin plays a major role in regulating many vital functions of the heart.

In this study, the researchers observed the hearts of mice, manipulating the level of calcineurin in their systems. Their data shows that “calcineurin in hearts of mice is directly linked to proper cardiac muscle contraction, rhythm and maintenance of heart activity.” When mice were almost completely stripped of calcineurin they displayed major heart problems which included “heart arrhythmia, failure and death” said Dr. Marjorie Maillet, one of the leading investigators in the study.

Prior to this, calcium has also been identified as necessary for a healthy heart. In this study, in addition to the aforementioned results, researchers found that the mice who were bred with a calcineurin deficiency displayed a severe reduction in the expression of these calcium related genes. Using this newfound link they have proposed a “feed-forward” mechanism, hypothesizing that when the calcineurin is activated by calcium, the effects of calcineurin on the heart will be increased.

While there are some drawbacks to this study, mainly that it is the first of it’s kind and was performed on mice, the results are still promising. Dr. Maillet certainly thinks so, saying that it “offers important insights for future studies that could lead to new approaches in diagnosis and treatment of heart patients.” It is still a little early to call, but things are starting to look up in the world of heart disease.

The original article can be found here.

Drugs That Kill Bacteria Can Also Make Them Stronger

By Johnathan Nieves ‘11

A recent study showed that exposure to low levels of antibiotics increased mutations in bacteria hundreds of times more than normal, making the creation of drug-resistant bacteria more likely. A drug under development by Radnor, PA-based PolyMedix, Inc. shows promise for addressing the serious threat of drug resistance by mimicking the human body’s defenses.

Click on the Image above to see Polymedix's Drug In Action (Sources: Image, World Health Organization; Video, Polymedix, Inc. )

If you don’t take your prescription antibiotics as your doctor advises, then listen up. Just last week (February 12) a paper published in the journal Molecular Cell described how exposure to low levels of antibiotics increased mutations in bacteria hundreds of times more than normal, making the creation of drug-resistant bacteria more likely. A drug currently under development by Radnor, PA-based PolyMedix, Inc., however, shows promise for addressing the serious threat of drug resistance by mimicking the human body’s defenses.

Drug resistance has been a growing health concern for decades now since the introduction of penicillin in the 1940s, the first available antibiotic of its kind. Drug resistance occurs because of bacteria’s natural ability to evolve through mutations it incurs as it reproduces. As it turns out, researchers have found that low antibiotic dosages are triggers for increasing the rate at which bacteria mutate, thus, increasing the likelihood of drug resistance.

“Like anything in nature, bacteria have ways to fight its opponents, and do so either by pumping antibiotics out of themselves through a process called efflux, or by rapidly mutating and changing the shape of the target of attack of the antibiotic drug. They can do this, even with large doses of antibiotics, it’s their innate way to try to survive,” explains Bozena Korczak, Vice President of Drug Development at PolyMedix Inc..”

“Upping the antibiotic dosage may be a viable solution but not the ultimate one,” adds Korczak. Driven by science conducted at the University of Pennsylvania, PolyMedix is investigating a new type of antibiotic drug that works by imitating the human immune system.

PolyMedix’s investigational antibiotic agent, called PMX-30063, is the first of its kind with a new approach to address the serious health implications of drug resistance by mimicking host defense protiens. Unlike most antibiotics, host defense proteins work fundamentally different. Rather than crossing the bacterial membrane to find a target like most antibiotics, they selectively target the cell membranes integrity by poking holes into it. This diminishes the bacteria’s ability to remain intact and the bacteria and its internal components become degraded (See video demonstration by clicking on the image above).

Polymedix purports that this unique mechanism of action makes drug resistance unlikely to develop. Korczak insists that “the best approach to preventing this phenomenon is by directly attacking the bacteria’s cell membrane, rendering them destroyed and dead in a way that there is little chance of resistance.”

To study the ability of bacteria to resist an antibiotic drug, a laboratory experimental method known as “serial passage” is used by intentionally trying to create bacterial drug resistance. Using this experiment, PolyMedix has shown that resistance did not appear to its compounds in contrast to traditional antibiotics.

So far, data from two Phase I clinical studies demonstrate that the compound is safe and well-tolerated. PolyMedix is on schedule to complete the third and final segment of the ongoing Phase 1 study with PMX-30063 early this year and commence Phase 2 studies later this year.

PolyMedix has received 9 grants and research contracts from the National Institutes of Health and branches of the military to help support the development of its antibiotic compounds.

To view the press release associated with this piece, please click here.

To learn more about PolyMedix, Inc., please visit www.polymedix.com.

Got milk? Vitamin D, a key player in multiple sclerosis

By Kelly Lohr

Drinking milk may do a lot more than just strengthen our bones. A study out of the Harvard School of Public Health in Boston recently suggested drinking milk during pregnancy may markedly reduce the chance of the child developing multiple sclerosis (MS) later in life.

Vitamin D can be found in dairy, fatty fish, and supplements. Exposure to sunlight also produces this helpful vitamin.

Lead by Fariba Mirzaei, MD, the study examined over 35,000 female nurses whose mothers had completed questionnaires recording their diets during their pregnancies with their now-grown daughters.  The work occurred over a 16-year period, during which 199 women developed MS.

MS is a degenerative disease that attacks the central nervous system (CNS), including the brain, spinal cord, and optic nerves. The symptoms vary, ranging from numbness in the arms and legs to paralysis and loss of vision. Unfortunately for its sufferers, the progress and severity of MS are often unpredictable. The neurons in our body are partially covered in a fatty substance called myelin in order to insulates the cells and  to allow them to transmit signals quickly. If the myelin is damaged, these signals can be delayed. MS results in the destruction of this insulating myelin in the CNS. This breakdown is thought to be caused by the body’s immune system attacking the myelin sheath.

Normal and damaged myelin in neurons.

The researchers lead by Dr. Mirzaei found that the risk of MS was lower in women whose mothers had high milk or vitamin D diets during pregnancy. Women whose mothers drank four glasses of milk per day had a 56% less chance of developing MS than those whose mothers drank less than three glasses per month. In general, women in the top 20% of vitamin D intake had a 45% less chance of having a child develop MS than those in the bottom 20% of vitamin D intake.

Vitamin D can come in many forms including fatty fish, milk and dairy products, and exposure to sunlight. Supplements could also be used to counter vitamin deficits in the diet. This study serves as evidence of a growing role for vitamin D in the pathology of MS. Prevention may play an important part in the disease, perhaps starting as early as pregnancy.

Source: http://www.medscape.com/viewarticle/716913