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Healing a “Broken” Heart March 4, 2011

Posted by Kyle in Biology, Chemistry, Health, Medicine, Physiology.
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Irreparable Harm

The majority of those reading this have probably experienced some sort of injury in their lifetime.  Injuries such as cuts and broken bones will soon heal with proper care, but there are certain tissues that if damaged, cannot repair themselves. Heart tissue and brain tissue are two examples that come to mind. This may be the case for most of us adult humans, but new research out of The University of Texas Southwestern Medical Center at Dallas is pointing out that some newborn mammals have the ability to heal completely when it comes to heart damage. The only problem is, at some point along the line, as we age, the heart loses this ability to heal itself. Still, this is a very important discovery for a society that suffers greatly from heart disease, which kills thousands of Americans every year.

Studying a Broken Heart

Researchers found that in newborn mice, when sections of heart were removed, the heart had completely healed within three weeks. The hearts then functioned as normal with no signs of damage. Understanding how this works and why the heart stops doing it after a certain amount of time is now the next step for researchers. Unlike when you tear a hamstring, damage to cardiac tissue after a heart attack doesn’t just heal with time. So for those who suffer from heart problems, a discovery like this brings them one step closer to a healthy heart in the future.

Of Mice & Men

Obviously mice, which help us a lot more than most people realize, and humans are a little different from each other, but seeing results like this in another mammal is still promising. If nothing else, it is definitely a huge step in the right direction for researchers looking to cut down on the number of heart related deaths. For now though, it is important for people to remember that they only have one heart, and taking care of it should be a priority.


Taking a Radioactive Drag: Polonium 210 and Cigarettes March 3, 2011

Posted by tsublett in Chemistry, Health, Medicine, Physiology, Policy.
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Radioactive Smoke: A Dangerous Isotope Lurks in Cigarettes

The Unknown and Known Dangers of Smoking

Many of us know the dangers of smoking. We see many friends and loved ones diagnosed with cancer and know of many who die from it each year. We have seen the warning labels on cigarette packages, but what is actually in that smoke? Research says, it’s polonium-210, a radioactive isotope found in fertilizers. The problem is, tobacco companies knew about this, a while ago. According to a 2011 article in Scientific American, “The tobacco industry has known about polonium in cigarettes for nearly 50 years.” Facts like these are disconcerting on many levels.

A Tobacco Plant

Ways We Are Exposed to Polonium 210

How exactly this isotope gets into the tobacco leaf is not entirely known, but it is thought to be a “daughter isotope of uranium 238 found in fertilizers. When the fertilizer is spread on the soil, it begins to decay into either an airborne isotope, such as radon 222, or into lead 210 in the soil. Both of these products enter through the roots or into the leaves and eventually decay into polonium 210. The leaves are then processed normally and eventually end up in cigarettes.

The History of Polonium 210 Detection

Now, then, there seems to be a problem. See, polonium 210 was detected first in the 1960s. This should be a BIG problem, because we are now considering its dangers even though it has been known about  for 50+ years! Through a series of papers published during the 1960s, namely a paper published in 1964 by Radford and Hunt, scientists demonstrated how polonium 210 can enter the soil.  Subsequently in a paper published in 1974, by John B. Little and William O’Toole, proved that smokers can develop “hot-spots” on their lungs where polonium 210 accumulates. The hot spots can cause mutations due to alpha decay . The problem is, tobacco farmers and cigarette manufacturers are not removing this isotope. The good news is… they may start doing so soon.

How much polonium do we get when we smoke?

Here is an excerpt from a New York Times article:

A fraction of a trillionth of a curie (a unit of radiation named for polonium’s discoverers, Marie and Pierre Curie) may not sound like much, but remember that we’re talking about a powerful radionuclide disgorging alpha particles — the most dangerous kind when it comes to lung cancer — at a much higher rate even than the plutonium used in the bomb dropped on Nagasaki. Polonium 210 has a half life of about 138 days, making it thousands of times more radioactive than the nuclear fuels used in early atomic bombs.

We should also recall that people smoke a lot of cigarettes — about 5.7 trillion worldwide every year, enough to make a continuous chain from the earth to the sun and back, with enough left over for a few side-trips to Mars. If .04 picocuries of polonium are inhaled with every cigarette, about a quarter of a curie of one of the world’s most radioactive poisons is inhaled along with the tar, nicotine and cyanide of all the world’s cigarettes smoked each year. Pack-and-a-half smokers are dosed to the tune of about 300 chest X-rays.

 

Is there any relief?

Maybe we should stop smoking, it’s likely the best approach. If you can’t quite kick the habit, the FDA may help. Recently the FDA has taken over the regulation of cigarettes in the wake of the Family Smoking and Tobacco Control Act passed in 2009. With the FDA’s help, the exact content of polonium 210 in cigarettes may soon be published. On a side note, one quick fix may come in tobacco leaf preparation. Simply washing the leaves after harvest may eliminate a large portion of the polonium 210 found in the air.

 

The Largest Preventable Cause of Death in the World.

It seems like a radioactive isotope found in smoke is just one of many carcinogens that continue to contribute to tobacco being the largest preventable cause of death in the world. According to Scientific American:

The World Heath Organization has made clear that smoking is the most avoidable cause of death. It estimates that 1.3 million people die of lung cancer worldwide every year, 90 percent because of smoking. If polonium has been reduced through methods known to the industry, many thousands of those deaths could have been avoided. The industry, many thousands of those deaths could have been avoided. The industry’s lawyers made the conscious choice not to act on the results of their own scientists’ investigations. But it is the customers who have had to live with-and die from- that decision.

So, cigarettes are bad, but how bad they may be for us is still up in the air. Perhaps we can make them a little less dangerous in the future by removing these dangerous isotopes. Hopefully, with the FDA regulating cigarettes, this dangerous vice will soon be put to rest.

Mysterious Melatonin December 18, 2010

Posted by Kyle in Biology, Chemistry, Health, Medicine, Neuroscience, Nutrition, Physiology.
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I am sure everyone has already heard of a little compound known as melatonin. Melatonin is a hormone that can be found in many different organisms including plants, although most people know melatonin for its actions in mammals. In humans, melatonin is produced in the brain by the pineal gland. Circulating melatonin levels have been found to be high at night and low during the day, which is consistent with research that has shown that light suppresses melatonin. Because melatonin plays a role in controlling the circadian rhythm, it has received much interest for its use as a treatment for various sleep disorders. Because melatonin is a hormone, supplementing melatonin can present some issues.

Many people have used melatonin supplements to help them sleep at night. If you take a trip to your local drug store you are likely to find melatonin on the shelf. The first time I came across melatonin supplements I couldn’t help but think about the potential negative aspects to selling melatonin over the counter, unregulated. As many of you know, the human body likes to maintain homeostasis. When this delicate balance is interrupted, the body will react to return to homeostasis. I started to wonder what happens when someone takes melatonin supplements. The first thing that comes to mind is a decrease in the amount of melatonin receptors or a decrease in the production of melatonin itself, or both. I also wondered about possible side effects of increasing melatonin levels. As we have seen with many other hormones, multiple pathways and mechanisms can be influenced by a single hormone. So someone taking melatonin to help them sleep could inadvertently throw off other pathways, like those involved in reproduction for example.

Melatonin has been shown protect against reactive oxygen species, which can wreak havoc inside cells. This could potentially be an obvious benefit to taking melatonin supplements, especially if it helps an individual sleep at night. While sifting through the literature, I was unable to find any studies specifically looking at the negative effects of taking melatonin supplements, if any. But just because it isn’t proven that something is bad, doesn’t mean the potential for bad isn’t there. Also, other countries have taken action to stop over the counter sale of melatonin. Of course, there is also the question, do melatonin supplements even work?  How much of the melatonin present in a melatonin pill is denatured by stomach acids or excreted in urine before it even has an effect?

I am skeptical of melatonin supplements, if you haven’t noticed yet. To each his own, but I don’t think I will be purchasing or taking any melatonin supplements in the near future.  Good luck to everyone on their upcoming finals. Make sure to get plenty of sleep, although if your to-do list looks like mine, that won’t be happening.

Stress and the GI Tract December 17, 2010

Posted by ljsteele in Behavior, Biology, Chemistry, Ecology, Environment/Conservation, Health, Neuroscience.
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The mechanics of stress and the gut.

Stress is shown to have a huge effect on the body, whether or not it is experienced as an acute or chronic stress.  A major topic of interest is what effects stress has on the gastrointestinal tract in organisms.  According to a multi-part scientific paper entitled “Stress and the Gastrointestinal Tract”, there are many different stressors that can be examined within a variety of organisms.  Examples of the stressors explored include food deprivation, fearful sounds, weather changes, and water avoidance ( an acute stressors explored in lab organisms such as mice, rats, and guinea pigs).  It has also been shown that acute stressors in humans, such as pain exposure, anger, fear, and intense exercise can cause gastrointestinal shut down.

From the stressors listed above, research has explored how stress influences gastro muscles to slow contraction,  thus inhibiting the processing of food.  An interesting reaction to this slowing of peristaltic movement is the fact that many organisms lose control of their colon, showing defecation in response to certain stimuli such as fear and water avoidance.  Corticotropin releasing hormone, also known as CRH  (or CRF, as identified in the aforementioned paper), is released from the hypothalamus, and blocks the effects of the vagas nerve, while also traveling through the solar plexus, and attaching to receptors in the stomach.

Stomach ulcer

Once bound, this hormone has been shown to inhibit gastro movement, and thus preventing emptying of the stomach. The difference between the stomach and the colon is that the stomach requires contraction of the muscles to push food through, whereas the colon requires contraction to keep bowel movements inside the body.  With the effect of CRH binding to the receptors, relaxation in gastrointestinal muscles occur, which is why the release of the colon sphincter results.  However, the results explored here were in response  to short term stressors.  The effects of long-term stressors have yet to be studied.

Stress and Ulcers

What does this research mean to you?  Well, the results we glean from research like this offer powerful implications for human medicine and today’s society.  Many people not only experience acute stress, but chronic stress as well.   Short term affects of acute stress include accelerated of heartbeat and an increase in metabolism, but it is only natural to ponder the long term effects of chronic stress.    We can extrapolate from the results of  acute stress that it would make sense that we, as humans, would not want these effects to be long lasting.  Major problems would arise with the decrease of gastro movement.  Problems manifest from a build up of bile and stomach acids in the stomach.  Since gut motility is decreased when stressed, less movement would mean that more bile, which is highly acidic, would sit in the stomach longer and could lead to stomach or intestinal ulcers.

Sympathetic Nervous System

Chronic stress can also lead to a decrease in the immune system of the organism as well as a decrease in the second messenger systems within the body.  An example of this effect on a second messenger system is the attachment of CRH to CRH-receptors in the solar plexus.  The binding of these receptors causes the effect of the decrease in gastro movement.

How much stress is too much stress?

Lastly, with chronic stress and chronic stimulation of the CRH/CRF system, we might see a scenario in that the more that these receptors are activated, the more desensatized they can become. This could cause problems for people and their response to stress.  If the are “desensitized” this may mean that these people have a problem when trying to   properly responding to an acute stressors when needed.

Frogger, More Than just a Game December 12, 2010

Posted by zach in Biology, Chemistry, Ecology, Environment/Conservation, Health.
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As a child you learned that a frog isn’t born as a litGraphic depicting life stages of a tadpole to a frogtle frog, but rather its life begins as an egg and develops into a frog through metamorphosis. This poses a lot of interesting questions for molecular biology because appendages have to grow at the same time the tadpoles tail is lost. The frog is an ideal model organism for how morphological changes can take place, since frogs are so easily kept in captivity it’s easy to manipulate their environment. When you are able to change their environment it makes it easier to identify what hormones, enzymes, or other environmental cues influence how the tadpole develops into a frog.

One hormone that has been shown to affect the metamorphosis of tadpoles is thyroid hormone (TH). In the presence of dilute concentrations of thyroid hormone the frog’s metamorphosis is accelerated.   The converse is also true, when TH is blocked by compounds such as goitrogens, tadpoles will not develop into frogs but, stay in the tadpole life stage.  We know that TH acts through nuclear receptors to activate transcription or, the process of DNA going to mRNA then translated into proteins.  With many advances taking place in the field of biochemistry my question is how is the structure of the chromatin affected through metamorphosis?  What chemical present in local ponds affect the structure of the chromatin?  There are many different mechanisms in which the structure of the chromatin can be altered.

 

Two of the most common ways the structure of the chromatin is altered is by methylation, which is adding a methyl group to a cytosine nucleotide, or acetylation, which is the process of adding an acetyl group on to the lysine residue on histones. Both methylation and acetylation can function to change gene expression. Methylation causes a steric hindrance for the transcriptional machinery and acetylation alters how much the gene is exposed to transcriptional machinery.  Both methylation and acetylation takes place through enzymes that cause a change in how the transcriptional machinery operates.  The enzymes can be influenced by a variety of different means, for example acetylation of histone H4 lysine acetylation can be blocked by Nickel compounds.

The question that I want t0 ask is what effects are on the epigenome, when frogs are exposed to pollutants at different life stages? When tadpoles are exposed to high levels of Ni2+ compounds they all die. Is the death of the tadpoles a result of an absence of H4 lysine acetylation or through a different molecular mechanism?  Since epigenetic mechanisms are critical to regulating gene expression it is plausible that the epigenome is tightly correlated with tadpole metamorphosis. Since the habitats of amphibians are becoming more and more polluted, it is urgent to discover the mechanisms in which their metamorphosis acts though in order to reduce a certain group of pollutants.

Dang My Appetite! December 8, 2010

Posted by wframe488 in Behavior, Biology, Health, Medicine, Nutrition, Physiology.
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The Biggest Loser

It wasn’t until recently America realized just how overweight people were getting in our country. I believe we are one of the most overweight countries of the world if I am not mistaken. It seems like new diet plans, weight-loss pills, and surgeries are developed everyday to help obese Americans shed those pounds. Weight-loss has definitely been growing its popularity, for example new reality television shows like The Biggest Loser , Weighing In, and Celebrity Fit Club, to name a few, have gotten people interested in getting up off the couch and exercising.

The fast food industry and video games can be partially blamed for helping Americans achieve the great honor of being one of the “biggest” countries in the world, but let’s not forget about our genetics. There are several hormones in our endocrine system that plays a role in weight regulation and weight-related behaviors like hunger and satiation. Two of the most popular and most talked about weight regulating hormones would have to be ghrelin and leptin.  We all typically produce these hormones, but in different amounts depending on the person. Ghrelin is a preprohormone that is normally produced in the stomach. It is a known appetite inducer and has also been known to slow down metabolism and decrease the body’s ability to burn fat. It stimulates the hypothalamus to release growth hormone via a GSH receptor. Leptin, on the other hand, is known to aid in appetite inhibition. It is expressed predominantly by adipocytes and contains highly expressed receptors in the hypothalamus region of the brain. It stimulates the hypothalamus via an Ob receptor to decrease appetite and body weight.

Ghrelin and Leptin Action Summary

One research article that I found about this particular topic, by J.P.H. Wilding, was titled “Food Fails to Suppress Ghrelin Levels in Obese Humans”. This research paper investigated the effects of a test meal on the plasma levels of both ghrelin and leptin. They sampled 13 lean and 10 obese subjects and found that the lean subjects exhibited a decrease in both ghrelin and leptin levels after a meal whereas the obese did not show any signs of decrease in concentration of these two hormones. The paper goes on to explain that the role of the decline in leptin of the lean subjects is unknown, but the lack of suppression following a meal of the obese subjects could lead to increased food consumption. This suggests that ghrelin is involved in the pathophysiology of obesity. This appetite inducing hormone is secreted by our bodies with out our control unfortunately and for those that secrete more will mostly likely tend to be bigger human beings just based off of overall caloric intake.

Food Groups

In regards to dieting, one major problem that almost all people possess after they diet is the regain of weight. This mainly is due to the idea that even though your weight is now maintained at a healthy level your appetite still remains the same as it once was, thanks to these two hormones mentioned previously. One interesting article that I read from the Journal of Clinical Endocrinology and Metabolism, was titled, “Appetite Hormones May Predict Weight Regain After Dieting”, which was by Ana B. Crujeiras. Her colleagues and her evaluated a group of 104 overweight men and women during an 8-week low-calorie diet and again 32 weeks after treatment. The scientists measured body weight and plasma ghrelin and leptin levels before, during, and after dieting. What is interesting about this article is that the researchers found that subjects with higher plasma leptin and lower ghrelin levels before dieting were the subjects that were more prone to regaining weight after they shed those pounds through dieting. Personally, I thought that the higher the ghrelin levels prior to dieting would cause the subject to be more prone to weight regain, but that’s not the case here, but that’s science. The article goes on to explain that this can be useful information and that these hormone levels can be proposed as biomarkers for predicting obesity-treatment outcomes.

In conclusion we know that virtually everyone produces ghrelin and leptin in there bodies and that these two hormones play a big role in regulating our appetite. Some of us are lucky enough to sustain the proper balance of these hormones, based solely on our genetics, for body weight maintenance. Although, others aren’t so lucky to possess such a talent. Just because someone is lean and skinny doesn’t mean that they are necessarily healthy, and just because someone totes around more body weight than others doesn’t mean that that person is necessarily unhealthy. In closing, all I have to say is that eating right and exercising is a big part of being healthy and maintaining weight despite what these pesky hormones are doing to our appetite. So, to everyone, eat healthy and exercise!

Don’t Get Tipsy Over Your Hormones October 21, 2010

Posted by jfalender232 in Behavior, Biology, Health, Physiology.
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Okay here’s the scoop, instead of boring you with the likely event that my fellow classmates might have bestowed upon you with their own blog posts, luckily for you, I pledge to make this the most exciting blog post that you will have the opportunity to read (that means you SHOULD click on the words that are highlighted in blue and underlined–you can thank me later for all the joy these links will give you). So enough with the chit-chat for now, let’s get ready to rumbbleeeee!

College is all about experiencing many new things such as moving away from your annoying parent(s), skipping class because it might be raining outside, meeting a myriad of new people, learning the art of mooching off your friends, and finally being exposed to your new best friend but your worst enemy. No I am not talking about Dean Wormer, hopefully you will never have to meet the dean. I am talking about alcohol, booze, liquor. It could make you the most popular person at night but then keep you strapped down to the bed with the worst hangover imaginable (unless you have to deal with Mike Tyson).  Please allow me to whet your educational appetite with this nugget of information:  “Alcohol dilates the blood vessels, or capillaries, that carry blood just below the surface of the skin. When they expand, the flow of blood to the skin is increased. The skin flushes, causing a warm feeling.” Alright so now that we are all warm and fuzzy inside lets jump in and explore this topic some more.

Alcohol and has many effects on the human body but one of the most important areas of research is the relationship between alcohol and hormones. WedMD defines hormones as “a chemical substance, formed in one organ or part of the body and carried in the blood to another organ or part where they exert functional effects; depending on the specificity of their effects, hormones can alter the functional activity, and sometimes the structure, of just one organ or tissue or various numbers of them.” Furthermore, alcohol has 4 primary areas that can effect: the regulation of blood sugar levels, reproductive functions, calcium metabolism, and bone structure.

Contrary to Def Leppards wish, I don’t want you to pour some sugar on me, so by realizing that your alcohol drinking can affect all three of your glucose sources and the functions of regulatory hormones will go a long way towards having a healthy relationship with your body. “Even in well-nourished people, alcohol can disturb blood sugar levels. Acute alcohol consumption, especially in combination with sugar, augments insulin secretion and causes temporary hypoglycemia. In addition, studies in healthy subjects and insulin-dependent diabetics have shown that acute alcohol consumption can impair the hormonal response to hypoglycemia (*More Info*)”. Maintaining normal blood sugar levels are crucial to the homeostasis of your body.

I would like to take a time-out here and impart some of facts of college life as told by yours truly (WARNING: please take all these facts with a grain of salt): You will spend more time thinking about sex than anything you might learn in a class. That being said, alcohol can have some potentially serious side effects on the reproductive system of both males and females. “In men, reproductive hormones are responsible for sexual maturation, sperm development and thus fertility, and various aspects of male sexual behavior. In women, hormones promote the development of secondary sexual characteristics, such as breast development and distribution of body hair; regulate the menstrual cycle; and are necessary to maintain pregnancy. Chronic heavy drinking can interfere with all these functions. Its most severe consequences in both men and women include inadequate functioning of the testes and ovaries, resulting in hormonal deficiencies, sexual dysfunction, and infertility (*More Info*)”. This is important to keep in mind because for males, extended low levels of testosterone can lead to the developing of feminization of males characteristics such as “breast enlargement”. Women need to be aware of alcohol effects because prolonged drinking can lead to “cessation of menstruation, irregular menstrual cycles, and menstrual cycles without ovulation, early menopause, and increased risk of spontaneous abortions (*More Info*)”. This leads to a creed that all should take to heart: ‘You can always dump your boyfriend or girlfriend, but never ever dump your hormones.’

The final two areas that we are covering in-depth, calcium metabolism and bone structure are closely correlated to one another. Calcium is the main building block of bones and is essential to the cell to cell communication. Speaking of communication relationships, ‘America’s favorite life-guru’ Dr. Phil can answer any communication issues you might have here.

 

I want YOU to meet me at the bar tonight!

The role of alcohol in calcium and bone metabolism can lead to several complications. “Acute alcohol consumption can lead to a transient parathyroid hormone (PTH) deficiency and increased urinary calcium excretion, resulting in loss of calcium from the body (*More Info*). Chronic heavy drinking can disturb vitamin D metabolism, resulting in inadequate absorption of dietary calcium (*More Info*)”.  These decreased calcium levels can potentially lead to bone diseases, most notably, osteoporosis. MedicineNet describes osteoporosis as, “a condition characterized by a decrease in the density of bone, decreasing its strength and resulting in fragile bones. Osteoporosis literally leads to abnormally porous bone that is compressible, like a sponge. This disorder of the skeleton weakens the bone and results in frequent fractures in the bones”. So yes it is possible that if you are not careful, excessive alcohol consumption could lead you to looking like this dashing fellow below.

 

Your other new drinking buddy likes to show off his awesome 'Bitter Beer Face'!!

So the next time you and your friends start to pour shots, shotgun beers, or do keg stands to the greatest 80s song of all time Here I Go Again, just remember that your hormones are relying on you as their designated driver for the night.

Cheers!

Please check out my friend, Wes’ blog, who examines more about alcoholism and its effects on the endocrine. It’s a great read!

The Science of Satiation October 16, 2010

Posted by Kyle in Behavior, Biology, Chemistry, Health, Nutrition, Uncategorized.
3 comments

Slow down or you’ll get a stomach ache!

My parents always told me that if I eat my food really fast, I may feel sick later. I am sure most people have experienced this at least once in their life. It seems that the reason for this is…that the faster you eat, the faster your stomach fills up. Your stomach ends up being full, or over-filled, before your body realizes it. By the time you do feel full, it is too late to stop eating and your stomach may feel like it’s going to explode.

It’s bad enough that your favorite meal can cause you pain after you devour it, but that’s not all it will do. Common sense should tell you that eating too much of something can potentially lead to being overweight. So if you’re eating too fast you can end up doing just that, gaining a lot of weight. An article from the British Medical Journal points out that eating too fast triples the risk of being overweight. Makes perfect sense…more food in equals more pounds put on.  But  the next question remains: what are the mechanisms behind all of this?

The science of satiation

An article out of The Endocrine Society’s Journal of Clinical Endocrinology & Metabolism (JCEM) points out that gut hormones my play a part in why people who eat fast end up overeating. As Alexander Kokkinos, MD, PhD, of Laiko General Hospital in Athens, Greece points out, gut hormones that signal the brain to stop eating may be impacted by the rate of eating.  The hormones that Kokkinos article examined were peptide YY (PYY) and glucagon-like peptide (GLP-1) which work to signal to us that we are full after a meal. For the study, the researchers took blood samples from participants after they had all eaten the same meal, however, the amount of time each participant took to eat the meal varied.  Their results showed that the participants who took longer periods of time to eat the meal had higher levels of the gut hormones and felt more full than those who ate their meals faster. So what does this all mean?

Fast food

Your body tries its best to tell you stop eating, but if you don’t get the signal in time it doesn’t matter.  As many Americans go about their day, they consume a massive amount of calories for very little cost. Going through the drive through doesn’t burn nearly as many calories as chasing down a woolly mammoth. Our early ancestors couldn’t go through the drive through for dinner, they had to work for their meal. Not only that, they probably didn’t eat nearly as much as we do today.  Consuming a ton of calories and burning very few  makes someone more likely to be overweight, but if you add in the fact that some people are consuming their meals in only a few minutes and eating large portions, these people are at a much higher risk of gaining weight. So next time you sit down for a meal, try and eat slowly. This will give your gut time to tell your brain that it’s time to quit eating.  Your gut will be happy, and you may just lose a few pounds in the long run.

Decreasing Ageing affect on Memory October 15, 2010

Posted by zach in Health, Medicine, Neuroscience, Physiology.
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Have you recently misplaced your car keys and spent hours trying to find them? A resent article from Science Daily explains how misplacing your keys may be a thing of the past.  A promising new drug candidate is currently being developed at the  University of Edinburgh to reverse age-related memory loss.  The researchers have developed a compound that has improved cognitive function and memory in aging mice. This compound works by blocking an enzyme known as 11beta-HSD1.  As we age our body changes, with these changes comes changes in the concentration of the enzymes in our body.  The cause of these enzymatic changes is not fully known but it can be linked to physiological effects such as stress.

The aging enzyme

11beta-HSD1 is an enzyme that is found in the brain which can produce stress hormones such as the glucocorticoids.  When there are high levels of glucocorticoids in the brain negatively affect memory.  Therefore, if we can find a way to block 11beta-HSD1 we could increase our memory by decreasing the negative pressure on memory. The problem with blocking 11beta-HSD1 is that until now it hasn’t been possible to find a molecule that has a high specificity for blocking only 11beta-HSD1.  After ingesting a synthetic compound that blocks 11beta-HSD1,  mice show a dramatic increase in memory after only ten days.  The increase in memory was quantified by the time it took mice to complete a Y maze.

A burgeoning field of research

The research in the biomedical world is very concentrated on developing medicines that will reduce or even try to eliminate the effects of aging.  In the past I have blogged about how targets of rapamycin act as a master regulator for protein synthesis.  If we could find a drug to regulate that regulated TOR we could in turn regulate aspects of how our body ages.  Maybe some day we will have a set of anti-aging drugs that will allow us to combat all the negative effects that come with growing old.  If researchers can keep developing synthetic compounds to stop memory loss there may be a day when you will never forget where you misplaced your keys.

Using Fish to Detect Estrogen-like Endocrine Disruptors October 15, 2010

Posted by Grace Dible in Biology, Chemistry, Ecology, Environment/Conservation, Genetics, Health, Medicine, Physiology.
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Endocrine disruptors, according to the EPA, are substances which mimic a hormone, stimulate a body to over respond to a stimulus, cause hormones to respond at inappropriate times, or cause an under/over production of a hormone.  The EPA is most concerned with endocrine disrupting chemicals that end up in the environment and affect the environment and wildlife.  Chemicals of more recent concern are synthetic, natural, and mimic estrogens.  These chemicals include 17α-estradiol (found in birth controls) and herbicides like atrazine.  Much of the recent research is trying to determine whether or not these endocrine disruptors are causing intersex fish, which could possibly lead to population declines.

This flow chart shows how endocrine disruptors may lead to sex changes in a fish population.

One way to determine the estrogenic endocrine disruptors in an aquatic environment is to use different transgenic fish as biomarkers, specifically zebrafish (Danio rerio) and medaka (Oryzia latipes).  Current research is underway in order to determine the affects of these different endocrine chemicals on bioactivity.  Both Medaka and Zebrafish can be transgenic with different fluorescent proteins, which were originally found in bioluminescent jelly fish.    At Marian University in Indianapolis, I am currently trying to determine the best methods for determining the affects of estrogen-like endocrine disruptors in transgenic medaka with green fluorescent protein (GFP).  This GFP is expressed in the liver of the fish when a large amount of vitellogenin, an estrogen inducible promoter, is in its system.  Ordinarily, vitellogenin is found in the female medaka liver, but if an endocrine disruptor is in the environment, then a male medaka may be able to express the GFP as well; the GFP is these medaka have a 100% binding affinity to 17α-estradiol.

Medaka fish expressing GFP in the liver

According to recent review on the effects of a supposed endocrine disruptor like atrazine (A Qualitative Meta-Analysis Reveals Consistent Effects of Atrazine on Freshwater Fish and Amphibians – Jason R Rohr and Krista A McCoy – January 2010  Environmental Health Perspectives), they “found little evidence that atrazine consistently caused direct mortality of fish or amphibians, but we found evidence that it can have an indirect and sublethal effects.”  These sublethal effects in fish may include a decrease in motor skills, perceiving predator risk, olfactory sensitivity, and gonadal morphology.  Atrazine may also lead to the body’s production of aromatase, an enzyme that converts testosterone into estrogen.   Studies still need to be done to see if this supposed endocrine disruptor is causing the fish population sex ratios to change or the production of aromatase.

How could this research be beneficial to human health?  Waste water treatment plants currently don’t filter out estrogen-like endocrine disruptors. Right now Dr. Paul Winchester, at the Indiana University School of medicine, is trying to determine whether there is a correlation between the supposed endocrine disruptor atrazine and birth defects.  Another focus of the research is whether or not areas with high amounts of atrazine can lead to higher rates of breast, ovarian, and prostate cancer.   Dr. Paul Winchester recently did an interview with Indianapolis based NUVO magazine to help spread information on this endocrine disruptor so that people are more aware of what is in drinking water.

To see his Dr. Winchester’s full interview click here.  To view the EPA statements on endocrine disruptors click here.