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Viruses: Friend or Foe?
What is invisible to the naked eye, can affect the Earth’s climate, has a tiny shell, and can causes cancer? Viruses are considered non-living, but play a major role in our bodies and environment. In fact, viruses kill half of the bacteria in the ocean every day. To get an idea of how much bacteria that is, a teaspoon of water contains approximately a billion bacteria. Recent estimates show there are 1031 viruses on this earth. That reads, 10 billion trillion, trillion. Although viruses are smaller than what the unaided eye is capable of viewing, if all viruses were stacked end to end, they would be lined up for about 100 million light years.
Viruses are constantly on the attack from the outside of our body desperately trying to get in, but 4 trillion viruses also reside inside our body. While some viruses are trying to find a host cell and cause harm, many viruses are necessary for a healthy life. Some of the viruses inside of us can protect us from detrimental bacteria, but can also help balance the population of bacteria vital to our health. A similar phenomenon occurs in the ocean. Without viruses consuming half of the bacteria day in and day out, the levels of bacteria in the ecosystem could hamper the living of certain species. Also, bacteria contain carbon and lots of nutrients. With the viruses consuming the bacteria, there is a constant recycling throughout the ocean. There is a hypothesis that because of all the carbon that’s coming out, it could be affecting the Earth’s climate. Any of the carbon that is sent back to the atmosphere is going to trap heat (greenhouse effect). It may be an extreme thought, but these tiny, non-living viruses are partially responsible for the weather.
Bacteriophages: the lifeless killers
Viruses that attack and dispose of bacteria are known as bacteriophages. Felix d’Herelle discovered the extraordinary conclusion that viruses can kill bacteria through treating a dish of bacteria with fluid from patients with dysentery! He actually began a business selling viruses that could cure bacterial infections. Hypothetically, there are viruses that exist in nature that can kill the most severe bacterial infections, but it’s a matter of discovering the right viruses. Each species of bacteria has a series of bacteriophages that can eliminate it.
Antibiotics and Viruses: An evolutionary arms race
Before antibiotics were discovered in the 1930s, a method called phage therapywas used to combat infections. However, once these antibiotic “magic pills” were discovered, phage therapy stood in the distance. The chemicals were reliable and scientists knew how to make them. However, with the current widening spread of antibiotic resistance caused by bacteria developing resistance to modern medicine’s most well-used antibiotics, it’s beginning to look like phage therapy wouldn’t be a terrible idea. One main argument phage therapy new found interest: antibiotics can’t evolve, while viruses can. Scientists have reached the point where viruses can be engineered and genes can be strategically placed to enhance their effectiveness. This genetic and evolutionary tinkering could allow scientists to develop viruses to strategically kill various bacteria that might be antibiotic resistant.
Viruses: Directors of Their Own Fate?
In the wake of the recent deadly avian flu virus, critics have questioned whether the spreading from mammal to mammal could have occurred on its own. A study completed at MSU by Justin Meyer was started with the thought that it would be a wild goose chase. Meyer wondered if lambda phages could evolve another way a new way to enter its host.
lambda was used to infect the gut bacterium E. coli. It is harmless to humans. The most common means for lambda to get into a cell is by attaching to its outer membrane. The genes and proteins contained by the lambda are then injected into the microbe. Meyer used E. coli that didn’t make the molecules necessary for the virus to grab onto. This meant that the only viruses that would survive were ones that mutated to use a different surface molecule. Shockingly, within 15 days, Meyer’s experiment showed that viruses were using a new channel in E. coli known as OmpF.
Meyer re-conducted the experiment with 96 lines of the virus and E. coli. Of those 96, 24 of the lines began to use OmpF as the pathway into the host. Because of the repeating phenomenon, the genomes of the evolved viruses were sequenced, finding that four mutations were required for the viruses to thrive. All four were required, not a single one, or even three out of the four. Meyer estimated the chance of all four mutations arising at once was nearly impossible: one in a thousand, trillion, trillion. However, the lambda viruses evolved to contain all four mutations in a couple weeks on a regular basis.
As incredible as this experiment is, it is somewhat frightening. Meyer showed how easily viruses can evolve completely new traits, which can lead to new diseases. This is exactly the reason why when treating a sickness with antibiotics, the patient MUST finish taking the dosage until it is gone, otherwise the virus can come back even stronger.
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Something in the Water
When we go to the sink to get a glass of water from the sink, we trust that what the water is comprised of is safe for us to drink. Most of us don’t give a thought as to what could be in it. This is one of the luxuries of living in a first world country. However, those in third world countries, such as Haiti, are not so fortunate. Shortly after the earthquake in Haiti in 2010, a cholera outbreak occurred. When an outbreak like this occurs, the goal is to not only check the spread of the disease among Haitians, but to prevent the bacteria from swapping DNA with other cholera strains in the country to form a more dangerous bug much harder to treat.
Antibiotic-resistant Cholera: Mechanisms explored
Bacteria reproduce asexually by a process called binary fission. Binary fission causes two genetically identical bacterial cells to be produced. If this was the only method bacteria had to procreate, treating a disease with antibiotics would be simple. Antibiotics aim to either kill bacteria directly or hamper their ability to grow and reproduce. This can be done by crippling the production of the bacterial cell wall and inhibiting protein, DNA, or RNA synthesis.
However, when we put our bodies on the attack with the use of antibiotics, bacteria respond by playing their side with different defensive mechanisms. Some of these mechanisms include changing the permeability of their membranes. For example, bacteria can decrease the number of channels available for the antibiotics to enter the cell. Another mechanism works by changing the actual physical structure of the antibiotic once it enters the cell so that the drugs can’t bind the way they were designed to in order to have an effect. Although both of these mechanisms prevent antibiotics from carrying out their job, bacterial recombination is the most common form of developing antibacterial resistance. When this happens, bacteria gain genetic variation by swapping DNA with other bacteria. This allows the bacteria to acquire resistance to the drug. A plasmid, which is a circular piece of DNA, can encode resistance to multiple antibiotics. Thus if one bacterial cell in the environment has evolved resistance to an antibiotic, it can easily share that information with other surrounding bacteria leading to an epidemic of widespread antibacterial resistance. A transposon, known as a “jumping gene”, can jump ship from DNA to DNA molecule. The transposon then becomes part of the plasmid.
Where did it come from?
Cholera, which had never been seen before in Haiti prior to the earthquake, had the advantage. Nations offering their help focused on the earthquake recovery while cholera entered Haiti under the radar. Reducing the fatality rate from cholera has been a success; however the response was slow to fully develop. The most likely story is that cholera spawned from a Nepalese volunteer at the Minustah base. Understandably, no one wanted to take responsibility for bringing an epidemic to a country that already needed all the help they can get.
To resolve the “blame-game”, Danish and American scientists collaborated to determine where the cholera came from. Haiti’s cholera strain and Nepal’s cholera strain of the bacteria were examined using the most comprehensive type of analysis: whole-genome sequence typing. Virtually identical, the Nepalese were forced to accept blame. Another method, pulse-field gel electrophoresis was also used as evidence. Scientists found that cholera erupted in Nepal in July 2010, but was under control the following month in August. Unfortunately, this was the same month that Nepalese soldiers left for a recovery mission in Haiti.
Through the application of genetics, the cholera strain has been identified. Unfortunately, this doesn’t solve Haiti’s problems. Only 12% of the population has access to piped, treated water. The rest find their water in rivers and wells. These are the same rivers that contain feces and that Haitians wash their clothes in. Vaccinations and supportive care will aid in the conquering of cholera, but until safe water is more readily accessible, the country needs to be prepared for round two.
Cramming: A Student’s Best Friend? March 4, 2011Posted by ljsteele in Behavior, Biology, Chemistry, Health, Medicine, Science & Culture, Uncategorized.
The night flies by…
As a senior undergraduate student, slowly over the past four years I have realized the importance of cramming before a test. Simply put, by this stage in my academic career, it has become routine to stay up all night before a test to study. In classes where there are multiple choice tests, it appears to be easier to stay up all night cramming, as is the belief that if you at least can recognize the question, ruling out the different choices for the answer becomes quite simple. It has been shown that over a third of students cram the night before a test.
However, although many students utilize the practice of cramming, whether or not it helps students is up for debate. There are different levels of cramming, and each appear to cause different results when it comes to grades and GPA. The issue that is starting to be seen is that although cramming may help in terms of short term memory, the retention of that information weeks after the course ends seems to be up in the air. Of course, when cramming is being utilized, it only makes sense that the information storage would be contained in the frontal lobe of the brain, while long term memory, which would be associated with studying that has taken place over numerous days or weeks, would be stored over multiple parts of the brain.
Many different universities have brought to light the health implications that one may bring upon him or herself when cramming. But, it is also shown that certain periods of acute stress are positive for the human body, which cramming would appear to fall under the category of acute stress. During acute stress, the body increases its fight or flight response (epinephrine and norepinephrine), shuts down digestion, reproductive systems, and boosts metabolism. Vasoconstriction and vasodilation also take place, therefore pumping blood into certain areas of the body and brain that during a normal day’s activities may not get stimulated very often. Especially during the fight or flight response, one becomes more attentive, which would seem to help with say, studying for a huge test.
Are there more effects than just retaining information?
Although cramming may not be ideal for certain people, research needs to continue in terms of stress and cramming, and even learning styles. Certain people are exposed to more stress than others, so possibly stress levels are compromised, leading to a decreased ability to study and cram the night before a test. Students continue to cram because results are obtained on tests and finals. Quite possibly cramming could do more than just get a student a good grade on a test-it could also help to train the body for different stress activities that otherwise may not be achieved.
Healing a “Broken” Heart March 4, 2011Posted by Kyle in Biology, Chemistry, Health, Medicine, Physiology.
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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, 2011Posted by tsublett in Chemistry, Health, Medicine, Physiology, Policy.
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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.
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, 2010Posted by Kyle in Biology, Chemistry, Health, Medicine, Neuroscience, Nutrition, Physiology.
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.
Dang My Appetite! December 8, 2010Posted by wframe488 in Behavior, Biology, Health, Medicine, Nutrition, Physiology.
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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.
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.
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!
Decreasing Ageing affect on Memory October 15, 2010Posted 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, 2010Posted by Grace Dible in Biology, Chemistry, Ecology, Environment/Conservation, Genetics, Health, Medicine, Physiology.
Tags: Biology, Biomonitoring, Endocrine Disruptor, Medaka Fish, Zebrafish
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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.
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.
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.
Beta-Blockers: Function and Effects October 15, 2010Posted by cassie in Health, Medicine, Physiology.
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Catecholamines such as epinephrine and norepinephrine are key players within the endocrine system that are stimulated in response to the “fight or flight” reaction. When stimulated, these hormones are rapidly released to bring about many physiological changes within the body. Physiologically, epinephrine and norepinephrine bind to adrenergic receptors found in various tissue target sites within the body- specifically in this case, the myocardial tissue of the heart causing a cascade of events. The cascade of events include vasoconstriction of the blood vessels due to increased cardiac output causing strain on the heart and vasculature. However, keep in mind that these effects can vary among target tissues due to the different adrenergic receptors located within each tissue area.
Beta blockers…a wonder-drug?
With the increased incidence of abnormal heart rhythms, hypertension, and heart attacks; a catergory of drugs known as beta-blockers have emerged within the pharmaceutical industry to act as preventative and relief measures for these diagnosed health issues. This specific class of drugs work to block the binding sites for epinephrine and norepinephrine on the adrenergic receptors (β1 and β2) found primarily on myocardial tissue- although they have other uses. By blocking the binding sites of these catecholamines, the overall effect is leads to reduced heart rate, along with increased vasodilation of blood vessels resulting in a lowering of blood pressure (see link for more information).
After learning about the stress response on a hormonal level, I became curious regarding efficiency of beta-blockers and how they bring about change in one type of target tissue versus another. Do these drugs have higher affinity for receptors in a specific target tissue? Or is their functionality strictly in terms of concentration? Are there any side-effects one should be aware of that could indicate harmful effects elsewhere in the body after usage?
A recent study in Circulation Research, addresses the specificity of beta-blockers and their varied results. According to the study, beta-blockers should be approached with caution and considered heavily before deciding upon treatment. After analysis of heart therapy combinations, researchers discovered that each beta-blocker has completely different outcomes based on which type of recepor is its target. With the alpha- and beta- receptors as targets, there seems to be an overall benefit to the patient. In contrast, those that target solely the beta- receptors seem to be detrimental in the long run because the heart becomes accustomed to being a more efficient pump but wears out in a shorter amount of time. Other data are congruent with the prior findings, stating that beta-blockers can be selective or non-selective. Non-selective beta-blockers affect all of the systems that epinephrine and norepinephrine interact with normally including the heart, lungs, and blood vessels. Selective on the other hand, involves a very specific target tissue only allowing for a narrow range of effects. Beta-blockers also have side-effects involving the nervous, digestive, and muscular system.
In conclusion, beta-blockers are beneficial and yet sometimes harmful depending on the specificity, severity of the symptoms, and other therapy combinations involved. Beta-blockers have made huge strides for the medical/pharmaceutical field, but ongoing research is necessary to evaluate the entirety of interactions within the body to ensure proper use and full understanding for the future of biomedical research.