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How To Treat Heat Rashes

Life Style

Sep 22, 2015

4983

Heat Rash

Heat rashes take place when people are outside under the sun for too long, causing them to sweat profusely. Heat rashes are common in hot regions and often cause symptoms such as tiny red blisters, itchiness and skin discomfort.

There are numerous treatment options available to ease the irritation and get rid of heat rashes:

Applying calamine lotion on the affected area can effectively relieve severe itching and burning.

Aloe vera gel is another cooling agent and a natural remedy to soothe heat rashes and their symptoms.

�It is best to avoid rubbing or scratching the rash affected area as much as possible. A physician may prescribe anhydrous lanolin in more severe cases. Anhydrous lanolin prevents the sweat ducts from blocking. Steroids may be prescribed if rashes are too severe.

People who develop heat rashes also experience severe heat exhaustion. Symptoms of heat exhaustion may include dizzy vision, weakness, low blood pressure, heart palpitations, nausea and headache. People who suffer from heat exhaustion are advised to seek medical attention immediately because it can lead to a heatstroke — a potentially life-threatening problem.

For babies, a lukewarm or cool bath is advisable, after which, the affected areas are air-dried as towel-drying may cause irritation. Avoid sharing towels with a contaminated person.

Keep the affected area moisture-free and avoid using any lotions or creams to prevent irritation.

Wear loose-fitting, airy clothing made of cotton to prevent the trapping of heat inside the clothing.

Make sure your babies have trimmed fingernails. To prevent itching, it may be helpful if your children wear mittens.

Stay in air-conditioned rooms until heat rashes subside. Monitoring the rash closely for any signs of infection is necessary and if signs of infection occur, a physician should be contacted immediately.

Natural Heat Rash Treatments

Heat rashes can be avoided by staying inside, but that is not always possible for all individuals considering the kind of work they do. If you must have to head outside into the heat, you will want to be prepared to prevent and treat your heat rash in case you counter one. You can treat your heat rashes even if you don’t have calamine lotion or aloe vera gel.

There are some natural ways to treat and cure heat rashes effectively without heading to the local pharmacy in the sweltering heat.

Surprisingly, something as simple and natural as taking a cool water bath can help soothe and cool your skin. However, since bathing all day is not practical, you’ll need to know what to get beyond a bucket. First, dressing in loose-fitting, lightweight, light-colored, cotton clothing is a must. It will not rub against and aggravate your skin. Until the heat rash clears, hot and humid weather should be avoided.

Staying in shaded places or air-conditioned buildings is an option and should be availed whenever at hand.� When you take a cold bath, air-drying your skin or patting it dry instead of rubbing it dry with a towel is a better way to stay away from and prevent further rashes.

The bumps and blisters developed from heat rash can cause discomfort. Applying ice on the area is one way you can relieve the burns either directly or wrapped in a soft cloth.

Increase your bath’s effectiveness by adding some oatmeal with a few teaspoons of baking soda in your tub to curb the itching sensation.

Dusting the affected area with baby powder or cornstarch might also work (a mild, unscented powder is best).

References

https://nomoredryscalp.com/

https://ajs.sagepub.com/content/35/8/1384.short

https://www.webmd.com/skin-problems-and-treatments/tc/heat-rash-topic-overview

Know your enemy: Combating whooping cough requires informed vaccine booster schedules

Aug 1, 2015

2561

In order to win any battle, it is important that you know your enemy. When it comes to fighting off diseases like the dreaded whooping cough, the big obstacle which the researchers realize today is an incomplete understanding of its underlying causes. This was stated by a University of Michigan population ecologist. The root causes of the resurgence of whooping cough remains a mystery which needs to be unraveled. However, public health officials in many countries�including the United States�have now introduced whooping cough booster shots into childhood immunization schedules.

In a paper published recently in the Proceedings of the National Academy of Sciences, Pejman Rohan, co-author of the study state that if the newly introduced booster schedules are based on a wrong diagnosis of the problem, the shots are likely to be “epidemiologically ineffective and economically costly. The first author the study is Maria Riolo. She is a former U-M doctoral student and presently is a postdoctoral researcher at the University of Chicago.

Rohani is a professor of ecology and evolutionary biology, a professor of complex systems, and a professor of epidemiology. He strongly thinks that childhood vaccinations are very important. In the U.S a series of five shots for whooping cough, also known as pertussis, for children under 7 is recommended by the Centers for Disease Control and Prevention. For older children and some adults, additional shots are recommended.

For their research, Riolo and Rohani made use of a mathematical model that identifies pertussis booster schedules which could result in the greatest reduction in disease for the lowest economic cost. Several potential causes of the pertussis resurgence were explored separately, even though they know that in the real world more than one of the mechanisms are likely to be at play simultaneously.

The mathematical model they used is based on a “genetic algorithm” that mimics how evolution by natural selection would operate on a population of diverse booster schedules. It was found that depending on the resurgence mechanisms, even the most effective booster schedules varied. Four possible mechanisms were explored which included: insufficient vaccine coverage, low vaccine efficacy, waning immunity and a leaky vaccine.

Insufficient vaccine coverage is when even a large-scale vaccination campaigns is unable to reach enough children. Low efficacy is the one that sometimes fails to provide adequate protection. In waning vaccine immunity, the vaccine is initially protective but the protection wanes over a period of time. For this particular vaccine scenario in their study, they studied booster strategies in cases where a pertussis vaccine protects for an average of 5, 15, 25, 35 or 45 years.

In case of a “leaky” vaccine the risk that a previously vaccinated person becomes infected is reduced but is not eliminated entirely. There is a possibility of this happening when all the microbial strains circulating in the general population are not used in the vaccine. It was found by Riolo and Rohani that simulated pertussis resurgence was primarily due to low coverage or low vaccine efficacy.� They also came to the conclusion that the most effective booster strategy was a single booster shot before children enter kindergarten.

In the case of waning immunity, it was found that the most successful schedules were the ones that administered a series of boosters between the age 5 and 45 to maintain population immunity. �The frequency of the vaccine actually depends on the duration of immunity provided by the vaccine. However, if the cause of the resurgence was leaky immunity, the team’s genetic algorithm found that no booster schedules could reduce the incidence of pertussis. Riolo said that in case a vaccine is to leaky, the pathogen can still continue to circulate in a fully vaccinated population, and that vaccine alone would not be effective in eliminating the pathogens.

There was a time when pertussis seemed under control because of the widespread childhood vaccination. However, since the 1980s, this bacterial illness is making a comeback in the United States and in some developed countries.

References

https://www.sciencedaily.com/releases/2015/01/150119154314.htm

https://medicalxpress.com/news/2015-01-enemy-combating-whooping-requires-vaccine.html

Your pain reliever may also be diminishing your joy

Jul 26, 2015

2447

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Acetaminophen is the main ingredient of some of the commonly used pain relievers used in the United States. A new study regarding it has revealed a previously unknown side effect � it blunts positive emotions. For this study, the emotional response of participants who took acetaminophen when they saw very pleasant and very disturbing photos was compared to those who took placebos. The results of the comparison revealed that those who took acetaminophen exhibited less strong emotions. The study results were published online in the journal Psychological Science.

Even though acetaminophen containing pain reliever Tylenol, has been in use in the United States for more than 70 years, but it is the first time that this side effect has been documented. Earlier research had established that acetaminophen works on physical pain as well as psychological pain. This study takes the findings of that research to a whole new level. Geoffrey Durso, lead author of the study and a doctoral student in social psychology at The Ohio State University said that acetaminophen reduces how much users actually feel positive emotions.

Durso opined that medicines like Tylenol and other such products have broader consequences than previously thought; it doesn't just act like a pain reliever but also as an all-purpose emotion reliever.

Andrew Luttrell, another graduate student in psychology at Ohio State, and Baldwin Way, an assistant professor of psychology at the Ohio State Wexner Medical Center’s Institute for Behavioral Medicine Research along with Durso conducted the study.

As per Consumer Healthcare Products Association (CHPA) reports, about 23 percent of American adults use a medicine containing acetaminophen and most of them are not aware about how this medicine can impact their emotions.

In order to study the effects of acetaminophen, two studies of college students were carried out. The first involved 82 participants, 50% of whom took an acute dose of 1000 milligrams of acetaminophen and other half took an identical-looking placebo. They then waited 60 minutes for the drug to take effect, after which they were showed 40 photographs selected from International Affective Picture System used by researchers around the world to elicit emotional responses. The photographs were varied and ranged from the extremely unpleasant (crying, malnourished children) to the neutral (a cow in a field) to the very pleasant (young children playing with cats).

Participants were asked to rate each and every photo on a scale of -5 (extremely negative) to +5 (extremely positive). They were then asked to view the same photos again and were asked to rate what emotional reaction it evoked on a scale of 0 to 10.

The analysis of the results showed that participants who were taking acetaminophen rated the pics less extremely than those who took the placebo that is positive pictures were not seen as positively and negative pictures were not seen as negatively. The analysis of their emotional response yielded similar results. People who took acetaminophen didn’t feel the same highs or lows as did the people who took placebos. It was also noted that neutral pictures were rated similarly irrespective of whether they look the drug or not.

To find out if intake of acetaminophen changes how people judge magnitude, the researchers carried out a second study in which 85 participants took part. They saw the same photos and were asked to rate them just like before. Additionally, they were also asked to report how much blue they saw in each photo. The evaluation and emotion response to negative and positive pictures were same as before, however, judgments of blue color content were similar irrespective of whether the participants took acetaminophen or not.

The results suggest that acetaminophen affects our emotional evaluations and not our magnitude judgments in general. Whether other pain relievers like ibuprofen and aspirin have the same effect can be a potential research topic.

References:

https://medicalxpress.com/news/2015-04-pain-reliever-diminishing-joy.html

https://news.osu.edu/news/2015/04/13/emotion-reliever/

How Immune Cells Facilitate the Spread of Breast Cancer

Jul 25, 2015

3182

The human body has its own system in place to fight off diseases and infections. Yes, we are talking about our body's immune system which acts like soldiers to protect against invaders and dissenters. It seems now that there are loopholes in our body's immune system which is why some immune cells turns out to be traitors! The findings of a study conducted by Dr. Karin de Visser and her team at the Netherlands Cancer Institute are published in the journal Nature recently. In the study, it was discovered by researchers that certain immune cells are persuaded by breast tumors to facilitate the spread of cancer cells.

Breast cancer is one of those common diseases in women in the Western countries. About one in every eight women is likely to develop breast cancer. Also, it is estimated that of the women who die of this disease, almost 90% die because the cancer has spread to other parts of their body resulting in metastases. One of the focuses of cancer researchers in the recent years has been to understand the process of metastasis. A previous study conducted a couple of years ago had reported that breast cancer patients with a high number of immune cells called neutrophils in their blood are at increased risk of developing metastases. Now, the obvious thing that comes to everyone's mind is – immune cells are supposed to protect our body. So, why high neutrophil levels are said to worsen outcome in women with breast cancer?

Dr. Karin de Visser, group leader at the Netherlands Cancer Institute, and her team found out that certain type of breast cancer tumor have the ability to create a domino effect of reactions within the immune system. Such tumors send out signals that results in the production of a lot of neutrophils by the immune system. Normally, neutrophils are produced as a part of an anti-inflammatory response. However, the neutrophils produced as a result of signals from tumor behave differently. They have the ability to block the actions of other immune cells, called T cells. T cells are the immune cells that can recognize and kill cancer cells.

The research team also discovered the signaling protein crucial to this process � interleukin 17 also known as IL17. De Visser said that in their experiment, they noticed that IL17 is vital for the increased production of neutrophils. She added that they also found that this is also the molecule that changes the behavior of the neutrophils, causing them to become T cell inhibitory.

Postdoctoral researcher Seth Coffelt, who is also the first author of the paper in Nature showed the importance of the IL17-neutrophil pathway by inhibiting this pathway in a mouse model that mimics human breast cancer metastasis. It was seen that the animals in which these neutrophils were inhibited developed much less metastases than animals from the control group, in which the IL17-neutrophil route was not inhibited. De Visser commented that it is to be noted that the blocking of the IL17-neutrophil route prevented the development of metastases, but did not affect the primary tumor. She is of the opinion that this could be a promising strategy to prevent the tumor from spreading.

Neutrophils have an important role to play in the body � they protect is from infections. So, inhibiting neutrophils altogether seem a bad idea as it would make the patient prone to all kinds of infections. So, inhibition of IL17 definitely sounds like a safer strategy. Anti-IL17 drugs are currently being tested in clinical trials as a treatment for inflammatory diseases, and the good news is that last month the first anti-IL17 based therapy for psoriasis patients was approved by the U.S. Federal Drug Administration. De Visser said that it would be interesting to find out how these drugs respond in breast cancer patients.

References

https://medicalxpress.com/news/2015-03-immune-cells-breast-cancer.html

https://www.sciencedaily.com/releases/2015/03/150330122354.htm

Team finds ‘exploding head syndrome’ more common in young people than thought

Jul 24, 2015

2409

�Exploding Head Syndrome' is a physiological ailment which is characterized by abrupt loud noises, sensation of an explosion in the head. It was previously assumed that it was a condition which occurred rarely in elderly people. But, a new study by the researchers at the Washington State University found that this condition is prevalent is young people in an unexpectedly high percentage. The results of the study were published online in the Journal of Sleep Research.

Brian Sharpless, a Washington State University assistant professor and director of the university psychology clinic, said that about one in five of the college students interviewed said that they had experienced it at least once. Some of them said that the experience was so bad that it significantly impacted their lives. The bad news for them is that at the moment there are no well-articulated or empirically supported treatments available. Also, only a few clinicians or researchers assess for it at present.

It was also found by the research team that more than 1/3^rd of the individuals who reported of experiencing exploding head syndrome also experienced isolated sleep paralysis � a scary experience in which one cannot move or speak when waking up. People who suffer from this condition literally dream with their eyes open. For this study, 211 undergraduate students were interviewed either by psychologists or graduate students trained in recognizing the symptoms of exploding head syndrome and isolated sleep paralysis. This is the largest study of its kind. In some of the previous less rigorous and smaller studies, some researchers had hypothesized that exploding head syndrome is a rare condition found mostly in people older than 50.

Sharpless said that he didn't believe the clinical lore that this condition occurred in people older than 50. He added that such assumption didn't sound biologically correct to him. He came to believe that exploding head syndrome was more widespread than assumed when he reviewed the scientific literature on the disorder for the journal Sleep Medicine Reviews previous year. He had concluded in his report that this disorder was an overlooked phenomenon which needed deeper study and analysis.

Exploding Head Syndrome comes into action when one is falling asleep. It is suspected by researchers that it stems from problems with the brain shutting down. Typically, when a brain shuts down, its motor, auditory and visual neurons should turn off in stages. But, when one suffers from this ailment, instead of shutting down properly the auditory neurons seem to fire all at once. Sharpless added that that is probably the reason why one hears the crazy loud noises that cannot be explained otherwise. These noises happen inside the brain and are not in the environment.

To understand isolated sleep paralysis, one needs to understand the same part of the brain as it seems likely that the brainstem’s reticular formation, is also involved in isolated sleep paralysis as well, which could answer for why some people experience both maladies.

Both these ailments are quite frightening. Even though the exploding head syndrome lasts just a few seconds, it can lead some people to believe that they’re having a seizure or a subarachnoid hemorrhage. In many instances, both exploding head syndrome and isolated sleep paralysis have been misinterpreted as unnatural events. Some people are so scared when they have such an experience that they do not even tell their spouse about it. Sharpless commented that some even think that they might be going crazy, but they have no idea that there are others like them who experience the same symptoms.

Even though these disorders do not have a well-established treatment yet, researchers have tried different drugs that may be promising.

References

https://medicalxpress.com/news/2015-03-team-syndrome-common-young-people.html

https://www.medicalnewstoday.com/articles/291741.php

How deep-brain stimulation reshapes neural circuits in Parkinson’s disease

Jul 23, 2015

3209

Dramatic and positive rapid effects are seen with deep-brain stimulation (DBS therapy) in treatment of movement disorders. However, it is surprising to note that scientists have little understanding of why and how DBS works. Even though there are huge prospects to improve the therapy further, lack of adequate understanding and knowledge have been holding things back.

For DBS, some devices are surgically implanted in the brain which sends electrical impulses to inner brain structures that are involved in movement. It is seen that Parkinson's disease (PD) patients who receive the treatment report a significant improvement in their symptoms. Symptoms like slow movement, tremor and rigidity diminishes to a great extent after the stimulation device is activated. Also, it is seen that when it is turned off, the symptoms returns quickly.

Even though DBS therapy has been a great success, still there are certain significant issues that still remain. Customizing the therapy for each and every patient is a cumbersome and challenging process and many a times patients do not derive its maximum benefit. That is why DVS has been a subject of interest for the scientific community. With a better understanding of how DBS acts on brain circuits, researchers hope to make DBS an even more effective treatment.

A new study, published online in Nature Neuroscience says that DBS is able to keep the symptoms of Parkinson's disease in check by minimizing excessive synchronization of brain activity in the motor cortex. Motor Cortex is a region on the outer surface of the brain which is responsible for the movements of the body.

Philip Starr, MD, PhD, the Dolores Cakebread Chair in Neurological Surgery and senior author of the new study said that even though the therapy is widely used these days for not only movement disorders but also many brain disorders, no one have a clue of how it works. The results of the new study are therefore significant because it answers this question on the level of brain networks, not just addressing where you’re actually applying the stimulation in the brain. The groundwork for this study has been laid by a previous research led by Coralie de Hemptinne, PhD, a postdoctoral fellow in Starr’s laboratory. It was found that a measure of synchronized rhythmic activity in the brain, which normally varies with movement or other behaviors, is excessively high in in the cortex in PD. It was hypothesized that it is likely that PD affects the flexibility needed by the brain requires to plan and execute movements, and that DBS might work by decoupling activity patterns in the motor cortex.

For the new study, the scientists decided to find out if there was a relationship between that synchrony and symptoms, and whether synchrony is lessened when symptoms are improved by DBS. �For that they measured synchrony in the motor area of the brain before, during, and after DBS, and while the patient was resting or engaged in a movement task in which they had to reach and touch a computer screen.

Their experiment showed that DBS eliminated excessive synchrony of motor cortex activity and facilitated movement without altering normal changes in brain activity that accompany movements.

Starr said that while their 2013 research revealed how Parkinson’s disease affects the motor cortex, their latest paper showed how DBS affects the motor cortex. The information revealed in these two studies can be crucial for developing new ways for stimulators to be automatically controlled by brain activity, which is the next innovation in the treatment of movement disorders.

References:

https://medicalxpress.com/news/2015-04-deep-brain-reshapes-neural-circuits-parkinson.html

https://www.sciencedaily.com/releases/2015/04/150413130814.htm

Unprecedented Germ Diversity Found In Remote Amazonian Tribe

Jul 22, 2015

2347

Is our Western lifestyle and diet stripping us of some of the beneficial bacteria that we would want back? Somewhere in a remote part of the Venezuelan Amazon, scientists have discovered an isolated village where some of the members are said to have the most diverse colonies of bacteria ever reported living in and on the human body.

The beneficial bacteria that share our bodies have a critical role to play in our health and well being. This study has raised some important questions about the microbial diversity of our ancestors. The most surprising finding about this group of Yanomami Indians is that they harbor bacteria containing genes that have the ability to resist antibiotic treatment � that is especially significant taking into account the fact that these villagers were never exposed to commercial western medications.

Jose Clemente, lead researcher and an assistant genetics professor at the Icahn School of Medicine at Mount Sinai Hospital in New York said that the isolated population offers a unique opportunity to put our microbial past under the microscope. Study's senior author M. Gloria Dominguez-Bello of NYU Langone Medical Center said that the results bolster a theory that reduced microbial diversity in Western populations and is linked to immune and metabolic diseases that are of the rise like – allergies, asthma, diabetes, etc.

The challenging part of the study is to find out which bacteria are important for humans to be healthy. Each of us have a microbiome on our body � there are sets of microbes living on our noses, mouth, skin, intestines, etc. This zoo of microbes starts right at the time of our birth and continues evolving and growing as we age. There are several factors that impact it � the way you were born � vaginal or C-section, diet, where you live and antibiotic exposure.

Most of the knowledge scientists have today of the human microbiome come from the studies of Americans or Europeans. That is why exploring non-western population that sticks to primitive lifestyle is likely to shed some more light on this subject.

The Yanomami still continue to live a hunter-gatherer lifestyle in rainforests and mountains along the border of Venezuela and Brazil. This particular research stems from the discovery of a Yanomami village in the mountains of southern Venezuela that was previously unmapped. The location of this village is not revealed by the researchers for privacy reasons. However, it is now known that it was first visited by a Venezuelan medical expedition in 2009 that collected fecal, skin and mouth swab samples from 34 villagers.

When the samples from the Yanomami population were compared to samples from U.S. populations, it was found that the Americans' microbiomes are about 40% less diverse. It was quite surprising to find that the Yanomami also harbored some unique bacteria that had certain health benefits like – prevent the formation of kidney stones, etc.

On further investigation, silent antibiotic-resistant genes lurking in some bacterial strains were also found. Guatam Dantas of Washington University School of Medicine in St. Louis and study's co-author said that antibiotics still could kill the bugs; however, when the genes were switched on, through antibiotic exposure, they could block activity of some common modern antibiotics.

Due to the rampant use of antibiotics in agriculture and medicines, germs are slowly becoming drug resistant. In early times, the bacteria in soil were also natural source of antibiotics which explains how these villagers might have picked up those bugs which had evolved resistance genes.

Dantas said that it is very important for us to ramp up our research for new antibiotics. If we do not take steps in the right direction, we’re going to lose this battle against infectious diseases.

References:

https://abcnews.go.com/Health/wireStory/unprecedented-germ-diversity-found-remote-amazonian-tribe-30396499

https://medicalxpress.com/news/2015-04-unprecedented-germ-diversity-remote-amazonian.html

Chemical tag marks future microRNAs for processing, study shows

Jul 21, 2015

2787

A DNA helix is formed when two DNA strands naturally arrange themselves into a helix. However, RNA doesn't form a helix; they form hairpin-like loops instead. Typically, DNA has a single job to handle, but RNA has multiple jobs to do which includes acting as a precursor for small molecules that block the activity of genes. In order to do this the RNA molecules must be trimmed from long hairpin-loop structures. The question that raises now is � how do the cells know which RNA loops need processing and which do not?

A new research conducted at the Rockefeller University and the findings of which were published in March 18^th publication of the Nature, shows how cells sort out the loops meant to encode small RNAs, known as microRNAs, by tagging them with a chemical group. Since, microRNAs help control various processes throughout the body, this discovery is quite important. It will have implications for development, health and disease, including cancer, the entry point for this research.

Sohail Tavazoie, Leon Hess Associate Professor, Senior Attending Physician and head of the Elizabeth and Vincent Meyer Laboratory of Systems Cancer Biology and the study's lead author said that the work in their lab and in many other researches earlier has shown that a number of changes happen in microRNAs in various types of cancer. In order to understand how and why this happens, a basic question need to be addressed – how cells normally identify and process microRNAs. Claudio Alarcón, a research associate in Sohail's lab discovered that cells can increase or decrease microRNAs by using a specific chemical tag.

RNAs have been long known to be something that lies between DNA and proteins. But, it turns out that they are quite versatile. A number of microRNAs have been discovered by scientists that regulate gene expression. MicroRNAs are encoded into the genome as DNA; they are later transcribed into hairpin loop RNA molecules, also known as primary microRNAs. These loops are then clipped to generate microRNA precursors.

In order to find out how cells know which hairpin loop to begin trimming, Alarcon started by looking out for modifications cells might make to the RNA molecules that are likely to transform into microRNAs.

Bioinformatics software was used to scan and find out any unusual patterns in the unprocessed RNA sequences. The sequence GGAC, code for the bases guanine-guanine-adenine-cytosine, stood out because it appeared in good number in the unprocessed primary microRNAs. The GGAC was of key importance as it led the researchers to an enzyme known as METTL3, which tags the GGAC segments with a chemical marker, a methyl group, at a particular spot on the adenine.

Once METTL3 was found, everything fell in place. Alarcon said that the methyl in adenosines (m6A tag) is the most common known RNA modification. METTL3 is known to contribute to stabilizing and processing messenger RNA, which is transcribed from DNA. �Now it is known that it has a role to play in the processing of primary microRNAs.

The researchers carried out a number of experiments through which they confirmed the importance of methyl tagging, finding high levels of it near all types of unprocessed microRNAs,. It suggests that it is indeed a generic mark associated with these molecules. When the researchers reduced expression of METTL3, it was seen that unprocessed primary microRNAs got accumulated meaning that the enzyme’s tagging action was important to the process. It was also found that in cell culture and in biochemical systems, primary microRNAs processed efficiently in the presence of the methyl tags.

Tavazoie added that cells can remove these tags, as well as add them. With the help of these experiments a switch has been identified that can be used to ramp up or tamp down microRNA levels, and alter gene expression. It could prove crucial in governing cancer progression.

References

https://medicalxpress.com/news/2015-03-chemical-tag-future-micrornas.html

https://newswire.rockefeller.edu/2015/03/24/chemical-tag-marks-future-micrornas-for-processing-study-shows/

Researchers Target Two Brain Sites Responsible For Anxiety

Jul 20, 2015

2340

Anxiety

Fear and anxiety are synonymous but there is a subtle difference between them when these terms are used scientifically. Fear is the response to an immediate actual threat meanwhile; anxiety is the fear that rises from expectation of the future. Today, scientists understand the typical anxiety disorder symptoms and also know how to treat those symptoms. But, what still remains challenging is the study of the neurology of anxiety. For example, it is known to the scientists that dysregulation of the orbitofrontal and ventrolateral prefrontal cortices are involved in such disorders, but it is known fully understood which are the specific contributions of each region.

A study was designed by a group of researchers at the University of Cambridge to assess the contributions of these regions of the brain in the anxiety responses of marmosets. Their findings were published in the Proceedings of the National Academy of Sciences.

Overreaction to Threat Conditions:

Anxiety and fear of unfavorable outcomes affects decision making in a person in a negative way. It often leads to stress, isolation and adverse health condition. It is important that an organism is threat for survival, but hypersensitivity to threat inhibit the right decision making capability in patients. There have been studies in the past which have suggested that this hypersensitivity is a result of dysregulation within the prefrontal cortex. However, it is not fully understood how this region affects aversive processing and how it has an impact on the negative emotional valence in decision making.

Since, it is known that the excitotoxic lesions on either the anterior orbitofrontal cortex or ventrolateral prefrontal cortex elevates anxiety and fear responses in marmosets, researchers designed an experiment to test on monkeys to study their responses before and after temporary inactivation of these regions.

Testing the Brain’s Threat Prediction Ability

The marmosets for the test were trained to respond to two identical visual stimuli. These stimuli were presented on each side of a touchscreen to gain a reward of banana juice. The way the visual stimuli were presented were independent but had identical variable-interval schedules. The response biases of individual monkeys were observed and it was seen that each monkey demonstrated a slight bias for one side of the screen or the other. Once per week, responses on one of the two stimuli would produce delivery of a punishment in the form of an aversive loud noise that was superimposed on the unchanged reward schedule. Such that spatial bias contributing to a punishment-induced bias could be avoided, the punishment was always introduced on the individual monkey’s “preferred” side.

It was seen that in the absence of reward, the punishment produced a strong aversive response. But, when the punishment and reward were delivered simultaneously, the monkeys did not alter their behavior. Hence, it was concluded by the researchers that the monkeys perceived the banana juice reward “worth” responding for, even though there was a possibility of the punishment.

The researchers then carried out the same experiment after inactivating either the anterior orbitofrontal cortex or ventrolateral prefrontal cortex with a GABA agonist 20 minutes before test sessions. It was seen that the inactivation of one of the two regions had no effect on responses when the test ended in a reward but no punishment. However, when punishment was introduced for responses, the monkeys with inactivated ventrolateral interior prefrontal cortex produced a strong, immediate response bias away from the punishment. These animals when tested again the next day for a reward only session did not show any anomaly from the previous behavior. So, it was understood that the bias developed in test animals during the reward-punishment sessions, but did not endure. But, it was seen that the animals with inactivated anterior orbitofrontal cortices showed did show a profound bias away from the previously punished side the next day. Thus, the researchers associate the activity of the vlPFC with cost-benefit analyses and the antOFC with the consolidation of memory for the punishment.

The researchers are of the opinion that in the future; cognitive behavioral therapy for patients suffering from anxiety disorders could be tailored according to the patient’s ability to make accurate cost-benefit analyses or to form memories that lead to strong antipunishment biases.

Looking or a solution for your anxiety? Try having a look at this.

References

https://medicalxpress.com/news/2015-03-brain-sites-responsible-anxiety.html

https://www.bioportfolio.com/news/article/2278736/Researchers-target-two-brain-sites-responsible-for-anxiety.html

How to Myelinate a Nerve?

Jul 19, 2015

2716

Human Brain

Demyelinating diseases are life altering. Such diseases are characterized by damages to the protective covering also called myelin sheath that surrounds nerve fibers in your brain and spinal cord. When this protective covering is damaged, nerve impulses slow or even stop, causing neurological problems. Take for example, Multiple Sclerosis (MS) or (ALS) which targets a healthy nervous system and cages the owner in his body. Most of the big pharma companies have put serious efforts in researches to discover miracle drugs that could cure the diseases. But, the hard truth wins every time � it may be possible to alleviate some of the symptoms for some time with the drugs, but no cure has been found yet. The researchers are now focusing on one fundamental question � how can be axons be physically remyelinated. To find that out, it is necessary to find out how they get myelinated in the first place.

Neuroscientists are focusing on various molecular pathways that seem to be critical to myelination. However, there is little they can tell us about how axons are myelinated. To understand how it happens, we need to watch it happen in slow-motion.

An interesting thing here is a recent review in the Developmental Cell titled ‘Dynamics and Mechanisms of CNS Myelination’. It took stock of the current state of the art in visualizing what is actually going on here. Even though there are many theories, there is no clear consensus about it. A central issue for Schwann cell myelination in the PNS � that is how do these cells tackle the problem of radial sorting, is elaborated in a complementary study published in Neuron.

The researchers for the study focussed on the role of the extracellular matrix in starting off the radial sorting. Schwann cells are to some extent responsible for secreting the various laminins, collagens, and heparin sulfate proteoglycans that make up the matrix. A critical level of spike activity in the axons is one of the main triggers to start secretion. The researchers also explored the role a newly defined family of receptors known as aGPCRs (adhesion G protein-coupled receptors) plays.

The highlight of the study is that the authors were able to connect the importance of the large N-terminal extracellular domains of these proteins in interacting with the basal lamina during radial sorting. They did thus by creating various mutants and looking at high resolution EM images. It is interesting to note that getting the makeup of the matrix right is just one small piece of the puzzle. In order to visually see myelination as it happens time lapse fluorescence microscopy is needed and the right labels on the things you want to see.

The good news is that Sue Barnett, from the University of Glasgow has been able to do this using ex vivo preparations of mouse spinal cord. Her group reported that once oligodendrocytes in the CNS get their axon, they spiral around it in a corkscrew fashion. After that there is focal expansion of these processes into short longitudinally extending cuffs which then overlap each other. They call their model, the ”ofiomosaic model”.

It is important to note that it is a spiraling corkscrew process as it has a handedness or polarity. Also, it could be a critical constraint which could influence how adjacent myelin segments interact and organize themselves. Sue added about an interesting thing they noticed, which classically isn’t supposed to happen at all, was the presence of ‘two myelin internodes’ on an axon in vitro.

Since, the detailed structure of myelinated nodes, paranodes, and internodes is now coming into full view, it will make it tad bit easier to understand what makes these unique membrane elements work, and the forms they take both in the PNS and the CNS.

Reference Links:

https://medicalxpress.com/news/2015-03-myelinate-nerve.html

https://girlscoutshopmaine.org/how-to-myelinate-a-nerve/

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