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What causes brain problems after traumatic brain injury? Studies have a surprising answer

Oct 11, 2015

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In a new research paper published in the latest issue of Neurotherapeutics by the researchers at the University Of Maryland School Of Medicine (UM SOM), it has been argued that our understanding about the true nature of traumatic brain injury and how it causes chronic degenerative problems is misunderstood.

The two authors of the paper – Alan Faden, MD, a neurologist and professor of anesthesiology, and David Loane, PhD, an assistant professor of anesthesiology are of the opinion that the cause of chronic brain damage and neuropsychiatric problems after trauma are more due to long-term inflammation in the brain. According to them, this inflammation is a key culprit behind the various symptoms that a person experiences after suffering traumatic brain injury and mild traumatic brain injury like brain atrophy, depression and cognitive decline.

Dr. Faden and Dr. Loane stated that in general more emphasis is given to a specific diagnosis like chronic traumatic encephalopathy (CTE). Some former football players have been diagnosed with it. They seriously think that this takes away the focus from other mechanisms, which are more common and hence more important and may be more treatable. There is no doubt that chronic traumatic encephalopathy is a very serious problem. However, relatively few people have been diagnosed with this condition. So, it definitely make sense for researchers and journalists to focus more things like repeated concussive impacts or mild traumatic brain injury which can also trigger chronic brain inflammation that can last for years and cause lasting irreversible damage.

Dr. Faden emphasized that brain inflammation is a very key issue and one that has been not taken very seriously. He added that in some recent brain imaging studies, which also includes those of former professional football players, it is indicated that persistent brain inflammation after a single moderate head injury or repeated milder traumatic brain injury may be very common, and that it may eventually contribute to cognitive problems. Some larger studies also reveal that brain inflammation actually stays for several months or years in many people with traumatic brain injury.

In their paper Dr. Faden and Dr. Loane also state that chronic brain inflammation related to traumatic brain injury may be treatable. There are recent researches that show that some experimental drugs, along with controlled exercise programs, can control brain inflammation caused by traumatic brain injury. That is why these avenues should be pursued on priority.

Prior to this there have been two groundbreaking publications were done by Dr. Faden. In these works, he studied and observed animal models of traumatic brain injury, examined the mechanisms by which even mild brain injuries can cause sustained cognitive and psychiatric problems. In his work he elucidated how this process occurs. One of the study was published in Cerebral Blood Flow and Metabolism and the other one in Journal of Neuropathology and Experimental Neurology. Dr. Faden opined that in these studies it was found how repeated mild injuries can lead to the injuries that are similar to those which occur after a single moderate or severe traumatic brain injury. The loss of brain cells and the brain inflammation look quite similar. He remarked that since the mechanism behind the damage is understood now, strategies to prevent or minimize the problems should be developed.

During the study for the paper published in the Journal of Cerebral Blood Flow and Metabolism, Dr. Faden and team studied the brains of animals with mild traumatic brain injury. It was seen that there was a substantial loss of neurons, and an increase a kind of inflammatory immune cell active in the brain called microalgia. �These changes were long-lasting and resulted in decreased function in the hippocampus.

In the other paper, it was found that traumatic brain injury triggers certain long-term molecular changes which results in increased inflammation lasting up to a year. Such inflammation causes death of brain neurons and result in cognitive loss.

Scientists Invent System to Improve Effectiveness of Cancer Surgery

Oct 10, 2015

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Cancers are infamous for making a comeback even after a surgery. So in a bid to reduce the rate of cancer re-occurrence, scientists have invented a new imaging system that makes the tumor �light up' when a hand-held laser is directed at them. This system can make it easier for surgeons to weed out any cancerous tissue during a surgery.

Aaron Mohs, Ph.D., assistant professor of regenerative medicine at Wake Forest Baptist Medical Center and a co-inventor of the system said that in such a surgery, the goal of a surgeon is to not only remove the tumor, but also enough surrounding tissue so that no malignant tissue is left behind. But, there is no means which can tell them that they have removed enough of it. The goal in building this system is to provide better real-time information to guide the surgery.

The details about the discovery were published online in IEEE Transactions on Biomedical Engineering (TBME). In this system a fluorescent dye that localizes in tumors with a real-time imaging system is used and it allows the surgeon to simply view a screen to distinguish between normal tissue and the “lighted” malignant tissue.

During their research on both mice and dogs, the scientists found that the fluorescent dye accumulated at higher levels in tumors than in the surrounding tissue. This helped the system to detect a distinct boundary between normal and malignant tissue. �Since, canine tumors are in many ways similar to human tumors, it is very likely that this system would work on human tumors as well. The scientists are working to further develop the system so that it can be safely used in human patients as well.

At present, cancer surgeons scan tumors prior to surgery with magnetic resonance imaging and other systems. However, there is no technology that can enable them to scan the tumor during surgery. Mohs remarked that this has long been an unmet clinical need. Even the pathology techniques that examine tumor tissue during surgery can take up to 20 minutes. The focus of such examination is the tissue that is removed during surgery and not the tissue that remains in the body.

Mohs was awarded a $1.37 million research grant from the National Institute of Biomedical Imaging and Bioengineering for a project to optimize the system and to test it in rodents.

In their report, the authors noted that the ideal system should be such that finds tumor boundaries with high sensitivity, have minimal impact on operative time and surgical technique, present findings in an intuitive manner and avoid the use of ionizing radiation or a specialized imaging environment, such as MRI machines.

The system, invented by Mohs, Michael C. Mancini at Spectropath�Inc., and Shuming Nie with Emory University and Georgia Institute of Technology, meets the needs to a large extent. It combines two types of imaging with a surgeon-controlled laser can be directed at any area of interest and an imaging system with three cameras that sits above the surgical field. The images recorded by both systems are processed to display a composite image.

With the help of this system, a surgeon can scan the tumor before a surgery to determine the boundaries following which the tumor can be surgically removed. The area can then be re-scanned to assess for any remaining malignant tissue. In case some diseased tissue is found, it can be surgically removed, and the process would be repeated until no diseased tissue is detected by the system.

In the prototype system indocyanine�green dye was used by the scientists as the source of fluorescence. They also noted that for future studies higher performance fluorescent dyes can be used and nanoparticles that can be targeted to specific tumors.

International Research Gives Neuroscientists Better Feeling about Sense of Touch

Oct 9, 2015

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We often take our sense of touch for granted. Even in neuroscience, scientists do not know much about how it works. However, in a recent study a group of researchers including Carnegie Mellon University’s Alison Barth, have tried to delve deeper into this crucial sensation. The research was published recently in an issue of Neuron. The researchers in this study have linked a group of neurons to a specific type of somatosensation. This finding can open the door for a heightened understanding about our sense of touch.

Carnegie Mellon has been a leader in the study of brain and behavior for more than 50 years. It is the birthplace of artificial intelligence and cognitive psychology. Today, it is building on its strengths in biology, computer science, psychology, statistics and engineering. The result of which is it's recently launched global initiative BrainHubSM. It focuses on how the structure and activity of the brain give rise to complex behaviors.

Barth, a professor of biological sciences and a member of Carnegie Mellon’s BrainHubSM research initiative opined that somatosensation is critical. As humans we can somewhat overcome losing our sense of smell, sight, taste, or hearing. However, if we lose our sense of touch, we will not be able to sit up or walk. In fact, one wouldn’t be able to feel pain or anything else. She added that even though it is such a critical sense, we know the least about it.

As the birthplace of artificial intelligence and cognitive psychology, Carnegie Mellon has been a leader in the study of brain and behavior for more than 50 years. Building on its strengths in biology, computer science, psychology, statistics and engineering, CMU recently launched BrainHubSM, a global initiative that focuses on how the structure and activity of the brain give rise to complex behaviors.

Somatosensation is actually our sense of touch. It occurs in a number of forms, like feeling texture, temperature, pressure, pain or vibration. It is what is responsible for proprioception, which helps us know where we are within our environment; it tells us if our feet are firmly planted on the floor, etc. Scientists have a good knowledge about the molecular receptors that mediate the different types of somatosensation. However, little is known about how it is represented in the brain.

Barth said that we know how information gets transmitted form the skin to the spinal cord when one gets pricked by a pin. What is not known is what happens inside the brain. Since, there are so many activities happening in the brain, everything is a jumble.

In some previous studies, Barth had observed that certain groups of neurons in the brain’s neocortex were more active than others. She used the fos-GFP mouse, a transgenic mouse model to study activity in live neurons. She and her colleagues wanted to find out if these neurons responded specifically to one stimulus or were generally more excitable. In their study, they found that the neurons reacted much more quickly and strongly when a puff of air was directed at the mouse’s whiskers, while other neurons had little or no response.

This showed that have different jobs to do in the cortex. The one they were observing responded when all of the mouse’s whiskers moved at once. It was also found by them that these particular neurons received direct synaptic input from the posteromedial nucleus of the brain’s thalamus. It confirms that the neurons that react to the puff-of-air stimulus have a dedicated, unique sub-network of connections that lets them communicate with one another and amplify the information they are receiving from the stimulus.

Barth said this knowledge have opened up avenues of understanding somatosensory functions. It is hoped that this finding will eventually lead to a work that will identify how somatosensory information is coded, which could be used to incorporate sensory information into brain-machine interfaces. Such a breakthrough could allow robotic limbs and prosthetics to actively sense and receive tactile input.

The research was funded by the Deutsche Forschungsgemeinschaft, the European Research Council, the Alexander von Humboldt Foundation, the European Union and the National Institutes of Health.

References

https://www.cmu.edu/news/stories/archives/2015/january/touch-and-neuroscience.html

https://medicalxpress.com/news/2015-01-international-neuroscientists.html

Living Forever May Never Be Possible, Study Says

Oct 2, 2015

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Living Forever

The thought of living forever might seem like something out of fairy tales. Now, though, men in most developed countries have a life expectancy of 75 years; women, 80 and more, it was not always the case.

A topic for brain storming is that if life expectancy from the 1800’s till now can be more than double, then can it become it double again? Could it be possible to do so infinitely?

Some researchers' strongly believe that humans are limited when it comes to life expectancy and the maximum limit is 125 years. Other researchers see a world in which we have people living to be 100 and more, i.e. centenarians. They are the walking examples of people who have incredible genes and have lived for 100 or more years.

Diseases like dementia and heart problems are common problems related to aging. These diseases block us from reaching the 100 year mark. Our body wears out from use. Scientists in their quest for immortality have been for years, focused on finding ways to prevent and slow down aging from occurring within the body. One method that has shown positive results in this field and increased the lifespan of small creatures such as mice or squirrels is a calorie-restrained diet.

Following this diet means cutting down on your daily food intake by 30 percent while consuming all the necessary nutrients that keep running healthy bodily functions. This diet plan is clearly difficult for humans to follow and maintain, so scientists and researchers all over the world are trying to find out how taking fewer calories helps to lengthen lives.

Anti-aging pills can slow down the effect of free radicals in our body to lengthen youth and prevent early onset of old age. Free radicals are the molecules present in our body that cause continuous damage within

our body as we age. Researchers claim that the compound resveratrol that is present in red wine might have the ability to slow down the aging process at the genetic level. Research is being carried on to make it available in pill form for use.

French researchers are also trying to find out the answer to this curiosity of living forever and have found two evidences so far. There are two categories of people in the world who have lived long lives that are the

closest to living forever. Athletes are considered among people that have the longest lives and researchers found that high life expectancy is more common among the athlete group. Although there have been no

findings that can support humans being able to live forever. Therefore, forming the premise of healthier lifestyle is to be followed.

Some would-be centenarians around the world have begun injecting human growth hormone into their bodies in the hopes of preventing the body from aging. There are many theories on how and why we age and on ways to prevent it. An anti-aging pill might present a solution but it is at least decades, if not centuries away in the future.

One challenge that an anti-aging pill poses is how long humans already live. Studies that are feasible with mice or yeast cells might not be possible with humans as no one is going to live long enough for the scientists

to be able to perfect them for human use.

An alternative way to live forever is to abandon the flesh and blood we are made of and turn to materials that are more durable. Futurists of the world envision a world in which a computer saves all the memories and

knowledge of our brain and portable silicone parts take the place of limbs. Scientists still have to figure out if the outcome will be part human part machine, but it is wise to say that it is not yet the time to abandon your

life’s legacy.

References

https://medicalxpress.com/news/2014-08-living-forever-may-never-be.html

https://www.thejournal.ie/cant-live-forever-1634332-Aug2014/

New Enzyme Targets For Selective Cancer Therapies

Oct 1, 2015

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Fight against many cancers has become easy thanks to important discoveries clinical research and scientific technological advances.

At a lab in the University of Alberta, there could be a possibility for finding a new and more selective therapy for cancer. Researchers claim to have developed a compound that effectively targets specific enzymes that are over expressed in specific cancers. The effectiveness of these tests have been proven with the help of cells from brain tumours. A first of its kind inhibitor has been synthesized by the scholar of chemistry Christopher Cairo and his team that will slow down the working of an enzyme neuraminidase.

Human cells also use their own forms of these enzymes that have the same mechanisms for various purposes in many biological purposes and k quantities in glioblastoma cells that are a form of brain cancer cells. A new study has revealed that glioblastoma cells that are found within a tumor and enhance cancer growth can be turned into normal cells. All this is possible with the help of Cairo’s inhibitor that was put under test by a team from the National Cancer Institute.

The compound is also believed to have the ability to stop the cells from growing further, pointing the importance of this mechanism for therapeutics. The Nature journal Cell Death & Disease also has the results of these efforts in the issue of 22 August.

A researcher added that this was the time that a selective neuraminidase deterrent was casting an impact in human cancer cells.

It seems like it would take a long time to reach the successful drug since justifying the compound deterring the neuraminidase enzyme in cancer causing cells is a concrete move in assuring its potential.

But presently, the compound is yet to take the form to be used as a drug. As explained by researchers, it was not meant to create gaps in the blood and brain making it all the more tougher to attain the required cells. The compound had to be used in high concentrations in Milan.

This research extends our understanding of the importance of carbohydrates in the functioning of cells. According to common belief, glucose i.e. blood sugar is the only important sugar in biology,

but little do we know that there is an entire area of research that is focused on understanding the working of complex carbohydrate in cells. It is known as glycobiology.

Carbohydrate structures in the human body cover the cell surface and affect how they interact with each other and with pathogens. Scientists claimed for decades that the carbohydrate structures found on cancer cells differ from those on found normal cells. For instance, many cancer cells have been found to contain different qualities of residues like salicylic acid, or have different arrangements of similar residues.

The carbohydrates present on the cell surface explain the mutual interaction of it with other cells that tends to hold them necessary in cancer.

The human cells experience four different iso-enzymes. One of them plays a huge role in promoting cancer and therefore it is important to target the right one. In case the wrong one is targeted, you are most likely to have adverse effects. Various kinds of side effects have been witnessed in the past which makes it important to be extra careful while focusing on the required cell.

These enzymes have been under consideration for the past 5 years. The achievements that we have had in our basket, have been rightful approval of our strategy, development of a selective neuraminidase inhibitor and a cell application underlining the enzyme.

References

https://uofa.ualberta.ca/news-and-events/newsarticles/2014/august/new-enzyme-targets-for-selective-cancer-therapies

https://www.firstwordpharma.com/node/1231562#axzz3LXBSSLsI

GIANT Study Reveals Giant Number of Genes Linked to Height

Sep 29, 2015

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Height

A study conducted by the International Genetic Investigation of Anthropometric Traits (GIANT) Consortium, provides a better insight into the biology of height. It also offers a model for investigating traits and diseases that are typically caused by many common gene changes acting together. The findings of the study were published online on October 5th by Nature Genetics. It is the largest genome-wide association study (GWAS) that has been conducted till date and involves more than 300 institutions and more than 250,000 subjects which is roughly double (around 400) the number of known gene regions which influences height.

Joel Hirschhorn, MD, PhD, of Boston Children’s Hospital and the Broad Institute of MIT and Harvard, leader of the GIANT Consortium and co-senior investigator on the study said that height is almost completely determined by genetics. However, the studies that have been conducted in the field were only able to explain just about 10% of this genetic influence. By doubling the number of participants in the study, the scientists are now able to have a much more complete picture of how common genetic variations have an influence on the height. It can also be ascertained to an extent how many genetic variants are there and how much influence they have.

Hundreds of GIANT investigators shared and analyzed data from the genomes of 253,288 people. They carried out the herculean task of checking about two million common genetic variants which showed up in at least 5 percent of their subjects. From this pool, 697 were chosen in 424 gene regions and were said to be related to height. This is the largest number to be associated with any trait or disease. With the results of this study, about 20% of the heritability of height can be explained.

The previous studies has hinted that a large number of genes influence height, and also pointed that the majority of heritability comes from common genetic variants, not rare ones. Since, the sample size was not big enough; a definitive conclusion could not be drawn. That is why it was decided to double the sample size; this way one is able to make new discoveries.

Co-senior investigator Peter Visscher, PhD, of the University of Queensland, Australia remarked that the study narrows down the genomic regions that contain a substantial proportion of remaining variation�to be discovered with even larger sample sizes. It is understood that height is a model trait that could explain how human genetics works � since this trait is not determined by one by many. It is estimated that 80% of height is due to genes.

Hirschhorn added that the result of the study was to prioritize many genes and pathways as important in skeletal growth during childhood. That is why it needed a collaborative model, to get the work done.

In 2007 the first paper was published that identified the first common height gene, and today the research team has identified nearly 700 genetic variants that determine height. It was seen that a number of the 697 height-related genetic variants were located near genes that were known to be involved in growth. However, there were also plenty of surprises as well. There were some pathways that had not been identified in previous studies but were important. Many of the genes identified in this research are likely to be important regulators of skeletal growth, but had not been known until now. As the sample size grows, there are more surprises from biology.

References

https://www.broadinstitute.org/news/6119

https://www.prnewswire.com/news-releases/giant-study-reveals-giant-number-of-genes-linked-to-height-278166091.html

To beet or not to beet? Researchers test theories of beet juice benefits

Sep 28, 2015

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You must have heard about the benefits of downing beet juice before exercising. It is a popular belief that it increases blood flow and improves performance. A study was conducted at the Penn State's Noll Laboratory to find out the real picture. The results of the study may surprise athletes. Beet juice is definitely rich in nitrates but, they do not seem to enhance muscle blood flow or vascular dilation during exercise. However, researchers did note that beat juice “de-stiffened” the blood vessels under resting conditions and thereby they eased the workload of the heart significantly.

So popular is the trend of drinking beet juice that you will find many endurance athletes consuming this crimson supplement to improve blood and oxygen flow in their muscles during training and competition. Some even think that it can improve their ability to withstand muscle fatigue during repeated bouts of high intensity exercise. In fact, some patients with high blood pressure are asking their doctors if drinking the juice can lower their high blood pressure.

To find out if these potential benefits of beet really hold good, David Proctor, professor of kinesiology and physiology at Penn State, decided to test the ability of the juice to enhance blood flow to exercising muscles. He along with other fellow researchers found that the belief regarding improved muscle blood flow did not hold up to their test. Their findings were reported in the journal Applied Physiology, Nutrition, and Metabolism.

For the study, subjects were given either a placebo drink containing beetroot juice minus the nitrate or a relatively high dose of nitrate-rich beetroot juice. Proctor and his colleagues found that the latter did not enhance the natural rise in blood flow to the forearm muscles during graded handgrip exercise. Jin-Kwang Kim, study's lead author and Penn State physiology graduate student said that the juice had no effect on the dilation of the brachial artery in these volunteers.

Green leafy vegetables like spinach and beetroot are a good source of nitrates. They are converted naturally in the body to nitric oxide – a molecule that relaxes and widens blood vessels and helps the cells in efficiently using oxygen. �These days a number of manufacturers liquefy beetroots and concentrate the nitrate into beetroot juice “shots.”

Proctor said that their study was the first of its kind that measured the blood flow to the contracting muscles after consuming nitrate-rich supplements such as beetroot juice. However, in some previous studies, improved muscle oxygenation during exercise after consuming nitrate-rich supplements have been reported.

Proctor said that the breakdown product of the nitrate in the participants’ blood was measured and it indicated that these participants absorbed the nitrate from the drink and converted it to nitrite – the precursor to nitric oxide. They however observed a direct correlation between nitrite levels in the blood and the slowing of participants’ arterial pulsation velocity. It indicates that the supplement did indeed have an artery de-stiffening effect.

Proctor said the reason for the null effects on muscle blood flow observed in this first study could be due to two factors. Firstly, the subjects were young individuals with blood pressure and cholesterol levels in the ‘very healthy’ range. So, it could be that these subjects already had well-preserved vascular endothelial function. The second contributor could be the relatively small range of forearm exercise intensities that were examined in this study. It is possible that any blood flow enhancing effect of dietary nitrate is measurable only during higher intensity and fatiguing work intensities.

Proctor and his colleagues are now working on an investigation of the effects of beet juice on vascular function in older adults � who have elevated blood pressure and those whose muscle blood flow during exercise is impaired.

References

https://medicalxpress.com/news/2015-01-beet-theories-juice-benefits.html

https://www.sciencedaily.com/releases/2015/01/150119083300.htm

Tumor Suppressor Protein Plays Key Role in Maintaining Immune Balance

Sep 27, 2015

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In a research published online in the scientific journal � Nature Immunology, it is revealed that scientists at the St. Jude Children's Research Hospital have discovered that a protein known to be suppressing tumor formation can also help in preventing autoimmune diseases and other problems by putting the brakes on the immune response.

The tumor suppressing protein PTEN is crucial for the proper functioning of regulatory T cells. This small population of white blood cells helps in maintaining the balance in immune system by suppressing specialized T cells called helper T cells that trigger distinct parts of the immune response. The helper T cells which were a part of this study included type 1 T helper (Th1) and follicular T helper (Tfh) cells.

In order to combat infections and to prevent misguided immune attacks that lead to autoimmune diseases and other problems, both regulatory T cells and helper T cells should play their roles. However, how the regulatory T cells control the diverse functions of various helper T cells was not known. The aim of this study was to fill in the gaps by understanding how the control process works, particularly PTEN’s role. This research also focussed on a new area to improve treatment of autoimmune diseases.

PTEN is one of the most frequently altered tumor suppressor genes in human cancers. Additionally, loss of the protein is also tied to autoimmune problems. According to this study, PTEN is required to maintain the stable population of regulatory T cells which in turn keeps the immune system in check. It is known that loss of PTEN in humans leads to the formation of tumors. Author Hongbo Chi, Ph.D., a member of the St. Jude Department of Immunology remarked that this study highlights another role and shows that PTEN is imperative for proper functioning of regulatory T cells and prevention of autoimmune diseases. He added that in mice, even the loss of one copy of the PTEN gene in regulatory T cells is enough to set the stage for autoimmune problems.

For this study, the researchers worked on specially bred mice and by deleting the PTEN gene in regulatory T cells they found that it was followed by a dramatic increase in the number of Tfh and related cells. Tfh cells typically help in production of antibodies, which combat infections. However, when they are produced inappropriately, antibodies trigger autoimmune disorders like lupus. �The mice used for this experiment developed kidney damage and immune changes associated with lupus. Even after the PTEN was restored to 50 percent of normal levels, it did not protect the mice from inflammatory disease.

On further research, it was found that Th1 cells influences the activity of Tfh cells. These cells produce a chemical messenger interferon gamma that triggers the immune response. on blocking the interferon gamma production in the specially bred mice, the researchers found that the number of Tfh cells fell and also there was a decrease in lupus-like immune abnormalities.

Sharad Shrestha, a graduate student in Chi’s laboratory and the study's first co-author remarked that by identifying the crucial role of PTEN in controlling Tfh cells and autoantibody production and by linking the role of PTEN to Tfh cells, they have opened doors for further investigation of Tfh related lymphomas.

Kai Yang, Ph.D., a staff scientist in Chi’s laboratory and also the study's co-first author said that the results of the study reveal a hierarchy of control that regulatory T cells use to simultaneously regulate Th1 and Tfh cells. They have found evidence that Th1 production of interferon gamma is a pre-requisite for the activity of Tfh cells.

This study also found insights into a cell signaling pathway that regulates many important functions, including T cell activity like the mTOR pathway, in which the protein complexes mTORC1 and mTORC2 play central roles. By deleting PTEN in regulatory T cells there was an increased activity of mTORC2 but not mTORC1. When scientists blocked mTORC2 activity in mice whose regulatory T cells lacked PTEN, immune system balance and activity returned to normal.

This PTEN-mTORC2 axis provides another avenue for scientists so that better treatments for autoimmune and other disorders can be developed.

Strategy Might Thwart Resistance to a Common Prostate Cancer Treatment

Sep 26, 2015

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It has been known for quite a while that high levels of testosterone lead to the growth of prostate cancer. However, there is a new study that challenges this conventional wisdom. A small recent study suggests that a treatment strategy known as bipolar androgen therapy can help in making prostate tumors more responsive to standard hormonal therapy. �In this therapy patients are made to alternate between low and high levels of testosterone.

The report of the study was published in the journal Science Translational Medicine recently.

Today, the primary treatment for advanced prostate cancer is hormonal therapy which typically aims to lower the levels of testosterone and prevent the tumor from growing. However, there is an issue with this treatment therapy. Prostate cancer cells eventually overcome the therapy by increasing their ability to suck up any remaining testosterone in the body. Through this new strategy, the tumor is forced to respond to higher testosterone levels again and thus it can aid in reversing its resistance to standard therapy.

Dr. Michael Schweizer, assistant professor of oncology at the University Of Washington School Of Medicine in Seattle and the study's lead researcher said that there are several larger trials that are going on and if confirmed it can lead to a new treatment approach for prostate cancers that have grown resistant to hormonal therapy. He also added that bipolar androgen therapy is still not ready for adoption into routine clinical practice as these studies have not been completed yet.

16 volunteers were chosen for the experiment. All of them had hormone therapy-resistant prostate cancer and they underwent bipolar androgen therapy. �These men didn’t have any symptoms from their cancer, like pain, and had been on standard hormonal therapy for an average of four years. Also, all of them had suffered impotence – a side effect of standard hormonal therapy for at least one year.

The results were encouraging – seven had their cancer go into remission, in four men the tumors shrank, and in one man, they disappeared completely. PSA (prostate specific antigen) levels are a standard signal of prostate cancer activity, as measured in a blood test. Schweizer said that about 50 percent of patients had declines in their PSA.

Dr. Samuel Denmeade, senior author of the study and co-director of the prostate cancer program at Johns Hopkins University in Baltimore said that he was of the opinion that the new approach has benefits beyond its effect on cancer cells. If a man’s testosterone levels are restored, many undesired side effects of effects of the hormone therapy like mood swings and not being able to have intercourse are also reduced.

Even though testosterone levels alternated between high and low, the participants seemed to tolerate the treatment well. Denmeade remarked that this treatment should not be thought of as a cure, but as a way to make men feel better and extend the time standard hormonal therapy remains effective. We hope that men taking this therapy will live longer, but we are not sure how long. �He also added that the bipolar androgen therapy might not be for “men who have not undergone any treatment for prostate cancer.

He also stressed that the long-term effects or dangers of the therapy are not known yet. Only longer studies and larger trials will help in finding out any risks associated with the treatment.

Dr. Anthony D’Amico, chief of radiation oncology at Brigham and Women’s Hospital in Boston is worried that alternating testosterone levels could actually shorten men’s lives. When a similar method was tried with estrogen in breast cancer, it caused early death.

References

https://medicalxpress.com/news/2015-01-strategy-thwart-resistance-common-prostate.html

https://health.usnews.com/health-news/articles/2015/01/07/strategy-might-thwart-resistance-to-a-common-prostate-cancer-treatment

Common Degenerative Eye Disease May Be Triggered By Tiny Mineral Deposits

Sep 24, 2015

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A new research article that appeared in the latest issue of the Proceedings of the National Academy of Sciences reveals that the scientists at the University Of Maryland School Of Medicine (UM SOM) have discovered that tiny lumps of calcium phosphate may significantly contribute to the triggering of age-related macular degeneration (AMD), a degenerative diseases of the eyes that can cause severe vision loss and blindness and which affects more than 10 million Americans. It is for the first time that the role of these mineral deposits has been found to be of significance in this disease.

For this study, retinal samples from a group of elderly patients, some of whom had AMD were studied by the researchers which included Biochemist Richard Thompson, PhD, Imre Lengyel, PhD – his colleague from University College, London, and a multidisciplinary international team. Their study revealed that the AMD samples contained hydroxyapatite, or HAP which are tiny spherules of a mineralized calcium phosphate. HAP is common in the body � it is what comprises the hard part of bones and teeth. However, never before it had been identified in that specific part of the eye.

It was known that AMD is characterized with the buildup of fatty protein deposits in the retina; however how they came about was not fully understood. When a significant deposit builds up in the eyes, it blocks the flow of nutrients into the light-sensitive portion of the eye and also hinders the way waste is flushed out of the eyes. In the study, Thompson and Lengyel discovered that the deposits seem to form around the tiny bits of HAP. Once these bits appear, the fatty protein material gets deposited around it and over years, these globules build up.

Prof. Thompson, who is an associate professor of biochemistry and molecular biology at the school, remarked that initially they had no idea about HAP being involved in the process. They made the discovery about its possible role by examining tissue samples from patients using X-ray diffraction and fluorescent staining chemicals.

AMD is so named because it affects the macula � which is the central area of the retina. This part of the eye is responsible for the sharp, direct vision necessary for reading and driving. AMD is typically found to affect older people � more than 11 percent of Americans over the age of 80 have AMD, and about 30 % people above the age of 75 are at the risk of getting advanced AMD. It affects tens of millions people worldwide and is the most common cause of blindness in older people in developed countries. Other factors that can increase the risk of AMD include smoking, some chronic infections, and chronic inflammatory diseases such as diabetes.

There is no cure for AMD. However, sometimes the damage can be slowed or halted by injections of medicines which stop the growth of the deposits. The cost of AMD is estimated at more than $340 billion.

Thompson and Lengyel are hopeful that the presence of HAP can be used as an early warning signal for AMD risk and that it can aid early intervention before patients have suffered irreversible vision loss. They are of the opinion that eventually it may be possible to devise methods that can reduce HAP deposits or limit the growth and progression of the disease.

This research have provided new insight into the deep mechanisms of this disease, and in doing so, new avenues of research have been created which has the potential to help millions of people around the world.

References:

https://medicalxpress.com/news/2015-01-common-degenerative-eye-disease-triggered.html

https://www.sciencedaily.com/releases/2015/01/150119154349.htm

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