Michigan State University researchers have identified a potential genetic target for treating an especially painful and invasive form of endometriosis.

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The new pill could be the answer to sleepless nights for many couples.

Only people with partners that snore throughout the night will understand how disrupting it can be to their sleep pattern.

And while there are a number of tricks and tips snorers can turn to for help, there is still no easy way to rid yourself of it for good.

However, scientists are hopeful a new pill being developed could be the answer.

The pill, called AD109, is being developed by pharmaceutical company Apnimed, and is a treatment for obstructive sleep apnoea.

The pill has been created to be taken once a night in order to stop symptoms such as snoring.

CEO of Apnimed, Dr Larry Miller said: “Obstructive Sleep Apnea represents a significant public health problem in the US and around the globe and current treatment options do not meet the needs of patients.”

He added: “We believe that AD109, an oral drug candidate dosed once-daily at bedtime, could be a significant breakthrough for these patients.”

So far, AD109 has gone through phase one of clinical trials, which saw 24 healthy volunteers given the drug once a night for seven days.

The results showed no side effects in the volunteers.

The next step for the pill is for it to be run through a phase two trial, where it will be tested on 140 people.

Apnimed have said they are looking to initiate this next phase this year.

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The world today may be on alert for the rampant Coronavirus, but scientists have not left out continuous research for a cure to HIV/AIDS, which has plagued millions of people everywhere. A new report reveals that another step has been taken towards a cure, as a few groups of researchers made a breakthrough.

A collaborative effort between the researchers from the University of North Carolina, Emory University, and Qura Therapeutics resulted in a breakthrough in HIV/AIDS research. The UNC Cure Center discovered a method of identifying and reactivating dormant cells that can be combined with other clearance strategies in order to clear the HIV reservoir that will end in a definitive, permanent cure.

This method was already tested on monkeys who suffer from SIV, which is a form of HIV, and the results were successful. With this result in animals, they continue to search for an effective cure for the HIV virus for humans, one that will not produce any side-effects nor necessitate maintenance medication. One of those methods will likely purge the HIV reservoir that the virus forms in the blood.

What makes the HIV virus so difficult to eradicate from a patient is because the virus forms a reservoir that returns once the patient stops using antiretroviral therapy or ART medication. Because the immune system cannot detect the virus when it is dormant, it cannot attack and kill the virus in that phase.

At the moment, the researchers are working on a drug that can identify and revive latent cells in humans. If this proves to be successful, then human trials may begin, and a cure will be developed to end the epidemic once and for all.

Aside from formulating drugs as well as identifying latent cells in humans, a group of researchers recently came up with a mathematical equation that could accurately predict when the virus would return once ART medication is stopped. Dr. Jessica Conway and her team explained their model at a conference in Hartford, Connecticut, back in January.

One challenge regarding this model is that the time the virus will rebound will vary from patient to patient as there are other factors to consider. As of now, Conway and her team are close to figuring out the model, and after a few more tests, they will have found the model that can be of big help to doctors for better clinical trials.

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Scientists at Yale University investigating the mechanisms at play in type-2 diabetes have discovered a new way they may be able to apply the brakes to the condition. The breakthrough centers on a new understanding of how fasting can drive the onset of type-2 diabetes, which led the researchers to unearth a way of intervening and switching the process off.

The research is described in a pair of studies published by Yale medical scientists, with the first focusing on a newly discovered connection between the body’s behavior when it is in a state of fasting, as it is while we sleep, and the development of type-2 diabetes.

The team found that fasting switches on a process whereby two proteins, TET3 and HNF4a, build up in the liver and elevate the production of blood glucose. In a healthy person, this process is switched off when the body exits fasting mode, but in those with type-2 diabetes that off-switch fails, leaving a surplus of glucose to build up in the blood.

By coming up with another way to switch it off, the scientists suspected they might be able to stop the disease from developing. In experiments designed to explore this theory, the team packaged genetic material called small interfering RNAs (siRNAs) inside viruses that target TET3 or HNF4 and injected it into mice. They found that this technique was effective at knocking down the levels of the proteins, along with blood glucose levels, “effectively stopping diabetes in its tracks.”

In the second study, the team explored the role TET3 plays in liver fibrosis, which is a scarring of healthy liver tissue that can lead to life-threatening conditions like cirrhosis. They found that TET3 plays a role at three different points along the fibrosis signaling pathway, meaning that drugs that can target these key proteins in type-2 diabetes could also be leveraged to treat fibrosis, for which there are currently very limited options.

“Right now, there are no effective drugs for the treatment of fibrosis,” says Xuchen Zhang, M.D., associate professor in pathology and co-author on the fibrosis study.

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Stem cells responsible for repairing the womb following menstruation can also promote endometriosis and endometrial cancer if they become dysfunctional, researchers have found.

Such malfunctioning stem cells also can reduce the chances of success for women undergoing in vitro fertilization (IVF), the study shows.

The researchers’ findings were reported in “Endometrial Axin2+ Cells Drive Epithelial Homeostasis, Regeneration, and Cancer following Oncogenic Transformation,” a study published in the journal Cell Stem Cell.

Using a technique called in vivo lineage tracing in female mice, investigators from the Hunter Medical Research Institute in Australia and their colleagues discovered that stem cells located at the base of special glands found throughout the inner lining of the womb (endometrium) are responsible for replenishing the endometrial tissue that is lost during menstruation.

In vivo lineage tracing is a technique that allows scientists to label and follow specific cells inside an organism. In so doing, the team discovered these stem cells contained high levels of a gene called Axin 2, which has been found to be active in cell types from other highly regenerative tissues.

When the researchers specifically destroyed Axin 2-positive stem cells in the wombs of female mice, they found the endometrium was no longer able to repair itself and became highly dysfunctional. Moreover, when investigators introduced cancer-associated mutations into these stem cells, the cells started to malfunction and to fuel the development of endometrial cancer.

“What we are able to show is that if you cause mutations in these cells, you get endometrial cancer,” Pradeep Tanwar, PhD, lead researcher and senior author of the study, said in a news story.

“What we now hypothesise is that when women have endometriosis, what they have is an expansion of these mutated cells. These cells end up going into the abdominal cavity. Because they are so highly regenerative — because these are the cells that are repairing the uterus in each cycle — they start making uterine-like tissues in the abdominal cavity — which is what endometriosis is,” said Tanwar, also an associate professor at the Hunter Medical Research Institute.

Tanwar also believes the malfunction of these stem cells could be the reason why women undergoing fertility treatments fail to conceive.

“Some women have repeated failed IVF cycles because their endometrium is too thin, and the embryos cannot implant,” he said. “We now know that these cells in these women are going to be defective, and that is why the repair is not happening properly,” he said.

The Hunter researchers spent seven years “exhaustively testing” their findings, Tanwar said. He said they collected and banked gynecological tissue samples from hundreds of women treated at the center.

Given the wide implications of these findings, many scientists around the globe have reached out to congratulate the team on their discovery, he said.

“There have been so many questions about these conditions, and this has given us a framework to start addressing those, and — hopefully — come up with some answers,” Tanwar said.

“There is huge potential in the study, and there is huge potential in what we are doing. This cell is affecting many of these gynaecological diseases, which are mainly uterine based,” he added.

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BioBuzz has reported that a new document submitted to the Food and Drug Administration from American Gene Technologies (AGT) may contain the cure to HIV/AIDS. The group submitted a 1,000 page document with their planned treatment.

The treatment would see an individual’s cells cultured and expanded outside the body, before being reintroduced back, with just a single dose. The aim of this immunotherapy is for the donor’s cells to stop the AIDS virus from progressing and thus build immunity from HIV.

The end goal of the treatment is to restore the body’s natural immunity to HIV, as cells that could prevent the spread of the illness are targeted first by the disease, and therefore the body’s immune system would treat it like any other disease if someone became infected.

In a statement, the CEO of the AGT, Jeff Galvin said: “We want to get these people out of jail and back to normal life. We see this as critically important. We need to move these people from anti-retroviral control to permanent immunity and we think our project may be able to do that.”

The Food and Drugs Administration should report back to the AGT on whether the treatment plan can move onto clinical trials by the end of the year. If successful, the AGT is looking to recruit patients by early next year.

Earlier this week, a research team at Abbott Laboratories published findings that a new strain of HIV had been discovered. This was the first time this had happened in almost 20 years.

The new strain, referred to as ‘HIV-1 Group M, Subtype L’, is one of dozens of mutations of the HIV virus to be discovered. There are currently known to be two main types of HIV and many subtypes which are constantly evolving over time, this is why ART (Anti-Retroviral Therapy) for HIV positive individuals may vary from person to person.   

Mary Rogers, principal scientist at Abbott said in a statement “Identifying new viruses such as this one is like searching for a needle in a haystack. This scientific discovery can help us ensure we are stopping new pandemics in their tracks.”

This new strain belongs to HIV-1 Group M, which has been responsible for the vast majority of infections in the HIV epidemic to date.

There are several ways to prevent HIV infection which include PEP, PrEP, condoms, and U=U (HIV positive people cannot pass on the virus). London based sexual health clinic 56 Dean Street are currently fundraising to help bring PrEP to more younger men, as although overall rates of new infections are declining, young men who have sex with men are increasingly accounting for a greater percentage of new diagnoses.

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Bernie Sanders became the first 2020 presidential candidate to come out in support of finding a global cure for AIDS. Scientists and researchers have been working toward a cure, but they insist that full support and additional resources from the government is necessary to find the solution. With his announcement, Sanders told the Research Foundation to Cure AIDS that “the U.S. can lead the world in finding the global cure for AIDS,” Block Toro reported.

Since Sanders’ announcement, almost every other presidential hopeful followed suit, supporting a cure for HIV/AIDS.

“We have all of the technology needed to end AIDS-related deaths and stop HIV transmission and develop a working cure for AIDS,” Sanders said. “All we need now is the political will to do it.”

In a series of questions asked by the Research Foundation to Cure AIDS (RFTCA), Sanders said that as president he would form a team of the top U.S. scientists, researchers and doctors to find a cure for HIV/AIDS, make sure every citizen had access to affordable treatment, work with the international community to help find a cure, as well as provide affordable medicine and hold Big Pharma accountable.

Sanders’ leadership and support of the cause won him praise by Kambiz Shekdar, Ph.D., RFTCA president.

“The cure for HIV/AIDS has been proven possible but the main struggle is to raise the funds needed to make it happen in real life,” Shekdar said. “We would need a presidential leadership like Bernie’s for developing the cure for all the patients in need.”

According to a transcript, Sanders “introduced curing AIDS as a new pillar” to his comprehensive AIDS address.

“Bernie believes that we can and we must end the AIDS epidemic in the United States and abroad, and we can lead the world by developing a cure for AIDS. Bernie will invest significant federal resources and convene experts, advocates, scientists, and researchers to ensure this goal is met. The United States has before come together to achieve things once thought impossible. What we need is a grassroots political movement that will stand up to the greed of the pharmaceutical industry and take the steps necessary to ensure we end the AIDS epidemic by 2025 and ensure no person in America dies because they cannot afford medication or health care. Bernie is proud to say he will, alongside a political movement, rise to this challenge.”

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Using genetic sequencing, scientists at the University of California, San Diego (UCSD), School of Medicine say they have identified a principal cellular player controlling HIV reproduction in immune cells which, when turned off or deleted, eliminates dormant HIV reservoirs.

“This is one of the key switches that the HIV field has been searching for three decades to find,” said Tariq Rana, PhD, professor of pediatrics and genetics at UCSD School of Medicine. “The most exciting part of this discovery has not been seen before. By genetically modifying a long noncoding RNA, we prevent HIV recurrence in T cells and microglia upon cessation of antiretroviral treatment, suggesting that we have a potential therapeutic target to eradicate HIV and AIDS.”

HIV spreads through certain bodily fluids attacking the immune system and preventing the body from fighting off infections. If left untreated, the virus leads to the disease AIDS.

Antiretroviral therapy is used to prevent and treat HIV. However, the medication does not cure patients. Instead, the virus remains inactive in the body. If therapy is discontinued, the virus awakens and multiplies rapidly.

In a study (“The Long Noncoding RNA HEAL Regulates HIV-1 Replication through Epigenetic Regulation of the HIV-1 Promoter”) published online in mBio, Rana and colleagues report the first genome-wide expression analysis of long noncoding RNA (lncRNA) in HIV-infected macrophages that promote tissue inflammation, stimulate the immune system, and rid the body of foreign debris. In general, lncRNAs do not encode the recipe for proteins the way other RNAs do, but instead help control which genes are turned “on” or “off” in a cell.

The team described how a single lncRNA dubbed HIV-1 Enchanced LncRNA (HEAL) is elevated in people with HIV. HEAL appears to be a recently emerged gene that regulates HIV replication in immune cells, such as macrophages, microglia, and T cells.

Using a combination of genomic, biochemical, and cellular approaches, they found that silencing HEAL or removing it with CRISPR-Cas9 prevented HIV from recurring when antiretroviral treatment was stopped. Additional research to confirm these effects in animal models will be performed.

“A major challenge in finding a cure for HIV-1/AIDS is the difficulty in identifying and eradicating persistent reservoirs of replication-competent provirus. Long noncoding RNAs (lncRNAs, >200 nucleotides) are increasingly recognized to play important roles in pathophysiology. Here, we report the first genome-wide expression analysis of lncRNAs in HIV-1-infected primary monocyte-derived macrophages (MDMs). We identified an lncRNA, which we named HIV-1-enhanced lncRNA (HEAL), that is upregulated by HIV-1 infection of MDMs, microglia, and T lymphocytes. Peripheral blood mononuclear cells of HIV-1-infected individuals show elevated levels of HEAL. Importantly, HEAL is a broad enhancer of multiple HIV-1 strains because depletion of HEAL inhibited X4, R5, and dual-tropic HIV replications and the inhibition was rescued by HEAL overexpression,” the investigators wrote.

“HEAL forms a complex with the RNA-binding protein FUS, which facilitates HIV replication through at least two mechanisms: (i) HEAL-FUS complex binds the HIV promoter and enhances recruitment of the histone acetyltransferase p300, which positively regulates HIV transcription by increasing histone H3K27 acetylation and P-TEFb enrichment on the HIV promoter, and (ii) HEAL-FUS complex is enriched at the promoter of the cyclindependent kinase 2 gene, CDK2, to enhance CDK2 expression. Notably, HEAL knockdown and knockout mediated by RNA interference (RNAi) and CRISPR-Cas9, respectively, prevent HIV-1 recrudescence in T cells and microglia upon cessation of azidothymidine treatment in vitro. Our results suggest that silencing of HEAL or perturbation of the HEAL-FUS ribonucleoprotein complex could provide a new epigenetic silencing strategy to eradicate viral reservoirs and effect a cure for HIV-1/AIDS.”

“Our results suggest that HEAL plays a critical role in HIV pathogenesis,” said Rana. “Further studies are needed to explain the mechanism that leads to HEAL expression after an individual is infected by HIV, but this finding could be exploited as a therapeutic target.”

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(Bloomberg) — Chinese researchers safely treated a man with leukemia and HIV using gene-edited stem cells, a step forward in a field that was shaken last year when another Chinese scientist used the same technology to create the world’s first genetically-edited babies.

The man’s medical case, published Wednesday in the New England Journal of Medicine, is the first detailed report in a major academic journal of how doctors are using the experimental tool Crispr to manipulate the DNA of a living patient in an effort to cure disease. But even before the earlier controversy in China, there’s been a heavy note of caution in the field about how far and fast to proceed with the technology.

The patient’s dual diseases — HIV and cancer — gave researchers at the Peking University Stem Cell Research Center in Beijing an opening. The man needed a transplant of stem cells to replace the damaged ones that were causing his blood cancer. That procedure also gave them the opportunity to re-engineer a gene called CCR5 in the donor cells to be resistant to HIV.

“This is a green light for the whole field of gene editing,” Carl June, a pioneer in the use of gene therapy to treat cancer and HIV at the University of Pennsylvania, said in an interview. He published a companion piece in the journal.

The work has some parallels to the highly controversial effort by scientist He Jiankui to alter the DNA in two embryos to make the babies resistant to HIV. That effort sparked an international backlash and calls to put a moratorium on using Crispr to create permanent changes in a subject’s DNA, especially in an embryo. The latest effort is a far more incremental but legitimate effort, especially given the imprimatur of one of the world’s foremost academic journals.

The work by Peking University’s Hongkui Deng and colleagues had several key differences from the earlier effort, including the controlled use of gene-editing on only select cells, the patient’s consent and the subsequent publication of the findings.

The experiment had mixed results. Nineteen months after the treatment, the young man’s cancer, an acute lymphoblastic leukemia, is in remission, and the modified cells integrated into his body and remain. The attempt to cure his HIV was a failure: Only about 5% of his infection-fighting lymphocytes are now resistant to HIV, making continued treatment of the virus necessary.

Even so, the results show a key proof of the concept that Crispr-edited cells can be transplanted into a person and persist long-term, Deng said in an emailed response to questions.

“We should all hope that this is a significant and powerful advance in scientific research, for if it can be tested safely and ethically — and it surely can — it could transform medicine,” said Laurie Zoloth, a professor of religion and ethics at the University of Chicago. “The first published paper is quite an historical moment.”

The researchers didn’t detect any adverse events from the gene-editing or signs that the man’s DNA had been damaged. Larger studies where more altered cells persist are needed to confirm the findings, Deng said. Concerns over unknown potential effects of Crispr has been one of the major hurdles standing in the way of more trials moving forward.

“If they had gone the other way, with a lot of off-target hits, that would have been chilling for the technology,” June said.

Data on three patients treated with Crispr-manipulated cells at the University of Pennsylvania, perhaps the first in the U.S., will be presented at the American Society of Hematology meeting in December.

Crispr has been compared to a word-processing system that allows writers to easily cut out extraneous words and correct typos. With DNA, it acts like molecular scissors, precisely trimming specific flaws in genes. Scientists are still trying to determine if tinkering with the genome can create stray errors elsewhere or lead to unexpected harms, such as cancers caused by uncontrolled cell growth.

There’s a biological rationale for targeting HIV in a leukemia patient, in part because of a handful of people cured of HIV who had bone-marrow transplants. Timothy Ray Brown became the first adult ever to be cured of HIV in 2007 after he received a bone marrow transplant to treat his leukemia. The donor cells had a rare mutation in the CCR5 gene, found in about 1 in 20 people, that makes it difficult for HIV to infect cells. Brown was known as the “Berlin patient,” and other researchers have tried to replicate his experience.

Researchers are now planning to try to increase the number of cells that are transformed and can thrive inside of a patient, Deng said. Other diseases with genetic causes, such as sickle cell anemia, muscular dystrophy, cystic fibrosis and cancer are likely to see a surge in interest based on the new results.

“Crispr technology is so flexible it can be used for all types of conditions,” June said. “You can rewrite the genetic code at will.”

But the China study also showed some of Crispr’s limits because only about 5% of the cells were affected, said Zoloth, the University of Chicago professor.

“This thoughtful honesty and modesty in scientific claims are an important part” of the project, Zoloth said. “It is a first step, if tentative, toward engineering naturally occurring constructs in nature in ways that benefit humanity.”

Leaders in the field agreed the safety findings are a critical first step, though they are hoping further refinement of the process will lead to better results. One key issue is that cells that have been altered using gene-editing or other types of technology are “finicky and tricky to transplant,” said Jennifer Doudna, professor of biochemistry and molecular biology at the University of California, Berkeley, who is credited as an inventor of Crispr.

“This plants the flag to say that at least in this one instance, this type of therapy appears safe,” she said. “The next step is showing that there is some efficacy, a therapeutic benefit to doing this.”

While the NEJM report is the first publication about the use of Crispr in humans, other pioneering researchers have been using it for years in China. The first trials started in 2016, when Lu You, a physician at Sichuan University, put gene-edited cells into a lung-cancer patient. Since then, scientists have launched multiple trials and reportedly treated dozens of patients. But little is known about some of those studies, and medical research is not as stringently regulated in China as it is in the West, prompting concerns about their safety and ethics.

“In the next 18 to 24 months, we’ll start to see published results from a number of these ongoing trials,” Doudna said. “That’s where the rubber hits the road. Does it benefit patients? Time will tell.”

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A cure for aging?

The research was carried out at University of Southern California and focuses on a kind of cell known as a senescent cell. Much aging-related research focuses on these, as they are key players in how humans grow old. Essentially, these are cells that have ceased the ability to divide and are therefore thought to be a key driver in age-related decline, along with conditions such as arthritis and heart disease.

“Senescent cells are effectively the opposite of stem cells, which have an unlimited potential for self-renewal or division,” says lead author Alireza Delfarah. “Senescent cells can never divide again. It’s an irreversible state of cell cycle arrest.”

While this is a well-established function of senescent cells, the biological processes underpinning this behavior aren’t so well understood. To investigate this, the team performed an analysis of the metabolic pathways in epithelial cells that had become senescent.

This led the researchers to discover that the cells had stopped producing a class of chemical compounds called nucleotides. These are the building blocks of DNA, and the researchers found through further experiments that when they intervened to stop the cells producing nucleotides, they indeed went on to become senescent.

“This means that the production of nucleotides is essential to keep cells young,” Delfarah says. “It also means that if we could prevent cells from losing nucleotide synthesis, the cells might age more slowly.”

That is easier said than done, but the discovery marks an important step in this direction. If we understand how and why cells become senescent, then we may be able to design drugs that target those particular machinations. But equally important, identifying what makes these cells unique will make it easier to design drugs that selectively target them and not other healthy ones.

These medications are part of a class of drugs called senolytics, which focus on eliminating senescent cells for healthier aging. Last year, scientists made a breakthrough in this area, demonstrating a new type of senolytic compound that could slow down the deterioration of aging mice with just three days of treatment.

The thinking with this kind of research isn’t necessarily to stop aging altogether, but to make aging in humans a more palatable experience by keeping us fitter and healthier for longer. Senescent cells are implicated in a range of age-related conditions, so new methods of clearing them away or preventing their buildup in the first place could open up some exciting possibilities.

“To drink from the fountain of youth, you have to figure out where the fountain of youth is, and understand what the fountain of youth is doing,” says study author Nick Graham. “We’re doing the opposite; we’re trying to study the reasons cells age, so that we might be able to design treatments for better aging.”

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Cartilage degeneration and damage treatment remain a major challenge in today’s society; hence, tissue engineering strategies are being developed to investigate new alternatives based on a combination of cell therapy and 3D scaffolds to support cartilage cells. Such therapies have emerged as a promising new approach to the treatment of cartilage injuries.

An international team of scientists, led by the University of Granada (UGR), has designed a new hydrogel using pioneering “polymer microarrays” technology, which successfully helps to regenerate cartilage.

The researchers evaluated the adhesion capacity and viability of healthy chondrocytes extracted from patients with osteoarthritis of the knee, screening over 380 different polyacrylate and polyurethane polymers. Of these 380 alternatives, they selected the ten polymers that presented the best properties in terms of facilitating the adhesion and viability of this cell type in particular. They also performed further assays to test the ability of these 10 polymers to support chondrocyte proliferation to produce cartilage matrix in long-term cultures.

The polymer poly (methylmethacrylate-co-methacrylic acid) was found to present the best biological and chemical characteristics, and was thus selected to synthesize hydrogels for use as 3D matrices. The analysis and characterization of the ultra-structural morphology, the microstructure, and the mechanical tests of this new hydrogel showed that it possessed the required characteristics to generate a support that mimics the environment that chondrocytes need in the cartilage.

Furthermore, biological characterization of this material showed that it has the capacity to generate the appropriate niche for growth in a number of chondrocytes, while retaining their characteristics in the long-term culture in the laboratory setting. This was demonstrated by the high expression of genes characteristic of chondrogenesis, such asType II collagen,SOX-9, and aggrecan. Not only that, these chondrocytes proliferated by colonizing the entire hydrogel, producing an extracellular matrix rich in proteoglycans, similar to that which they produce in native cartilage.

Subsequent studies on mice verified the tremendous potential of this polyacrylate. First, the implantation of the hydrogel in immunocompetent mice showed that the material is totally biocompatible, presenting no signs of rejection by the organism. Furthermore, mouse cells colonized the hydrogel and secreted extracellular matrix. Second, the implantation of the hydrogel after it had previously been in culture with patients’ chondrocytes for 21 days showed that, when taken from the mice, the chondrocytes continued maintaining their viability, proliferating, and expressing chondrogenesis genes, producing the matrix typical of the aforementioned cartilage.

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Scientists at the National Institutes of Health are linking genetics to the risk of high blood pressure among black patients by analyzing genomic research databases.

The scientists believe variants in a gene known as ARMC5 may be associated with higher blood pressure among blacks, following a study that found 17 variants in the ARMC5 gene that were associated with high blood pressure.

However, researchers also found one variant gene that appears to be protective and associated with a role in regulating blood pressure and seems to be limited to people of African descent, but more study is needed.

“High blood pressure increases a person’s risk for heart disease and stroke,” says Constantine Stratakis, MD, scientific director at the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD). “The condition is more common among blacks, who also tend to get it at a younger age than whites do, and we are studying the underlying causes of this health disparity.”

Use of information technologies to support multiple large genomic research databases, including access to human genome research databases, are helping scientists collaborate in the United States and United Kingdom. For example, work on the new variant gene also may suggest a new predisposition to tumor formation also in blacks with high blood pressure. “Until now, we knew nothing about the new variant gene,” Stratakis says.

Earlier work by the Eunice Kennedy Shriver National Institute of Child Health and Human Development group linked some variants of ARMC5 to primary aldosteronism, a hormonal disorder that causes high blood pressure among black patients.

In a newer study, analyzed datasets containing genomic information from large numbers of people were accessed via existing databases from the National Institutes of Health’s Minority Health Genomics and Translational Research Bio-Repository Database, and the Genomics, Environmental Factors and Social Determinants of Cardiovascular Disease in African-Americans Study in the United States, as well as from the United Kingdom Biobank.

The UK biobank is being used as another large dataset to confirm some results based on data from 3,000 people, and the researchers found the same results in both nations.

For now, the exact function of the ARMC5 gene is unclear, and more work is needed to understand what the gene does and how variants may protect or predispose a person to high blood pressure.

Today, researchers cannot definitively say there is a link between high blood pressure in black persons and the presence of a tumor, but the new gene does play a role in formation of tumors in the adrenal gland, Stratakis explains.

The new gene regulates early adrenal growth and likely affects how cells in adrenal glands proliferate and die. So now, researchers are looking for an on-off switch that may or may not affect blood pressure and tumors.

“Collectively, our research suggests that ARMC5 may play an important role in regulating blood pressure in blacks,” concludes Mihail Zilbermint, MD, and one of the lead authors of the study. “Because the gene is linked to primary aldosteronism (high blood pressure), ARMC5 may be involved in how the adrenal glands function with the hormones that are important for regulating blood pressure.”

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In recent years, scientists have witnessed a disturbing trend regarding the health condition of teenagers. Apparently, more and more teenagers are falling prey to high blood pressure. This is reason for worry as developing this condition so early in life can have serious health implications in the long run.

The health complications that teenagers with high blood pressure can have later on in life are many. A study of adolescent obesity and hypertension in urban India, published in the International Journal of Community Medicine and Public Health,discovered that out of 1,486 adolescent respondents, 7.5 per cent suffered from pre-hypertension symptoms and 5.4 per cent had hypertension.

What exactly is blood pressure?
It is a system of measurement in medical terms. In medicine, blood pressure is measured by the force of blood pushing against the artery walls. Your body works in a complex system. When your heart beats, blood is pumped through your arteries round your body to give it the energy and oxygen it needs. This blood pushes against the sides of the blood vessels or against the artery walls. If the force or pressure is too high, it can harm the arteries and weaken the heart. When you check somebody’s blood pressure, you will see two numbers. The higher number is systolic pressure and the lower number is diastolic pressure.

What causes blood pressure in a teenager?
But just one reading will not be enough to confirm that your teenage son or daughter is suffering from this condition. There can be temporary spikes due to anger, anxiety or physical activities. Usually, if doctors don’t know the cause of this condition, they refer to it as primary. But if the cause is known, i.e., if it is due to illness or lifestyle choices, it is called secondary.

Most secondary BP issues are due to medical conditions like kidney and heart diseases, hormonal or endocrine disorders, stress and anxiety. It could also result from substance abuse and the use of prescription drugs like corticosteroids or birth control pills.Hormonal changes and rapid growth spurts can also cause a temporary spike in cholesterol and blood pressure levels. But since this is temporary, there is nothing to worry about.

Risk factors for high BP
High blood pressure is often triggered by some external factors. It could also be the result of some underlying health condition. Usually, overweight teens, especially boys, fall in the high-risk category. A family history of high BP or cardiovascular disease as also a mother who smoked during pregnancy significantly increases the risks.

Symptoms to watch out for
This condition is also known as ‘the silent killer’. There are usually no symptoms at all to warn a person that something might be wrong. But if BP levels go up very high, then you will notice a flushed and red face. Hot flashes are also very common with this condition.Other symptoms to look out for are headaches, heaviness in the head, pain in the chest, breathlessness and palpitation. If BP shoots up really high, it can also cause seizures.

Diagnosis of the condition
The doctor will, first of all, rule out any family history of high BP. He will take notice of medical history, diet, level of physical activity and also his or her activity level at school. He may also recommend a physical examination of his patient. This can involve urine tests, blood tests, and ultrasound examination of the kidneys. This will help him to figure out the cause of the condition.

Line of treatment
Treatment depends on symptoms, age and general health. It will also depend on the severity of the problem. If it is due to any medical reasons, that has to be taken care of first. If your teen has an unhealthy lifestyle, you need to have a serious talk with him about changing his habits.

A doctor will not prescribe medicines immediately if he can avoid it. Instead, he may just prescribe a few changes in lifestyle and diet.

On the diet front, your doctor may ask you to have lots of fruits and vegetables, whole grains and low-fat or non-fat dairy products. He may also ask you to cut down on salt and sugar and limit your intake of rich, fatty foods. Lose weight, exercise more, avoid smoking and drinking. Learn how to manage your stress and anxiety issues. You will soon see a drop in you BP.

What are the complications?
High blood pressure increases a person’s risk of coronary heart disease and stroke. However, this is rare in children and teenagers. But as they grow older, complications can manifest themselves because of this problem. And, by the time they are in their twenties, they may display a thickening of their arteries, which can cause heart attacks and even strokes. According to researchers from the American Heart Association, organ damage from high blood pressure doesn’t only occur in adults.It can happen to teenagers too. They are of the view that imaging of the heart may be useful to determine how aggressive treatment should be.

What you can do
Take up some physical activity even if it means just going for a walk round the block. You can easily lower your blood pressure by doing this daily for 20 to 30 minutes. Also keep an eye on your salt intake and eat more potassium-rich foods. Try to avoid caffeine and don’t get pressured in having alcohol by your peers. The best thing to do if you have high blood pressure is to manage your stress levels. Take professional help if needed. But try to get a grip on our stress and anxiety issues. Eating dark chocolate also helps. But the most important thing to do here is lose weight.

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