Since the 1970s, genetic screening has been standard practice during pregnancy. The goal of this kind of genetic testing has historically been to understand the likelihood an embryo carries a heritable disease, the classic example being the recessive genes for autosomal recessive disorders like cystic fibrosis, sickle cell anemia, and Tay Sachs, or tests that determine developmental disorders like Down Syndrome. This allows parents to make informed choices about ending pregnancies and planning ahead for potential issues. But as genetic technologies develop and gene editing becomes more widely practiced the possibilities are not limited to observation. As Dr. Robert Klitzsman writes inDesigning Babies: How Technology is Changing the Way We Create Children, genetic testing in the context of IVF is already giving us a glimpse of the ways in which the proliferation of new technologies could affect the genome of future children and future generations. And its not all good news.

Klitzman, Director ofColumbia Universitys Masters of Bioethics Program, suggests that progress has not been accompanied by adequate oversight or regulation. What are the limits of genetic screening, genetic testing, and gene editing technologies? The answer has as much to do with what risks are deemed acceptable and what risks are not. Designer babies are no longer the stuff of science fiction, but would-be parents arent exactly in a DNA Build-a-Bear. A transition is underway and Klitzman believes that parents need to understand the bleeding edge of whats possible to have the necessary context to understand the technologies they are using even in the process of basic screenings.

Fatherly spoke to Dr. Klitzman about the current state of genetic testing and the potential risks of emerging technologies.

Expecting parents likely understand one side of genetic testing, screening for heritable diseases. But new technologies and new discoveries mean that we can do more with genetic information and with genes themselves than ever before. So what are the limits of the current technologies?

A few years ago people thought wed find the cancer gene or the fat gene. But now we know that for most common diseases and most complex traits there are many genes involved. Sure there are certain genes that increase the risk of cancer from, say, 5 or 10 percent. But in genetic screening for diseases people should realize that, for a lot of diseases, the world is more complicated than just screening an embryo.

So its the old debate: nature or nurture? The answer is both. For a lot of traits, genetics explains the part but not all of the risk of the disease. So you may undergo genetic testing or you may screen embryos and the child may still get certain diseases. So its not always foolproof.

But its better than nothing.

Its important for parents to get tested to see if they have recessive conditions particularly if its in their family. If anyone has cystic fibrosis in their family, they should be tested to know. If theyre a carrier, they should see if their spouse is a carrier. If anyone has breast cancer in their family, they should be tested to see if they have that mutation. I think people with sickle cell disease should be tested for that. I think any woman who is over 35 should have the embryo tested for down syndrome and other chromosomal abnormalities. So I think there are certain diseases.

But, through evolution, most diseases for which there is a very predictive genetic test tend to be rare. If there was a terrible gene that was wiping out people, it wouldnt be getting passed on. The only genes that get passed on are not going to be from really terrible mutations because they would kill the people and by and large they wouldnt have any kid.

Its interesting that you point out the limits of genetic testing technologies because youre also a strong advocate for increased access.

I think insurance should pay for genetic testing. If a couple is concerned because their cousin has cystic fibrosis or someone in their family has sickle cell disease and wants to get tested, that should be covered. It may not be covered now so I think thats another set of policies that need to change. And part of that I think there needs to be more genetic counseling, which insurance also doesnt cover. The laws havent kept up with the technology. Our technologies advanced way ahead of our legal system and our duty to understand and figure out what to do with that of ethical legal and social questions involved.

A lot of the thornier issues you write about involve preimplantation genetic diagnosis, which is genetic testing post-conception and prior to pregnancy in the context of IVF. How are the decisions made by would-be parents undergoing PGD different than the decisions being made in the context of normal genetic testing?

Right now, we genetically screen embryos. When a couple undergoes IVF, lets say they create eight embryos. Doctors could say, These four are the girls, these four are the boys. Now, lets say a family has a history of breast cancer or the mother has the BRCA gene which carries breast cancer. The doctors could say, These three embryos have breast cancer gene these five dont. And the couple can choose the ones that dont.

Also, increasingly couples can say, Well, I just want a boy. And that creates a number of ethical challenges as opposed to letting Mother Nature do whatever it would do.

So theres potential in that specific context to take action in a way thats not possible in typical screenings. How much of that action is embryo selection versus actual gene manipulation?

We can take genes out. Theres a gene associated with Huntingtons disease or the BRCA breast cancer gene. We now have the technology to take them out.But these technologies are still in an experimental phase. And Im concerned that theyll soon be made fairly widely available even though there still may be risks involved and people may or may not fully appreciate those risks.

A few years ago, a doctor in China used CRISPR to edit the genes of twin girls. That opened brought a lot of criticism but also raised awareness of what can be done with this technology.

Thats right. So what Dr. He Jiankui did is that he worked with fathers who had HIV. There was a concern that the father could potentially pass HIV onto the child. And so he took the embryo and disabled the CCR5 gene that is involved in letting HIV get into a cell. The problem is that when you disable that gene, the risk of getting HIV goes down but the risk of getting influenza getting in goes up as do other risks.

DNA consists of three billion molecules. Each of us is a shelf of books in an office that has three billion letters in them. Well, if you go in and rip out some letters, you want to make sure you rip out the right ones. And so it looks like Dr. He didnt do it so precisely. So in fact what he said he took out wasnt exactly what he took out. In other words, if a child is born and missing part of the DNA, that part might be the next gene thats involved for, say, brain development or something like that.

You need to be very, very careful.

Presumably, the ethical questions get more complicated when gene editing becomes a more widely available procedure.

Until 60 years ago, we didnt even know what DNA did. We now have the ability to identify genes and were increasingly finding genes that are associated with not only various diseases but also human traits those associated with blonde hair and blue eyes, those associated with height and perfect pitch.

I think CRISPR probably will be used for people wanting or not wanting certain socially desirable or undesirable traits in their children.

A Gattaca situation.

Yes, exactly.

This interview has been condensed and edited for clarity.

The post Gene Editing Is Creating a New World of Designer Babies. Are We Ready For It? appeared first on Fatherly.

Read the rest here:
Gene Editing Is Creating a New World of Designer Babies. Are We Ready? - Yahoo Lifestyle

Recommendation and review posted by Bethany Smith

Genetic testing has become a hot topic with patients, families, health care providers and many others within the inherited retinal disease (IRD) community. Eye Want 2 Know brought to you by Spark Therapeutics, is pleased to bring you a special educational evening featuring genetic testing stories and experiences as told from the patient, advocate and health care professional perspectives.

Join the IRD community at this limited-seating event on World Sight Day, October 10 in San Francisco to hear first-hand genetic testing accounts, including:

Danelle Umstead, blind Paralympian and former Dancing with the Stars contestant

Elias Traboulsi, MD, M.Ed., Head of the Department of Pediatric Ophthalmology, Director of the Center for Genetic Eye Diseases at Cleveland Clinic's Cole Eye Institute

Chris Moen, MD, Chief Medical Officer of the Choroideremia Research Foundation

Meghan DeBenedictis, MS, LGC, M.Ed., Licensed, Certified Genetic Counselor and Coordinator at Cleveland Clinic's Cole Eye Institute

WHEN: Thursday, October 10, 5:00PM-7:00PM

WHERE: Town Hall at Galvanize, San Francisco

Genetic testing has become a hot topic with patients, families, health care providers and many others within the inherited retinal disease (IRD) community. Eye Want 2 Know brought to you by Spark Therapeutics, is pleased to bring you a special educational evening featuring genetic testing stories and experiences as told from the patient, advocate and health care professional perspectives.

Join the IRD community at this limited-seating event on World Sight Day, October 10 in San Francisco to hear first-hand genetic testing accounts, including:

Danelle Umstead, blind Paralympian and former Dancing with the Stars contestant

Elias Traboulsi, MD, M.Ed., Head of the Department of Pediatric Ophthalmology, Director of the Center for Genetic Eye Diseases at Cleveland Clinic's Cole Eye Institute

Chris Moen, MD, Chief Medical Officer of the Choroideremia Research Foundation

Meghan DeBenedictis, MS, LGC, M.Ed., Licensed, Certified Genetic Counselor and Coordinator at Cleveland Clinic's Cole Eye Institute

WHEN: Thursday, October 10, 5:00PM-7:00PM

WHERE: Town Hall at Galvanize, San Francisco

Read more here:
Beyond the Science: Perspectives on Genetic Testing for IRDs - NBC Bay Area

Recommendation and review posted by Bethany Smith

New guidelines for genetic testing should help more women and their relatives take steps to improve their odds against cancer that might run in the family.

All women who have had cancer of the breast, ovary, Fallopian tubes or peritoneum tissue in the walls of the abdomen should be offered a screening tool to determine their risk of mutation, new U.S. Preventive Services Task Force guidelines say.

The new recommendation removes a wording that limited testing to those diagnosed at younger ages.

Thats a pretty big thing, genetic counselor Kimberly Knapp said at Joyce Murtha Breast Care Center in Windber.

In the past, screening for breast cancer susceptibility genes BRCA1 and BRCA2 was recommended for women who developed breast or ovarian cancer before age 50 and others who had certain types of cancer before age 60.

Now, we dont have to age discriminate, Knapp said.

Anyone with a significant family history of breast or ovarian cancer should also consider genetic screening, which begins with a thorough review of family cancer history with a trained counselor, Knapp said.

Those women can contact breast cancer programs at several of the regions hospitals to find out more about their risk.

Genetic counselors will be able to help determine if they are eligible for genetic testing for the BRCA1 or BRCA2 gene mutations.

BRCA is shorthand for breast cancer, but the mutations are also associated with an increased risk of other cancers.

Genetic testing at Joyce Murtha Breast Care Center at Chan Soon-Shiong Medical Center at Windber tests for the BRCA gene, Knapp said.

Because researchers continually find more genetic links, Windber offers a genetic screening for a panel of almost 50 different mutations.

The new guidelines expand the pool of patients who are eligible for insurance coverage of the test, she said.

At Indiana Regional Medical Center, breast surgeon and genetic counselor Dr. Dan Clark works with families to screen for 24 gene mutations.

Screening is not just a yes or no. You get a report with four pages of results, he said at the hospital.

The report may recommend additional screenings for hereditary cancers, including breast, ovarian and colon cancer.

We know there are a lot of other cancers associated with genetics, he said.

But most cancer is not hereditary, he warned.

The American Cancer Society estimates between 5 percent and 10 percent of all cancers come from gene mutations passed on through families.

Clark fears heightened attention on genetic risk may cause women with breast cancer in their families to think they are not at risk, noting most breast cancer patients have no family history of the disease.

Link:
Genetic testing expanded to help those with disease in their families - Oskaloosa Herald

Recommendation and review posted by Bethany Smith

Von Willebrand disease (VWD) is the most common hereditary bleeding disorder but one of the most difficult to diagnose, especially type 1 VWD. Recurrent challenges include the need to complete several assays of von Willebrand factor (VWF) activity and lack of consensus surrounding the acceptable standard for diagnosis. Consequently, improving current diagnostic techniques, as well as implementing new methods, is essential to ensure patients are provided optimal care.

In a review article published in Current Opinion in Hematology, Veronica H Flood, MD, of the department of pediatrics at the Medical College of Wisconsin in Milwaukee, and colleagues summarized the current literature surrounding the diagnosis of type 1 VWD. They also reviewed new advances in genetic testing for VWF, which could serve as a potential alternative to conventional laboratory methods.

Overview of Genetic Dysfunction

In contrast to type 2 VWD, type 1 VWD may include genetic defects in the coding region of the VWF gene. These mutations vary from insertions and deletions to point mutations that produce missense or nonsense mutations. With conventional sequencing methods, insertions and deletions can be missed, which has historically precluded the clinical use of genetic-based diagnostic techniques. These limitations are not typically seen in type 2 VWD as genetic defects are usually present in the DNA region specific to the impacted functional region.

Because of the high degree of polymorphism seen in the VWF gene, entire genome or exome sequencing may be required for diagnosis; in other instances, the VWF gene may be analyzed directly if a particular coagulation defect is suspected. In type 1 VWD, certain high frequency variants have been linked to disease etiology, but recent data have highlighted the potential role of novel variants in type 1 VWD. The high degree of variability seen in the VWF gene is certainly a key contributor to the disease phenotype, but not all defects will ultimately lead to VWD.

Modifier Genes and Diagnosis

In addition to defects in VWF, several genes independent of the VWF locus have been shown to affect VWF levels. The most described modifier gene is ABO, though others such as CLEC4M, STAB2, and STXBP5 also exist. Blood group O levels of less than 50 IU/dL are routinely used to establish a diagnosis of VWD, but some individuals with blood type O also meet this criteria despite being healthy. Some experts have proposed that low VWF may be more suitably described as a risk factor for bleeding instead of as the basis for bleeding.

Read more:
Advances in the Diagnosis of Type 1 von Willebrand Disease: Genetic Testing - Hematology Advisor

Recommendation and review posted by Bethany Smith

The globalmarket for testosterone replacement therapyis characterized by the presence of a large number of small and large scale manufacturers. All of the manufacturers have been steadfast in filling the meagre market gap in order to enhance their prospects of growth. Furthermore, research and development has been the central characteristic of al the market players operating in the global market.

In 2015, it was found that 80% of the total market share was held by the top five market vendors with AbbVie Inc. taking the lead. The large scale vendors are focusing on establishing an iconic brand for their product by resorting to rigorous marketing and advertising tactics. The smaller companies are expected to concentrate on capturing the local and regional markets to sustain themselves in the current scenario of stiff competition.

A negative implication for the leading market players in recent times has been the loss of patents for their products. This has not only plundered them of revenues but has also affected the workflow of these companies. The market players are expected to launch awareness campaigns about testosterone replacement therapies in order to educate and inform the consumers. Hence, the market for testosterone replacement therapies is expected to witness the emergence of several new trends and opportunities over the forthcoming years. Some of the key players in the global testosterone replacement therapy market include Bayer AG, Endo Pharmaceuticals, Inc., Novartis AG, and Allergen plc.

Get Sample with Latest Research @https://www.transparencymarketresearch.com/sample/sample.php?flag=S&rep_id=1097

The CAGR for theglobal testosterone replacement therapy marketis estimated to be -4.20% over the period between 2016 and 2024. The negative growth rate of the global market is expected to take the market value from US2.0 bn in 2015 to a decreased value of US$1.3 bn by 2024-end.

High Incidence of Hypogonadism to Drive Market Demand

Research studies suggest that around 30% of all men suffer from testosterone deficiency, which has driven demand within the global market for testosterone replacement therapy. Furthermore, the population demographic of men in the age range of 40-79 years is more likely to suffer from testosterone deficiency. The need for mutation or having an offspring amongst men in the aforementioned age range has driven demand within the global market. Moreover, the geriatric population has been on a rise, which underhandedly contributes to market growth. Several campaigns aimed at educating people about the benefits of testosterone replacement therapy have been an important propeller of demand within the global market. It is anticipated that more people suffering from testosterone deficiency would resort to these therapies over the coming years.

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Side Effects of Testosterone Replacement Therapy Could Obstruct Market Growth

Despite the rising awareness amongst the masses about the advantages of testosterone replacement therapies, the market growth is hindered by the apprehension of the people. The chances of developing metabolic disorders are higher in men who undergo testosterone replacement therapies. Furthermore, the risk of developing cardiovascular diseases also discourages people from resorting to testosterone replacement therapies. The FDA has also cautioned people about the use of such therapies by issuing strict warnings, which has further obstructed the growth of the global market.

See original here:
Testosterone Replacement Therapy Market: An Insight on the Important Factors and Trends Influencing the Market - Online News Guru

Recommendation and review posted by Bethany Smith

An individuals experiences during early life can influence their risk for disease as an adult. Dr. David Barker first postulated this in the 1980s following his observations that infants born with low birth weight were at significantly increased risk for developing cardiovascular disease as adults. This idea was controversial at the time because it challenged the conventional thinking that unhealthy lifestyle was the primary cause of cardiovascular disease. However, subsequent epidemiologic studies confirmed Barkers findings and the concept that early-life experiences are an important determinant of adult disease risk became known as the Barker hypothesis.

While the Barker hypothesis was derived from evidence linking foetal malnutrition to cardiovascular disease risk in adulthood, the concept has since expanded to include a broader spectrum of risk factors, diverse disease states targeting different organ systems, and developmental periods extending beyond gestation. In recognition of this paradigm shift, the Barker hypothesis was renamed the developmental origins of health and disease (DOHaD) hypothesis. Several decades of DOHaD research have identified at least four categories of early-life risk factors: the nutritional status of the pregnant woman and young child, psychosocial stress, immunological stress, particularly infection during pregnancy, and chemical exposures. It is now also appreciated that the risk of most, if not all, adult-onset diseases are influenced by early-life stress, but only if exposures occur during specific periods of development. These high-risk periods are referred to as critical periods or critical windows of development, and these vary depending on the early-life insult and the target organ. For many organ systems, however, the foetal period is the primary critical window.

The nervous system is particularly vulnerable to early-life stressors, perhaps because human brain development continues after birth, throughout early childhood and into adolescence. To date, research supports an association between early-life environmental insults and increased risk of neuropsychiatric disorders like schizophrenia, demyelinating diseases, such as multiple sclerosis (MS), and neurodegenerative diseases, such as Alzheimers and Parkinsons diseases (AD and PD, respectively). Whether an early-life stressor increases an individuals risk for neuropsychiatric or neurologic disease depends on numerous factors. What is the type and magnitude of the stressor? Is the insult continuous, intermittent, or a single isolated incident? What is the timing of exposure relative to critical windows of development, which vary across different brain regions? Does the affected individual carry genes that confer increased susceptibility or increased resistance to the adverse effects of the stressor? Sex also influences the impacts of early-life stressors, perhaps because gonadal sex hormones influence many of the organisational aspects of neurodevelopment. Examining the sex-specificity of early-life stressors may be important for understanding why many neurological and neuropsychiatric diseases exhibit a sex bias in their incidence and clinical profile.

Maternal infection during pregnancy is strongly linked to increased risk of schizophrenia, though it does not appear that any specific pathogen or class of pathogens is responsible. While there is disagreement as to whether a specific trimester of pregnancy is most vulnerable, the pro-inflammatory environment created by maternal infection is thought to alter the pattern of cellular connections made in the foetal brain, laying the groundwork for altered behavior in adulthood. Emerging evidence also suggests that early-life exposure to the lead (Pb) may increase risk for schizophrenia, particularly in individuals that express a mutation in the disrupted in schizophrenia 1 (DISC-1) gene, a gene that is strongly associated with schizophrenia and related mental disorders. AD is the most common cause of progressive dementia in elderly adults and it is rapidly increasing in global incidence; PD is the second most common neurodegenerative disease after AD. Only a small percentage of cases of either disease can be attributed to solely genetic causes, supporting a role for environmental factors in determining individual risk. Recent studies have identified early-life risk factors for AD and PD, including low birth weight, premature birth, living in a rural area, low socioeconomic status during childhood, and prenatal or early childhood exposures to environmental pollutants, including heavy metals, pesticides, and air pollution. Air pollution has also been linked to an increased risk of MS.

A key question in the field is how do early-life events influence risk of adult-onset disease? It is believed that environmental stressors disrupt the organisational patterning and/or function of the developing brain by altering cell numbers or interfering with the differentiation of neurons or glial cells. So why do these changes not manifest as functional deficits or disease until adulthood? One explanation is that the affected cells are not functional until later in life. For example, exposure of the developing brain to high concentrations of the food additive monosodium glutamate (MSG) causes excessive death of neurons in the hypothalamus by triggering apoptosis, a form of programmed cell death. However, functional deficits associated with the foetal loss of these hypothalamic neurons (hypogonadism and infertility) become evident only in adolescence when the neuroendocrine function of these neurons is normally activated. Alternatively, the adverse impacts of the early-life stressor are masked or initially attenuated due to compensatory mechanisms or plasticity of the brain. However, these developmental perturbations predispose the individual to neural deficits following subsequent insults, such as chemical exposure, disease, or aging due to decreased brain reserve capacity. This phenomenon has been demonstrated in both animal models and humans following developmental exposures to methyl mercury or pesticides.

In summary, the experimental evidence indicates that early-life insults can fundamentally change the trajectory of brain development, thereby diminishing the ability of the brain to protect against subsequent insults, which increases susceptibility to disease in adulthood. A significant challenge in the field is to identify early-life stressors that increase adult-onset disease in humans. Detecting effects in the human population is difficult because the effects do not manifest until well after the developmental exposure. However, the effort to identify these associations merits investment of research dollars because preventing disease by identifying and reducing or eliminating risk factors is more effective than treating disease in terms of both individual and societal costs.

Please note: This is a commercial profile

Editor's Recommended Articles

Read more here:
Environmental exposures during early life influence adult disease risk - Open Access Government

Recommendation and review posted by Bethany Smith

The report provides a basic overview of the Androgen Replacement Therapy industry including its definition, applications and manufacturing technology.with leading business players.

Androgen replacement therapy, often referred to as testosterone replacement therapy, is a form of hormone therapy in which androgens, often testosterone, are replaced. ART is often prescribed to counter the effects of male hypogonadism. Rising aging male population with disease and increasing awareness about disease and therapy benefits dominating the market.

Augmented demand for the global Androgen Replacement Therapy market has been increased in the last few years. This informative research report has been scrutinized by using primary and secondary research.

Get a Sample Copy of Global Androgen Replacement Therapy Market Report @ https://inforgrowth.com/sample-request/4914309/androgen-replacement-therapy-market

Top Key Players: AbbVie, Endo International, Eli lilly, Pfizer, Actavis (Allergan), Bayer, Novartis, Teva, Mylan, Upsher-Smith, Ferring Pharmaceuticals, Kyowa Kirin, Acerus Pharmaceuticals

The Global Androgen Replacement Therapy Market Report represents highly detailed data including recent trends, Market demands, supply and distribution chain management strategies which will help to identify the workflow of Global Androgen Replacement Therapy Market Industry.

Global Androgen Replacement Therapy Market Report provides critical and detailed data for investment plans with research and development budgets, raw material budgets, labor cost, and other funds. Global Androgen Replacement Therapy Market industry is large enough to build a sustainable business, so this report helps you to identify the opportunities in Global Androgen Replacement Therapy Market by region: North America, Europe, Asia-Pacific, North America and Middle East and Africa.

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Androgen Replacement Therapy Market by Type: Gels, Injections, Patches, Others

Androgen Replacement Therapy Market by Application: Hospitals, Clinics, Others

Major highlights of the global research report:

Finally, the researchers throw light on the different dynamics of the market such as drivers, restraints, and opportunities. Additionally, it offers exhaustive information about new products, developments, and investment.

Key Content of Chapters

1:Market Overview, Development, and Segment by Type, Application and Region2:Company information, Sales, Cost, Margin etc.3:Global Market by company, Type, Application and Geography4:Asia-Pacific Market by Type, Application and Geography5:Europe Market by Type, Application and Geography6:North America Market by Type, Application and Geography7:South America Market by Type, Application and Geography8:Middle East and Africa Market by Type, Application and Geography9:Market Features10:Investment Opportunity11:Conclusion

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We are a market-intelligence company formed with the objective of providing clients access to the most relevant and accurate research content for their growth needs. At InForGrowth, we understand Research requirements and help a client in taking informed business critical decisions. Given the complexities and interdependencies of market-intelligence, there is always more than one source to explore and arrive at the right answer. Through our smart search feature and our reliable andamp; trusted publishing partners, we are paving way for a more simplified and relevant research.

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Androgen Replacement Therapy Industry Analysis, Business Opportunities and Future Forecast 2024 by Top Key Players - Infonews Box

Recommendation and review posted by Bethany Smith

Parent Project Muscular Dystrophy (PPMD) has awarded two grants, one to further development of agene therapy to prevent heart failure linked to Duchenne (DMD) and Becker muscular dystrophy (BMD), and another to create better measures of treatment responses in DMD clinical trials.

PPMD, a nonprofit organization leading the fight against DMD, awarded $1 million to the professor and researcher H. Lee Sweeney, PhD, and his team at theUniversity of Florida to continue developing gene therapies to address the causes of heart failure in Duchenne and Becker MD.

The grant is part of PPMDs Cardiac Initiative, which draws on contributions from theDuchenne community, as well as the support of other Duchenne families and foundations.

For people with Duchenne, cardiac disease is a great concern. The absence of dystrophin contributes to a progressive deterioration of the hearts muscle, leading to dilated cardiomyopathy (DCM).

In this disease, the muscle and chambers of the heart begin to dilate and can reach a point where the muscle cannot contract enough to pump blood well. As heart muscle weakens, heart failurecan occur.

The funding will support the development of a heart-specific gene therapy using viral vectors (AAV vectors) to deliver two genes engineered to correct calcium handling and prevent the malfunction of mitochondria (the cells energy powerhouses) in the heart of Duchenne and Becker patients.

Sweeney and his team have been studying what happens in the heart during DMD, and found there is a calcium overload straining the organ. They have been treating animal models with the potential gene therapy, so far with positive results.

If successful, the therapy could treat the heart in a way that is independent of, or complementary to, micro-dystrophin based gene therapy.

Heart issues dont just affect some people with Duchenne; they affect ALL people with Duchenne. And while we have improved cardiac care in Duchenne, we still need treatments that repair our childrens hearts, PPMDs president and CEO, Pat Furlong said in a press release. Furlong lost both of her sons to heart failure as a result from DMD.

Chris and Patrick died of heart failure, so the heart is at the center of Duchenne for me, Furlong added. Thats why I am extremely proud to announce this $1 millioninvestment into a gene therapy with the potential to heal the hearts of our loved ones. I am grateful to Dr. Sweeney and the amazing team atUniversity of Florida, as well as the families in our community who believe in our mission and gave generously to help fund the fight to end Duchenne.

PPMD is also partnering with Duchenne UK to fund a project to create a set of highly sensitive and validated patient-reported outcomes (PROs) for use in Europe and the U.S.

The$200,000 grant was awarded to Chad Heatwole, MD, MS, the projects leader and a neuromuscular clinician at theUniversity of Rochester. Its goalis to develop outcome measures for clinical trials that are able to better capture treatment benefits from a patient and caregiver perspective.

Building on their experience in developing health indices for other diseases, Heatwole and his team will conduct a series of interviews with patients from Europe and the U.S. to identify relevant symptoms, and develop a comprehensive set of patient-reported outcomes according to regulatory guidelines from the FDA (in the U.S.) and EMA (in Europe).

We believe that incorporating the voice of the patient through PROs is an extremely powerful tool to support and accelerate drug development. We are grateful to be working with the Duchenne UK team to develop tools that ensure patients are heard, Abby Bronson, PPMDs senior vice president for Research Strategy, said in a press release.

Ana is a molecular biologist enthusiastic about innovation and communication. In her role as a science writer she wishes to bring the advances in medical science and technology closer to the public, particularly to those most in need of them. Ana holds a PhD in Biomedical Sciences from the University of Lisbon, Portugal, where she focused her research on molecular biology, epigenetics and infectious diseases.

Total Posts: 307

Margarida graduated with a BS in Health Sciences from the University of Lisbon and a MSc in Biotechnology from Instituto Superior Tcnico (IST-UL). She worked as a molecular biologist research associate at a Cambridge UK-based biotech company that discovers and develops therapeutic, fully human monoclonal antibodies.

Read more from the original source:
PPMD Grants to Promote Gene Therapy for Heart Disease and Patient Outcomes Research - Muscular Dystrophy News

Recommendation and review posted by Bethany Smith

DUBLIN--(BUSINESS WIRE)--The "Growth Opportunities in the Neurodegenerative Disorder Therapeutics Market, Forecast to 2024" report has been added to ResearchAndMarkets.com's offering.

As one lives longer, one needs to increasingly battle age-related disorders. Neurodegenerative disorders are the most worrisome because they impact millions of people around the world and lack any curative therapy. While companies continue their search, they are also battling declining revenues from marketed products used to manage symptoms. Heavy genericization, followed by price erosion, reliance on patient-reported data for diagnosis and measuring outcomes, and elusive R&D success, has put unprecedented pressure on pharma companies and prompted several to shed their assets mid-way.

This research service, in addition to quantifying the market, provides details of future products and the expected revenue generation from them. While the therapy market is marred by high rates of pipeline attrition, there are several parallel areas of growth. For instance, the study covers regenerative medicine, which has grown by leaps and bounds and offers the promise of curative therapies.

The study also dives deep into different technological advancements, geographical trends, and potential partnership opportunities for Alzheimer's and Parkinson's diseases. The study covers opportunities in prevention facilitated by digital solutions integration, in conjunction with an understanding of disease diagnosis and progression, expedited drug development, and, most importantly, delivery of the required outcome to the patient.

The study captures the competitive landscape and the different strategies employed by companies to stay ahead of the curve and identifies the game-changing companies leading innovation from the front. Acknowledging the high cost of failure, the study investigates the need and growing acceptance of open innovation to curate data, ask better questions, extract meaningful insights, and create more accurate and predictable solutions.

In addition to collaboration with peers, companies will seek partnership with digital partners. Given the growing availability of data, technologies and tools, and research expertise there are several companies seeking clinically validated solutions, which have been profiled in the study. The study lays down strategic imperatives for companies to recalibrate their business models based on collaboration and be future-ready.

Information is also provided on some of the leading M&A activities impacting the market, as well as unconventional collaboration agreements laying the foundation for propelling innovations toward licensure and delivery. Furthermore, present and future market trends such as regulatory support, focus on wellness, and value chain convergence, which would shape the market, are discussed.

Key Issues Addressed

Key Topics Covered:

1. Executive Dashboard

2. Market Overview and Dynamics

3. Forecast and Trends - Total Neurodegenerative Disorder Therapeutics Market

4. Alzheimer's Disease Segment Analysis

5. Parkinson's Disease Segment Analysis

6. Competitive Landscape - Total Neurodegenerative Disorder Therapeutics Market

7. Visioning Scenarios

8. Growth Opportunities

9. The Last Word

10. Appendix

Companies Mentioned

For more information about this report visit https://www.researchandmarkets.com/r/igkntv

Continue reading here:
Global Neurodegenerative Disorder Therapeutics Market 2019-2024: Opportunities in Digital Biomarkers, Microbiome Therapeutics, Cell and Gene Therapy,...

Recommendation and review posted by Bethany Smith

Recently developed gene therapy seems to be a promising alternative for treating one of the most common causes of blindness, wet age-related macular degeneration (AMD), claims a study.

Data presented at the 123rd Annual Meeting of the American Academy of Ophthalmology showed that six patients with wet age-related macular degeneration (AMD) went at least six months without the need for continued injections to control a disease that typically requires treatment every four to six weeks.

Researchers said the hope is that gene therapy will free patients from nearly monthly eye injections by offering a potential "one-and-done" treatment. It's not just about convenience; a more consistent treatment may also help people keep more of their vision.

"This is potentially paradigm-shifting," said lead researcher, Szilard Kiss, M.D., director of Clinical Research and chief of the Retina Service in the Department of Ophthalmology at Weill Cornell Medical College in New York City.

"It's the next evolutionary leap in treating AMD. When you think about what science fiction is and what science reality is; gene therapy for AMD is becoming a clinical reality," added Dr Kiss.

AMD is a degenerative eye disease that happens when part of the retina is damaged. The damage happens when new, weak blood vessels form behind the retina at the back of the eye. These abnormal vessels leak, causing scarring and killing off the cells that allow us to see.

One main reason why is that patients are undertreated. This is because most people with AMD must go to the ophthalmologist's office every four to eight weeks for an injection directly into their eye (oftentimes in both eyes).

This can be a difficult schedule to maintain for many elderly patients struggling with other maladies and reliant on others to get them to their ophthalmologist visits. It's also unsustainable for the health care system.

Last year alone, ophthalmologists performed more than 8 million anti-VEGF injections in the United States.

Researchers have been searching for a better alternative to monthly injections almost from the moment anti-VEGFs were introduced. Gene therapy is emerging as one of the more promising alternatives to long-term anti-VEGF treatment.

The goal of Dr Kiss' research is to develop a gene therapy that allows the eye to make its own anti-VEGF medicine. The ideal gene therapy would be administered not through a surgical procedure in an operating room, but through an injection into the eye that can be done in the doctor's office, just like routine anti-VEGF treatment is done today.

To do this, Dr Kiss and colleagues have developed a next-generation vector that can insert into the cells of the eye, the genetic material that makes a molecule similar to a widely used anti-VEGF medicine called aflibercept. Once inside the cells, the DNA sequence begins making the aflibercept protein.

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Gene therapy effective for treating wet age-related macular degeneration: Study - DNA India

Recommendation and review posted by Bethany Smith

Using its brain mapping platform, Inscopix will team up with researchers at the Broad Institute of MIT and Harvard to investigate how changes in brain activity alter the functioning of nerve cells. The goal is to identify new therapeutic targets for Parkinsons disease.

Thecollaboration will be led by Evan Macosko, MD, PhD, of the Broad Institutes Macosko Lab, an expert in single-cell transcriptomics a next-generation sequencing approach that assesses how gene activity changes in a single cell.

This research builds on a previous study that used Inscopixs miniature microscope, called nVoke, which allows simultaneous imaging and manipulation of nerve cells circuit dynamics in real time. The technology allows researchers to image cell activity for months with single-cell resolution in a living animal.

The previous study, Diametric neural ensemble dynamics in parkinsonian and dyskinetic states, published in Nature, used nVoke to identify alterations in neural activity patterns in brain circuits that regulate movement in a Parkinsons mouse model. This model mimics the human disease by gradually losing dopaminergic neurons a hallmark of Parkinsons.

Dopaminergic neurons release the neurotransmitter dopamine a chemical substance produced in response to nerve signals that allow nerve cells to communicate. In Parkinsons disease, dopamine-producing neurons are mainly lost in a brain region known as the substantia nigra, which plays a key role in reward and movement.

Now, the researchers will investigate whether the observed changes in neuronal activity in the Parkinsons mouse model can be correlated to changes in the expression of genes detected in single cells, which may have occurred as a result of the loss of dopamine. Gene expression is the process by which information in a gene is synthesized to create a working product, like a protein.

By analyzing neuronal activity and gene activity, the researchers hope to gain further insights into the mechanisms of Parkinsons disease. This may allow the identification of new, cell-type specific therapeutic targets.

According to Inscopix, real-time mapping of neural activity in brain circuits has been shown to more accurately predict the efficacy of a therapy to work on the brain, when compared with analyzing animal behavior.

Single-cell transcriptomics and brain mapping have each demonstrated the potential to increase our understanding of neurological conditions, such as Parkinsons disease, and bringing them together could help us make even greater strides forward, Kunal Ghosh, CEO of Inscopix, said in a press release.

We look forward to expanding our research into PD [Parkinsons disease] with the Macosko Lab, with the goal of paving the way for therapeutic programs that can be de-risked at earlier stages of development, Ghosh added.

Patricia holds a Ph.D. in Cell Biology from University Nova de Lisboa, and has served as an author on several research projects and fellowships, as well as major grant applications for European Agencies. She has also served as a PhD student research assistant at the Department of Microbiology & Immunology, Columbia University, New York.

Total Posts: 208

Ana holds a PhD in Immunology from the University of Lisbon and worked as a postdoctoral researcher at Instituto de Medicina Molecular (iMM) in Lisbon, Portugal. She graduated with a BSc in Genetics from the University of Newcastle and received a Masters in Biomolecular Archaeology from the University of Manchester, England. After leaving the lab to pursue a career in Science Communication, she served as the Director of Science Communication at iMM.

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Real-time Brain Mapping Used to Search for Therapeutic Targets in PD - Parkinson's News Today

Recommendation and review posted by Bethany Smith

NEW YORK, Oct. 14, 2019 /PRNewswire/ -- According to the current analysis of Reports and Data, the Global Gene Expression market is expected to reach USD 11.37 billion by the year 2026, in terms of value at a CAGR of 8.1% from 2019-2026. Gene expression promises to tap into a previously unexplored segment in the vast and burgeoning genetic engineering industry. Gene expression is the process by which the genetic code - the nucleotide sequence - of a gene is used to direct protein synthesis and produce the structures of a cell. It is the process by which instructions in the DNA are converted into a functional product like protein. The commercial applications of gene expression have been studied and researched upon extensively in recent years. Many diverse and wide ranging applications have been found for this novel technique. With the increased availability and lowering costs of DNA technologies, gene expression has become a more readily used tool indispensable in drug discovery and development.

Increase in investments in the market, which are supporting the technological advancements, and rise in healthcare expenditure are estimated to shape the growth of the gene expression market. Drug discovery & development and increase in demand for personalized medicine in chronic diseases such as cancer will be observed as the most lucrative applications for gene expression analysis in the forecast period. Application of gene expression in clinical diagnostics, on the other hand, will reflect a moderate growth throughout the analysis period. Moreover, the falling costs of sequencing have facilitated the integration of genomic sequencing into medicine. With the increased availability and lowering costs of DNA technologies, gene expression has become a more readily used tool indispensable in drug discovery and development. Many companies and educational institutions are collaborating to make gene expression publicly accessible through databases such as the Connectivity Map (CMap), Library of Integrated Network-based Cellular Signatures (LINCS) and the Tox 21 project.

New product development has been the consistent strategy undertaken by majority of the players to expand their product portfolio for serving a larger consumer base. For example, in September 2019, Qiagen N.V., launched the newly enhanced GeneGlobe Design & Analysis Hub, which integrates the company's manually curated knowledge base on over 10,000 biological entities with the industry's most comprehensive portfolio of tools for next-generation sequencing (NGS), polymerase chain reaction (PCR) and functional analysis. Other companies like Thermo Fisher Scientific and Illumina Inc. have launched new products in the last few months which are being used in the gene expression market.

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Further key findings from the report suggest

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Segments covered in the report:

For the purpose of the study, this Reports and Data has segmented the Gene Expression Market on the basis of product type, platform type, prescription mode, end user and the regional outlook

Product and Services (Revenue, USD Million; 20162026)

Capacity (Revenue, USD Million; 20162026)

Application (Revenue, USD Million; 20162026)

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Regional Outlook: (Revenue, USD Million; 20162026)

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Gene Expression Market to Reach USD 11.37 Billion by 2026 | Reports and Data - PRNewswire

Recommendation and review posted by Bethany Smith

Mart Research new study, Global Gene Therapy MarketReport cover definite aggressive standpoint including the piece of the overall industry & profiles of the key members working in the worldwide market.

The global Gene Therapy market will reach Volume Million USD in 2019 and with a CAGR xx% between 2020-2026.

Gene Therapy Product Type Coverage (Market Size & Forecast, Major Company of Product Type etc.):

Ex vivo

In vivo

Get a free sample report: https://martresearch.com/contact/request-sample/1/83572

Gene Therapy Demand Coverage (Market Size & Forecast, Consumer Distribution):

Cancer Diseases

Monogenic Diseases

Infectious Diseases

Cardiovascular Diseases

Others

Gene Therapy Company Coverage (Sales data, Main Products & Services etc.):

Sangamo

Spark Therapeutics

Dimension Therapeutics

Avalanche Bio

Celladon

Vical

Advantagene

Gene Therapy Major Region Market

North America

Europe

Asia-Pacific

South America

Middle East & Africa

Place the Order of Global Gene Therapy Market Research Report: https://martresearch.com/paymentform/1/83572/Single_User

Some Points from Table of Contents:

Chapter 1 Industry Overview

1.1 Gene Therapy Industry

1.1.1 Overview

1.1.2 Products of Major Companies

1.2 Market Segment

1.2.1 Industry Chain

1.2.2 Consumer Distribution

1.3 Price & Cost Overview

Chapter 2 Gene Therapy Market by Type

2.1 By Type

2.1.1 Ex vivo

2.1.2 In vivo

2.2 Market Size by Type

2.3 Market Forecast by Type

Chapter 3 Global Market Demand

3.1 Segment Overview

3.1.1 Cancer Diseases

3.1.2 Monogenic Diseases

3.1.3 Infectious Diseases

3.1.4 Cardiovascular Diseases

3.1.5 Others

3.2 Market Size by Demand

3.3 Market Forecast by Demand

Chapter 4 Major Region Market

4.1 Global Market Overview

4.1.1 Market Size & Growth

4.1.2 Market Forecast

4.2 Major Region

4.2.1 Market Size & Growth

4.2.2 Market Forecast

Chapter 5 Major Companies List

5.1 Sangamo (Company Profile, Sales Data etc.)

5.2 Spark Therapeutics (Company Profile, Sales Data etc.)

5.3 Dimension Therapeutics (Company Profile, Sales Data etc.)

5.4 Avalanche Bio (Company Profile, Sales Data etc.)

5.5 Celladon (Company Profile, Sales Data etc.)

5.6 Vical (Company Profile, Sales Data etc.)

5.7 Advantagene (Company Profile, Sales Data etc.)

Chapter 6 Conclusion

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List of Table

Table Global Gene Therapy Market 2016-2019, by Type, in USD Million

Table Global Gene Therapy Market 2016-2019, by Type, in Volume

Table Global Gene Therapy Market Forecast 2020-2026, by Type, in USD Million

Table Global Gene Therapy Market Forecast 2020-2026, by Type, in Volume

Table Global Gene Therapy Demand 2016-2019, in USD Million

Table Global Gene Therapy Demand 2016-2019, in Volume

Table Global Gene Therapy Demand Forecast 2020-2026, in USD Million

Table Global Gene Therapy Demand Forecast 2020-2026, in Volume

Table Global Gene Therapy Market Size & Growth 2016-2019, in USD Million

Table Global Gene Therapy Market Size & Growth 2016-2019, in Volume

Table Global Gene Therapy Market Forecast 2020-2026, in USD Million

Table Global Gene Therapy Market Forecast 2020-2026, in Volume

Table Global Gene Therapy Market 2016-2019, by Region, in USD Million

Table Global Gene Therapy Market 2016-2019, by Region, in Volume

Table Global Gene Therapy Market Forecast 2020-2026, by Region, in USD Million

Table Global Gene Therapy Market Forecast 2020-2026, by Region, in Volume

Table Sangamo Overview List

The key insights of the report:

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Research is and will always be the key to success and growth for any industry. Most organizations invest a major chunk of their resources viz. time, money and manpower in research to achieve new breakthroughs in their businesses. The outcome might not always be as expected thereby arising the need for precise, factual and high-quality data backing your research. This is where MART RESEARCH steps in and caters its expertise in the domain of market research reports to industries across varied sectors.

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Global Gene Therapy Market Size, Share, Growth Rate, Revenue, Applications, Industry Demand & Forecast to 2026 - Galus Australis

Recommendation and review posted by Bethany Smith

In 2006, Shinya Yamanaka shook stem cell research with his discovery that mature cells can be converted into stem cells, relieving a longstanding political-ethical blockage and throwing open medical research on everything from curbing eye degeneration to organ printing.

But that process still has pitfalls, including in risk and scalability, and some researchers are exploring another way first hinted at years ago: new technology to convert mature cells directly into other mature cells without the complex and time-consuming process of first making them into stem cells.

One of those companies, Mogrify, just raised $16 million in Series A financing to bring its overall funding to over $20 million since its February launch. Led by CEO Darrin Disley, the funding will help expand their new base in Cambridge to a 60-strong staff and push forward their direct-conversion approach to cell therapy through research and licensing. Investors include Parkwalk Advisors and Ahren Innovation Capital.

They list potential applications as treatments for musculoskeletal and auto-immune disorders, cancer immunotherapy, and therapies for ocular and respiratory diseases. For example, you could use it regenerate cartilage in arthritis patients.

If you could take a cell from one part of the body and turn it into any other cell at any other stage of development for another part of the body, you effectively have the Holy Grail of regenerative medicine, Disley told Labiotech.eu in April.

Mogrifys advantage over the Yamanaka method called induced pluripotent stem cells (iPS), is that in theory it can be more scalable and avoid the problems associated with iPS. These include instabilities arising from the induced immature state and an increased risk of cancer if any pluripotent cells remain in the body.

The concept behind Mogrify actually predates, by nearly 19 years, Yamanakas discovery, which fast won him the 2012 Nobel Prize in Medicine. A 2017 Nature study on transdifferentiation, as the process is called, of fibroblasts into cardiac tissue traced the idea to a 1987 findingthat a master gene regulator could convert mice fibroblasts into skeletal muscle.

The problem though, according to Mogrify, is that most current efforts rely on an exhausting guess-and-check process. With hundreds of cell types and an even greater number of transcription factors the program that recodes the cell finding the right factor for the right cell can be like a custodian with a jangling, unmarked key ring trying to get into a building with thousands of locks.

Mogrifys key tech is a computer model they say can predict the right combination. The scientists behind the platform published a 2016 study in Nature applying the model to 173 human cell types and 134 tissues.

Before Mogrify, Disley led the Cambridge-based gene-editing company Horizon Discovery.

Continued here:
Cell therapy startup raises $16 million to fund its quest for the Holy Grail in regenerative medicine - Endpoints News

Recommendation and review posted by Bethany Smith

GlaxoSmithKline announced a five-year collaboration agreement with Lyell Immunopharma, a San Francisco, US-based company, working on methods to prevent inhibition of T cells by tumors and relapses due to loss of T cell functionality.

The agreement will see the two companies working on the advancement of GSKs cell therapy pipeline, specifically on GSK3377794, a potential treatment for multiple cancer types currently in Phase II clinical development, which targets the NY-ESO-1 antigen.

According to GSK, although the first two chimeric antigen receptor (CAR)-T cell therapies, Yescarta (axicabtagene ciloleucel) and Kymriah (tisagenlecleucel), have now reached the market, engineered T cells have not yet delivered strong clinical activity in common solid tumours.

Improving the fitness of T cells and delaying the onset of T cell exhaustion could help engineered T cell therapies become more effective, the company stated.

Further than GSKs cell therapy candidate, the research partnership will look to advance Lyells approach of enhancing initial T cell response against solid tumours into a platform technology for future cell and gene therapies development projects to treat rare types of cancer.

Lyells technology, according to Rick Klausner, the companys CEO, looks to tackle three barriers to T cell efficacy in solid tumours.

We are redefining the ways we prepare patient cells to be made into therapies, modulating cells functionality so that they maintain activity in the tumour microenvironment, and establishing methods of control to achieve specificity and safety for solid tumour-directed cell therapies, Klausner explained.

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GSK partners with Lyell on cell therapies development - BioPharma-Reporter.com

Recommendation and review posted by Bethany Smith

Catabasis Pharmaceuticals and the Jain Foundation have started a preclinical research collaboration to study edasalonexent as an oral treatment candidate for dysferlinopathy, a group of muscle diseases that includes limb-girdle muscular dystrophy (LGMD) type 2B.

Edasalonexent, formerly CAT-1004, is a small molecule designed to block the NF-kB cell signaling route a potential driver of muscle dystrophy, with a key role in skeletal and cardiac muscle breakdown. Through this mechanism, edasalonexent is thought to help preserve muscle function and slow disease progression. The experimental therapy is currently in Phase 3 clinical testing in boys with Duchenne muscular dystrophy (DMD).

Dysferlinopathy, which also includes Miyoshi myopathy, is a group of rare muscle disorders characterized by slowly progressive muscle weakness and wasting. The disorders are caused by mutations in the gene DYSF, which provides instructions for making dysferlin, a protein that normally works to provide structure to muscle fibers, and protect them.

In people with dysferlinopathy, muscles lack that key dysferlin protein, which results in chronic activation of the NF-kappa B pathway, muscle fiber damage, and failure to repair injured fibers.

Through the collaboration of Catabasis with the Jain Foundation, a non-profit dedicated to finding a cure for muscular dystrophy caused by dysferlin deficiency, researchers will conduct a preclinical study to evaluate the therapeutic potential of edasalonexent in dysferlinopathy.

The study will measure disease progression in dysferlin-deficient mice treated with edasalonexent, and use magnetic resonance imaging (MRI) and magnetic resonance spectroscopy to assess muscle volume, fat accumulation, and other changes. The initial results are expected in the first half of 2020.

We look forward to working with Catabasis to advance research for Dysferlinopathy, Laura Rufibach, PhD, and Doug Albrecht, PhD, co-presidents of the Jain Foundation, said in a press release.

Patients with dysferlinopathy (LGMD2B / Miyoshi myopathy) experience a progressive and debilitating decline in muscle function which significantly impacts their lives, Rufibach and Albrecht said. We are excited to explore the potential of edasalonexent to benefit those living with this disease.

In Duchenne research, results of the MoveDMD Phase 1/2 trial and its open-label extension (NCT02439216) showed that treating boys ages 4-7 with edasalonexent slowed disease progression and preserved muscle function compared with an off-treatment period. Biomarkers of muscle health and inflammation also showed significant improvements.

Evidence of NF-kB activation in both dysferlinopathy and DMD suggests a similar disease mechanism and opportunity for intervention, said Andrew Nichols, PhD, Catabasis chief scientific officer.

Through this collaboration, we look forward to learning more about the potential of edasalonexent in dysferlinopathy, he added.

The treatments efficiency and safety are being evaluated in children with Duchenne in the Phase 3 trial PolarisDMD (NCT03703882). Enrollment was just completed and exceeded the target number of participants, Catabis said. A total of 130 boys, ages 4 to 7, with any mutation type, have been enrolled in the U.S., Canada, Europe, Israel, and Australia.

We are thrilled to reach this important milestone. The interest and feedback from families and trial sites has been overwhelmingly positive, Joanne Donovan, MD, PhD, Catabasis chief medical officer, said in another press release.

Edasalonexent has the potential to be a foundational therapy, providing benefit to boys, regardless of their underlying mutation, with the potential to benefit muscle function, as well as cardiac function and bone health, she added.

Participants in PolarisDMD will be randomly assigned to receive either edasalonexent capsules three times per day (dose of 100 mg per kg per day) or a placebo, for 52 weeks, after which all boys and their eligible siblings may continue through an open-label extension study called GalaxyDMD.

Top-line results from PolarisDMD are expected in the fourth quarter of 2020. The findings are anticipated to support aNew Drug Application filing with the U.S. Food and Drug Administration in 2021.

We look forward to completing the trial next year and are working diligently toward the goal of making edasalonexent available to patients, Donovan said.

Ana is a molecular biologist enthusiastic about innovation and communication. In her role as a science writer she wishes to bring the advances in medical science and technology closer to the public, particularly to those most in need of them. Ana holds a PhD in Biomedical Sciences from the University of Lisbon, Portugal, where she focused her research on molecular biology, epigenetics and infectious diseases.

Total Posts: 42

Jos is a science news writer with a PhD in Neuroscience from Universidade of Porto, in Portugal. He has also studied Biochemistry at Universidade do Porto and was a postdoctoral associate at Weill Cornell Medicine, in New York, and at The University of Western Ontario in London, Ontario, Canada. His work has ranged from the association of central cardiovascular and pain control to the neurobiological basis of hypertension, and the molecular pathways driving Alzheimers disease.

Continued here:
Catabasis and Jain Foundation Study Edasalonexent for Dysferlinopathy - Muscular Dystrophy News

Recommendation and review posted by Bethany Smith

Zacks Investment Research upgraded shares of Axovant Gene Therapies (NASDAQ:AXGT) from a hold rating to a buy rating in a research report released on Wednesday morning, Zacks.com reports. The brokerage currently has $6.50 target price on the stock.

According to Zacks, Axovant Sciences Ltd. is a biopharmaceutical company which focuses on the acquisition, development and commercialization of therapeutics for the treatment of neurodegenerative disorders. Its product candidate includes RVT-101 which is in different clinical trial for the treatment of Alzheimers disease and other forms of dementia. Axovant Sciences Ltd. is based in Hamilton, Bermuda.

Other equities analysts also recently issued reports about the stock. ValuEngine raised shares of Axovant Gene Therapies from a sell rating to a hold rating in a research note on Thursday, August 1st. Leerink Swann assumed coverage on shares of Axovant Gene Therapies in a research note on Friday, June 21st. They issued an outperform rating and a $5.79 price target for the company. Svb Leerink assumed coverage on shares of Axovant Gene Therapies in a research note on Friday, June 21st. They issued an outperform rating and a $18.00 price target for the company. Robert W. Baird raised shares of Axovant Gene Therapies from a neutral rating to an outperform rating and decreased their price target for the stock from $16.00 to $13.00 in a research note on Monday, August 12th. Finally, Cowen reissued a hold rating on shares of Axovant Gene Therapies in a research note on Tuesday, July 9th. Two research analysts have rated the stock with a hold rating and nine have given a buy rating to the company. Axovant Gene Therapies has a consensus rating of Buy and a consensus price target of $26.91.

Shares of NASDAQ:AXGT opened at $5.72 on Wednesday. Axovant Gene Therapies has a 12 month low of $3.81 and a 12 month high of $20.80. The company has a 50-day moving average price of $6.84 and a 200-day moving average price of $5.49. The company has a quick ratio of 1.70, a current ratio of 1.70 and a debt-to-equity ratio of 0.60.

Axovant Gene Therapies (NASDAQ:AXGT) last released its quarterly earnings results on Friday, August 9th. The company reported ($1.23) earnings per share (EPS) for the quarter, topping the Zacks consensus estimate of ($1.34) by $0.11. Equities analysts expect that Axovant Gene Therapies will post -4.25 earnings per share for the current year.

A number of institutional investors and hedge funds have recently made changes to their positions in AXGT. Sphera Funds Management LTD. purchased a new stake in Axovant Gene Therapies in the first quarter worth about $6,794,000. Primecap Management Co. CA purchased a new stake in Axovant Gene Therapies in the first quarter worth about $1,400,000. BlackRock Inc. purchased a new stake in Axovant Gene Therapies in the second quarter worth about $1,482,000. Marshall Wace LLP purchased a new stake in Axovant Gene Therapies in the first quarter worth about $272,000. Finally, Jane Street Group LLC grew its holdings in Axovant Gene Therapies by 28.8% in the second quarter. Jane Street Group LLC now owns 46,455 shares of the companys stock worth $289,000 after purchasing an additional 10,375 shares during the period. Institutional investors and hedge funds own 13.48% of the companys stock.

About Axovant Gene Therapies

Axovant Gene Therapies Ltd., a clinical-stage gene therapy company, focuses on developing a pipeline of product candidates for debilitating neurological and neuromuscular diseases. The company's current pipeline of gene therapy candidates targets GM1 gangliosidosis, GM2 gangliosidosis, Parkinson's disease, oculopharyngeal muscular dystrophy, amyotrophic lateral sclerosis, and frontotemporal dementia.

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Axovant Gene Therapies (NASDAQ:AXGT) Lifted to Buy at Zacks Investment Research - Riverton Roll

Recommendation and review posted by Bethany Smith

(CN) Why do birds of a feather stick together, even when it would be better for both if they set one another free? Research published in the Proceedings of the National Academy of Sciences on Monday analyzes the costs of cooperation in long-term mating birds to explain the evolutionary origin of post-coital couples.

From the peacocks feathers to the red-crowned cranes dance, male birds often create elegant displays to attract a female mate. In the case of monogamous birds, some males only display after theyve mated an act often anthropomorphized as a display of affection, but in biology simply called a display. Even then, rather than fly off to be woo other lady birds while the weathers warm, male birds commonly remain with their mate and continue their displays.

I caught a female goldfinch, placed her in a bird bag and carried it back to the banding station. All the way back to the station, her mate followed, calling, said University of Chicago biologist Trevor Price, a senior author of the study, in a statement.

He waited impatiently in a nearby tree as I banded the female, and when I released her the pair flew off together in close company, twittering, Price continued. This kind of thing happens in many other species, too, so forming a strong pair bond and emotional attachments between a male and female is evidently not only a feature of humans.

But this devotion can come at a cost.

Picture a male, singing love songs rather than foraging for his offspring. While this costs him and his nest precious food for energy, he is also losing out on other mating opportunities.

Females can produce more eggs or larger eggs, and often work harder at raising them when her mate remains and continues his song. But this extra mothering affects her chances of survival: If a female is raising too many babies or skipping too many meals to feed them, she might not live to mate another season.

If a males display leads his mate to overinvest in her nest so much it reduces her survival rate, selection eventually favors females who ignore the males display. When females stop responding, the display no longer gives males an advantage and, like a bad fashion trend, the trait can disappear.

To understand the benefits of displaying and long-term relationships, biologists at University of Chicago and the University of North Carolina developed a model with haploid genetics to show when and how the couple and their chicks benefit.

Taking into account death and divorce, the model looks at genetic success over several generations and mating pairs. The model assumes males and females pair at random but stick to strict social and genetic monogamy thereafter.

We find that a stable equilibrium can indeed be attained where all males display and all females respond to the display, the researchers wrote. Pair bond is strengthened, and displays between the sexes accumulate over evolutionary time, even in the absence of sexual selection.

The males display is most beneficial if it pushes a female to optimum capacity, rather than beyond her ability.

Say the environment is changing, maybe humans are building a road next to a park where birds nest. The change stresses the female, causing her to produce below optimum, or maybe she spends less time foraging and more time on guard. In this case, her mates display pushes her back on track to provide better care to her offspring within but not beyond her capacity increasing survival chances for both her and her young in the new environment.

Over time, females may come to rely on cues from the males display in order produce an optimum number of offspring, and in his absence, she would under-produce or under-care for her clutch.

This balance of benefits is necessary for both the male display and the female response to remain in the gene pool.

The models enable us to see the wide ranges of conditions that can cause displays to become stuck in the population, evolutionarily, and that can lead to this result, noted Dr. Maria Servedio of the University of North Carolina at Chapel Hill in a statement. Servedio specializes in the evolution of premating isolation and sexual selection.

The study, Evolution of Sexual Cooperation From Sexual Conflict, was supported by the National Science Foundation and the Norwegian Research Council.

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Investing in Love & Affection Pays Off - Just Ask Birds - Courthouse News Service

Recommendation and review posted by Bethany Smith

The weather was hot and muggy as the 2019 Texas Archery Only season for white-tailed deer got underway in late September, but the weekend turned out super cool for Chris Barrilleaux of Splendora.

Hunting on a private lease along the Trinity River in San Jacinto County, the 58-year-old grocery store owner arrowed a whitetail buck sporting a really peculiar set of antlers.

The buck is a main frame 8 pointer with thick main beams. The left antler is particularly odd with several knots, curls and a split G2 that pokes outward and forms a distinctive T at the end. What really makes the deer interesting is its antlers are still fully wrapped in velvet.

Velvet is the word often used to describe the thin layer of hairy skin that covers the antlers throughout the growing process, which begins in early spring. The soft skin is lined with tiny blood vessels to fuel fast growth of the cartilage until it calcifies into hardened antlers, usually by the end of August.

Thats when testosterone begins to flow and the blood supply to the velvet ceases, causing it to dry and peel away from the bone. Bucks help things along by rubbing on trees and bushes to polish their new antlers ahead of the fall breeding season. Those bucks that survive through the winter will cast their antlers the following spring and the growing process starts all over again. Or at least thats the way things normally work in the wild.

Barrilleauxs deer was an oddball. It had retained the velvet on its antlers long after other bucks had shed theirs. Closer examination of the 5 1/2-year-old whitetail explained why.

The hunter said the deer had only one testicle. The abnormality may have come about as the result of birth defect, or the deer may have injured itself at a younger age, possibly by getting hung in a fence. Either way, the deer lacked the surge in male hormones needed to shed its velvet and spark the desire to do other things the normal guys do when the testosterone high sets in each fall.

Wildlife experts refer to the condition as cryptoridism. Cryptorchids are frequently called stags.

Stags dont make rubs, ground scrapes, chase does, spar with other bucks to establish themselves in a pecking order and they dont engage in breeding activity. Nor do they drop their antlers in the spring or shed their velvet ever. Their male hormones are just too out of whack.

The antlers on a stag just continue to grow, said Alan Cain, white-tailed deer program leader with the Texas Parks and Wildlife Department. Most of the growth occurs during the peak antler growing time from around April through August. They may grow a little outside that time frame, but its minimal.

Barrilleauxs stag wont score very high on the Boone and Crockett scale, but it is a once-in-a-lifetime trophy just the same. Most hunters will go a lifetime and never see such a deer. Capitalizing on the opportunity to take one with archery gear represents a special feather in a deer hunters cap.

Barrilleaux claims he had collected game camera pictures of the stag earlier in the month, so it didnt come as a surprise when the animal showed up in front of his bow stand on opening day. What does come as somewhat of a shock is that he chose to let the freak buck hed nicknamed Ol Velvet walk the first time he saw it.

I passed on him opening day, he said. After that I kept asking myself what the heck were you thinking you may never see something like that again. Luckily, he showed up again the next morning.

Cryptorchidism represents just one of the strange anomalies known to occur in North Americas favorite big game animal. Mother Nature sometimes throws some genetic curveballs into the mix that can cause weird things to happen with whitetails and other wildlife.

Melanism is one such condition. Researchers say it occurs when an animal produces excessive amounts of hair, skin and retina pigment called melanin. The result is a coat that is noticeably darker than normal. Some deer appear almost charcoal in color, while others may look chocolate brown or dark grey.

The condition has been known to occur in a wide variety of animals, including squirrels, birds and members of the feline family. The recessive trait has even been documented in penguins.

Cain says genetic mutations also can result in albinism (all white) or a piebald coat, which consists of spotty patches of white and brown. Of the three conditions, melanism is believed to be the rarest of all.

While melanistic whitetails deer have been documented in several states, Texas is considered to be "melanism central" by many whitetail researchers. Melanistic deer may show up just about anywhere in the state, but it seems to be the most prevalent in parts of Central Texas. Cain says Hays, Travis, Comal, Williamson, Blanco, Guadalupe, Burnet and Bastrop counties are known hotspots for deer with abnormally dark coats.

We see them in certain pockets, Cain said.

Melanistic deer also have been documented in eastern Texas, but not very often. The only one Im aware of belongs to Bobby Tuttle of Beckville.

Tuttle shot the Panola County buck early during the 2012 season, when it appeared in a pasture behind his house shortly after daybreak on Nov. 7. The buck had a 10-point typical rack and wore a beautiful dark brown coat.

The hunter he said started collecting game camera pictures of the buck three years earlier, but had never seen it in person until that fateful Wednesday morning. Interestingly, Tuttle said it wasn't his first encounter with a dark-colored whitetail on his property. Four years earlier, he saw a melanistic doe in same field where he killed the buck he called Blackie.

"She jumped over into a feed pen with another doe," he said. "She didn't have speck of white on her, either. Even the underside of her tail was black. She was black as an angus cow."

Genetics can be a confusing thing. In extreme cases, DNA may get so twisted that a deer somehow winds up with both male and female sex organs. These are called hermaphrodites. Its also possible for a doe to grow antlers.

There are all kinds of oddball things that can happen out there, Cain said. In 10 years in this position, with millions of deer killed across the state, Ive probably heard of no more than five antlered does or hermaphrodites. Genetic anomalies like that are pretty rare.

But they do happen from time to time.

One of the most impressive antlered does ever reported in Texas was taken in 2003 McMullen County by Alan Woodward. The 17 pointer was still in full velvet and sported an 8 1/2 inch drop tine, according to reports in North American Whitetail Magazine. Former TPWD wildlife biologist Macy Ledbetter said the deer had a complete set of female organs. It was aged at 6 1/2 years old.

Another freak show surfaced in Fall 2007 in McCulloch County, where Cliff Smallwood of White Oak was hunting on a 550-acre lease near Brady. Smallwood shot a tall-tined 7 pointer that would have been a 9 pointer if not for two broken tines. Smallwood, who was accompanied by TPWD game warden Jeff Cox, made an interesting discovery when he approached the dead deer.

"It's neck was swollen and had cuts on it," Smallwood said. "It also had dried blood and hair on the tips of its antlers. It was pretty obvious the deer had been fighting with another buck and inflicted some injury, probably within the last 24-48 hours."

Closer examination of the buck led to an even more bizarre discovery. The tarsal glands located on the inside of the deer's hind legs were snow white, not urine-stained, as is the case with many rutting bucks.

"We thought that was kind of weird," Smallwood said. "Then I lifted a rear leg and saw it had no male genitals. Instead, it had female genitalia and teats. It was a doe with antlers -- the strangest thing I have ever seen."

Major League Fishing announces plans to acquire Fishing League Worldwide

Major League Fishing rocked the fishing industry last fall when it announced the formation of the Bass Pro Tour an invitation-only bass tournament circuit that subsequently lured some of sports biggest names away from competitive fishings most prominent leagues the Bassmaster Elite Series and FLW Tour on the promises of bigger and better things, including more lucrative paydays.

On Oct. 10, the organization announced another bold move indicating it has reached an agreement supported by a Letter of Intent to purchase Fishing League Worldwide, better known as FLW. Based in Benton, Ky., FLW is a grassroots fishing organization that has been hosting bass tournaments catering to anglers on all levels from weekenders to tour level pros for nearly a quarter century.

The company is regarded as the largest of its kind in the world, hosting nearly 300 tournaments across five circuits each year. Among them are the FLW Tour, Costa FLW Series, T-H Marine Bass Fishing League, YETI College Fishing and Bass Pro Shops High School Fishing.

The announcement of the merger came on the heels of months of rumors hinting that changes were coming. A joint press release from the two organizations indicated the deal will be finalized by the end of the month.

Were thrilled about welcoming FLW to the MLF team, said Jim Wilburn, President and CEO of Major League Fishing. FLW shares our commitment to creating tournaments and opportunities centered on the success of the angler. Through this acquisition, we are better positioned to support anglers and sponsors at all levels.

According to FLW President of Operations Kathy Fennel, the merger marks the "beginning of a new era in the sport."

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Freaks of Nature: Mother Nature, genetics sometimes play strange tricks on white-tailed deer - Athens Daily Review

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A black cloth was placed over thesharkseyes,a tube pumped water through the gillsandsix scientists descended to the platform, allowing themselves15 fast-paced minutes to take blood, parasite, muscle, fecaland semen samples.

Veterinarian Mike Hyatt of the New York Aquariumcut the shining whitebellyto install an acoustic tag,as University of Windsor research associate Dan Madigan drilled thesatellitepositioning tag referred to as a SPOT tag to the dorsal fin. Its this tag which will allows thousands of peoplewhove downloaded an app to follow the sharks movements online.

But behind the excitement, an unresolvedscientific debate has bubbled away over how sharks, notoriously sensitive to handling, are impacted.

During a briefing, Hyatt saidblood tests taken at the beginning and end of such intense captures show the animals stress levels dont rise.Whats quite astonishing is working with them out of the water their stress levels stay the same and sometimes actually improve, heexplained.

However,while marine biologists interviewed by The Canadian Press concur withHyatts view ofthe sharks short-term reaction,they wonder what will happen to internal organs and reproductive systems in the months and years to come. Some shark researchers refuse to use the method.

At the federal Bedford Institute of Oceanography in Halifax, Heather Bowlby, the research lead at the federal Canadian Atlantic Shark Research Laboratory, has shifted away fromsystems that involves hooking sharks or bringing them aboard ships.

This season, her teamused a lureto attract a four-metre female and then a harpoon torapidly attach a pop-up archival tagnear its dorsal fin.

Therecording devicewill later detach and float to the surface and provide light, temperature and depth data that will helpBowlby study its habitat and habits.

Theres been a general shift in the shark research community to move away from bringing sharks on board a boat, she said in an interview. All of their muscle is concentrated in their back and it does press down. They dont have a rib cage.Theyre not designed to be out of the water, and thats why we have moved to tagging inside the water.

Gregory Skomal, wholeads a Massachusetts Division of Marine Fisheries study group off Cape Cod, says he uses a spotter plane and harpoon methods like Bowlbys to minimize invasive handling.

Hesaid he has questions aboutthe impact of Ocearchs method. It could be creating long-term problems for the future reproductive success of the animal . Its an area that people arevery worried about.

Chris Lowe, a veteran shark researcher with the University of California at Long Beach,says he observed the impact on a younger shark after hebolted a SPOT tagto it, and the fin bent over and deformed over time.

At that point I elected not to use them any more due to damage to the fin . I dont think weve developed a good enough tag design thats designed to come off or to minimize damage, he said.

Still, Lowe says this may not hold true of more mature sharks, and there are tradeoffs for scientists who dontuse the Ocearch methods.

He saysthe pop-up tags he harpoons onto sharks are less accurate in tracking the sharks precise journeys and he cant collect thevolume of data on blood, genetics and parasites.

Meanwhile, Ocearchs method cancombine the positioning provided by the SPOT tags withthe archival depth and temperature information from the pop-off tags.Its a practicethe grouphasused for females the last two years, providing a potentially rich source of data.

Chris Fischer, the expedition leader and founder of Ocearch, firmly disagrees with criticsand sayshes gatheringa whole suite of valuableinformationwidely available for scientists to examine and whichwill lead to improved fisheries management.

These will be the most comprehensively studied individual white sharks in history here in Canada, he said during an interview after the expedition ended its work, which ranfrom Sept. 13 to Oct. 4 off Cape Breton and Lunenburg.

The precision of his taggingmethodscould help researchers locate the holy grail of the nursery where mature females reproduce and give birth, he said aboard his research ship.

Meanwhile, Robert Hueter, the chief scientist with Ocearch, says photos of great whites tagged in the eastern Pacific that were observed years later after the SPOT tagscame off show no significant effect on the shark or its dorsal fin.

The shark biologist at Floridas Mote Marine Laboratorysayscriticisms about unknown, long-term impactsarespeculation without data,and he notes that during the operation, their team does ultrasound imaging of internal organs and has found no evidence of damage.

Finally, we put the resulting movements of our sharks on the Ocearch Tracker for all the world to see; clearly our sharks are moving as we know white sharks to do, south in winter and north in summer, with key stops along the way, he wrote in an email.

Still, Aaron MacNeil, the Canada Research Council chair in fisheries conservation at Dalhousie University,has become a critic ofthe scientific methodologies.

Herecently raised theissue ofthe vesselfishing for sharksnear waters where Nova Scotians surf and dive, saying hes concerned it could draw the animals closer to people.

In my view, the federal Fisheries Department still needs to establish a safe distance for shark-fishing to occur relative to recreational users and exclude shark-fishing within this zone, he said.

Fischercontends that it is not that simple to alter shark behaviour.

A federal Fisheries Department spokeswoman said great white sharks are normally found in waters around Nova Scotia this time of year and in close proximity to coastal areas, and therefore, it is considered that these research activities are unlikely to significantly increase risks.

Meanwhile, as the season wrapped up, Fischer said he intends tocontinue his relationship with the federal Fisheries Department, which has granted him permits under the Species At Risk Act anda foreignvessel license.

He says under the conditions of its permit, Ocearch will provide the federalauthorities with its tracking information, along with blood, semen, diet, genetic and other valuable information.

The question for DFO is Where do you need us to go next for you?'said Fischer, noting he would like to return to Cape Breton next year to validate this years findings.

Alain Vezina, the Maritimes region director of science at the federal Fisheries Department, declined a request for an interview. In written responses, thedepartment said Ocearchis required to provide it with an outline ofits activities and the tagging data they collect, and that the organization is to submit a report by the end of this year.

The methods are intended to minimize any potential impacts to these sharks. Monitoring will be undertaken to ensure compliance with the permit conditions, the email from the communications department said..

This report by The Canadian Press was first published Oct. 14, 2019.

Michael Tutton, The Canadian Press

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Great white tagging program off N.S. stirs debate over treatment of sharks - CFJC Today Kamloops

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The Miss America 2020 pageant is getting a new home and date this year, but women from all 50 states, as well as Washington D.C., are still getting ready to compete for the national title and take the crown.

This years competition is getting two new homes this year, with both a return to NBC after several years airing on ABC, as well as a move from Atlantic City, New Jersey. The competition will now air live from the Mohegan Sun Arena in Uncasville, Connecticut, on Thursday, Dec. 19 at 8 p.m. EDT. This is a change from a previous air date in September when the show aired on ABC.

The Miss America Organization is proud to partner with Mohegan Sun as we return to our longtime NBC home, Regina Hopper, President & CEO of The Miss America Organization said in a press release. We are looking forward to a fresh take on this historic competition that will showcase theincrediblewomen vying for the job of Miss America 2020.

Sowho are the women who are participating in this years competition and looking to take the title from Miss America 2019, Nia Franklin? Check the list below for moreinformation andfun facts about the women competing in this years pageant.

51 New ladies will compete for the title of Miss America 2010 at this years pageant. Pictured is Miss America 2019 winner Nia Franklin as she receives her crown from Miss America 2018, Cara Mund at Atlantic City Boardwalk Hall in Atlantic City, New Jersey on Sept. 9, 2018. Photo: Donald Kravitz/Getty Images

Miss Alabama-TiarraPennington

Miss Alaska-MaileJohnston

Miss Arizona-Jacqueline Thomas

Miss Arkansas-DarynneDahlem

Miss California-Eileen Kim

Miss Colorado-Monica Thompson

Miss Connecticut-Jillian Duffy

Miss Delaware-Hillary May

Miss District of Columbia-KatelynneCox

Miss Florida- MichaelaMcLean

Miss Georgia-Victoria Hill

Miss Hawaii-Nicole Holbrook

Miss Idaho-Grace Zimmerman

Miss Illinois-Ariel Beverly

Miss Indiana-TiarraTaylor

Miss Iowa-Emily Tinsman

Miss Kansas-Annika Wooton

Miss Kentucky-Alex Francke

Miss Louisiana-Meagan Crews

Miss Maine-Carolyn Brady

Miss Maryland-CaitlynStupl

Miss Massachusetts-Lyndsey Littlefield

Miss Michigan-Mallory Rivard

Miss Minnesota-KathrynKueppers

Miss Mississippi-Mary Margaret Hyer

Miss Missouri-Simone Esters

Miss Montana-Mo Shea

Miss Nebraska-Allie Swanson

Miss Nevada-NasyaManchini

Miss New Hampshire-Sarah Tubbs

Miss New Jersey-Jade Glab

Miss New Mexico- Misa Tran

Miss New York-LaurenMolella

Miss North Carolina-Alexandra Badgett

Miss North Dakota-Haley Wolfe

Miss Ohio- CarolineGrace Williams

Miss Oklahoma-Addison Price

Miss Oregon-Shivali Kadam

Miss Pennsylvania-Tiffany Seitz

Miss Rhode Island-Molly Andrade

Miss South Carolina-Morgan Nichols

Miss South Dakota-Amber Hulse

Miss Tennessee-Brianna Mason

Miss Texas- Chandler Foreman

Miss Utah-DexonnaTalbot

Miss Vermont-Jillian Fisher

Miss Virginia-Camille Schrier

Miss Washington-Abbie Kondel

Miss West Virginia-TorianeGraal

Miss Wisconsin-Alyssa Bohm

Miss Wyoming-Jordan Hardman

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Miss America 2020: Meet The 51 Ladies Competing For The Crown - International Business Times

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The author aged 10, playing Hamlet in a school play.

One hundred and sixty days ago, one Friday afternoon in May, I went to my doctor.

Im transgender, I told him, and I want to be referred to a gender clinic.

His response was perfect: apologising for not knowing much about trans healthcare, he pulled up the referral form on his computer and asked if I would stay so that we could fill it in together.

When prompted by the form, I explained that I identify as non-binary, and he said hed come across the term before but didnt know much about what it meant. He ran through the form twice, checking every response with me, and then sent it off to the gender clinic in London.

The whole process took less than 10 minutes. I walked out of the GP surgery ecstatic; immediately called my sister to tell her, happy and shaky and relieved, what Id done.

And then the wait began.

As a reporter at PinkNews, I write about trans healthcare pretty often.

Sometimes its about the length of time trans people have to wait for an appointment at a gender clinic in different parts of the UK. In Devon, it currently takes three years between going to your GP for the first time, like I did, and going for your first appointment with a gender specialist.

Sometimes I write about how few gender clinics there are. There are just eight, in the whole of England and Wales, for who knows how many trans people half a million? A million? We dont know, because no one counts us.

Ive written about trans peoples joy at getting their gender legally recognised; about the gender recognition act in the UK that the government has promised to reform, again and again, but keeps delaying; about non-binary gender markers on driving licenses; and people crowdfunding for their top surgery or buying hormone treatment on the internet because the wait for the gender clinic is just too long to bear.

Mostly, the separation between myself as a journalist covering these issues and myself as someone directly affected by them is a boundary that, while fluid and permeable, I manage to maintain to some degree.

But its when trans children are pulled into the mainstream medias transphobic narrative that I think about the number of days it has been since I went to my doctor and asked to be referred to a gender clinic.

Im 29, and I can tell you without a single drop of doubt that I would be happier today had I been able to explore my gender identity, with the support of qualified professionals, as a teenager when the rest of society, cisgender society, explores theirs.

That opportunity is lost for me now, but it is not too late for trans kids. But instead of supporting them instead of campaigning for more gender clinics (there is only one gender clinic for under 18s in the entire country) and better support for them the UK media uses faux concern for trans kids to tell trans people like me, whove been where they are, that we are the powerful trans lobby seeking to do them harm. It paints the few organisations that exist to support these children and their parents as child mutilators, and says offering them counselling and peer support is child abuse.

Most of the time, when I write about these stories stories that come out predominantly in two or three UK papers, written by a handful of journalists, none of whom are trans I can remain, if not dispassionate, then at least calm. Writing from a trans-inclusive, LGBT+ perspective on trans issues the gift given to me by PinkNews is useful, I tell myself. Every time a transphobic journalist writes a column attacking trans people in a major newspaper, I can write a piece discrediting it, if I choose.

Sometimes, though, when the onslaught of outright transphobia in the UK not directed at me, necessarily, but directed at whichever trans person or organisation is the villain in the right-wing press that week feels particularly intense, I catch myself thinking about how many days its been since I was referred to the gender clinic.

I catch myself with my toes too close to the edge of the Tube platform with a train approaching, and I think about the awful statistics about how many trans people try to kill themselves, and I take a step back.

And I keep taking antidepressants, and going to therapy, and I keep waiting.

If I wasnt a journalist, I might not know that it will be at least another 19 months until I go to the gender clinic for the first time, but I do. And every time I see a gender-critical feminist talk about the powerful trans lobby, I think about this. If were so powerful, how come it takes years, literally, to get to a doctor? How come the press can openly call us predators and child molesters and freaks? How come trans children cant always get the help that they need in time?

Were there a powerful trans lobby, the first thing I would want it to do would be to put Piers Morgan on a planet very far away. And then, Id like for trans children to be unreservedly loved and affirmed. And Id like everyone waiting for an appointment at a gender clinic to get one, so that no trans person reaches the point where life becomes unbearable. Weve waited long enough.

Original post:
This World Mental Health Day, spare a thought for the trans children whose lives have become unbearable - PinkNews

Recommendation and review posted by Bethany Smith

Resisting over-consumption of our favorite high-calorie treats is about more than mere willpower for the severely obese.

LOS ANGELES (PRWEB) October 10, 2019

An October 1 article on Medical Xpress reports on the evermore evident fact that failed weight-loss attempts are not the result of weak willpower. Severely obese individuals who are attempting to lose weight may be extremely motivated and determined, and quite disciplined in most areas of their lives, but they are fighting against their own bodys innate biological processes. In some cases, these individuals may be able to rapidly lose significant amounts of weight, but thats when the real challenge starts. As the body recognizes that it is deviating from its normal state, complex chemical processes start to encourage overeating in a number of ways largely involving the production of hormones. The feelings of appetite these hormones stimulate are essentially indistinguishable from hunger and are extremely difficult to ignore even for the most determined individual. Worse, they only increase as more weight is lost. Southern California weight loss clinic West Medical says weight loss surgery is the one proven method of short-circuiting this metabolic catch-22.

West Medical notes that there are a number of ways to take advantage of this kind of medicine. For severely obese individuals, the clinic continues, sleeve gastrectomy surgery may be the most effective method of fighting hunger hormone production. The weight loss clinic notes that, during the surgery, the patients stomach is reconfigured into a pouch-like chamber that is reduced to about one-tenth of its original size. West Medical explains that, as the remaining portion of the stomach is removed, production centers for most hunger hormones are either removed or significantly hampered. The clinic says that by hindering this biological process, patients are much less likely to splurge their way back to obesity after they have lost significant weight although, of course, having a much smaller stomach also makes overeating far more unpleasant.

The weight loss specialists acknowledge that serious lifestyle changes must occur after any weight loss procedure for it to be a long-term success but the surgery makes them easier. Of course, as the benefits of weight loss accrue, life can become a lot more enjoyable. Moreover, the weight loss clinic notes that a wealth of studies have provided an exceptional amount of evidence stating that patients are far less likely to suffer premature death and the serious health problems that cause it. While medical science has reduced the mortality rate on many of these illnesses significantly, most of them can also greatly reduce an individuals overall quality of life. West Medical concludes that the benefits of weight loss operations such as sleeve gastrectomy surgery are more than worth the effort.

Patients who qualify for a sleeve gastrectomy typically have a body mass index (BMI) of 40 or more or 35 or more with related health problems such as type 2 diabetes. Other patients may take advantage of a growing number of alternative procedures. For more information about West Medical and all of its weight loss services visit their website at https://westmedical.com/ or call (855) 690-0565.

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Weight Loss Surgery Gives Willpower the Help it Needs to Defeat Obesity, says West Medical - PR Web

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According to a new study, an additional 1.7 million Canadians will be living with obesity by 2023.

Our growing girth is already at historic levels, and were among the heaviest countries in the world. Over the past decade, rates of overweight and obesity have increased in Canada, France, Mexico, Switzerland and the U.S., according to a 2017 report by the Organization for Economic Co-operation and Development. More than one in four adults is obese in Canada. Within three years, there will be a total of 8.5 million people in a weight class considered a serious threat to health.

All of this leaves virtually no chance of meeting World Health Organization targets for a zero increase in obesity from 2010 to 2025, a global goal set to address the health impacts of weight gain (such as high blood pressure, type 2 diabetes, heart disease, stroke and certain cancers) as well as the cost to health-care systems, estimated at $5 to $7 billion in Canada alone.

The burden surprised me, says Laura Rosella, co-author of the modelling study and an associate professor in epidemiology at the University of Torontos Dalla Lana School of Public Health. I thought, optimistically, that we have actually been making progress in terms of awareness and efforts to reduce obesity.

Its going to get worse before it gets better.

Why?

Its not, as comedian Bill Maher recently put it,because people are eating like aholes.

Try to lose weight and the brain fights back, aggressively. Higher levels of the hunger hormone ghrelin are released, sending a single-minded message to the nerves in the hypothalamus: Get food. At the same time, the brain blocks satiety, or Im full, signals from the gut and slows downthe rate at which calories are burned.

This famine effect can last a year or longer as people struggle to keep the lost weight off.

It is an incredible and efficient response to weight loss, obesity specialist Dr. David Macklin says with awe.

But Mahers fat-shaming quip taps into acommon misperception: that obesity comes down to some kind of moral failing, a lack of discipline and self-control, and that the solution is as simple as finding the right diet and working out a ton, Macklin says.

In fact, it goes much deeper.

We now have great clarity that obesity is a chronic and complex, progressive, primarily genetically conferred, centred-in-the-brain, environmentally influenced, real medical condition, sums up Macklin, the medical director of a weight management program for high-risk pregnancies at Torontos Mount Sinai Hospital.

The DNA of obesity

The tendency is to blame obesity primarily on poor food choices sugary drinks, salty, greasy processed foods, staggering portion sizes.

But a growing body of research suggests that the appeal of these foods, as well as the drive to overeat, is rooted in our DNA.

Genome-wide studies have identified hundreds of genes associated with body mass index, waist-to-hip ratios and other traits of obesity, most of them expressed meaning whether theyre turned on or off in the brain.

Many of these genes evolved over millions of years to collect and store excess calories as fat whenever food was available, and to keep early humans from starving whenever food was scarce. Except as weve shifted from hunter-gatherers to farmers, then farmers to factory workers, food is no longer so scarce.

In this part of the world, for most people, we dont have famine anymore, we have only a feast, says Dr. Sue Pedersen, of the C-ENDO Diabetes and Endocrinology Clinic in Calgary.

Instead of a survival mechanism, gaining excess weight is now a liability. And as scientists are discovering, some of us are more genetically vulnerable to packing on the pounds than others, says Macklin.

Part of this is how the brain responds to the hunger hormone ghrelin. In people with a genetic predisposition to obesity, the gut also tends to release fewer quantities of the hormones tied to fullness.

Either way, If you take people who are the same weight and they have the same metabolic rate and you put everyone on (a) diet, people will lose weight unequally, based on their genetics, says Macklin.

Furthermore, some people who consume excess calories gain fat. Other people, their body responds by burning more, by increasing their metabolic rate and taking anything extra and putting it into muscle.

Even more frustrating for those less prone to burning fat, the further people get from their highest weight, Macklin says, the harder the body fights against losing it.

How strongly we respond to cues in the environment that generate the fundamental drive to eat the psychological state known as wanting and our ability to control that wanting, Macklin says, is heritable as well.

The gut microbiome

The environment inside our digestive tract may also play a critical role in weight gain.

Each of us plays host to trillions of different bacteria, which colonize our intestines immediately after birth and continue to evolve as we age based on what we eat and where we live. These bacteria impact our digestion, the production of certain vitamins and our immune system.

Theres now evidence that people living with obesity have different gut flora than those who are not. According to some scientists, it may be that mircobiota not just our genes are reducing the expression of gut satiety hormones.

Although researchers are still exploring exactly how gut bacteria interact with our intestines and the brain, the link appears clear:When mice free of intestinal bugs are fed stool from either obese mice or humans, they put on more weight and body fat than those fed bacteria from the guts of lean mice or humans.

The chemical context

Some antidepressants and newer generation anti-psychotics, drugs Canadians are being prescribed in record numbers,may be behind ourrapid and dramatic weight gaintoo.

Antipsychotics can trigger hedonic hyperphagia eating to excess for pleasure, not hunger. Two years ago, Montreal researchers reported that, after 24 months of treatment, the mean weight of children prescribed antipsychotics for ADHD and other behavioural problems increased by 12.8 kg.

One study published last year in the British Medical Journal found people taking any of the 12 most commonly used antidepressants had an increased risk of weight gain that persisted over at least five years of follow-up. Its not clear why. Depression, in and of itself, can cause weight gain. And people might eat more as their mood improves. Some believe the drugs may affect metabolism or trigger cravings for carbohydrates. But there are options, Pedersen says. Some anti-depressants are weight neutral or even induce weight loss.

The chemicals in our food particularly artificial sweeteners may also react with taste receptors or gut bacteria in ways that stimulate more food intake, Pedersen adds.

Recent studies suggest theres something about the sheer textural and sensory properties of ultra-processed foods that make us eat more of them, and more quickly. (Again, it could be that foods with hyper-palatable amounts of sugar, fat and salt are irresistible to the ancient brain.)

Obesityultimately still comes down to physics, Pedersen says. If calories in are higher than calories out, weight will go up.But managing the factors that contribute to that equation is much more complicated than simply sticking to a diet. And a lack of education means that fat-shaming and weight discrimination are as prevalent in medicine as everywhere else.

Why are obesity rates getting worse? says Macklin. When youre talking about a real disease, and youre only offering up advice like, Eat less, move more, its like saying, Listen, I see you have asthma, and its severe asthma, but just breathe deeper. Just pull yourself up by your bootstraps and I dont want to see you back here wheezing.

Not only is obesity real, but treatments exist. That should be the messaging to someone with obesity.

Read the National Posts ongoing focus on Canadas obesity epidemic at nationalpost.com/obesity.

Subscribe to our podcast, 10/3, on Apple Podcasts or Spotify

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The biology of obesity: How our ancient brain conspires to make us overeat - National Post

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Photo: Anh Nguyen

To mark World Mental Health Day, HONG KONG BUZZ takes a look at depression. It is a serious matter when you see that one in three Hong Kong youngsters suffers from stress, anxiety or depression (Hong Kong Playground Association) and the suicide rate for people aged 15 to 24 is 9.5 per 100,000 (Centre for Suicide Research and Prevention). Depression can strike at any age.

On medical matters go to a reputable source. Here is the USAs Mayo Clinic on depression:

SYMPTOMS:

The illness is also called major depressive disorder or clinical depression, the Mayo Clinic says. Most people with depression will feel better with medicine or psychotherapy or both.

CAUSES

People with depression appear to have physical changes in their brains. Neuro-transmitters are naturally occurring chemicals in the brain that effect mood. Changes in the bodys hormone balance can trigger depression, such as pregnancy or after giving birth. Other causes: thyroid problems, menopause and others. People are more likely to develop depression if their relatives have suffered from it.

RISK FACTORS

Still with the Mayo Clinic they include:

PREVENTION AND TREATMENT

The clinic says you can prevent depression by controlling your life and avoiding anything that will cause you stress. Reach out to family or friends and get treatment. The safest medicine with the least side effects is a serotonin reuptake inhibitor such as Celexa or Prozac. These must be prescribed by a medical professional. Other medicines include serotonin-norepinephrine reuptake inhibitors, atypical anti-depressants, tricyclic anti-depressants and monoamine oxidase inhibitors.

HOME REMEDIES

Study the illness by reading reputable books and websites, so you will understand what is happening to you. Pay attention to warning signs such as the onset of symptoms (above). Avoid alcohol and drugs. Eat healthily and be physically active, walking, running or swimming. You may use supplements but be careful because they can interfere with medicines and dont overdose. Mayo Clinic mentions two, St Johns Wort and Omega 3 fatty acids.

Read more from the original source:
A terrible illness: Who do you know who looks melancholic, feels worthless and hopeless, and often thinks of death? - Hong Kong Buzz

Recommendation and review posted by Bethany Smith