StemCell Therapy

The spread of coronavirus seems to be slowing down in China as the country continues to put proper measure in place to slowdown the spread of the disease. However, the virus outbreak in Iran, Italy, and South Korea are raising fears of a broader epidemic. The coronavirus (COVID-19), caused by SARS-CoV-2 started in Whuan China started in December 2019. To date, coronavirus has claimed 2,701 human lives and wreck havoc to global markets.

As of 25 February 2020, around 80,149 cases have been confirmed, including in all provinces of China and more than two dozen other countries. Of these, 11,569 cases were classified as serious. There have been 2,701 deaths attributable to the disease, including 38 outside mainland China, surpassing that of the 2003 SARS outbreak.

As the virus spread around the world so are the rumors about the origin of the virus. Weve written many stories about the virus ranging from Chinese scientists arguing that the the virus originated from Chinas Wuhan laboratory. Some media outlets also pointed to comments from Chinas Presidentabout the need to contain the coronavirus and set up a system to prevent similar epidemics in the future. President Xi said a national system to control biosecurity risks must be put in place to protect the peoples health because lab safety is a national security issue.To add to the suspicion, NY Post also pointed toa newly release directive from Chinese Ministry of Science and Technology titled: Instructions on strengthening biosecurity management in microbiology labs that handle advanced viruses like the novel coronavirus.

The problem, however, is these news storieshave very little scientific merit. According to a new study published in ScienceDirect titled: Full-genome evolutionary analysis of the novel corona virus (2019-nCoV) rejects the hypothesis of emergence as a result of a recent recombination event, their findings show that theCOVID-19 is 96 percent similar to the bat virus RaTG13. The 2019-nCoV although closely related to BatCoV RaTG13 sequence throughout the genome (sequence similarity 96.3%), shows discordant clustering with the Bat_SARS-like coronavirus sequences, the authors said.

The study concludes with the statement: The levels of genetic similarity between the 2019-nCoV and RaTG13 suggest that the latter does not provide the exact variant that caused the outbreak in humans, but the hypothesis that 2019-nCoV has originated from bats is very likely. Their conclusion supports the widely accepted claim that coronavirus originated from Whuan meat market where bats are snakes were sold for food.

The question is, what do we make of the study published by Chinese scientists in The Lancet?The wider scientific community, upon seeing the paper, were also less than impressed with the speculations and conclusions drawn by the Chinese scientists. The scientist at the forefront of an international effort to track the deadly coronavirus outbreak shot down claims about the diseases origins, including that it escaped from a Wuhan laboratory after being genetically engineered.Trevor Bedford, of the Fred Hutchinson Cancer Research Center in Seattle, said:There is no evidence whatsoever of genetic engineering that we can find. He made the statement at the American Association for the Advancement of Science meeting in Seattle. The evidence we have is that the mutations (in the virus) are completely consistent with natural evolution.

Finally, on February 2, the World Health Organization (WHO)called the new coronavirus a massive infodemic, referring to an overabundance of informationsome accurate and some notthat makes it hard for people to find trustworthy sources and reliable guidance when they need it.

Due to the high demand for timely and trustworthy information about 2019-nCoV, WHO technical riskcommunication and social media teams have been working closely to track and respond to myths and rumours.Through its headquarters in Geneva, its six regional offices and its partners, the Organization is working 24 hours aday to identify the most prevalent rumors that can potentially harm the publics health, such as false preventionmeasures or cures. These myths are then refuted with evidence-based information. WHO is making public healthinformation and advice on the 2019-nCoV, including myth busters, available on its social media channels (includingWeibo, Twitter, Facebook, Instagram, LinkedIn, Pinterest) and website, WHO said.

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Coronavirus was not genetically engineered. Instead it is the first Infodemic - TechStartups.com

Whenever Harry Wuest has a doctors appointment in northern Atlantas hospital cluster dubbed Pill Hill, he makes sure to stop by the office of Dr. Douglas Doug Murphy for a quick chat.

And Murphy, unless hes tied up in the operating room, always takes a few minutes to say hello to his former patient. Remember when ... ? is how the conversation typically starts, and its always tinged with laughter, often joyful, sometimes bittersweet.

Its a reunion of two men who shaped a piece of Georgias medical history.

Almost 35 years ago, Murphy opened the chest of Wuest and sewed in a new heart, giving him a second shot at life. Wuest was the third heart transplant patient at Emory University Hospital.

Tall, lanky, with short curly hair and a quiet demeanor, Wuest is the longest-surviving heart transplant recipient in Georgia and one of the longest-surviving in the world. The 75-year-old accountant still plays golf twice a week and only recently went from working full-time to part-time. My heart is doing just fine, he says.

Murphy is now the chief of cardiothoracic surgery at Emory Saint Josephs Hospital and still in the operating room almost every day. He has moved on to become the worlds leading expert in robotically assisted heart surgery.

Harry Wuest is originally from Long Island, New York. After a stint in the Air Force, he moved to Florida to work and go to school. He wanted to become a physical education teacher. Then, in 1973, he fell ill. It started with some pain on his left side. He didnt think much of it, but when he got increasingly winded and fatigued, he went to see a doctor.

Several months and numerous specialists later, he received the diagnosis: Cardiomyopathy, a disease of the heart muscle that can make the heart become enlarged, thick and rigid, preventing it from pumping enough blood through the body.

They didnt know how I got it, says Wuest, sitting back in a brown leather armchair in the dark, wood-paneled living room of his Stone Mountain home. Maybe it was a virus. And back then, there wasnt much they could do to treat it, except bed rest.

For the next 12 years, Wuest lived life as best as he could. He got a degree in accounting from the University of Central Florida and worked for a real estate developer. There were good days, but there were more bad days. He was often too weak to do anything, and his heart was getting bigger and bigger.

Emorys first transplant surgeon

The first successful human-to-human heart transplant was performed in Cape Town, South Africa, in 1967 a medical breakthrough that catapulted the surgeon, Dr. Christiaan Barnard, onto the cover of Life magazine and to overnight celebrity status.

This highly publicized event was followed by a brief surge in the procedure around the world, but overall, heart transplants had a rocky start. Most patients died shortly after the surgery, mainly due to organ rejection. Back then, immunosuppressive drugs, which can counteract rejection, were still in their infancy. Many hospitals stopped doing heart transplants in the 1970s.

That changed with the discovery of a highly effective immunosuppressive agent. Cyclosporine got FDA approval in 1983 and altered the world of organ transplants.

It was shortly thereafter when Emory University Hospital decided to launch a heart transplant program, but none of the senior surgeons wanted to do it. Even with the new drug, it was a risky surgery, and mortality was still high.

Its an all-or-nothing operation, Murphy says, as he sits down in his small office overlooking the grayish hospital compound. Hes wearing light blue scrubs from an early morning surgery. At 70, he still has boyish looks, with a lean build and an air of laid-back confidence. If you have a number of bad outcomes initially, it can be detrimental to your career as a surgeon, he says.

But Murphy didnt really have a choice. He remembers that during a meeting of Emorys cardiac surgeons in 1984, he was paged to check on a patient. When he returned, the physicians congratulated him on being appointed the head of the new heart transplant program. He was the youngest in the group and had been recruited from Harvards Massachusetts General Hospital just three years before.

Yeah, thats how I became Emorys first transplant surgeon, says Murphy.

He flew to California to shadow his colleagues at Stanford University Hospital, where most heart transplants were performed at the time. Back home at Emory, he put together a team and rigorously rehearsed the operation. The first transplant patient arrived in April 1985. The surgery was successful, as was the second operation less than a month later.

Around the same time, Harry Wuest wound up in a hospital in Orlando. He needed a transplant, but none of the medical centers in Florida offered the procedure. One of his doctors recommended Emory, and Wuest agreed. I knew I was dying. I could feel it. He was flown to Atlanta by air ambulance and spent several weeks in Emorys cardiac care unit until the evening of May 23, when Murphy walked into his room and said, Weve got a heart.

I could finally breathe again

The heart, as the patient later learned, came from a 19-year-old sophomore at Georgia Tech who had been killed in a car crash.

Organ transplants are a meticulously choreographed endeavor, where timing, coordination and logistics are key. While Murphy and his eight-member team were preparing for the surgery, Wuest was getting ready to say farewell to his family his wife and three teenage sons, and to thank the staff in the cardiac ward.

I was afraid, he recalls, especially of the anesthesia. It scared the heck out of me. He pauses during the reminiscence, choking briefly. I didnt know if I was going to wake up again.

The surgery took six hours. Transplants usually happen at night because the procurement team, the surgeons who retrieve different organs from the donor, only start working when regularly scheduled patients are out of the operating room.

Despite the cultural mystique surrounding the heart as the seat of life, Murphy says that during a transplant surgery, its not like the big spirit comes down to the operating room. Its very technical. As the team follows a precise routine, emotions are kept outside the door. We dont have time for that. Emotions come later.

Waking up from the anesthesia, Wuests first coherent memory was of Murphy entering the room and saying to a nurse, Lets turn on the TV, so Harry can watch some sports.

Wuest spent the next nine days in the ICU, and three more weeks in the hospital ward. In the beginning, he could barely stand up or walk, because he had been bedridden weeks before the surgery and had lost a lot of muscle. But his strength came back quickly. I could finally breathe again, he says. Before the surgery, he felt like he was sucking in air through a tiny straw. I cannot tell you what an amazing feeling that was to suddenly breathe so easily.

Joane Goodroe was the head nurse at Emorys cardiovascular post-op floor back then. When she first met Wuest before the surgery, she recalls him lying in bed and being very, very sick. When she and the other nurses finally saw him stand up and move around, he was a whole different person.

In the early days of Emorys heart transplant program, physicians, nurses and patients were a particularly close-knit group, remembers Goodroe, whos been a nurse for 42 years and now runs a health care consulting firm. There were a lot of firsts for all of us, and we all learned from each other, she said.

Wuest developed friendships with four other early transplant patients at Emory, and he has outlived them all.

When he left the hospital, equipped with a new heart and a fresh hunger for life, Wuest made some radical changes. He decided not to return to Florida but stay in Atlanta. Thats where he felt he got the best care, and where he had found a personal support network. And he got a divorce. Four months after the operation, he went back to working full-time: first in temporary jobs and eventually for a property management company.

After having been sick for 12 years, I was just so excited to be able to work for eight hours a day, he recalls. That was a big, big deal for me.

At 50, he went back to school to get his CPA license. He also found new love.

Martha was a head nurse in the open-heart unit and later ran the cardiac registry at Saint Josephs Hospital. Thats where Wuest received his follow-up care and where they met in 1987. Wuest says for him it was love at first sight, but it took another five years until she finally agreed to go out with him. Six months later, they were married.

Harry Wuest and his wife, Martha. She was a head nurse in the open-heart unit and later ran the cardiac registry at Saint Josephs Hospital. Thats where Wuest received his follow-up care and where they met in 1987. Wuest says for him it was love at first sight, but it took another five years until she finally agreed to go out with him. Six months later, they were married.

Having worked in the transplant office, I saw the good and the bad, Martha Wuest says. A petite woman with short, perfectly groomed silver hair, she sits up very straight on the couch, her small hands folded in her lap. Not every transplant patient did as well as Harry. And I had a lot of fear in the beginning. Now he may well outlive her, she says with a smile and a wink.

Wuests surgeon, meanwhile, went on to fight his own battles. Two and a half years into the program, Murphy was still the only transplant surgeon at Emory and on call to operate whenever a heart became available. Frustrated and exhausted, he quit his position at Emory and signed up with Saint Josephs (which at the time was not part of the Emory system) and started a heart transplant program there.

At St. Josephs, Murphy continued transplanting hearts until 2005. In total, he did more than 200 such surgeries.

Being a heart transplant surgeon is a grueling profession, he says, and very much a younger surgeons subspecialty.

He then shifted his focus and became a pioneer in robotically assisted heart surgery. He has done more than 3,000 operations with the robot, mostly mitral valve repairs and replacements more than any other cardiac surgeon in the world.

Heart transplants "remain the gold standard"

Since Murphy sewed a new heart into Wuest 35 years ago, there has been major progress in the field of heart transplants, but it has been uneven.

There is improved medication to prevent rejection of the donor heart, as well as new methods of preserving and transporting donor hearts.

Yet patients requiring late-stage heart failure therapy, including transplantation, still exceed the number of donor hearts available. In 2019, 3,551 hearts were transplanted in the United States, according to the national Organ Procurement and Transplantation Network. But 700,000 people suffer from advanced heart failure, says the American Heart Association.

New technologies and continued research are providing hope to many of these patients. There has been significant progress in the development of partial artificial hearts, known as Left Ventricular Assist Devices, or LVADs. They can be used as bridge devices, to keep patients alive until donor hearts are available, or as destination therapy, maintaining patients for the remainder of their lives.

Also, total artificial hearts have come a long way since the first artificial pump was implanted in a patient in 1969. The technology is promising, says Dr. Mani Daneshmand, the director of Emorys Heart & Lung Transplantation Program. But its not perfect.

Long-term research continues into xenotransplantation, which involves transplanting animal cells, tissues and organs into human recipients.

Regenerative stem cell therapy is an experimental concept where stem cell injections stimulate the heart to replace the rigid scar tissue with tissue that resumes contraction, allowing for the damaged heart to heal itself after a heart attack or other cardiac disease. Certain stem cell therapies have shown to reverse the damage to the heart by 30 to 50 percent, says Dr. Joshua Hare, a heart transplant surgeon and the director of the Interdisciplinary Stem Cell Institute at the University of Miamis Miller School of Medicine.

All of these ideas have potential, says Daneshmand. But none of them are ready to replace a human donor heart. A heart transplant remains the gold standard, because you cant accommodate the same success with a machine right now, he says.

Efforts around expanding the donor pool are really the best way to address this problem, while we wait for technology to catch up, he adds.

Besides Emory, other health care systems in Georgia that currently have a heart transplant program are Piedmont Healthcare, Childrens Healthcare of Atlanta and Augusta University Health.

Organ rejection remains a major issue, and long-term survival rates have not improved dramatically over the past 35 years. The 10-year survival is currently around 55 percent of patients, which makes long-term survivors like Harry Wuest rare in the world of heart transplants.

The United Network of Organ Sharing, or UNOS, which allocates donor hearts in the United States, doesnt have comprehensive data prior to 1987. An informal survey of the 20 highest-volume hospitals for heart transplants in the 1980s found only a scattering of long-term survivors.

In for the long haul

Being one of the longest-living heart transplant recipients is something that Wuest sees as a responsibility to other transplant patients, but also to the donors family, which hes never met. If you as a transplant recipient reject that heart, thats like a second loss for that family.

Part of this responsibility is living a full and active life. Both he and Martha have three children from their previous marriages and combined they have 15 grandchildren. Most of their families live in Florida, so they travel back and forth frequently. Wuest still works as a CPA during tax season, and he does advocacy for the Georgia Transplant Foundation. In addition to golf, he enjoys lifting weights and riding his bike.

Hes had some health scares over the years. In 2013, he was diagnosed with stage 1 kidney cancer, which is in remission. Also, he crossed paths with his former surgeon, and not just socially. In 2014, Murphy replaced a damaged tricuspid valve in Wuests new heart. That operation went well, too.

Murphy says there are several reasons why Wuest has survived so long. Obviously, his new heart was a very good match. But a patient can have the best heart and the best care and the best medicines and still die a few months or years after the transplantation, the surgeon says. Attitude plays a key role.

Wuest was psychologically stable and never suffered from depression or anxiety, Murphy says. Hes a numbers guy. He knew the transplant was his only chance, and he was set to pursue it.

Wuest attributes his longevity to a good strong heart from his donor; good genetics; great doctors and nurses; and a life that he loves. Im just happy to be here, he says.

Quoting his former surgeon and friend, he adds: Doug always said, Having a transplant is like running a marathon. And Im in for the long haul.

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34 years with a new heart and counting - MDJOnline.com

CAMP HILL, PA (WPMT) A family in Cumberland County has turned to stem cells to treat their two-year-old son diagnosed with cerebral palsy. The only problem: stem cell treatment for the disease hasnt been approved by the FDA.

The day he was born, when he wheeled him down the hall and he was only a pound, and I started to cry and said, will he live? And he said, of course Hes only small, said Danielle Maxwell, Lances mom.

The words, hes only small, are what Lances mom and father Rob have lived by since the day he was born. The preemie, born three months early, has been through several surgeries and complications along the way. But, Lance has always been a fighter.

Lance fought so hard just to survive the beginning of life, and come home with us, said Danielle. And he is just so happy and loving and amazing.

About a year ago, Lance was diagnosed with cerebral palsy. Doctors told his family, he will never walk, talk or take care of himself.

We just dont believe that, said Danielle. We dont.

Lance receives a lot of different therapies but, his parents did not want to just stop there.

We both overwhelmingly feel, he never gave up, he never gave up on us, he never gave up on himself, said Rob. So, we owe it to him to give him the opportunity. Its really that simple, he deserves the opportunity.

Danielle began researching stem cell therapies, even speaking to doctors in countries overseas where treatment with stem cells is more readily accessible than in the U.S. The FDA has approved stem cell treatments for some conditions but not cerebral palsy. However, trials to determine the effectiveness of stem cell treatment for the disease are underway.

What weve seen is a small but real appearing improvement in motor function, said Doctor Charles Cox with University of Texas Health in Houston, began a trial in 2013 on the safety and effectiveness of banked cord blood or bone marrow stem cells in children with cerebral palsy, and is now just wrapping up the results from the trial.

The overall results of this study depend if youre a glass half full or half empty kind of person, said Dr. Cox. It is not a compelling miraculous result. Its not, Oh my God, this child was treated and look at this profound benefit.'

Because stem cell treatment for cerebral palsy is still in trial phases, its not approved treatment by the FDA. However, the Maxwells did find a doctor in Harrisburg willing to transfer stem cells from a full-term babys umbilical cord to Lance. But, since it isnt FDA approved, we were not allowed to be there to show Lance receiving the stem cells. The Maxwells are hopeful following this procedure Lance may someday walk and more importantly be able to communicate with them.

He wants to be involved, said Rob. You can tell hes trying to communicate he just cant get over that hump. We believe stem cells could be that bridge to help him move a little faster.

Danielle says it will take about six months to see if the stem cells will have any definitive benefits for Lance. But, already says shes seeing progress. She says Lance is not able to stand on his own

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Cumberland County family turns to non-FDA approved stem cell treatment to help two-year-old son with cerebral palsy - fox2now.com

Treatment for sickle cell disease has come a long way since the 1970s when the life expectancy of people living with it was less than 20 years.

People with sickle cell disease are not only living longer life expectancy is now 42 to 47 years of age but are enjoying a better quality of life, too.

"In the Philadelphia area, there has been great pediatric care for sickle cells disease and because of that people who have it are living very well," said Dr. Farzana Sayani, a hematologist at Penn Medicine.

Sayani is the director of a comprehensive sickle cell program focusing on adults living with the disease. Penn also has an active transition program for youth transitioning from a pediatric institution to adult care.

Sickle cell disease is an inherited red blood cell disorder that affects about 100,000 Americans.It is most often found in people of African or Hispanic descent.About 1 in 365 African-American babies are born with sickle cell disease, according to Sayani.

People who have the disease inherit an abnormal type of hemoglobin in their red blood cells, called Hemoglobin S, from both their mother and father.When only one parent has the hemoglobin S gene, a child will have the sickle cell trait, but usually does not develop the disease. But they may pass it on to their children.

Hemoglobin is the protein in the blood responsible for carrying oxygen to the rest of the body. Hemoglobin S causes red blood cells to become stiff and sickle-shaped. Instead of being round in shape, they look like crescent moons.

Sickle cells are sticky and can bind together, blocking the flow of blood and preventing oxygen from getting where it needs to go in the body. This causes sudden attacks of pain referred to as a pain crisis.

There are severaldifferent types of sickle cell disease.Hemoglobin SS, also known as sickle cell anemia, is the most common and most severe type of sickle cell disease.

Anemia occurs when red blood cells die at a rate faster than the body can replace them. Normal red blood cells generally live for 90 to 120 days. Sickled cells only live for 10 to 20 days. This shorter life-to-death cycle is harder for the body to sustain.

Another form,Hemoglobin SC, is not as severe as sickle cell anemia, but it can still cause significant complications, Sayani said.Other forms include Hemoglobin S0 thalassemia, Hemoglobin S+ thalassemia, Hemoglobin SD and Hemoglobin SE.

Sickle cell disease screening is a mandatory part of newborn screenings in Pennsylvania.

If the screening is positive, the family is informed and plugged into the health care system in order to receive the proper care.

If the disease is not diagnosed at birth, a blood test can confirm it at any age in which symptoms start to surface.

The severity of sickle cell disease can vary.

Each individual is affected differently, making it difficult to predict who will get what complications, Sayani said. That is why a comprehensive sickle cell program is so important.

Early signs include a yellowish tint to the skin or jaundice, fatigue and a painful swelling of the hands and feet.

"Young children with sickle cell disease may be tired, not eat very well and have delayed growth," Sayani said. "They may also develop anemia, be at greater risk of infection and start to experience pain crises."

Acute pain crises, also known as vaso-occlusive crises, can lead to long stays in the hospital to manage the crippling pain. Children with sickle cell disease also tend to experience delayed growth and puberty.

As a person with sickle cell disease grows older, the sickled red blood cells start to affect various organs, bones and joints.

This can lead to acute chest syndrome, which occurs when damaged lung tissues makes it difficult to breathe. Brain complications, including stroke, are possible.People with sickle cell disease are also prone to heart damage, eye problems, and infections like chlamydia, salmonella and staphylococcus. Chronic and acute pain is common.

There are different types of medicine that can help manage sickle cell disease.

Last year, an oral medicine was approved that makes sickle cells less likely to sickle. So was an intravenous medicine that has been shown to reduce pain crises and hospitalizations by 50%. Some people living with sickle cell disease also may need regular blood transfusions.

Hydroxyurea has also been used successfully for many years to reduce pain crises and the need for blood transfusions and hospitalizations.

Currently, blood and bone marrow transplant is the only way to cure the disease. But it is not an option for everyone because of the difficulty of finding a well-matched stem cell donor.

A related donor is best but only about a third of sickle cell patients have a donor that is related and fully-matched, Sayani said.

While these transplants have a 85% or more success rate, they also are associated with significant risks, including organ dysfunction, infection and graft vs. host disease which can be quite debilitating.

Transplants completed in children have the best results, Sayani said. But because of the risks involved, doctors only suggest it for patients with severe forms of the disease.

Early clinical trials with gene therapy are also showing promise, she added.

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New sickle cell disease treatments are helping people live longer and giving them a higher quality of life - PhillyVoice.com

The newly released Dish Life: The Game is described as "part Sims, part Tamagotchi". It sees you starting out as an undergraduate student, gradually rising through the scientific ranks to become a professor. You'll do this while helping your colleagues and managing the day-to-day running of your lab. It ultimately aims to showcase the laboratory as a social world, where strong relationships are key to achieving great science.

I first played developer Pocket Sized Hands' latest back in January at Pocket Gamer Connects London, and I felt it was one of the most interesting titles on the show floor. What first appeared to be a fairly straightforward educational game funded by the University of Cambridge, no less quickly revealed itself to be a surprising and layered, though still very accessible, sim with some intriguing role-playing elements.

The basic idea is that you'll work to run and expand your lab, dealing with the various complications and challenges that arise over time. Your stem cells need to be cared for, your colleagues may require your support, and you're going to have to consider a number of tough decisions that could make or break your research and friendships. You may also have to deal with things like bullying in the workplace, media controversies, and challenging ethical quandaries.

It's the sim aspects and enjoyable minutia of running a lab that makes Dish Life feel so very distinctive. Caring for your stem cells scratches that Tamagotchi itch, and managing the lab and its staff is satisfying work.

If you hear the term "educational game" and instantly switch off, know that it easily sidesteps the tedium of the genre to deliver an experience with personality to spare. There are definitely moments where your knowledge will be tested, such as the little reports you have to write, but they feel natural and dare I say it? quite fun.

It was developed in collaboration with Cambridge sociologists and stem cell scientists from the university's Stem Cell Institute, including producerDr. Lucy van de Wiel (Cambridge Department of Sociology's ReproSoc group), giving it a certain level of authenticity. The game follows on from a short film directed by Chloe Thomas and produced by Dr. Karen Jent (ReproSoc) and stem cell scientist Dr. Loriana Vitillo. I've embedded it above for you to give it a watch.

Dish Life: The Game is now available for download from both the App Store and Google Play as a free-to-play title.

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Dish Life: The Game, available now for iOS and Android, challenges you to run your very own stem cell lab - Pocket Gamer

AN EXTRAORDINARY teenager recovering from a fresh round of lifesaving treatment as she battles bone cancer is in line for the Young Scot of the year award.

Brave Molly Cuddihy from Gourock has won the hearts of people in Inverclyde and beyond as she fights the extremely rare Metastatic Ewing's Sarcoma.

The remarkable Clydeview Academy pupil has kept a smile on her face throughout her ordeal and raised an incredible 250,000 at a fundraising ball to help younger children battling cancer.

Earlier this month she underwent a stem cell transplant which left her in intensive care.

Her dad John, of Doune Gardens, said: "Molly is unable to physically speak at the moment because of side effects.

"She was so surprised by her nomination and over the moon.

"She found out on the day she went in for her transplant.

"It lifted her spirits and it lifts us all.

"Molly is incredible and an inspiration.

"She never feels sorry for herself, she just gets back up again and gets on with it.

"Again we have to thank everyone for their support - we are overwhelmed by the support of everyone out there.

"If love and kindness was a pill, Molly would be cured."

After the stem cell transplant Molly was in intensive care because of a series of complications caused by the treatment.

But her dad told the Telegraph: "The signs from the stem cell transplant are good."

Molly now faces a spell in isolation because the treatment has left her body with the protection of an unborn child.

Since her fundraising ball in October Molly has been undergoing treatment for cancer while also working with health chiefs to put plans in place for a special room in the Royal Hospital for Sick Children for children aged eight to 12 year olds.

Schoolgirl Molly was only 15 when she diagnosed with cancer in January 2018 and spent nearly a year in hospital.

She had bone cancer in her ribcage, which presented itself as a mass on her side but it had spread to her lungs and her spine.

She faced many months of gruelling chemotherapy and radiotherapy to blast the cancer.

The one in her spine is inoperable and has to be treated with radiotherapy.

On top of that there was the added complication of a bacterial infection contracted in hospital which threatened her life.

Despite all of this, during her first year in hospital Molly sat her Nationals exams in hospital and scored straight As.

In August last year she achieved straight As in her Highers and won a place at Oxford University's international summer school through all her hard work.

Weeks later Molly was told she would have to have another operation to remove one tumour, with chemo to target two more and stem cell bone marrow transplants.

During her cancer battle Molly has won the hearts of a number of celebrities, including Simon Cowell, Gary Barlow and Paulo Nutini, thanks to her fundraising exploits.

Together with her best friend Sara Millar she organised a fundraising ball last October to say thanks to all the hospital staff who have helped her.

Molly was also the first ever winner of the Rosie Mitchell Memorial Award at the Greenock Telegraph's Community Champions night last year.

Molly has now been shortlisted for Young Scotswoman of the Year hosted by Newsquest, which owns the Greenock Telegraph.

The public vote is open now and locals can back Molly up until until 5pm today.

The winner will be announced at the glittering gala in association with the St Enoch Centre, at the Grand Central Hotel on March 26.

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Brave Gourock teen battling bone cancer is in line for the Young Scot of the year award - Greenock Telegraph

Michael Schumacher turned 51 in January and as he became a year older, his fans are hoping that he is doing fine. Apparently, fans did not stop supporting him even if he not visible since his sustained massive brain injury due to a freak accident while he was skiing in December 2013.

A few weeks after the accident, Schumachers family refused to release information about the F1 champs health recovery. The family completely shut down the media so fans were deprived of information as to what is going on and any development in Schumis health. The secrecy went on for years and up to now, they remained secretive when it comes to the motorsport legends condition.

Secret treatment

It has been over six years since Micheal Schumacher had an accident and since then, some new treatments were developed. It was reported that the former sportsman tried out one of the latest procedures available today and it is called the stem cell treatment.

The Telegraph reported that Schumi was brought to Paris and admitted at the Georges-Pompidou hospital in September. The procedure was supposedly carried out by cardiovascular surgeon Philippe Menasch and it was said that one of the medical staff attested that Schumacher is conscious after the stem-cell procedure, a treatment dubbed as the pioneer in cell surgery."

It was said that Michael Schumacher stayed at the hospital for three days and on the last day, he was transported back to his home in Switzerland via ambulance. The question is - did he improved after the treatment?

How is he today?

As per The Daily Mail, even the surgeon who performed the procedure on Michael Schumacher said that he doesnt perform miracles. It appears he is saying that even though the treatment is considered a breakthrough in the medical field today, it may not work for everyone. With the racers condition, he may have developed some kind of complications that could have made his health situation worst and this treatment may have not affected Schumi as it should.

It is believed that Michael Schumacher is still paralyzed and being nursed on his bed. His movements are still limited and If there are improvements, perhaps, he could talk a bit and move some parts of his body like his head.

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Michael Schumacher reportedly underwent breakthrough treatment; Here are details of the secret procedure - EconoTimes

There have been a number of deaths from the coronavirus among doctors who are young and, as far as we know, otherwise healthy.

According to Dr Bharat Pankhania, an expert on communicable disease control at the University of Exeter Medical School, it is not surprising that some young, healthy people die after contracting the virus, noting the risk of infection and even death is not zero for any demographic.

All of us are at risk, and hence the superlative efforts at keeping containment in place, and keeping the virus from circulating as much as we can do, he said.

David Heymann, professor of infectious disease epidemiology at the London School of Hygiene and Tropical Medicine, agreed. This is a new disease in humans, so no-one has immunity health workers, like everyone else, dont have immunity, he said.

What is Covid-19 - the illness that started in Wuhan?

It is caused by a member of the coronavirus family that has never been encountered before. Like other coronaviruses, it has come from animals. Many of those initially infected either worked or frequently shopped in the Huanan seafood wholesale market in the centre of the Chinese city.

Have there been other coronaviruses?

Severe acute respiratory syndrome (Sars) and Middle Eastern respiratory syndrome (Mers) are both caused by coronaviruses that came from animals. In 2002, Sars spread virtually unchecked to 37 countries, causing global panic, infecting more than 8,000 people and killing more than 750. Mers appears to be less easily passed from human to human, but has greater lethality, killing 35% of about 2,500 people who have been infected.

What are the symptoms caused by the new coronavirus?

The virus can cause pneumonia. Those who have fallen ill are reported to suffer coughs, fever and breathing difficulties. In severe cases there can be organ failure. As this is viral pneumonia, antibiotics are of no use. The antiviral drugs we have against flu will not work. Recovery depends on the strength of the immune system. Many of those who have died were already in poor health.

Should I go to the doctor if I have a cough?

UK Chief Medical Officers are advising anyone who has travelled to the UK from mainlandChina, Thailand, Japan, Republic of Korea, Hong Kong, Taiwan, Singapore, Malaysia or Macau in the last 14 days and who is experiencing a cough or fever or shortness of breath to stay indoors and call NHS 111, even if symptoms are mild.

Is the virus being transmitted from one person to another?

Chinas national health commission has confirmed human-to-human transmission, and there have been such transmissions elsewhere.

How many people have been affected?

As of 20 Februrary, China has recorded 2,118 deathsfrom the Covid-19 outbreak.Health officials have confirmed74,576 casesin mainlandChinain total. More than 12,000 have recovered.

The coronavirus has spread to at least 28 other countries. Japan has 607 cases, including 542 from a cruise ship docked in Yokohama, and has recorded one death. There have also been deaths in Hong Kong, Taiwan, France and the Philippines.

There have been nine recorded cases and no fatalities to date in the UK. As of 17 February, a total of 4,501 people have been tested in the UK, of which 4,492 were confirmed negative.

Why is this worse than normal influenza, and how worried are the experts?

We dont yet know how dangerous the new coronavirus is, and we wont know until more data comes in. The mortality rate is around 2% at the centre of the outbreak, Hubei province, and less than that elsewhere. For comparison, seasonal flu typically has a mortality rate below 1% and is thought to cause about 400,000 deaths each year globally. Sars had a death rate of more than 10%.

Another key unknown is how contagious the coronavirus is. A crucial difference is that unlike flu, there is no vaccine for the new coronavirus, which means it is more difficult for vulnerable members of the population elderly people or those with existing respiratory or immune problems to protect themselves. Hand-washing and avoiding other people if you feel unwell are important. One sensible step is to get the flu vaccine, which will reduce the burden on health services if the outbreak turns into a wider epidemic.

Is the outbreak a pandemic?

A pandemic, in WHO terms, is the worldwide spread of a disease. Coronavirus cases have been confirmed outside China, but by no means in all 195 countries on the WHOs list. It is also not spreading within those countries at the moment, except in a very few cases. By far the majority of cases are travellers who picked up the virus in China.

Should we panic?

No. The spread of the virus outside China is worrying but not an unexpected development. The WHO hasdeclared the outbreak to be a public health emergencyof international concern. The key issues are how transmissible this new coronavirus is between people, and what proportion become severely ill and end up in hospital. Often viruses that spread easily tend to have a milder impact. Generally, the coronavirus appears to be hitting older people hardest, with few cases in children.

Sarah Boseley,Hannah DevlinandMartin Belam

Heymann said that who succumbs to the infection and who shrugs it off is often down to individual differences in the bodys response to the virus.

Some groups have a greater risk than others. At the moment it appears that people who are at greater risk are the elderly and probably the very young, said Pankhania.

But, he added, you cannot have that only the elderly and the very young will die, it is part of the natural history of such infections that we will get deaths across the age ranges The same pathophysiology can happen in the young as in the old.

In short, yes. It is not surprising that fellow clinical colleagues have got infected and some have died, said Pankhania, noting that medical professionals were in a special situation as they had multiple potential exposures to infection.

You have got infection control in place, however if you are forever being targeted, on the one rare occasion where your guard slipped, you get infected, he said. It is like being in the battlefield no matter how much protection you have, a stray bullet can catch you sometimes.

Such a slip, he added, was not surprising. A minor slip is eminently possible, especially when you are working under stress, you are tired, you have done long hours and your guard falls and you get infected, he said.

Pankhania said that at present it was thought there was only one form of the virus in circulation, so doctors were not being exposed to a more serious strain.

But Heymann said that if doctors did become exposed to the virus, it might be in a higher dose than would have occurred in a social context for example, they might come into contact with bodily fluids. If there is a massive inoculum of virus, that could make it a more overwhelming infection, he said.

That is a tricky question. Heymann said there was evidence that some patients in China infected with coronavirus also had flu at the same time. If that were the case, this could possibly increase the severity of a coronavirus infection, just because the body is already fighting [flu], and it might overwhelm the system, he said, but added that remained a theory.

However Heymann noted prior exposure to all sorts of bugs meant that health workers in general tended to have quite robust immune systems.

In a clinical setting you need full personal protective equipment, so you would be fully gowned, said Pankhania, adding that airtight masks were also used. You can only breathe through the filter on that mask.

Goggles were used, he added, noting it was possible to be infected through the eyes, while gloves were also important.

A colleague has to watch you put [the equipment] on and a colleague has to watch you take it off, and you would systematically put it on and systematically take it off, said Pankhania. Otherwise you risk contaminating yourself in the process of taking it off. But he added that under stress, mistakes could happen.

Pankhania said the 1918 flu pandemic offered one possibility, noting that some young people showed an exuberant immune response in other words, their immune system reacted too strongly to infection. In some cases, as yet poorly explained, poorly understood, the immune response is over the top that immune response then turns itself upon the persons body itself, he said, adding that could lead to fluid loss and organ damage. Buthe said it was not yet clear if this was at play in the current coronavirus outbreak.

The question remains open, but this week the World Health Organization director-general, Tedros Adhanom Ghebreyesus, told reporters that a number of trials were under way looking at the potential use of two HIV drugs as well as another antiviral called remdesivir that was developed to tackle haemorrhagic fevers including Ebola. Results, it seems, may be expected in three to four months. Meanwhile Columbia University researchers have received a $2m (1.5m) grant to work on possible antivirals drugs and antibodies to tackle coronavirus.

There are a lot of unknowns, including whether the virus could mutate to a more virulent form, while Pankhania said experts were still looking at the rate of deaths among those infected.

One key number is known as the R0, or basic reproduction number, which indicates how many new cases an infected person generates. At present it is thought to be about 2.6.

However, Pankhania said there was reason to be cautiously optimistic, noting that the figure might be lower outside of China, not least since other countries have had prior warning of the virus, while Wuhan is a densely populated city. He urged people in the UK to stay calm and said there was no reason to give up social events, quit the gym or keep children from playdates.

That is absolutely overreacting, he said. At this point in time there is no coronavirus circulating in the UK in a free way.

No, it is important to try to contain the coronavirus. A new virus has emerged out of the blue, said Pankhania, adding that it was believed to have started in bats, entered another animal and then passed to humans. It can not only infect humans, but be transmitted among humans and cause disease, he said. The upshot is the potential for a new virus circulating around the globe causing illness and death.

It is an extra burden on humanity, an extra infection in addition to influenza, and there is also an unknownness about it, which is we dont know how many people it could make very ill, we dont know how many people it will take, hence our concerns, he said.

Excerpt from:
Who is most at risk of contracting coronavirus? - The Guardian

Trial to evaluate safety and tolerability of PT101, as well as expansion of regulatory T cells

Pandion Therapeutics, Inc., a biotechnology company developing modular protein therapeutics for autoimmune disease, today announced the dosing of the first subject in a Phase 1 clinical trial of PT101, a novel and proprietary interleukin 2 (IL-2) mutein Fc fusion protein therapy. PT101 has shown potential to treat autoimmune diseases by expanding populations of regulatory T cells.

"PT101, the lead program in our pipeline of modular protein therapeutics, has the potential to transform the standard of care for patients with a wide array of autoimmune diseases by modulating the immune system through the bodys natural mechanisms, rather than suppressing it," said Rahul Kakkar, MD, chief executive officer of Pandion. "We are extremely pleased to announce the commencement of this first-in-human trial less than three years after we launched Pandion and began discovery work on PT101."

The Phase 1 clinical trial will assess the safety, tolerability, and pharmacokinetics of PT101 in healthy volunteers and will include measures of its pharmacodynamic and immuno-modulatory activity. The trial is designed to demonstrate the safety of PT101 and confirm its ability to expand regulatory T cell populations in human subjects. Pandion intends to investigate PT101 as a treatment for patients with ulcerative colitis and other autoimmune diseases.

In preclinical studies, PT101 demonstrated highly potent and selective expansion of regulatory T cells across a broad dose range. Toxicology studies with PT101 further support a wide therapeutic window and no evidence of toxicity associated with treatment.

"Significant need remains in the treatment of many autoimmune and inflammatory conditions," said Jo Viney, PhD, chief scientific officer of Pandion. "Treatment with low doses of interleukin 2 to expand regulatory T cells has shown promise in treating autoimmune diseases, but a narrow therapeutic index and frequent dosing make such therapy challenging. PT101s novel, proprietary design has achieved high selectivity for the expansion of regulatory T cells. We look forward to evaluating PT101s safety and selectivity in the clinic this year."

About PT101PT101 is an interleukin 2 (IL-2) mutein Fc fusion protein therapy designed to potently and selectively expand regulatory T cells for the treatment of autoimmune disease. Pandions Phase 1 trial of PT101 is designed to assess the safety, tolerability, and pharmacokinetics of PT101 after subcutaneous administration, and will also include measures of regulatory T cell expansion and other pharmacodynamic measures.

About PandionPandion Therapeutics is developing modular biologics for autoimmune regulation that are designed to achieve lasting therapeutic outcomes for patients with autoimmune and inflammatory diseases. The company is developing its lead drug candidate, PT101, an IL-2 mutein Fc fusion protein that preferentially expands regulatory T cells, as well as a robust pipeline of systemic immune modulators and tissue-targeted therapeutics focused on the gut, liver, skin, kidneys, and pancreas. Pandions approach to developing modular proteins, antibodies and bispecifics includes two key elements: first, the innovative biologics are based on cutting-edge immunomodulators such as an IL-2 mutein or PD-1 agonist that work systemically by activating regulatory pathways of the immune system that suppress uncontrolled autoimmune responses; and second, these immunomodulators can be combined with tissue-selective tethers, building modular proteins and antibodies that target the precise location within the organ to deliver the desired effect. Pandion is backed by leading life sciences investors including Polaris Partners, Versant Ventures, Roche Venture Fund, SR One, BioInnovation Capital, and the JDRF T1D Fund. The company is headquartered in Cambridge, Massachusetts. Please visit http://www.pandiontx.com.

View source version on businesswire.com: https://www.businesswire.com/news/home/20200224005192/en/

Contacts

Media:Kathryn MorrisThe Yates Network914-204-6412kathryn@theyatesnetwork.com

Investors:Sarah McCabeStern Investor Relations, Inc.212-362-1200Sarah.mccabe@sternir.com

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Pandion Announces First Subject Dosed in a Phase 1 Clinical Trial of PT101, an IL-2 Mutein Fc Fusion Therapy for Autoimmune Disease - Yahoo Finance

She is studying three of the different types of pregnancy in syngnathids, a fish family including seahorses, pipefish and seadragons as part of a project called MALEPREG. One type is when eggs are glued to the body of the male, who then carries them; the second is full male pregnancy, with transfer of nutrients and oxygen in a placenta-like system including one in which a pouch closes with a skin fold upon egg deposition; and the third is similar to the second but with a closed pouch.

Beyond the novelty value, what is so interesting about studying male pregnancy?

When its a normal pregnancy system, egg production and pregnancy all intermingle with the mother, so its very difficult to differentiate what happens during egg development and pregnancy.

(Another) reason is that when we want to understand the evolution of a trait, when we only have the absence or presence of this trait then its very difficult to study how it has evolved. In syngnathids, what we have is that male pregnancy has evolved on a gradient so we have closely related species that do display different forms.

If we compare those, then we can understand, OK, these genes have (provided) the function for this and this, and now this has happened.

What exactly are you looking at?

One of the main issues were studying is the problem of the immune system. If you accept a non-self embryo because half is from the father and half from the mother in your body, then your body would in principle (reject it). (So for pregnancy to evolve), somehow this rejection has to be circumvented.

In mammalians, (certain immune system) genes are downregulated (during pregnancy) this is why we see that pregnant individuals are often sick. Then there are specific adaptations in the placenta that prevent the rejection of this non-self tissue. We are studying this in syngnathids.

We are doing a comparative genomics approach, so we have sequenced genomes of these different (syngnathid) forms. What we have found is that those genes are lost (in syngnathids with a part-closed pouch and changed in those with a closed one). So one arm of the immune system thats really important for vertebrates is (functionally) entirely lost.

What are the implications of that finding?

Our hypothesis is that this has permitted the evolution of male pregnancy.

When we look at fishes, in general, the parental investment strategies are completely different from humans males have a more important role. For the syngnathids, the problem is that they dont have a stomach, so they have to feed more or less permanently. They are always hunting food. So probably thats why they started to carry (their eggs) with them.

When we look at those species that are only carrying these embryos with them on the belly, those still have a (fully) functional immune system. Only with the evolution of this placenta-like structure full male pregnancy is this part of the immune system lost. Potentially, this (loss) has permitted this extreme evolution.

(Also), we have (here) a system that basically is immunologically deficient. (This) can ultimately help human medicine, because there are so many immunodeficiency diseases (such as HIV) and we are not able to cope with them. (It suggests that theres) a lot more flexibility in the adaptive immune system or in the evolution of adaptive immunity than we thought earlier.

What else have you found so far?

We did transplant experiments to understand better this self/non-self recognition. We transplanted fins (tissue) of the syngnathids to the belly of (themselves and others) to see if they rejected it or not and what we have found there is that those that have lost parts of their immune system are a lot better-accepting of non-self tissues.

We compared (syngnathid pregnancy) genes to the mammalian pregnancy genes, and we actually do find that these are genes from the very same pathways: similar genes have been co-opted in their function towards pregnancy.

(This) suggests that there are not probably so many options in what things have to be changed in their functions (to allow pregnancy). It doesnt really give us an idea of why (pregnancy) has evolved, but more that convergent evolution can come with a similar mechanistic basic.

What are you looking at next?

Now we know which genes might be involved (in the evolution of male pregnancy), but we dont know their function yet. The next step will be to (definitively) identify these.

Then we can study how (these genes) have evolved across the phylogeny (family tree of organisms) and see, for example, where there are mutations involved. We know that in (male) pregnancy they seem to have a role, but not if this is the same function as they have in female pregnancy.

Were (also) working on all the microbiota involved (in syngnathids brood pouches). Weve cultivated these microbes and now were going to deplete all the microbes on the male side and then add them again to see what their function is, to really understand this co-evolution of pregnancy with the immune system, but also with these microbes.

(With parts of the immune system lost, were studying in addition) how is it possible that these fishes can survive and fight against diseases? And what kinds of compensatory mechanisms might they have?

What wider lessons can we draw from studying male pregnancy in syngnathids?

In reproduction, I think we still (often) have the understanding that males are the ones giving the sperm and they dont then have a big function in parental investment. But we know now in terms of epigenetics (gene expression) that fathers are providing a lot more than just the sperm.

In the syngnathids, we really have the chance to see, OK, the males have this and this function. There are so many classical perceptions about how males have to behave and how females have to behave, (but it may not always be the case). We should really go beyond model systems. When we are driven to go and look at these weird creatures, we can (better) understand nature.

The research in this article was funded by the European Research Council. If you liked this article, please consider sharing it on social media.

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Q&A: The curious case of male pregnancy in seahorses and pipefishes - Horizon magazine

Nes-Ziona, Israel, Feb. 24, 2020 (GLOBE NEWSWIRE) -- Enlivex Therapeutics Ltd. (Nasdaq: ENLV), a clinical-stage immunotherapy company, today announced that it is initiating a plan to increase its manufacturing capacity of AllocetraTM, following the first confirmed coronavirus (COVID-19) case in Israel, in preparation for potential requests for treatment of coronavirus (COVID-19) patients who are hospitalized with diagnosed organ dysfunctions or failures related to coronavirus.

AllocetraTM is an experimental therapy being investigated for treatment of patients with organ failure associated with sepsis, a syndrome whose lethal pathophysiology cytokine storm followed by organ failure is similar to that of the coronavirus (COVID-19).

Sepsis is the 3rdleading cause of mortality in the United States. One of every three patients who die in U.S. hospitals dies from sepsis. Organ failure resulting from sepsis, as well as in coronavirus (COVID-19), is considered the result of an exaggerated response of the immune system (cytokine storm) in the human body to an infection by a virus or a bacteria.

This exaggerated immune response results in organ damage. The immune attacks typically occur in vital organs such as lungs, heart, kidney and liver. When the organs become distressed, they begin to slowly dysfunction, which can result in organ failure, multiple organ failure, and mortality. Mortality rates from sepsis vary upon the degree of organ failure with which the patient arrived at the hospital. The literature describes an average of 20-40% mortality within 28-90 days for sepsis patients admitted to the ICU in a state of organ failure. Similarly, a cytokine storm was recently reported in patients with COVID-19 that were hospitalized in the ICU, (Huang et al. http://www.thelancet.com Published online January 24, 2020 https://doi.org/10.1016/S0140-6736(20)30183-5) and patients admitted to ICU had higher plasma levels of cytokines and chemokines.

There is no currently approved treatment for sepsis or for complicated corona virus infections. Enlivex recently announced the interim results from its first clinical trial in patients with sepsis. When compared with matched historical controls with sepsis from the same hospital, there were clear differences in (i) mortality -- none of the six Allocetra-treated patients died, vs 29% mortality in 28 days for the matched controls group; (ii) organ failure measures 78% of the matched controls had an increase of organ failure markers post admission to the hospital, while none (0%) of the six treated patients had any increase in organ failure score, despite similar presentation, and the average organ failure state of the matched controls worsened by a factor of two, while the treated group had not a single case of any organ failure increase; (iii) all the treated patients had their organ failures eliminated and they were subsequently released from the hospital. Each of the patients had organ dysfunction in two to five systems prior to administration of Allocetra. A Full summary of this trial is expected to be published in March 2020.

Enlivex has publicly announced its plan to initiate in 2020 two clinical studies: (i) a Phase II/III clinical trial for sepsis later in the year, and (ii) a Phase II/III for the prevention of GvHD in patients who undergo bone-marrow transplantations. The manufacturing capacity of Allocetra was planned to match the expected recruitment rate of patients in those two clinical trials.

To accommodate potential requests for treatment of COVID-19 patients who are hospitalized with diagnosed organ dysfunctions and/or failures, Enlivex has initiated a plan to increase the production capacity of Allocetra.

ALLOCETRATMby Enlivex was designed toprovide a novel immunotherapy mechanism of actionthat targets life-threatening clinical indications that are defined as unmet medical needs, includingprevention or treatment of complications associated with bone marrow transplantations (BMT) and/or hematopoietic stem cell transplantations (HSCT); organ dysfunction and acute multiple organ failure associated with sepsis; and enablement of an effective treatment of solid tumors via immune checkpoint rebalancing.

ABOUT ENLIVEX

Enlivex is a clinical stage immunotherapy company, developing an allogeneic drug pipeline for immune system rebalancing. Immune system rebalancing is critical for the treatment of life-threatening immune and inflammatory conditions which involve an out of control immune system (e.g. Cytokine Release Syndrome) and for which there are no approved treatments (unmet medical needs), as well as solid tumors immune-checkpoint rebalancing. For more information, visit http://www.enlivex.com.

Safe Harbor Statement: This press release contains forward-looking statements, which may be identified by words such as expects, plans, projects, will, may, anticipates, believes, should, would, intends, estimates, suggests, has the potential to and other words of similar meaning, including statements regarding expected cash balances, market opportunitiesfor the results of current clinical studies and preclinical experiments, the effectiveness of, and market opportunitiesfor, ALLOCETRATMprograms, which are made pursuant to the safe harbor provisions of the Private Securities Litigation Reform Act of 1995. Investors are cautioned that forward-looking statements involve risks and uncertainties that may affect Enlivexs business and prospects, including the risks that Enlivex may not succeed in generating any revenues or developing any commercial products; that the products in development may fail, may not achieve the expected results or effectiveness and/or may not generate data that would support the approval or marketing of these products for the indications being studied or for other indications; that ongoing studies may not continue to show substantial or any activity; and other risks and uncertainties that may cause results to differ materially from those set forth in the forward-looking statements. The results of clinical trials in humans may produce results that differ significantly from the results of clinical and other trials in animals. The results of early-stage trials may differ significantly from the results of more developed, later-stage trials. The development of any products using the ALLOCETRATMproduct line could also be affected by a number of other factors, including unexpected safety, efficacy or manufacturing issues, additional time requirements for data analyses and decision making, the impact of pharmaceutical industry regulation, the impact of competitive products and pricing and the impact of patents and other proprietary rights held by competitors and other third parties. In addition to the risk factors described above, investors should consider the economic, competitive, governmental, technological and other factors discussed in Enlivexs filings with the Securities and Exchange Commission, including under the heading Risk Factors contained in Enlivexs most recently filed Annual Report on Form 20-F. The forward-looking statements contained in this press release speak only as of the date the statements were made, and we do not undertake any obligation to update forward-looking statements, except as required under applicable law.

ENLIVEX CONTACT:Shachar Shlosberger, CFOEnlivex Therapeutics, Ltd.shachar@enlivex-pharm.com

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Enlivex Therapeutics Announces Plan for Increased Production Capacity of AllocetraTM in Preparation for Potential Treatment of Coronavirus (COVID-19)...

AB Sciencesmasitinib significantly slowed disability progression in people with primary progressive multiple sclerosis (PPMS) and non-active secondary progressive MS (SPMS) at a lower dose of 4.5 mg/kg a day, top-line results from a Phase 2b/3 clinical trial show.

Masitinib, formerly known as AB1010, is an oral therapy that inhibits the activity of cells in the innate immune system, specifically mast cells, microglia, and macrophages. In doing so, the therapy is expected to limit the inflammatory processes that cause damage to the nervous system in MS.

It may also have applications in other conditions, including other neurological diseases and certain cancers.

People with primary progressive (PPMS) and non-active secondary progressive (nSPMS) forms of multiple sclerosis account for half of all MS patients, Patrick Vermersch, PhD, a professor at University of Lillein France and a trial investigator, said in an AB Science press release.

PPMS is estimated to affect about 15% of all MS patients, while non-active SPMS affects about 30% to 35%.

While numerous treatments based on targeting of B-cells and T-cells of the adaptive immune system are available for patients with relapsing forms of MS, these strategies have failed or had inconclusive results in PPMS and nSPMS. Consequently, there remains a very high medical need for people with progressive MS forms, Vermersch added.

In the AB07002 Phase 2b/3 clinical trial (NCT01433497), a group consisting of 301 MS patients were enrolled, with 200 randomized to 4.5 mg/kg of masitinib daily, and 101 to a placebo. The trials primary endpoint (goal) was changes in disability, measured through the Expanded Disability Status Scale (EDSS) score, from the studys start (baseline) through week 12 to week 96 of treatment.

Results showed the primary endpoint was met, with significantly lower increases in EDSS seen in the masitinib-treated group compared to the placebo group. This treatment effect was maintained for both the PPMS and non-active SPMS subpopulations. (Higher EDSS score represent worsening disability levels.)

Treatment also significantly delayed disease progression, as measured by the time to reach an EDSS score of 7.0 functionally, this score means a person requires the use of a wheelchair.

[T]he results from this study represent a scientific breakthrough because this is the first time that the novel strategy of targeting the innate immune system via mast cells and microglia has been able to significantly slow progression of clinical disability in progressive forms of MS, Vermersch said. These data are extremely encouraging, and may provide new hope for progressive MS patients.

Added Olivier Hermine, MD, PhD, president of AB Sciences scientific committee:This positive result in progressive MS is an important new finding that further validates the mechanism of action of masitinib in neurodegenerative diseases.

Masitinibs safety was consistent with the therapys known profile. Overall, 95% of people on 4.5 mg/kg masitinib daily, and 87.1% of those in the corresponding placebo group, experienced at least one reported adverse event. AB Science did not specify what these events were.

People in another trial arm were given masitinib a daily dose of 6.0 mg/kg, with titration starting at 4.5 mg/kg/day. This group consisted of 310 people, with 203 treated with masitinib and 107 given a placebo. No significant beneficial effects over placebo with masitinib at this higher dose were seen.

Further details were not released, which AB Science said would be given at an upcoming scientific conference. The company also announced a new patent filing for masitinib based on AB07002 trial results, and said it will be in contact with regulatory authorities to discuss further development of masitinib as a treatment for progressive forms of MS.

Masitinib is also being tested patients withamyotrophic lateral sclerosis (ALS), where a single-site Phase 3 trial (NCT03127267) is expected to open in March in Montreal, Canada. A Phase 3 trial (NCT01872598) in people withAlzheimers diseaseor probable Alzheimers also recently concluded.

This MS trial is the second piece of supportive evidence delivered by the masitinib clinical program. The first one was thepositive Phase 2B/3 study with masitinib in amyotrophic lateral sclerosis, Hermine said.

The two studies taken together clearly demonstrate that targeting the innate immune system via macrophage/microglia and mast cells, as masitinib does, is one of the right strategies to treat neurodegenerative disorders, Hermine concluded.

Marisa holds an MS in Cellular and Molecular Pathology from theUniversity of Pittsburgh, where she studied novel genetic drivers ofovarian cancer. She specializes in cancer biology, immunology, andgenetics. Marisa began working with BioNews in 2018, and haswritten about science and health for SelfHacked and the GeneticsSociety of America. She also writes/composes musicals and coachesthe University of Pittsburgh fencing club.

Total Posts: 1,053

Patrcia holds her PhD in Medical Microbiology and Infectious Diseases from the Leiden University Medical Center in Leiden, The Netherlands. She has studied Applied Biology at Universidade do Minho and was a postdoctoral research fellow at Instituto de Medicina Molecular in Lisbon, Portugal. Her work has been focused on molecular genetic traits of infectious agents such as viruses and parasites.

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Masitinib Slows Disability Progression in PPMS and Non-active... - Multiple Sclerosis News Today

The Harvard epidemiology professor Marc Lipsitch is exacting in his diction, even for an epidemiologist. Twice in our conversation he started to say something, then paused and said, Actually, let me start again. So its striking when one of the points he wanted to get exactly right was this: I think the likely outcome is that it will ultimately not be containable.

Containment is the first step in responding to any outbreak. In the case of COVID-19, the possibility (however implausible) of preventing a pandemic seemed to play out in a matter of days. Starting in January, China began cordoning off progressively larger areas, radiating outward from Wuhan City and eventually encapsulating some 100 million people. People were barred from leaving home, and lectured by drones if they were caught outside. Nonetheless, the virus has now been found in 24 countries.

Despite the apparent ineffectiveness of such measuresrelative to their inordinate social and economic cost, at leastthe crackdown continues to escalate. Under political pressure to stop the virus, last Thursday the Chinese government announced that officials in the Hubei province would be going door to door, testing people for fevers and looking for signs of illness, then sending all potential cases to quarantine camps. But even with the ideal containment, the viruss spread may have been inevitable. Testing people who are already extremely sick is an imperfect strategy if people can spread the virus without even feeling bad enough to stay home from work.

Lipsitch predicts that, within the coming year, some 40 to 70 percent of people around the world will be infected with the virus that causes COVID-19. But, he clarifies emphatically, this does not mean that all will have severe illnesses. Its likely that many will have mild disease, or may be asymptomatic, he said. As with influenza, which is often life threatening to people with chronic health conditions and of older age, most cases pass without medical care. (Overall, around 14 percent of people with influenza have no symptoms.)

Lipsitch is far from alone in his belief that this virus will continue to spread widely. The emerging consensus among epidemiologists is that the most likely outcome of this outbreak is a new seasonal diseasea fifth endemic coronavirus. With the other four, people are not known to develop long-lasting immunity. If this one follows suit, and if the disease continues to be as severe as it is now, cold and flu season could become cold and flu and COVID-19 season.

At this point, it is not even known how many people are infected. As of Sunday, there have been 35 confirmed cases in the U.S., according to the World Health Organization. But Lipsitchs very, very rough estimate when we spoke a week ago (banking on multiple assumptions piled on top of each other, he said) was that 100 or 200 people in the U.S. were infected. Thats all it would take to seed the disease widely. The rate of spread would depend on how contagious the disease is in milder cases. On Friday, Chinese scientists reported in the medical journal JAMA an apparent case of asymptomatic spread of the virus, from a patient with a normal chest CT scan. The researchers concluded with stolid understatement that if this finding is not a bizarre abnormality, the prevention of COVID-19 infection would prove challenging.

The rest is here:
Youre Likely to Get the Coronavirus - The Atlantic

Ever since the earliest reports of a pneumonia-like illness spreading within Hubei province in China, the resemblance to the SARS outbreak of 2002-2003 has been uncanny: probable origins in the wild-animal markets of China; an illness that in some people resembles the common cold or a flu, but in others leads to pneumonia-like symptoms that can cause respiratory failure; community transmission that often occurs undetected; super-spreader events; and reported vertical transmission in high-rises or other living spaces where the waste systems are improperly engineered or drain catch-basins are dry, allowing aerosolized particles to pass from one floor of a building to another (see The SARS Scare for an in-depth description of the epidemiology and virology of the SARS outbreak of 2002-2003 and the four independent zoonotic transmissions of 2003-2004).

At first, this latest outbreak was referred to as a novel coronavirus, then in the media as COVID-19 (formally, the name for the disease in an infected person who has become sick, a distinction analogous to that between a person who is HIV positive and one who has developed AIDS). Now that the virus has been characterized and its relationship to SARS firmly established, its designation is SARS-CoV-2severe acute respiratory syndrome coronavirus 2.

Will public-health measures be sufficient to contain its spread? How infectious is it? What is the incubation period? Is this a pandemic? What role does the immune-system response play in the progression of the disease? Which populations are most at risk? Can scientists develop a vaccine, and how quickly? These are some of the questions that scientists worldwide are asking, and that a collaboration among Harvard University and Chinese researchers will address as part of a $115-million research initiative funded by China Evergrande Group, which has previously supported Universitygreen-buildings research at the Graduate School of Design, research onimmunologic diseases, and work inmathematics. (See below for the University press release describing the initiative.)

Harvard Magazinespoke with some of the researchers involved in fighting the first SARS outbreak, and those who will be collaborating with Chinese colleagues, in what is already a worldwide effort to control SARS-CoV-2.

Michael Farzan 82, Ph.D. 97, who in 2002 was an assistant professor of microbiology and molecular genetics at Harvard Medical School (HMS) studying the mechanism that viruses use to enter cells, was the first person to identify the receptor that SARS used to bind and infect human cells. SARS-CoV-2 is a close cousin to SARS, and uses the same human receptor, ACE2, reports Farzan, who is now co-chair of the department of immunology and microbiology at Scripps Research. The ACE2 receptor is expressed almost exclusively in the lungs, gastrointestinal tract, and the kidneys, which explains why the disease is so effectively transmitted via both the respiratory and fecal-oral routes.

But there are subtle differences in the new virus behind the current outbreak, he explained in an interview. The viruss receptor binding domainthe part that attaches to the human receptorhas undergone a lot of what we call positive selection, meaning there has been a good deal of evolutionary pressure on that region from natural antibodies, probably in bats or some other animal host that is a reservoir for this disease. So while the virus retains its ability to bind ACE2, Farzan explains, it no longer binds the same antibodies. That is unfortunate, because as the first SARS epidemic wound down, HMS professor of medicine Wayne Marasco had identified a single antibodyfrom what was then a 27-billion antibody librarythat blocked the virus from entering human cells. (Marasco is actively testing new antibodies, hoping to find one that will have the same effect on SARS-CoV-2.) Still, we are not starting from square one, says Farzan.

In animal studies,Remdesivir [a new and experimental antiviral drug] has seemed to work against SARS-like viruses, he says. Its effectiveness will probably hinge on getting it early enough, in the same way that the antiviral drug Tamifluis most effective against the seasonal flu when given to patients early in the course of infection.

And there is a reasonable hope that a vaccine canbe developed, Farzan adds, because the part of the virus that binds the human receptor is exposed and accessible, making it vulnerable to the immune systems antibodies. In addition, the viral genome is relatively stable. That means SARS CoV-2 wont evolve much over the course of an epidemic, so a vaccine that is relatively protective at the beginning of an epidemic will remain effective until its end.

Another reason for optimismdespite the long road to deploying any vaccine in humansis that the science that allows researchers to understand the viruss structure, life cycle, and vulnerabilities is progressing far more rapidly today than during the first SARS outbreak 17 years ago. So, too, is the understanding of the human immune response to the virus, and of the most effective public-health strategies based on the epidemiology of the disease.

When epidemiologists assess the severity of an epidemic, they want to know how effectively the disease can propagate in a population. The first measure they attempt to calculate is the reproductive number (R0)the number of people that an infected individual will in turn infect in an unexposed population, in the absence of interventions. When the reproductive number is greater than 1 (meaning each infected person in turn infects more than one other person), more and more people become infected, and an epidemic begins. Public-health interventions are therefore designed to lower the rate of transmission below 1, which eventually causes the epidemic to wind down. The second number epidemiologists focus on is the serial intervalhow long it takes one infected person at a particular stage of the disease to infect another person to the point of the same stage of the disease. The serial interval thus suggests how rapidly the disease can spread, which in turn determines whether public-health officials can identify and quarantine all known contacts of an infected individual to prevent their retransmitting the disease to others.

Marc Lipsitch, a professor of epidemiology at the Harvard Chan School of Public Health (HSPH), and director of the schoolsCenter for Communicable Disease Dynamics, helped lead one of the two teams that first calculated the reproductive number of SARS in the 2002-2003 outbreak. SARS had an R0 of 3, he recalls: each case led to three others. In that outbreak, about 10 percent of those who became sick died. The good news is that SARS CoV-2 appears to have a much lower R0 than SARS, ranging from the high ones to low twos, and only 1 percent to 2 percent of those who become sick have died. On the other hand, the serial intervalstill being worked outappears to be shorter, meaning the new virus has the potential to spread faster.

In the current epidemic, Lipsitch notes a further concern: the fact that the incubation-period distribution and the serial-interval distribution are almost identical. Thats a mathematical way of saying that people can start transmitting the virus even when they are pre-symptomatic, or just beginning to exhibit symptoms. That makes tracing and quarantining contacts of infected individualsa classic, frontline public-health measurenearly impossible.

Tracing, quarantining, and other public-health interventions, such as distancing measures (closing workplaces or asking employees to work from home, for example) proved sufficient to defeat SARS in the early 2000s. But with SARS-CoV-2, public-health measures alone may prove inadequate. Controlling this version of SARS may require antivirals, stopgap antibody therapies, and ultimately, vaccines, deployedtogetherwith robust public-health containment strategies.

Unfortunately, SARS-CoV-2 is almost certainly already a pandemic, Lipsitch continues: demonstrating sustained transmission in multiple locations that will eventually reach most, if not all places on the globe. The disease appears to be transmitting pretty effectively, probably in Korea, probably in Japan, and probably in Iran. He has estimated that 40 to 70 percent of the adult global population will eventually become infected.

That said, Infected is different from sick, he is careful to point out. Only some of those people who become infected will become sick. As noted above, only about 1 percent to 2 percent of those who have becomesickthus far have died, he says. But the number of people who areinfectedmay be far greater than the number of those who are sick. In a way, he says, thats really good news. Because if every person who had the disease was also sick, then that would imply gigantic numbers of deaths from the disease.

I'm very gratified, Lipsitch continues, to see that both China and Harvard recognize the complementarity between public health and epidemiology on the one hand, and countermeasure-development on the other hand. We can help target the use of scarce countermeasures [such as antivirals or experimental vaccines] better if we understand the epidemiology; and we will understand the epidemiology better if we have good diagnostics, which is one of the things being developed in this proposal. These approaches are truly complementary.

In the short term, Lipsitchwho has sought to expand the modeling activities of the Center for Communicable Disease Dynamics to better understand the current outbreaks epidemiologysays, It would be great toexpand collaborations with Chinese experts. Longer term, I see a really good opportunity for developing new methods for analyzing data better, as we have in previous epidemics. After the first SARS outbreak, for example, epidemiologists developed software for calculating the reproductive number of novel diseases; that software now runs on the desktop computers of epidemiologists around the world. And in 2009, during an outbreak of swine flu in Mexico, Lipsitch and others developed a method for using the incidence of the disease among awell-documented cohort of travelerswho had left Mexico, to estimate the extent of the disease among amuch larger and less well surveyedpopulation of Mexican residents.

What they found then was that the estimated number of cases in Mexican residents likely exceeded the number of confirmed cases by two to three orders of magnitude. The same method is being used to assess the extent of SARS-CoV-2 in China right nowso far without any hiccups. In the Mexican case, Lipsitchreports, the estimates suggested that severe cases of the disease were uncommon, since thetotal numberof cases was likely much larger than the number ofconfirmedcases. So I think we have learned from each epidemic how to do more things. And in between them, you solidify that less visible, less high-profile research that builds the foundation for doing better the next time. His group, for example, has been developing ways to make vaccine trials faster and better once a vaccine candidate exists.

A vaccine is the best long-term hope for controlling a disease like SARS-CoV-2. Higgins professor of microbiology and molecular genetics David Knipe, who like Lipsitch will participate in the newly announced collaboration, works on vaccine delivery from a molecular perspective. Knipe has developed methods to use the herpes simplex virus (HSV) as a vaccine vector and has even made HSV recombinants that express the SARS spike proteinthe part of the virus that binds the human ACE2 receptor. He now seeks to make HSV recombinants that express the new coronavirus spike protein as a potential vaccine vector.

But Knipe also studies the initial host-cell response to virus infection, which is sometimes called the innate immune response. And he has used HSV vectors that expressed the first SARS spike protein to study how it activates innate immune signaling. That is important because inSARS 1, initial symptoms lasted about a week, but it was the second phasecharacterized by a massive immune-system response that began to damage lung tissuethat led to low levels of oxygen saturation in the blood, and even death.The inflammation in the lungs is basically a cytokine storm, an overwhelming and destructive immune response thats the result of innate signaling, Knipe explains. So were going to look at that with the new coronavirus spike protein, as well. This could help to determine the actual mechanism of inflammation, and then we can screen for inhibitors of that that might be able to alleviate the disease symptoms.

The idea, he says, is to stop theinflammatoryresponse now killing people in the respiratory phase of the disease by targeting the specific molecular interaction between the virus and the host cell. This, he explains, aligns with one of the principal initial goals of the collaboration, which is to support research both in China and at Harvard to address the acute medical needs of infected individuals during the current crisis.

In the last days of 2019 and the first days after the New Year, we started hearing about a pneumonia-like illness in China, says Dan Barouch, an HMS professor of medicine and of immunology known for his anti-HIV work, whose lab has developed a platform for rapid vaccine development. (During the Zika virus outbreak of 2016, for example, his group was the first to report, within a month, a vaccine protective in animal models.) When the genome of the virus was released on Friday, January 10, we started reviewing the sequence that same evening, working through the weekend. By Monday morning, we were ready to grow it.

His concern about this latest outbreak was that the rate of spread seemed to be very rapid. In addition, the outbreak had the clinical features of an epidemic. We reasoned that this might make it difficult to control solely by public-health measures, he says, particularly because the virus can be transmitted by asymptomatic individuals. Thus, if the epidemic is still spreading toward the end of this year or early 2021, by which point a vaccine might be available, Barouch explains, such a remedy could prove essential. Historically, when viral epidemics don't self-attenuate, the best method of control is a vaccine.

Although Barouchs Beth Israel Deaconess Medical Center lab is working on DNA and RNA vaccines, a new technology that has the potential to cut vaccine development times in half, large-scale manufacturing using so-called nucleotide vaccines is unproven. That's why I think there needs to be multiple parallel vaccine efforts, he emphasizes. Ultimately, we don't know which one will be the fastest and most protective. At the moment, he reports, there are at least a half dozen scientifically distinct vaccine platforms that are being developed and he believes that vaccine development for this pathogen will probably go faster than for any other vaccine target in human history.

Ever since I graduated from medical school, he points out, there have been new emerging or re-emerging infectious disease outbreaks of global significance with a surprising and disturbing sense of regularity. There is Ebola. There was Zika. There were SARS, MERS; the list keeps growing. With climate change, increasing globalization, increasing travel, and population shifts, the expectation is that epidemics will not go away, and might even become more frequent.

In this global context, Barouch emphasizes the importance of a collaborative response that involves governments, physicians, scientists in academiaandin industry, and public-health officials. It has to be a coordinated approach, he says. No one group can do everything. But I do think that the world has a greater sense of readiness this time to develop knowledge, drugs, and therapeutics very rapidly. The scientific knowledge that will be gained from the vaccine efforts [will] be hugely valuable in the biomedical research field, against future outbreaks, and in the development of a vaccine to terminate this epidemic.

University provost Alan Garber, a physician himself, adds that Global crises of such magnitude demand scientific and humanitarian collaborations across borders. Harvard and other institutions in the Boston area conduct research on diagnostics, virology, vaccine and therapeutics development, immunology, epidemiology, and many other areas.With its tremendous range of expertise and experience, our community can be an important resource for any effort to address a major global infectious disease outbreak. Our scientists and clinicians feel an obligation to be part of a promising collaboration to overcome the worldwide humanitarian crisis posed by this novel virus.

The official Harvard press release follows:

Harvard University Scientists to Collaborate with Chinese Researcherson Development of Novel Coronavirus Therapies, Improved Diagnostics

At a glance:

Since its identification in December, the novel coronavirus has quickly evolved into a global threat, taking a toll on human health, overwhelming vulnerable health care systems and destabilizing economies worldwide.

To address these challenges, Harvard University scientists will join forces with colleagues from China on a quest to develop therapies that would prevent new infections and design treatments that would alleviate existing ones.

The U.S. efforts will be spearheaded by scientists at Harvard Medical School, led by DeanGeorge Q. Daley, working alongside colleagues from the Harvard T.H. Chan School of Public Health. Harvard Medical School will serve as the hub that brings together the expertise of basic scientists, translational investigators and clinical researchers working throughout the medical school and its affiliated hospitals and institutes, along with other regional institutions and biotech companies.

The Chinese efforts will be led by Guangzhou Institute of Respiratory Health and Zhong Nanshan, a renowned pulmonologist and epidemiologist. Zhong is also head of the Chinese 2019n-CoV Expert Taskforce and a member of the Chinese Academy of Engineering.

Through a five-year collaborative research initiative, Harvard University and Guangzhou Institute for Respiratory Health will share $115 million in research funding provided by China Evergrande Group, aFortuneGlobal 500 company in China.

We are confident that the collaboration of Harvard and Guangzhou Institute of Respiratory Health will contribute valuable discoveries to this worldwide effort, said Harvard University President Lawrence Bacow. We are grateful for Evergrandes leadership and generosity in facilitating this collaboration and for all the scientists and clinicians rising to the call of action in combating this emerging threat to global well-being.

Evergrande is honored to have the opportunity to contribute to the fight against this global public health threat, said Hui Ka Yan, chair of the China Evergrande Group. We thank all the scientists who responded so swiftly and enthusiastically from the Harvard community and are deeply moved by Harvard and Dr. Zhongs teams dedication and commitment to this humanitarian cause. We have the utmost confidence in this global collaborative team to reach impactful discoveries against the outbreak soon.

While formal details of the collaboration are being finalized, the overarching goal of the effort is to elucidate the basic biology of the virus and its behavior and to inform disease detection and therapeutic design. The main areas of investigation will include:

With the extraordinary scale and depth of relevant clinical and scientific capabilities in our community, Harvard Medical School is uniquely positioned to convene experts in virology, infectious disease, structural biology, pathology, vaccine development, epidemiology and public health to confront this rapidly evolving crisis, Daley said. Harnessing our science to tackle global health challenges is at the very heart of our mission as an institution dedicated to improving human health and well-being worldwide.

We are extremely encouraged by the generous gesture from Evergrande to coordinate and supportthe collaboration and by the overwhelmingly positive response from our Harvard colleagues, said Zhong, who in 2003 identified another novel pathogen, the severe acute respiratory syndrome (SARS) coronavirus and described the clinical course of the infection.

We look forward to leveraging each of our respective strengths to address the immediate and longer-term challenges and a fruitful collaboration to advance the global well-being of all people, Zhong added.

Harvard University ProvostAlan M. Garbersaid outbreaks of novel infections can move quickly, with a deadly effect.

This means the response needs to be global, rapid and driven by the best science. We believe that the partnershipwhich includes Harvard and its affiliated institutions, other regional and U.S.-based organizations and Chinese researchers and clinicians at the front linesoffers the hope that we will soon be able to contain the threat of this novel virus, Garber said. The lessons we learn from this outbreak should enable us to respond to infectious disease emergencies more quickly and effectively in the future.

Read more here:
Harvard and the Guangzhou Institute of Respiratory Health Team to Fight SARS-CoV - Harvard Magazine

Scientists have implicated toll-like receptor 2 (TLR2) in age-related macular degeneration and shown that knocking it out can improve symptoms in animal models.

Researchers have shown that toll-like receptor 2 (TLR2) may play a role in age-related macular degeneration (AMD), the most common cause of central-vision blindness in adults. The scientists suggest targeting TLR2 in the eye may be a future therapy for AMD.

The paper, published in Cell Reports, stated that AMD is associated with two biological processes; uncontrolled oxidative stress resulting in the formation of a bleach-like chemical in the retina and the tagging of cell contents with complement protein. These tags signal for the elimination of the cell contents.

The scientists suggest in this paper that these two processes are linked by TLR2. Found on cell surfaces, TLR2 recognises chemical signals from bacterial infections in the environment outside the cell and activates the immune system.

In the case of the eye, TLR2 appears to act as a sensor of oxidative-stress, recognising a chemical pattern that is generated during oxidation, rather than infection and triggering a signal cascade that ends in promoting the laying down of complement, explained first author on the paper, Dr Kelly Mulfaul, from Trinity College Dublin, Ireland.

Dr Sarah Doyle, study leader and assistant professor of immunology at Trinity, said: A function for TLR2 has not previously been reported in retinal neurodegenerative disease pathology but it is likely to play an important role, because when we remove TLR2 from our experimental model systems we reduce the level of complement and this has the effect of protecting cells that are essential for vision from dying.

With the continual increase in life expectancy outpacing the rate at which drugs for age-related conditions are developed new avenues of therapy are badly needed, so the fact that blocking this single protein can have such a protective effect in the eye is a particularly exciting discovery.

Read the rest here:
TLR2 could be targeted to treat age-related macular degeneration - Drug Target Review

By Christine Gelley, Agriculture and Natural Resources Educator, Noble County, Ohio State University Extension

We finally got some snow and freezing temperatures! At our house, we didnt get snow a single day that our Christmas decorations were up, but snow on Valentines Day was appreciated. Fresh snow provides a refreshing look to the landscape when it covers up all the muck and brown underneath it. However, those cold temperatures are still not lasting long enough to firm up the ground and as soon as we track through that snow, our break from reality is over.

Mud creates challenges with mobility both for our animals and equipment. Aside from complicating the logistics of caring for the farm, mud increases our risks for herd health complications too. Many producers have babies on the farm right now. It is important to watch out for signs of mastitis with the mothers and scours with the young.

Lactating animals are at greater risk of mastitis infections when it is muddy. Contaminants on the udder tissue can enter the mammary glands through the milk ducts and cause inflammation. Mothers with mastitis may not allow their young to nurse at the needed length of time or frequency due to pain. The udder may feel hard or hot. Many cases of mastitis occur and pass before we ever notice, but some more acute cases can cause lasting damage to the mothers mammary tissue and reduce the growth of her young.

As soon as possible after birth and if you are able, check that each teat produces colostrum (the first and most crucial milk). Getting colostrum into a newborn within the first few hours is critical for the long-term health of the animal. The best source of colostrum is from the newborns mother. If this is not possible, the next best choice is another mother of the same species from your farm. After that, the next best choice is a colostrum replacer. The nutrient composition of milk is different from species to species and there are diseases that can be passed through milk from farm to farm. Therefore, do not substitute across species or with milk from another farm.

In addition, do not pasteurize colostrum. It will denature the components that make it so special. If you have a mother that produces extra colostrum or in the unfortunate event that a mother dies giving birth or shortly after, milks as much colostrum from her as you can and freeze it. Thaw frozen colostrum/milk in a warm water bath, never in the microwave. For more tips consult https://u.osu.edu/beef or https://u.osu.edu/sheep by typing colostrum into the search bar. There are many helpful articles available on the OSU Extension Team websites that you can access 24/7.

Another very helpful article is by my colleague in Belmont County Dan Lima about scours. It can be viewed online at https://go.osu.edu/scoursbydan. In his article, Dan reminds us that muddy conditions put calves (and other young) at a higher risk of developing scours, which is most obviously noticeable as diarrhea. Scours can be caused by a variety of organisms present in mud. The most common being E. coli. Often the young will pick up the bacteria (or other pathogens) from mothers udder tissue while nursing. Scours can be very detrimental to young animals because it causes dehydration and weight loss.

Young that receive adequate amounts of colostrum at birth receive helpful antibodies from their mothers that provide the immune system responses needed to combat the pathogens that cause scours. Vaccines can be administered to mothers in the weeks before calving that can also increase immunity in their young to scours.

In both mastitis and scours cases, the best way to keep issues at bay is through prevention. Do everything in your power to provide a relatively clean birthing environment and promote healthy immune systems.

Cull mothers that do not adequately care for their young or that have poor udder structure. If the udders are not conformed to aid the young nursing, they will struggle. If the udder bag is abnormally saggy, there is a greater chance of contamination of manure on the teats. Make notes at birth and after regarding mothering capabilities and resist the urge to give too many chances to mothers that create problems for you. A mother that does not do her job is a liability rather than an asset and will likely pass those traits on to her young. For lasting success, only keep the assets on your farm.

Read the original:
Muddy issues: Mastitis and scours Ohio Ag Net - Ohio's Country Journal and Ohio Ag Net

The most advanced study released by AMR on the Diabetic Neuropathy market comprising key market segments such as Type, Application, Sales, Growth, Comprises details of companies manufacturing field, production volume, capacities, value chain, product specifications, raw material sourcing strategies, concentration rate, organizational structure, and distribution channel.

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Some of the key and emerging players profiled in this market study profiled are Johnson & Johnson (Janssen Global Services LLC), Boehringer Ingelheim GmbH, NeuroMetrix Inc., Eli Lilly and Company, GlaxoSmithKline plc, Pfizer Inc., Lupin Limited, Astellas Pharma Inc., Glenmark Pharmaceuticals Ltd, Arbor Pharmaceuticals LLC, Depomed Inc..

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Focuses on the key global Diabetic Neuropathy players, to define, describe and analyze the value, market share, market competition landscape, SWOT analysis, and development plans in the next few years.

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Some of the players have a stellar growth track record for 2014 to 2018, some of these companies have shown tremendous growth by sales and revenue while net income more than doubled in the same period with performing as well as gross margins expanding. The growth in gross margins over the years points to strong pricing power by the company for its products, over and above the increase in the cost of goods sold.

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According to AMR, key market segments sales will traverse the $$ mark in the year 2020. Unlike classified segments by Type (), by End-Users/Application.

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Diabetic Neuropathy market will increase from $XX million in 2019 to strike $YY million by 2026, with a compound annual growth rate (CAGR) of xx%. The most robust growth is anticipated in Asia-Pacific, where CAGR is presumed to be ##% from 2019 to 2026. This prediction is good news for market players, as there is good potential for them to continue developing alongside the industrys projected growth.

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Market players have determined strategies to offer a whole host of new product launches within several markets around the globe. Remarkable models are variant to be launched in eight EMEA markets in Q4 2019 and 2020. Acknowledging all-around exercises some of the players profiles that would be worth reviewing are Johnson & Johnson (Janssen Global Services LLC), Boehringer Ingelheim GmbH, NeuroMetrix Inc., Eli Lilly and Company, GlaxoSmithKline plc, Pfizer Inc., Lupin Limited, Astellas Pharma Inc., Glenmark Pharmaceuticals Ltd, Arbor Pharmaceuticals LLC, Depomed Inc..

Although recent years might not be that inspiring as market segments have registered reasonable gains, things could have been better if manufacturers would have plan-driven move earlier. Unlike past, but with a decent estimate, investment cycle continuing to progress in the U.S., many growth opportunities ahead for the companies in 2020, it looks like a good for today but stronger returns can be expected beyond.

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Global Diabetic Neuropathy Market 2020: What Will Be Total Market Size By 2025? - Chronicles 99

The market study on the global Neuropathy Screening Devices Market will include the entire ecosystem of the industry, covering five major regions namely North America, Europe, Asia Pacific, Latin America and Middle East & Africa, and the major countries falling under those regions. The study will feature estimates in terms of sales revenue and consumption from 2019 to 2025, at the global level and across the major regions mentioned above. The study has been created using a unique research methodology specifically designed for this market.

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Quantitative information includes Neuropathy Screening Devices Market estimates & forecast for an upcoming years, at the global level, split across the key segments covered under the scope of the study, and the major regions and countries. Sales revenue and consumption estimates, year-on-year growth analysis, price estimation and trend analysis, etc. will be a part of quantitative information for the mentioned segments and regions/countries. Qualitative information will discuss the key factors driving the restraining the growth of the market, and the possible growth opportunities of the market, regulatory scenario, value chain & supply chain analysis, export & import analysis, attractive investment proposition, and Porters 5 Forces analysis among others will be a part of qualitative information. Further, justification for the estimates for each segments, and regions will also be provided in qualitative form.

Major Players included in this report are as follows NeuroMetrixOwen MumfordBeijing OERHUATAI TechnologyDongguan City Xinben Industrial

Neuropathy Screening Devices Market can be segmented into Product Types as Non-Electrinic DevicesElectrinc Devices

Neuropathy Screening Devices Market can be segmented into Applications as HospitalsClinicsDiagnostic CentersDrug Stores

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Neuropathy Screening Devices Market: Regional analysis includes: Asia-Pacific (Vietnam, China, Malaysia, Japan, Philippines, Korea, Thailand, India, Indonesia, and Australia) Europe (Turkey, Germany, Russia UK, Italy, France, etc.) North America (United States, Mexico, and Canada.) South America (Brazil etc.) The Middle East and Africa (GCC Countries and Egypt.)

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This study will address some of the most critical questions which are listed below: What is the market size of the Neuropathy Screening Devices Market at the global level? Which mode of distribution channel is most preferred by the manufacturers of Neuropathy Screening Devices? Which is the preferred age group for targeting Neuropathy Screening Devices for manufacturers? What the key factors driving, inhibiting the growth of the market, and what is the degree of impact of the drivers and restraints? What is the impact of the regulations on the growth of the Neuropathy Screening Devices Market? Which is the leading region/country for the growth of the market? What is the anticipated growth rate of the leading regions during the forecast period? How are the emerging markets for Neuropathy Screening Devices expected to perform in the coming years? How is the consumption pattern expected to evolve in the future? Who are the major players operating in the global Neuropathy Screening Devices Market? What is the current market position of the key players? Who are the emerging players in this industry? Who are the major distributors, traders, and dealers operating in the Neuropathy Screening Devices Market?

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Neuropathy Screening Devices Market Trends, Key Players, Overview, Competitive Breakdown and Regional Forecast by 2025 - News Parents

Dear Doctor: I had a rough spot on the back of my hand that turned into a wart. What caused it? How do I get rid of it?

Dear Reader: Youre describing what is known as a common wart. Its a small, raised skin growth caused by one of the estimated 150 different varieties of the human papilloma virus, or HPV. Other types of HPV cause different kinds of warts. These include plantar warts, which are callouslike growths on the soles of the feet; genital warts; and smooth, flat-topped growths known as flat warts, often seen on the face and forehead.

Common warts dont present any health dangers. However, they can be unsightly and cause embarrassment. Theyre typically about the size of a pencil eraser or smaller, may be circular or oval, and can appear anywhere on the body. Common warts may grow a smooth, domed top, or they can have a wrinkled appearance, like a head of cauliflower. Theyre often a different color than the surrounding skin, including brown, gray, pink or beige. Some may contain what look like small black dots, which are actually tiny blood vessels filled with clotted blood.

If you get a common wart, youve come into physical contact with the virus that causes it, either on someones skin, or on a surface an infected person has touched. The virus can enter the body through a break in the skin, and if your immune system cant fight it off, a wart will soon appear. Common warts are painless, but when they crack, or if you pick at them, they can bleed.

In most cases, your bodys immune system will rally, and the wart will eventually vanish, usually within a year or two. Those who would rather not wait have several treatment options. Most people can try over-the-counter wart medications available at the drug store. These are made up of salicylic acid, which is delivered either as a gel, liquid or in a patch. The acid gradually removes the layers of skin until the wart is gone. Its helpful to soak the wart in warm water prior to applying the salicylic acid, as it will allow the medication to penetrate deeper into the many layers of tissue. In between treatments, use an emery board or pumice stone to remove the dead skin. Be sure to isolate these tools since they can transmit the virus. Side effects of this treatment can include skin irritation and discomfort. Never use salicylic acid on the face or on the genitals. People living with neuropathy or diabetes should not try at-home wart removers and should see a doctor instead.

If you try a home-based treatment and its unsuccessful, your doctor also has several options available. One is that same salicylic acid, but in a higher concentration, which requires a prescription. Another approach is cryotherapy, which uses liquid nitrogen to freeze the wart. Warts may also be removed with a laser, burned off or cut away.

Any time that a wart changes shape or color, or if it becomes painful or infected, its important to seek medical attention.

Eve Glazier, M.D., MBA, is an internist and associate professor of medicine at UCLA Health. Elizabeth Ko, M.D., is an internist and assistant professor of medicine at UCLA Health.

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There are many ways to get rid of warts - Journal Review

Global Medical Foods Market: Overview

One of the key factors boosting the growth of the global medical foods market is the rising awareness among the people regarding medical foods. The rising focus of the regulatory bodies on the manufacturing and labelling of medical foods will also be a key factor fuelling the growth of the medical foods market. In addition to this, the high focus by manufacturers on developing disease-specific formulas effective patients nutrition or diet care are also anticipated to result in the growth of the global medical foods market.

The report also enlists various factors which are anticipated to pose a challenge for the growth of the market. The current trends in the market and those that are anticipated to shape the future of the market have been discussed in detail in the report.

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By product, the medical food market is segmented into powder, pill, and others. Of these the powder segment has held a key share in the market as many medical food products are manufactured in powdered form and consumed in a semi solid or liquid form. By application, the global medical foods market is segmented into depression, diabetic neuropathy, ADHD, Alzheimers disease, and nutritional deficiency. Of these, diabetic neuropathy has been accounting for key shares within the market. The risk of neuropathy is boosted with age, diet changes, and unhealthy lifestyle.

In the years to come, it is anticipated that the nutritional deficiencies segment will develop a strong CAGR, as patients being treated for ADHD, autoimmune diseases, and cancer are likely to have high nutritional requirements, which is subsequently anticipated to boost the demand for medical foods.

Global Medical Foods Market: Snapshot

The global medical foods market has become increasingly important in the healthcare sector in recent years due to the rising awareness about its importance in complementing the treatment. Medical food comprises diets designed specifically to overcome the nutritional deficiencies caused by some diseases or to fulfill the specific dietary needs in the management of some diseases. The global medical foods market is likely to receive steady support from the healthcare sector in the coming years due to the rising prevalence of diseases such as Alzheimers among the elderly and ADHD among children, as these diseases are among the prime diseases that necessitate specific diet plans.

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Global Medical Foods Market: Key Trends

The rising geriatric population is a major driver for the global medical foods market. Old people are more likely to develop nutritional disorders as well as to fall prey to other diseases that affect their ability to absorb nutrients from their diet. Nutrition deficiency disorders are also more common among the geriatric demographic than in other patient classes, leading to the geriatric population becoming a key consumer segment for the global medical foods market.

The increasing prevalence of diabetes across the world is another key driver for the global medical foods market. Diabetic neuropathy is the leading application of the global medical foods market and is likely to retain dominance in the coming years. Diabetic neuropathy is becoming common among diabetic patients due to their often unhealthy lifestyles, with close to three-quarters of all diabetes likely to also suffer from some form of neuropathy. This is a key driver for the global medical food market, as the rising prevalence of diabetes in emerging regions has, in conjunction with the rising investment in the healthcare sector, created a conducive environment for growth of the market.

The rising prevalence of ADHD among children is also likely to remain a key driver for the global medical foods market. The growing prevalence of the disease has led to intensive research into its causation and treatment. The role of nutrition in the management of psychological problems such as ADHD has thus come under the scanner. On the opposite end of the spectrum, the rising prevalence of neurodegenerative conditions among the geriatric population is also likely to remain a key driver for the global medical foods market in the coming years.

Global Medical Foods Market: Market Potential

The global medical foods market is likely to witness a steady shift towards pills and away from powders. While powders can be easily mixed with various types of food, many patients dont enjoy their taste. This has led to pills becoming a preferred mode of delivery for many, and are thus likely to rise in demand in the global medical foods market in the coming years.

Apart from leading diseases such as diabetic neuropathy and Alzheimers, other diseases such as phenylketonuria (PKU) are also likely to come under the ambit of the medical food market in the coming years. In April 2017, PKU Sphere, a new medical food for patients of PKU was launched. PKU Sphere is claimed to contain a balanced mix of amino acids and glycomacropeptide, a protein essential for patients of PKU, who cant digest phenylalanine and have to fulfill their protein requirements in alternate ways.

Global Medical Foods Market: Geographical Dynamics

North America is likely to remain the leading regional contributor to the global medical foods market in the coming years due to the ready availability of advanced healthcare technology and a solid database regarding the dietary needs of patients suffering from various diseases. The rising prevalence of diabetes in North America, due primarily to the unhealthy lifestyle practiced by citizens in developed countries such as the U.S., is also likely to be crucial for the medical foods market in North America in the coming years.

Global Medical Foods Market: Competitive Dynamics

The leading players in the global medical foods market include Abbott, Fresenius Kabi AG, Targeted Medical Pharma Inc., Danone, and Primus Pharmaceuticals Inc. The steady support to development of sophisticated disease-specific formulas is likely to benefit the medical foods market in the coming years.

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Excerpt from:
Medical Foods Market Analysis Trends and Dynamic Demand by Forecast 2017 to 2025 - Jewish Life News