Category Archives: Colorado Stem Cells

DENVER (KDVR) Most kids want toys under the tree this Christmas, but one Colorado 4-year-old just wants her brother to have a chance at a longer life.

Amber Freed has four-year-old twins, one girl and one boy. Her daughter is completely typical but her son has a rare disease.

Her son Maxwell got the terminal diagnosis just months into his life. Childrens Hospital Colorado broke the news that his disease is so rare that less than 50 people in the world have the disease and Maxwell was one of them.

Her son Maxwell was diagnosed at childrens hospital with a disease so rare it only had a number, not a name SLC6A1.

Maxwell suffers Parkinsons-like symptoms, seizures, severe movement and speech disorders, and intellectual disability.

Also, doctors told her other doctors couldnt do anything to help; she was advised to start calling scientists. She called 300 of them in one month.

You can actually replace the gene in a childs body that is not working well. I finally met the scientists that I trusted my sons life with. And we made a plan to cure this disease together. It was going to take a lot of hard work, hunting scientists from all over the world. To work on this and you descend, but I was also going to need to raise $4 million, said Amber Freed.

Amber didnt waste any time, she started a foundation nicknamed Milestones for Maxwell. So far she has raised $3.5 million, mostly through small increments on gofundme. Now she needs just $500,000 more by the end of the year.

Since summer 2018 mom Amber Freed has been fighting to raise money for a clinical trial and gene replacement therapy.

She explains how a global pandemic set them back 18 months.

COVID has been terrible for rare diseases because all of a sudden, it makes the most sense to fund COVID related scientific projects. And at the beginning of the pandemic, nobody could go in to take care of our mouse colonies and our stem cells. And so our experiment started dying. COVID set us back 18 months if youre in competition with COVID, that probably every person will get at some point, over a super rare pediatric disease, of course the funding will go to COVID.

Until they can raise this money, Amber said Maxwell is living on borrowed time and worries every day could be his last.

You can donate to their GoFundMe Page here

Read more:
Christmas Wish: 4-year-old just wants life-saving treatment for her twin brother - FOX 31 Denver

Conventional wisdom says that if youre vaccinated and you get a breakthrough infection with the coronavirus, you can transmit that infection to someone else and make that person sick.

But new evidence suggests that even though that may happen on occasion, breakthrough infections might not represent the threat to others that scientists originally thought.

Ross Kedl, an immunologist at the University of Colorado School of Medicine, will point out to anyone who cares to listen that basic immunology suggests the virus of a vaccinated person who gets infected will be different from the virus of an infected unvaccinated person.

Thats because vaccinated people have already made antibodies to the coronavirus. Even if those antibodies dont prevent infection, they still should be coating that virus with antibody and therefore helping prevent excessive downstream transmission, Kedl says. And a virus coated with antibodies wont be as infectious as a virus not coated in antibodies.

In Provincetown, Mass., this summer, a lot of vaccinated people got infected with the coronavirus, leading many to assume that this was an example of vaccinated people with breakthrough infections giving their infection to other vaccinated people.

Kedl isnt convinced.

In all these cases where you have these big breakthrough infections, theres always unvaccinated people in the room, he says.

In a recent study from Israel of breakthrough infections among health care workers, the researchers report that in all 37 case patients for whom data were available regarding the source of infection, the suspected source was an unvaccinated person.

Its hard to prove that an infected vaccinated person actually was responsible for transmitting their infection to someone else.

I have seen no one report actually trying to trace whether or not the people who were vaccinated who got infected are downstream and certainly only could be downstream of another vaccinated person, Kedl says.

Theres new laboratory evidence supporting Kedls supposition. Initially, most vaccine experts predicted that mRNA vaccines like the ones made by Pfizer and Moderna that are injected into someones arm muscle would generate only the kinds of antibodies that circulate throughout the body.

But that might not be the whole story.

I think what was the big surprise here is that the mRNA vaccines are going beyond that, says Michal Caspi Tal, until recently an instructor at Stanford Universitys Institute for Stem Cell Biology and Regenerative Medicine and now a visiting scientist at the Massachusetts Institute of Technology.

What Tal has found is that in addition to the circulating antibodies, there was a surprisingly large amount of antibodies in mucosal membranes in the nose and mouth, two of the primary entry points for the coronavirus.

Immunologist Jennifer Gommerman of the University of Toronto found this as well.

This is the first example where we can show that a local mucosal immune response is made, even though the person got the vaccine in an intramuscular delivery, Gommerman says.

If there are antibodies in the mucosal membranes, they would likely be coating any virus that got into the nose or throat. So any virus that was exhaled by a sneeze or a cough would likely be less infectious.

Gommerman says that until now, it seemed likely that a vaccine that was delivered directly to the mucosal tissue was the only way to generate antibodies in the nose or throat.

Obviously a mucosal vaccination would be great too. But at least were not sitting ducks, Gommerman says. Otherwise everyone would be getting breakthrough infection.

Now, these studies by Gommerman and Tal have yet to undergo peer review, and some have already suggested that the antibodies they have described may not confer true mucosal immunity.

But theres other evidence that a vaccinated persons breakthrough infection may not transmit efficiently to others.

Marion Pepper, an immunologist at the University of Washington, says a recent study from the Netherlands looked at how well virus from vaccinated people could infect cells in the lab.

Pepper says the answer was not well.

If you actually isolate virus from people who are getting a secondary infection after being vaccinated, that virus is less good at infecting cells, Pepper says. Its not known why. Is it covered with an antibody? Maybe. Has it been hit by some other kind of immune mediators, cytokines, things like that? Maybe. Nobody really knows. But the virus does seem to be less viable coming from a vaccinated person.

More studies are emerging that suggest theres something different about the virus coming from a vaccinated person, something that may help prevent transmission.

Whatever it is, the University of Colorados Kedl says its one more reason that getting vaccinated is a good idea.

Because youre going to be even more protected yourself. And youre going to be better off protecting other people.

Kedl says thats what you call a win-win situation.

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Breakthrough infections might not be a big transmission risk. Heres the evidence. - WBEZ

Misfolded proteins (orange) in the endoplasmic reticulum may play a role in Wolfram syndromes many symptoms.

By Mitch LeslieFeb. 11, 2021 , 2:00 PM

Maureen Marshall-Doss says the first sign that her vision was deteriorating came when she misidentified the color of a dress. At a backyard get-together about 20 years ago, the Indianapolis resident pointed out an attractive yellow dress another woman was wearing. You see that as yellow? Shes wearing a pink dress, Marshall-Doss recalls her husband responding.

Today, Marshall-Doss is virtually blind. With help from custom made eyeglasses that magnify objects 500 times, I can see shapes, she says. But she can no longer drive and had to quit the job she loved as a school librarian. Along with her dimming vision, she has type 1 diabetes and has lost her sense of taste and smell.

Marshall-Doss is one of 15,000 to 30,000 people around the world with Wolfram syndrome, a genetic disease. For decades, the condition remained enigmatic, untreatable, and fatal. But in the past few years, insights into its mechanism have begun to pay off, leading to the first clinical trials of drugs that might slow the illness and sparking hopes that gene therapy and the CRISPR DNA-editing tool might rectify the underlying genetic flaws. Here is a rare disease that the basic science is telling us how to treat, says physiologist Barbara Ehrlich of the Yale School of Medicine.

The research could also aid more than the relatively few patients with Wolfram syndrome. Driving the diseases many symptoms is a malfunction of the endoplasmic reticulum (ER), the multichambered organelle that serves as a finishing school for many cellular proteins. Known as ER stress, the same problem helps propel far more common illnesses, including type 2 diabetes, amyotrophic lateral sclerosis (ALS), Parkinsons disease, and Alzheimers disease. Wolfram syndrome is the prototype of an endoplasmic reticulum disorder, says medical geneticist Fumihiko Fumi Urano of Washington University School of Medicine in St. Louis. Because Wolfram syndrome is simpler, says Scott Oakes, a cell biologist and pathologist at the University of Chicago, researchers think it could illuminate the mechanisms of other ER-disrupting diseases, which affect hundreds of millions of people worldwide.

In the late 1930s,four children with diabetes were going blind, and doctors were stumped. Like many other people in the United States struggling through the Great Depression, the siblings ate a paltry diet, subsisting on potatoes, bread, oatmeal, and a little milk. But after examining three of the children, Donald Wolfram, a physician at the Mayo Clinic in Rochester, Minnesota, and an ophthalmologist colleague ruled out malnutrition as the cause of their puzzling condition. Lead poisoning and syphilisthough common enoughwerent to blame, either. When Wolfram and his partner wrote up the cases in 1938, they concluded that the symptoms could be manifestations of an hereditary or acquired cerebral lesion.

The physicians were right that the syndrome eventually named for Wolfram is hereditary. Recessive mutations in the gene for a protein called wolframin are responsible for most cases, with glitches in a second gene causing most of the rest. However, the pair was wrong to think the defect lies only in the brain. Instead, the symptoms stem from widespread cell death. Its definitely a disease that affects the whole body, Marshall-Doss says.

The first sign of the illness, appearing when patients are children, is usually diabetes mellitus, or faulty sugar metabolism, sparked by the demise of insulin-secreting beta cells in the pancreas. Most patients also develop the unrelated condition diabetes insipidus, in which the pituitary gland doesnt dole out enough of a hormone that helps control the bodys fluid balance, causing the kidneys to produce huge amounts of urine.

Mutations in the gene for wolframin disrupt the endoplasmic reticulum and lead to cell death throughout the body, causing a range of symptoms.

V. Altounian/Science

Ellie White, 19, of Centennial, Colorado, who was diagnosed with Wolfram syndrome 12 years ago, says she hasnt had a full night of sleep since she was 3 years old. She gets up again and again to use the bathroom and monitor her blood sugar.

Yet she and other patients say that as disruptive as those problems are, they are not the diseases most dismaying consequence. The biggest symptom of Wolfram syndrome that affects me the most is my vision, White says. Because neurons in the optic nerve perish, patients usually go blind within 10 years of their first visual symptoms.

Other neurons die as well. As the disease progresses, brain cells expire, and walking, breathing, and swallowing become difficult. Most people with Wolfram syndrome die before age 40, often because they can no longer breathe. At 57, Marshall-Doss is one of the oldest patients; one of her mutated genes may yield a partly functional version of wolframin, triggering a milder form of the disease, Urano says.

Two advanceshave made it possible to begin to tackle those symptoms. The first was Uranos discovery nearly 20 years ago that linked Wolfram syndrome to ER stress. The ER is where about one-third of a cells newly made proteins fold into the correct shapes and undergo fine-tuning. Cells can develop ER stress whenever they are under duress, such as when they dont have enough oxygen or when misfolded proteins begin to pile up inside the organelle.

In test tube experiments, Urano and his colleagues were measuring the activity of genes to pinpoint which ones help alleviate ER stress. One gene that popped up encodes wolframin, which scientists had shown in 1998 was mutated in patients with Wolfram syndrome. Following up on that finding, Urano and his team determined that wolframin takes part in whats known as the unfolded protein response, which is a mechanism for coping with ER stress in which cells take steps including dialing back protein production.

Scientists think wolframin plays a key role in the unfolded protein response, though they havent nailed down exactly how. When wolframin is impaired, cells become vulnerable to ER stress. And if they cant relieve that stress, they often self-destruct, which could explain why so many neurons and beta cells die in the disease.

Defective wolframin may harm cells in other ways. The ER tends the cells supply of calcium, continually releasing and absorbing the ion to control the amount in the cytoplasm. Changes in calcium levels promote certain cellular activities, including the contraction of heart muscle cells and the release of neurotransmitters by neurons. And wolframin affects calcium regulation.

Beta cells genetically engineered to lack functional wolframin brim with calcium, Ehrlich and colleagues reported in July 2020 in theProceedings of the National Academy of Sciences. When exposed to lots of sugar, the altered cells release less insulin and are more likely to die than healthy beta cells, the team found. The cells share that vulnerability with beta cells from patients with Wolfram syndrome. We think that excess calcium is leading to excess cell death, Ehrlich says.

ER malfunctions could hamstring other organelles as well. The ER donates calcium to the mitochondria, the cells power plants, helping them generate energy. In 2018, a team led by molecular biologist Ccile Delettre and molecular and cellular biologist Benjamin Delprat, both of the French biomedical research agency INSERM, discovered that in cells from patients with Wolfram syndrome, mitochondria receive less calcium from the ER and produce less energy. Those underpowered mitochondria could spur the death of optic nerve cells, the researchers speculate.

Fumihiko Urano holds dantrolene, a muscle relaxant drug he helped test as a treatment for Wolfram syndrome.

The link between ER stress and Wolfram syndrome has been crucial for identifying potential treatments because otherwise we would have nothing to target, Urano says. But a second development was also key, he says: the advocacy and support of patient organizations, such as the Snow Foundation and the Ellie White Foundation, headed by its namesakes mother. The foundations have stepped up with money for lab research and clinical trials when other sources, including government agencies, didnt come through.

Scientists, patients, and their advocates say Urano also deserves much of the credit. Besides treating patients, he heads the international registry of cases and has taken the lead in organizing clinical trials, screening compounds for possible use as treatments, and devising potential therapies. Fumi is clearly the driving force, says Stephanie Snow Gebel, co-founder of the Snow Foundation, who about 10 years ago helped persuade him to forgo a plum job as department chair at a Japanese university and take over the Wolfram program at Washington University.

Patients could soonstart to reap the benefits. In 2016, Urano and colleagues started the worlds first clinical trial for the disease: a phase 1/2 study of dantrolene, an approved muscle relaxant. The molecule was a top performer when they screened 73 potential treatments for their ability to save cells with terminal ER stress. Dantrolene didnt improve vision in the 22 participants, including White, the scientists reported in an October 2020 preprint. But in some patients, beta cells appeared to be working better and releasing more insulin. The drug is safe, but Urano says it will need to be chemically tweaked to target its effects before future trials are warranted.

Researchers are pursuing other possible treatments targeting ER stress or calcium levels. In 2018, U.K. scientists launched a trial that will include 70 patients to evaluate sodium valproate, a therapy for bipolar disorder and epilepsy that, in the lab, prevents cells with faulty wolframin from dying. Last year, another compound that emerged from Uranos screens, the diabetes drug liraglutide, entered a clinical trial. Also last year, an experimental drug developed by Amylyx Pharmaceuticals for Alzheimers disease and ALS received orphan drug designation from the U.S. Food and Drug Administration for Wolfram syndrome because it curbs ER stress. That designation offers tax breaks and other incentives, and it will get trials started sooner, Urano says.

Ehrlich and her team have a candidate of their own that they have begun to test in rodents: the drug ibudilast, which is approved in Japan to treat asthma. The researchers found it reduces calcium levels in beta cells lacking wolframin and boosts their survival and insulin output. New screening projects may reveal still more candidates.

But Urano knows that even if a treatment receives approval, it would be only a Band-Aid for Wolfram syndrome. Hoping to develop a genetic cure, he and colleagues are introducing replacement genes into cells from patients and from mice engineered to replicate the disease. The researchers are endowing the cells with healthy copies of the gene for wolframin or the gene for a protein that reduces ER stress to determine whether they restore cellular function and reduce cell death. At INSERM, Delettre and colleagues are also evaluating whether directing a working gene into optic nerve cells can curtail vision loss in mice with faulty wolframin. The scientists are still gathering data, but early results suggest the treatment can halt the deterioration.

Urano and his collaborators have also turned to the genome editor CRISPR, deploying it to correct the gene defect in patients stem cells and then growing them into beta cells. When the researchers transplanted the revamped cells into mice with diabetes, the animals blood sugar returned to healthy levels, the team reported in April 2020 inScience Translational Medicine.

Stem cell biologist Catherine Verfaillie of KU Leuven is collaborating on the CRISPR research. But she notes that because the faulty wolframin gene affects so many tissues, researchers will have to figure out how to deliver the CRISPR components to most cells in large organs such as the brain and livera prospect she calls pretty daunting. Urano agrees, predicting that CRISPR-based Wolfram therapies might take 10 to 20 years to develop. The alternative approach, gene therapy, could reach clinical trials more quickly, in 3 to 10 years, he says, because researchers have more experience with gene therapy and have created several treatments that have already been approved for other illnesses.

Because it stems from a single genetic glitch, Wolfram syndrome could also help scientists tease out the role of the ER in more complex diseases, including neurological conditions, type 2 diabetes, and cancer. The ER also falters in those diseases, causing cells to die, but the mechanism is harder to discern because they stem from myriad genetic and environmental factors. In Alzheimers disease, for instance, neurons develop ER stress as misfolded proteins accumulate inside and outside the cells.

Besides deepening researchers understanding of other conditions, the research on Wolfram syndrome might even deliver candidate treatments. Everyone would be very excited if we can make advances in targeting ER stress in Wolfram syndrome, Oakes says. It would open up the whole field to doing this in other degenerative diseases.

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The race to treat a rare, fatal syndrome may help others with common disorders like diabetes - Science Magazine

Fort Collins, Colorado: A new informative report on the Stem Cell Therapy Market has recently published by Reports Globe to its massive repository. The primary and secondary research techniques have been used to compile data from different sources such as websites, media publications, and press releases. The Stem Cell Therapy market offers up-to-date information on different market segments and sub-segments. It offers an all-inclusive study of different key factors affecting the growth of the Stem Cell Therapy market. The global market research report offers extensive research on different technologies, tools, and standard methodologies that are fueling the growth prospect of the Stem Cell Therapy market.

Global Stem Cell TherapyMarketwas valued at 117.66 million in 2019 and is projected to reach USD255.37 million by 2027, growing at a CAGR of 10.97% from 2020 to 2027.

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The global informative report begins with a brief introduction of Stem Cell Therapy market and market overview, classification, application, technologies, products or services, and key players operating across the globe. The global informative report elaborates on the global market scope, market scope at the present, and prediction of demand from global clients in the future. The global market research report has been presented in a clear and professional manner for easy and better understanding to readers. The driving forces, limitations, and global opportunities are listed for the Stem Cell Therapy market to get the gist of different dynamics of the global market. It has been compiled through proven research techniques such as primary research and secondary research.

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Adipose Tissue-Derived Mesenchymal Stem Cells Bone Marrow-Derived Mesenchymal Stem Cells Cord Blood/Embryonic Stem Cells Other Cell Sources

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Musculoskeletal Disorders Wounds and Injuries Cardiovascular Diseases Surgeries Gastrointestinal Diseases Other Applications

3.Stem Cell Therapy Market, By Type:

Allogeneic Stem Cell Therapy Market, By Application Musculoskeletal Disorders Wounds and Injuries Surgeries Acute Graft-Versus-Host Disease (AGVHD) Other Applications Autologous Stem Cell Therapy Market, By Application Cardiovascular Diseases Wounds and Injuries Gastrointestinal Diseases Other Applications

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North America (USA, Canada)Latin America (Chile, Brazil, Argentina, rest of Latin America)Europe (UK, Italy, Germany, France, rest of the EU)Asia Pacific (India, Japan, China, South Korea, Australia, rest of APAC)Middle East and Africa (Saudi Arabia, United Arab Emirates, South Africa, rest of MEA)

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Stem Cell Therapy Market Size, Top Key Players, Applications, Business Statistics, Trends and Forecast 2021-2027 The Bisouv Network - The Bisouv...

Kindly readers keep responding to my recent columns about advanced weather forecasting and the great Nebraska blizzard in 1888 that killed hundreds of school children who died from exposure trying to make to their prairie homes from their one-room schoolhouses.

This weeks response to those columns comes from Irene, the egg woman, with a family story about another deadly blizzard other than the one in 1888. Heres her story:

Your column on the 1888 blizzard in Nebraska reminded me of what my mother told me about a blizzard in early March of 1927. My mother, age 20, was the second of seven children. Her mother, my grandmother, was in the hospital at McCook, Neb., after giving birth to the seventh child.

The younger sister of my grandmother and her young son from Colorado were visiting the family on their farm about 30 miles from McCook. My mother, her aunt, her older brother, and her 4-year-old brother decided to visit my grandmother and the new baby at the hospital in McCook. The school-age children including the aunts son were left at the one-room country school.

When they began the trip home, it was snowing hard. They came upon two children trying to walk home, so they put them in the car and took them to the childrens home. As they proceeded after letting off the children at their home, the group realized they would not be able to reach their farm, so they went back to the house where they had left the children and asked to stay. The childrens father said, No. He gave no reason. There were two salesmen at the house, and they, too, were not allowed to stay.

The group, which now included the salesmen, decided to go back to the hospital in McCook. Soon the Model T would go no farther, so they began walking. One of the salesmen was carrying a heavy suitcase. It probably contained his wares. He refused to give it up, so my mother grabbed it and threw it into the ditch. After walking a while, my mother thought she saw the hospital on the other side of a field. The others thought she was hallucinating, but they followed her across the field. She had been correct. They knocked on the hospital door, however no one came, so my mother used her knee to break the glass. That got some attention, and my mother and her companions were given supper and warm beds.

Several years later the hospital suffered minor damage from a cyclone. The Catholic sisters who ran the hospital jokingly told my grandfather, We thought it was your daughter.

What happened to the children at school? The neighbors took them to their own homes. My mother told me no one worried about the children, as they knew the neighbors would take care of them. Would that happen in todays society?

***

I read an article recently where some bio-scientists were growing actual wood in their laboratory using a gene-manipulating technique similar to that of growing fake meat.

The scientists were making plant-growing cells similar to stem-cells in animals. Their basic cells came from a common flower. And then some way they were programming those cells to morph into tree wood cells.

As if that bit of science isnt crazy enuf to wrap your brain around, how about this? The scientists believe that ultimately they can grow the fake wood material into any size and shape they desire.

So, the future of buying one-piece wooden furniture might be to order a lab-grown chair or table direct from the fake wood store grown into the size/shape you order.

I swear I read the story. Ill leave it to you to believe it will happen sometime.

***

It wuz take your child to work day at the local short-line farm machinery factory where a young farmer worked as a welder during the day shift. The farmer/welders 8-year-old daughter was all excited about the visit and had been for weeks. In preparation to the visit, her dad had done his best to explain in advance all about his job, his work place and his co-workers.

On the big day, as the farmer/daughter pair were meandering around the factory floor, the daughter began to cry and get cranky.

Her concerned father bent over and asked his daughter what wuz wrong. The little gal continued sobbing so loudly that a group of co-workers gathered around.

Finally, the little gal sobbed out why she wuz so unhappy. She sobbed loudly, Daddy, where are all the goofy, ignorant clowns you said you worked with?

***

Ol Jay Esse from Colorado sends me lots of wise words to end my columns with. Heres a few off of his stack thats accumulated on my desk:

Life is too short to drive boring cars.

If a cow doesnt produce enuf milk, is she a milk dud or an udder failure?

Advice to men: You should always look both ways before crossing a woman.

Why do TV news reporters spend a half hour giving us bad news and, yet, end their programs by telling us to Have a good evening?

At my age Im old enough to not believe everything I read including the bathroom scales.

Have a good un.

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More on deadly blizzards | TheFencePost.com - Fence Post

REGINA -- Saskatchewans hockey community is mourning the loss of Rick Schwartz, who died suddenly in his Regina home on Monday evening from a heart attack at age 59.

To the public, Schwartz is known as the father of a Stanley Cup champion. His son, Jaden, is a member of the St. Louis Blues who won the cup in 2019.

Schwartz is also known for the dedication that he and his wife, Carol, have for the Mandi Schwartz Foundation. It is named after their daughter who lost a public battle to cancer in 2011. The foundation has focused on advocating for bone marrow drives and donations.

However, to those closest to Schwartz, hes being remembered as a man who put family and community before anything.

FAMILYS FIRST

Ramona and Patrick Vigneron, who are long-time close family friends of the Schwartzes, say theyll remember Ricks jokes, smile and laughter the most.

And just how much he absolutely loves his family, Ramona said. He always said familys first.

Schwartz had three children: Jaden, Rylan and Mandi.

The two families would travel together, often to watch their children play hockey. Some of their trips took them to Colorado, North Dakota, St. Louis and Germany.

With the celebrations hed always include family and friends, Ramona said.

Whether it was during the kids minor hockey days in Wilcox or watching a Stanley Cup Championship, Schwartz always provided a fun time for those around him.

One of the most entertaining things you could do is watch a hockey game with Rick with one of the kids playing, Patrick said.

It was great watching games with Ricky because he got pretty emotional as he watched the boys and Mandi play, Ramona said. It was really part of Rickys life, you could just see him come to life watching the kids play.

BONE MARROW DRIVES

In honour of Mandi, the Schwartz family launched a foundation that is often involved in bone marrow drives in hopes of helping people who need a donor find their perfect match.

Rick was determined to make sure Mandis foundation continued on with the stem cells, and match program was very important, Ramona said.

Bone marrow drives continue at Yale University, where Mandi played. The St. Louis Blues also held a drive in 2013. Four years later, an 18-year-old woman was able to find her perfect match from a man who was swabbed at that Blues game.

The Schwartz family hosted both the donor and the recipient, both from the United States, in 2019 for the annual Run for Mandi in Saskatchewan.

ATHOL MURRAY COLLEGE OF NOTRE DAME

Rick and Carols three children all attended Athol Murray College of Notre Dame in their childhood and teenage years.

They participated in multiple sports, but hockey was the biggest. Its been about a decade since any of the kids played there, but the Schwartzes have always stayed involved in the community.

The great thing about Rick was that he loves hockey, Rob Palmarin, the president of Athol Murray College of Notre Dame, said. Hed still come out to our arena and would visit with our coaches who were the coaches of his sons and daughter, and our hockey staff. He was a frequent visitor to our arena so he was just one of the family.

After Mandis passing in 2011, the Schwartz family helped to honour her at the school.

The Schwartz family has set up an endowment fund and that supports a number of our female athletes, particularly hockey players, on an annual basis, Palmarin said. That came out of the tragedy of Mandi Schwartz dying of cancer in 2011. So its been almost a decade of them working to keep her memory alive.

Palmarin said Rick and Carol were role models of parents who had children playing hockey.

One of the mottos painted in the rink at Notre Dame reads Never Lose Heart.

That motto is painted up there not only as an inspiration to our student athletes when they practice and play, but its also an inspirational motto for all of us to remember the Notre Dame Hounds family, both living and deceased, Palmarin said. Rick is now going to be part of that.

RECENT MEMORIES

Most recently, Schwartz worked with the Saskatchewan Safety Council. Patrick worked there with him for the past five years.

Weve got a couple of projects on the board right now and Im not sure where theyre going to end up, but well try to make them work for him, Patrick said.

Ramona said right now, the Schwartz family is cherishing the time they were able to spend together over the summer.

One of the blessings of COVID-19 was that Rylan came home from Germany and then Jaden came home from St. Louis and they were with their parents for literally four months, Ramona said. Carol kept repeating these last few days it has been awesome how much time Rick got to spend with his sons for the last four months.

She said the memories of playing golf and cards will long be remembered by the family.

The death is a shock. Theres a lot of people who have been affected by Ricky and just how passionate he is, Ramona said. He has a heart of gold.

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'A heart of gold': Rick Schwartz remembered for his commitment to family, community - CTV News

Jeopardy host Alex Trebek died Sunday of pancreatic cancer, over a year after he was diagnosed with stage IV cancer. NBC News said he died at 80 after a battle with cancer. CBS News implied it was a battle that he lost.

Trebek himself used similar language to describe his future plans when he was diagnosed with the disease back in March 2019. Im going to fight this, Trebek said. Im going to keep working, and with the love and support of my family and with the help of your prayers also I plan to beat the low survival rate statistics for this disease.

When it comes to discussing this disease, many people use words like battle, fight, survive and beat language that would not be out of place when describing a war zone.

At the time of Trebeks diagnosis, well-wishers took to social media offering messages of support to him that often used this pugnacious language.

Indeed, words like battle and fight often arise when a celebrity or other public figure discloses a cancer diagnosis. That was the case when Sen. John McCain, who died in August 2018, first revealed he had been diagnosed with a primary glioblastoma, the same aggressive form of brain cancer that killed former Vice President Joe Bidens son Beau and Sen. Edward Kennedy, a Democrat from Massachusetts.

At the time of McCains diagnosis, supportive tweets and statements from politicians and other dignitaries referenced this idea of cancer as a war or fight to be won, while also acknowledging McCains stellar career and the service he had given to this country. House Speaker Paul Ryan referred to McCain as a warrior. Others, including former Presidents George H.W. Bush and Barack Obama, referenced McCains service to the country, including his experience as a prisoner of war during the Vietnam War.

When it comes to discussing this disease, many people use words like battle, fight, survive and beat language that would not be out of place when describing a war zone. Of course, in this context it represents a persons stamina and state of mind, and optimism. But without knowing whether the person was comfortable with a word like fight to show their will to go on living and their resilience, as Trebek was, you may want to think twice before using it.

When my grandmother was diagnosed with cancer in December 2013 at the age of 83, I initially figured that she would fight it valiantly. After all, this was a woman who had already beaten cancer twice before to say nothing of how fervently she looked after my family, including my grandfather, who is wheelchair-bound.

But after one round of chemotherapy, my grandmother decided to forego treatment and eventually entered hospice care. When she died about five months later, I struggled with her decision not to continue receiving chemo after that first round. A selfish part of me privately felt like she had given up and let cancer win.

I wasnt alone in how I thought about cancer.

For some cancer patients and their loved ones, these battle metaphors are comforting, said Len Lichtenfeld, deputy chief medical officer for the American Cancer Society. The perspective for a lot of people is that youre entering a battle, and youre trying to deal with a foe you would rather not have to consider, he said. But battling cancer may hit the wrong note for some patients and their loved ones, just like sufferer or victim is rejected by people who have other chronic or aggressive diseases.

Hundreds of thousands of people die from cancer in America every year and many of those who die fought the disease extensively. In 2020, there have been an estimated 1.8 million new cancer cases diagnosed in the U.S. and more than 600,000 Americans died of the disease, according to the American Cancer Society. The five-year survival rate for stage IV pancreatic cancer, which Trebek was diagnosed with, is just 3%.

We still lose too many people to cancer, Lichtenfeld said. If things work out and people do well, are they any more a hero than somebody who did everything they needed to do, but unfortunately the disease was stronger than they were?

We still lose too many people to cancer. If things work out and people do well, are they any more a hero than somebody who did everything they needed to do, but unfortunately the disease was stronger than they were?

The metaphor can be disconcerting even for individuals who go into remission. Krystle McGrady, a social worker who lives in Colorado, was diagnosed with Hodgkin lymphoma at 16. She initially went through six months of chemotherapy followed by radiation treatment. When that was unsuccessful, she had a stem cell transplant. After roughly two years, her cancer went into remission and it was only then, she said, that people began to use these battle-like metaphors around her, something that made her uncomfortable.

It was really uncomfortable for me because it made it seem like I had some sort of choice in the matter, she said. This is what I had to do if I wanted a life. Over a decade later, McGrady now works with cancer patients, and she said she consciously avoids using such terminology particularly when it comes to the word survivor. Treatment isnt necessarily a cure, she said.

The battle language can make having cancer seem like a one-time event that the patient controls, then moves on from. The reality isnt so simple. For a growing number of people diagnosed with cancer, advancements in medicine have made living with it closer to having a chronic condition, Lichtenfeld noted.

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The language used when talking about cancer doesnt just have an emotional impact on people it can also influence how they make choices surrounding treatment and medical care.

A 2015 study compared womens reactions to different terminology used when diagnosed with ductal carcinoma in situ (DCIS), a condition thats considered to be the earliest form of breast cancer. Women who were initially told that they had abnormal cells and then later found out they had pre-invasive breast cancer cells were more likely to choose treatment over watchful waiting.

Using a metaphor like journey takes into account patients ability to choose, how treatment may be short- or long-term and how the going may not always be so easy.

As the study points out, research has shown that some over-diagnosis and over-treatment of breast lesions such as DCIS does occur though evidence shows screenings to detect breast cancer also reduce the number of fatalities caused by the disease. Even minor alterations in terminology can change the way we feel or behave in the face of cancer, Anne Moyer, a professor at Stony Brook University, wrote in Psychology Today.

In place of such war-themed language, some have suggested using the journey metaphor or allowing the person with cancer to define their own situation.

The travel-themed metaphor takes into account patients ability to choose, how treatment may be short- or long-term and how the going may not always be so easy. The journey metaphor does not countenance such concepts as winning, losing, and failing, Gary Reisfield and George Wilson from the University of Florida wrote in a 2004 article in the Journal of Clinical Oncology. Rather, there are only different roads to travel, various avenues to be explored, and, always, there are exits.

That said, it is also important to be careful about casting people with cancer as inspiring figures or angels. Putting them on a pedestal can also be discomfiting. Cancer patients are still people they want to share in lifes more mundane experiences. As McGrady points out, she made many good friends and got to have plenty of rewarding life experiences after her diagnosis. Loved ones shouldnt forget to continue talking about the small things in life or be afraid to discuss their own happy life events.

It took me a while, but Ive come to terms with my grandmothers choice. Her cancer carcinoma of unknown primary, a form of cancer in which the location in the body where the disease began isnt known has an average survival time of nine to 12 months, according to data from the American Cancer Society.

Today, I see my grandmothers decision to end treatment as remarkably sagacious. With her prognosis in mind, she ultimately chose to spend her remaining time with my family in comfort, rather than endure uncomfortable treatments that may not have given her much more time in the end. Who knows? Had my family pushed her to fight harder or to try to battle cancer, she might have lost that precious time with us.

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Alex Trebek died of pancreatic cancer think twice before saying he lost his battle with the disease - MarketWatch

October 2, 2020| Genetic variations not driving outcomes, bio-sensing viral translation, pursuit of a passive vaccine, an Android app that analyzes the SARS-CoV-2 genome, potential antibody cocktails, targeting the hairpin, spike protein may be superantigen, implicating MAIT cells, three mutations common to COVID cases in the U.S., naturally occurring lipid and enzyme hold promise, research using breathing human lungs cells, widespread preexisting immunity, and a Neandertal gene variant that triples the risk of severe disease. Plus, an interactive exhibition about COVID-19 and an international team of experts will study how viral diseases "spill over" from animals to humans.

Research Updates

A comprehensive search of genetic variation databases has revealed no significant differences across populations and ethnic groups in seven genes associated with viral entry of SARS-CoV-2, according to a study published in Infection, Genetics and Evolution. Researchers from Boston Childrens Hospitaland Hokkaido University(Japan) surveyed publicly available databases of genomic variants, including gnomAD, the Korean Reference Genome Database, TogoVar (a Japanese genetic variation database) and the 1000 Genomes Project. Genetic variants were found in each of the seven implicated proteins, the largest number in the ACE2 receptor on the cell surface, but very few of the variations altered the functions of the proteins. The overall variation frequency was also extremely low (less than 0.01%). Findings suggest that differences in COVID-19 morbidity and mortality are not the result of genetic variationsacross populations but more likely due to preexisting medical conditions, individual medical histories, environmental factors and healthcare disparities. DOI: 10.1016/j.meegid.2020.104507

Researchers from the University of Montpellier (France) and Princeton Universityreport in Proceedings of the National Academy of Sciencesthat air emitted during plosive speech sounds(e.g. P) forms vortical puffs that travel out approximately one meter. Speech containing a train of such puffs forms a continuous, turbulent, jet-like flow capable of transporting exhaled air and droplets out to two meters or more during 30 seconds of conversation. The information could inform public health strategies for mitigating airborne disease transmission, the authors say. DOI: 10.1073/pnas.2012156117

At Colorado State University, scientists have has shown an important mechanism in the host-attacking process of infectious viruses at the single-molecule level in living cells and have reproduced these behaviors in computational models. Their experiments and models, published in Nature Structural and Molecular Biology, reveal in unprecedented detail how viruses initiate translation of genetic material into proteins. Researchers invented a biosensor that lights up blue when viral translation is happening, and green when normal host translation is happening, allowing differentiation between normal and viral host processes in real time. The biosensor also permits the effects of different types of stress that cells undergo when being attacked by a virus to be visualized, and how, where and when normal versus viral translation increase or decrease. In cells under stress, internal ribosome entry sites (IRES) translation dominates. Although SARS-CoV-2 does not contain IRES, the biosensor is modular and can easily incorporate pieces of the virus to explore how it uniquely hijacks host replication machinery during infection. DOI: 10.1038/s41594-020-0504-7

Researchers at the German Center for Neurodegenerative Diseases(DZNE) and Charit - Universittsmedizin Berlinhave identified highly effective antibodies against SARS-CoV-2 and are now pursuing the development of a passive vaccine. Thye have also discovered that some SARS-CoV-2 antibodies bind to tissue samples from the brain, heart muscle and blood vessels, which could potentially trigger undesired side effects. Their findings are reported in Cell. The scientists isolated almost 600 different antibodies from the blood of individuals who had overcome COVID-19 and then narrowed this number down to a few that were particularly effective at binding to the virus. Next, they produced these neutralizing antibodies artificially using cell cultures. Studies in hamsters confirmed the high efficacy of the selected antibodies. Development of a passive vaccine, focused on three antibodies that look particularly promising for clinical development, is now underway via a collaboration with Germany-based global biotechnology company Miltenyi Biotec. Planning has already started for clinical trials, although none are expected to begin any earlier than the end of this year. DOI: 10.1016/j.cell.2020.09.049

A newmobile app Genopodeveloped by the Garvan Institute of Medical Research(Australia) in collaboration with the University of Peradeniya(Sri Lanka)has made it possible to analyze the genome of the SARS-CoV-2 virus on a smartphone in less than half an hour. This makes genomics more accessible to remote or under-resourced regions, as well as the hospital bedside. Until now, genomic analysis has required the processing power of high-end server computers or cloud services. The new app could execute bioinformatics workflows on nanopore sequencing datasets that are downloaded to a smartphone and combines several miniaturized versions of available bioinformatics tools that work on the processing power of a consumer Android device. Researchers tested their app on different Android devices, including models from Nokia, Huawei, LG and Sony. The app is a free, open-source application available through the Google Play store and described in Communications Biology. DOI: 10.1038/s42003-020-01270-z

As reported in Science, an international team of researchers has shown that a mix of ultrapotent antibodies from recovered COVID-19 patients can recognize and lock down the infection machinery of the pandemic coronavirus and keep it from entering cells. Each of the antibody types performs these overlapping tasks slightly differently. Low doses of these antibodies, individually or as a cocktail, were also shown to protect hamsters from infection when exposed to the coronavirus by preventing it from replicating in their lungs. The presence of the antibodies additionally seems to set off the infection-fighting actions of other immune cells that arrive to clear out the virus. Besides directly preventing interactions with the host receptor, one of two discovered antibodies prevented the virus from fusing with the host membrane on the surface of the cell. Findings could pave the way to implement antibody cocktails for prophylaxis or therapy that might have the advantage of circumventing or limiting the emergence of viral escape mutants. DOI: 10.1126/science.abe3354

Small molecules that target a structure within the RNA genome of SARS-CoV-2, interfering with viral gene expression and targeting the RNA for destruction, have been identifiedby researchers from TheScripps Research Institute and Iowa State University. The so-called frameshifting element of the RNA contains a hairpin that helps the virus translate its genes into proteins, and the team found a moleculecompound 5 (C5)which decreases the hairpin's efficiency in doing its job by about 25% in cell culture experiments. To enhance the potency of C5, they attached a molecule called a ribonuclease-targeting chimera (RIBOTAC) that recruits a human enzyme to degrade the viral RNA. In cultured cells, RIBOTAC increased the potency of C5 by about 10-fold. Study findings appear in ACS Central Science. DOI: 10.1021/acscentsci.0c00984

Researchers at the University of PittsburghSchool of Medicine and Cedars-Sinaiidentified a putative T-cell receptor binding motif in the SARS-CoV-2 spike protein that is absent from other beta-coronaviruses, the sequence and structure of which resemble a bacterial superantigenic peptide that causes toxic shock syndrome. COVID-19 patients with severe hyperinflammation exhibited a T cell receptor repertoire distinct from that of patients with mild/moderate disease, suggesting that the SARS-CoV-2 spike may act as a superantigento cause multisystem inflammatory syndrome in children and cytokine storm in adults. The study published in Proceedings of the National Acadamy of Sciences. DOI: 10.1073/pnas.2010722117

Mucosa-associated invariant T (MAIT) cells, which account for a small fraction of T cells in the blood of healthy people, are strongly activated in people with moderate to severe COVID-19 disease, according to a study by researchers at Karolinska Institute(Sweden) that published in Science Immunology. MIAT cells are primarily important for controlling bacteria but can also be recruited by the immune system to fight some viral infections. Study results indicate that the number of MAIT cells in the blood of 24 patients with moderate to severe COVID-19 disease sharply decline and the remaining cells in circulation are highly activatedsuggesting they are engaged in the immune response against SARS-CoV-2. Pro-inflammatory MAIT cells also accumulated in the airways of COVID-19 patients to a larger degree than in healthy people (14 individuals), which partly explains the reduced number of MAIT cells in their blood. In convalescent patients (45 individuals), the number of MAIT cells in the blood recovered at least partially in the weeks after disease and, among four patients who had died, the MAIT cells tended to be extremely activated with lower expression of the receptor CXCR3 than in those who survived. DOI: 10.1126/sciimmunol.abe1670

Researchers in China have identified potential therapeutic effects of the anticoagulation agent dipyridamolein the severely ill patients with COVID-19. In an analysis of a randomly collected cohort of 124 patients with COVID-19, the authors found that hypercoagulability (as indicated by elevated concentrations of D-dimers) was associated with disease severity. By virtual screening of an FDA-approved drug library, they identified dipyridamole in silico, which suppressed SARS-CoV-2 replication in vitro. The original research, available online since April, appears in a recent special issue of Acta Pharmaceutica Sinica B. DOI: 10.1016/j.apsb.2020.04.008

In the same publication, Chinese researchers also report that that crystal structure of SARS-CoV-2 nucleocapsid protein RNA binding domain reveals potential unique drug targeting sites. The structural information of SARS-CoV-2 nucleocapsid protein remains unclear. A third group of researchers separately report on a molecular docking-based webserverthey have developed, called D3Targets-2019-nCoV, for predicting drug targets and for multi-target and multi-site-based virtual screening of drugs against COVID-19. Both articles were originally published online in April. DOI: 10.1016/j.apsb.2020.04.009and DOI: 10.1016/j.apsb.2020.04.006

After analyzing protein sequences for COVID-19 samples from all over the world, researchers at the University of Missouri identified three specific mutationsD614G, P323L and C241Uco-existing in every single case in the U.S.This could suggest why the virus seems to be so infectious in the country. (Their newest unpublished research indicates that resurgent COVID-19 viruses in European countries also have all three of the identified mutations in nearly all European cases.) A UM undergraduate student and middle school student in Columbia, Missouri used their computer programming skills to identify patterns in the sequences. Antiviral drugs currently being made to treat COVID-19 are developed based off the current model for the virus, but these mutations are co-evolving and causing the virus' structure to change so that those drugs may become less effective. DOI: 10.1007/s11481-020-09954-3

Researchers at Colorado State University report that neither domestic dogs nor cats developed clinical disease after being infected with SARS-CoV-2 and that infected dogs did not shed virus, whereas infected cats shed infectious virus orally and nasally for five days after infection and could infect other cats via direct contact. Cats re-exposed to the virus mounted an effective immune response and were not re-infected, suggesting that cats may be a useful model for vaccine development. Findings appeared in Proceedings of the National Academy of Sciences. DOI: 10.1073/pnas.2013102117

By examining preexisting research for other conditions, researchers at the University of Cincinnatiand multiple institutions in Germany report in the Journal of Biological Chemistrythat they have found a potential treatmentthat could be applied to COVID-19. Its a naturally occurring lipid in the human body called sphingosine known to be important in the lipid metabolism of all cells and the local immune defense in epithelial cells. Sphingosine has been shown in past studies to prevent and eliminate bacterial infections of the respiratory tract. Here, in experiments using cultured human cells with SARS-CoV-2 particles added, scientists show it binds into the cellular lock, the receptor ACE2, for the virus to prevent infection. Sphingosine could potentially be delivered as a nasal spray to prevent or treat infections, they say. DOI: 10.1074/jbc.RA120.015249

Scientists at Boston University's National Emerging Infectious Diseases Laboratories and the Center for Regenerative Medicine joined forces to develop a research model for understanding how SARS-CoV-2 impacts the lungsby engineering living, "breathing" human lung cells from stem cells for the task. According to their new findings, published in Cell Stem Cell, the trouble starts soon after the air sacs in the lungs are infected with virus, activating one of the body's biological pathways known as NFkB. Simultaneously, the virus also suppresses the lungs' ability to call in the help of the immune system to fight off the viral invaders. When the signal for help finally goes out days later, an army of immune cells swarms into lung tissue heavily laden with infected, dead, and dying cells and with unchecked levels of inflammation triggered by the early activation of NFkB. In attempting to destroy every infected cell in their path, the incoming immune cells add more fuel to the fire and can help send the lungs and other organs into total failure. The discovery of NFkB's role in this deadly cascade makes it a promising target for new therapeuticsthat could tamp down its activity early on after COVID-19 infection. Neither remdesivir nor camostat were found to completely control the inflammation unleashed by NFkB. DOI: 10.1016/j.stem.2020.09.013

Researchers from the University of California Los Angelesand China have found that catalase, a naturally occurring enzyme, holds potential as a low-cost therapeutic drugto treat hyperinflammation that occurs due to COVID-19 and suppress the replication of coronavirus inside the body. A study detailing the research was published in Advanced Materials. Inside cells, the antioxidant enzyme kick starts the breakdown of hydrogen peroxide into water and oxygen. The team first demonstrated the enzyme's anti-inflammatory effects and its ability to regulate the production of cytokines, next showed that catalase can protect alveolar cells lining the human lungs from damage due to oxidation, and finally that catalase can repress the replication of SARSCoV2 in rhesus macaques without noticeable toxicity. DOI: 10.1002/adma.202004901

Research by infectious disease experts at the University of RochesterMedical Center suggests that past colds may provide some protection from COVID-19. In fact, immunity to COVID-19 is likely to last a long timemaybe even a lifetime. Their study, published in mBio, is the first to show that SARS-CoV-2 induces memory B cells to create antibodies to destroy the viral pathogen and remember it in the future, clearing infection before it starts. The study is also the first to report cross-reactivity of memory B cells, which could mean that anyone who has been infected by a common coronaviruswhich is nearly everyonemay have some degree of pre-existing immunityto COVID-19. Findings are based on a comparison of blood samples from 26 people who were recovering from mild to moderate COVID-19 and 21 healthy donors whose samples were collected six to 10 years ago, specifically levels of memory B cells and antibodies that target specific parts of the spike protein (S2 subunits) common to all coronaviruses. DOI: 10.1128/mBio.01991-20

The COVID-19 pandemic has created a flood of potentially substandard research amid the rush to publish, with a string of papers retracted or under a cloud and a surge in submissions to pre-print servers where fewer quality checks are made, a leading ethicist from Bond University(Australia) has warned in the Journal of Medical Ethics. As of May 7, 2020, 1,221 studies on COVID-19 were registered on the international clinical trial registry site, ClinicalTrials.gov, and as of July 31, 2020, 19 published articles and 14 preprints about COVID-19 have been retracted, withdrawn, or had serious doubts raised about the integrity of their data. Most of these papers came from Asia (57.5%), with over half coming from China (58%). The reason for known in three of the 33 cases that have come under scrutinyunverifiable data (common across publications) and undisclosed conflict of interest. The authors also offer suggestions for remedying the situation. DOI: 10.1136/medethics-2020-106494

A study by researchers at Karolinska Institute(Sweden) and Max Planck Institute for Evolutionary Anthropology(Germany) that published in Natureshows that a Neandertal gene variant triples the risk of severe COVID-19. Their large international study linked a gene cluster on chromosome 3 to a higher risk of hospitalization and respiratory failure upon infection with the SARS-CoV-2 virus. The cluster is very similar to the corresponding DNA sequences of a roughly 50,000-year-old Neandertal from Croatia. The genetic risk variant is particularly common among people in South Asia(about half of the population carry the Neandertal risk variant). In Europe, one in six people carry the risk variant, while in Africa and East Asia it is almost non-existent. DOI: 10.1038/s41586-020-2818-3

Industry Updates

In Sweden, SciLifeLab(one of the largest molecular biology research laboratories in Europe) and the Visualization Center(research and science center) are collaborating to set up an interactive exhibition about COVID-19. The project is designed to facilitate communication about complex data to the public in an attractive and educational fashion using interactive multi-touch display tables and 3D technology of Interspectral AB. The visualization combines four different types of research datasets on COVID-19: the SARS-CoV-2 virus architecture, the atomic structure of the spike protein, influenced human lungs, and global aspects of the pandemic. Press release.

Tufts Universitywill lead a $100 million, five-year program to understand and address threats posed by zoonotic viral diseases that can "spill over" from animals to humans, such as SARS-CoV-2, in an effort to reduce risk of infection, amplification, and spread, the United States Agency for International Development has announced. Strategies to Prevent Spillover (aka STOP Spillover) will involve wildlife and human disease experts from both the university and organizations across the globe. These include the Africa One Health University Network; Broad Institute of the Massachusetts Institute of Technology and Harvard University; Humanitarian OpenStreetMap Team; International Centre for Diarrhoeal Disease Research, Bangladesh; Internews; JSI Research and Training Institute, Inc.; Southeast Asia One Health University Network; Tetra Tech ARD; the University of California, Los Angeles; the University of Glasgow Institute of Biodiversity, Animal Health, and Comparative Medicine; the Global Center for Health Security at the University of Nebraska Medical Center; and the University of Washington Institute for Risk Analysis and Risk Communication. Press release.

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Culprit Mutations, Risky (Neandertal) Variants, Genomic Analysis App: COVID-19 Updates - Bio-IT World

Fort Collins, Colorado Reports Globe recently added the Stem Cell Therapy Market Research Report that provides a thorough investigation of the market scenario of the market size, share, demand, growth, trends, and forecast from 2020-2027. The report covers the impact analysis of the COVID-19 pandemic. COVID-19 pandemic has affected the export-import, demands, and trends of the industry and is expected to have some economic impact on the market. The report provides a comprehensive analysis of the impact of the pandemic on the overall industry and offers insights into a post-COVID-19 market scenario.

The report primarily mentions definitions, classifications, applications, and market overview of the Stem Cell Therapy industry. It also covers product portfolios, manufacturing processes, cost analysis, structures, and gross margin of the industry. It also provides a comprehensive analysis of the key competitors and their regional spread and market size.

Global Stem Cell TherapyMarketwas valued at 117.66 million in 2019 and is projected to reach USD255.37 million by 2027, growing at a CAGR of 10.97% from 2020 to 2027.

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Competitive Analysis:

The report provides a comprehensive analysis of the companies operating in the Stem Cell Therapy market, along with their overview, business plans, strengths, and weaknesses to provide a substantial analysis of the growth through the forecast period. The evaluation provides a competitive edge and understanding of their market position and strategies undertaken by them to gain a substantial market size in the global market.

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The report covers extensive analysis of the key market players in the market, along with their business overview, expansion plans, and strategies. The key players studied in the report include:

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Additionally, the report is furnished by the advanced analytical data from SWOT analysis, Porters Five Forces Analysis, Feasibility Analysis, and Investment Return Analysis. The report also provides a detailed analysis of the mergers, consolidations, acquisitions, partnerships, and government deals. Along with this, an in-depth analysis of current and emerging trends, opportunities, threats, limitations, entry-level barriers, restraints and drivers, and estimated market growth throughout the forecast period are offered in the report.

Market Breakdown:

The market breakdown provides market segmentation data based on the availability of the data and information. The market is segmented on the basis of types and applications.

1.Stem Cell Therapy Market, By Cell Source:

Adipose Tissue-Derived Mesenchymal Stem Cells Bone Marrow-Derived Mesenchymal Stem Cells Cord Blood/Embryonic Stem Cells Other Cell Sources

2.Stem Cell Therapy Market, By Therapeutic Application:

Musculoskeletal Disorders Wounds and Injuries Cardiovascular Diseases Surgeries Gastrointestinal Diseases Other Applications

3.Stem Cell Therapy Market, By Type:

Allogeneic Stem Cell Therapy Market, By Application Musculoskeletal Disorders Wounds and Injuries Surgeries Acute Graft-Versus-Host Disease (AGVHD) Other Applications Autologous Stem Cell Therapy Market, By Application Cardiovascular Diseases Wounds and Injuries Gastrointestinal Diseases Other Applications

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The report provides additional analysis about the key geographical segments of the Stem Cell Therapy Market and provides analysis about their current and previous share. Current and emerging trends, challenges, opportunities, and other influencing factors are presented in the report.

Regional analysis includes an in-depth study of the key geographical regions to gain a better understanding of the market and provide an accurate analysis. The regional analysis coversNorth America, Latin America, Europe, Asia-Pacific, and the Middle East & Africa.

Objectives of the Report:

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Stem Cell Therapy Market Size, Analytical Overview, Key Players, Growth Factors, Demand, Trends And Forecast to 2027 - thedailychronicle.in

Fort Collins, Colorado The Cancer Stem Cells Market research report offers insightful information on the Cancer Stem Cells market for the base year 2019 and is forecast between 2020 and 2027. Market value, market share, market size, and sales have been estimated based on product types, application prospects, and regional industry segmentation. Important industry segments were analyzed for the global and regional markets.

The effects of the COVID-19 pandemic have been observed across all sectors of all industries. The economic landscape has changed dynamically due to the crisis, and a change in requirements and trends has also been observed. The report studies the impact of COVID-19 on the market and analyzes key changes in trends and growth patterns. It also includes an estimate of the current and future impact of COVID-19 on overall industry growth.

Cancer stem cells market garnered a revenue of USD 798.6 million in the year 2019 globally and has been foreseen to yield USD 2,045.4 million by the year 2027 at a compound annual growth (CAGR) of 8.8% over the forecast period.

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The report has a complete analysis of the Cancer Stem Cells Market on a global as well as regional level. The forecast has been presented in terms of value and price for the 8 year period from 2020 to 2027. The report provides an in-depth study of market drivers and restraints on a global level, and provides an impact analysis of these market drivers and restraints on the relationship of supply and demand for the Cancer Stem Cells Market throughout the forecast period.

The report provides an in-depth analysis of the major market players along with their business overview, expansion plans, and strategies. The main actors examined in the report are:

The Cancer Stem Cells Market Report offers a deeper understanding and a comprehensive overview of the Cancer Stem Cells division. Porters Five Forces Analysis and SWOT Analysis have been addressed in the report to provide insightful data on the competitive landscape. The study also covers the market analysis and provides an in-depth analysis of the application segment based on the market size, growth rate and trends.

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The research report is an investigative study that provides a conclusive overview of the Cancer Stem Cells business division through in-depth market segmentation into key applications, types, and regions. These segments are analyzed based on current, emerging and future trends. Regional segmentation provides current and demand estimates for the Cancer Stem Cells industry in key regions in North America, Europe, Asia Pacific, Latin America, and the Middle East and Africa.

Cancer Stem Cells Market Segmentation:

Cancer Stem Cells Market, By Cancer Forms (2016-2027)

Cancer Stem Cells Market, By Mode Of Action (2016-2027)

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Overview of the table of contents of the report:

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How Reports Globe is different than other Market Research Providers

The inception of Reports Globe has been backed by providing clients with a holistic view of market conditions and future possibilities/opportunities to reap maximum profits out of their businesses and assist in decision making. Our team of in-house analysts and consultants works tirelessly to understand your needs and suggest the best possible solutions to fulfill your research requirements.

Our team at Reports Globe follows a rigorous process of data validation, which allows us to publish reports from publishers with minimum or no deviations. Reports Globe collects, segregates, and publishes more than 500 reports annually that cater to products and services across numerous domains.

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Cancer Stem Cells Market is Thriving Worldwide 2020-2027 | Top Companies Merck KGaA, ONCOMED PHARMACEUTICALS INC, Bionomics, MacroGenics, Inc.,...