Cell Biology

The cell-based meat company will use the money to expand its pilot production facility. | 2020-09-28 – Meat & Poultry

MAASTRICHT, THE NETHERLANDS Mosa Meat has raised $55 million as part of a larger Series B funding round.

The Netherlands-based food technology company, which in 2013 created the worlds first cell-based hamburger patty, will use the funds to expand its current pilot production facility in Maastricht, develop an industrial-sized production line and introduce cultivated beef to consumers. No timeline has been set to bring the products to market, but the company said it is working with regulators in Europe to demonstrate the safety of cultivated beef.

The Series B funding round was led by Luxembourg-based food tech fund Blue Horizon Ventures, with participation from Bell Food Group and M Ventures.

Mosa Meat also announced Regina Hecker, partner at Blue Horizon Ventures, joined its board of directors with a special focus on science, scaling and technology. She holds a PhD in molecular and cellular biology from the University of Zurich, a masters degree in biotechnology management from the IE Business School in Madrid, a masters of engineering in biotechnology and is certified in plant-based nutrition from the T. Colin Campbell Center for Nutrition Studies.

We are excited to be joining Mosa Meat as lead investor in this round, Hecker said. Following a thorough investigation of its technology and team, we are convinced that Mosa Meat is strongly placed to pioneer the scale-up of cultured meat.

The company has reached several technical milestones recently. In 2019 it removed fetal bovine serum (FBS) from its cell culture media, the nutrient rich broth that feeds cells so they can proliferate. FBS comes from unborn calves and is the standard used in cell culturing. Mosa Meat also has lowered the cost of its animal-free media, the most expensive part of its production process, by 88%.

We are very excited to welcome our new partners and see existing partners continue our journey together, said Maarten Bosch, chief executive officer of Mosa Meat. With their support and capabilities, we have the opportunity to take the next concrete steps to scale production, make progress toward a cleaner, kinder way of making real beef and ultimately increase the resilience, sustainability and safety of our global food system.

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The cell-based meat company will use the money to expand its pilot production facility. | 2020-09-28 - Meat & Poultry

Cell Biology

University of the Cumberlands students recognized for scholarship, service – The News Journal

Students Noah Thornberry (junior; Bowling Green, KY) and Mallory Allen (junior; Corbin, KY) were recently chosen as the recipients of service awards at University of the Cumberlands.

Thornberry received the 2020 T.E. Mahan Service Award, and Allen received the 2020 A.T. Siler Service Award. These awards are given to the male and female candidate from the junior class at University of the Cumberlands who best manifest the qualities which indicate the potential for becoming someone who will make an outstanding contribution to his/her community in the future. Each candidate must also have an academic standing in keeping with the standards of the University.

Noah William Thornberry, son of Mark and Ellaine Thornberry, has demonstrated exceptional service ethics and community service. His passions are service to others and real estate.

Since 2015, Thornberry has served children as a Bible school teacher at Sunday school and on summer vacations. Furthermore, he has served children in the Williamsburg area through the Mountain Outreach childrens Christmas program. While successfully balancing a demanding academic load and athletic duties, Thornberry has had the perseverance to pursue his second passion, the development of his own real estate organization. The combination of his service and leadership models both Cumberlands focus Think for tomorrow and the Universitys strategic vision to prepare students for a future life of responsible service and leadership.

Mallory Elizabeth Allen, daughter of Steve and Dawn Allen, is currently pursuing a Biology major and has maintained a 4.0 GPA. She has a heart for serving others and is deeply rooted in Cumberlands campus community.

On campus, Allen served as a volunteer resident assistant for a womens dormitory for a semester. She has served in a number of honor societies and as president of the Pre-health club. She has also volunteered for Shoes for the Soul, campus service projects, and assembling donated backpacks for food-insecure children at a local food pantry. Off campus, Allen participates in numerous volunteer activities at the Creek Church and in the Corbin Independent school system. She has volunteered for three summer mission trips to Haiti and has tutored high school students.

Professionally, Allen desires to be a physician. She has served as a teaching assistant for cell biology lab and chemistry lab, as well as being a lab technician for microbiology laboratory. In preparation for her medical school application, Allen has also attended the University of Kentucky Rural Physician Leadership Program Application Bootcamp, University of Kentucky College of Medicine Medical Education Development for Underrepresented Populations, and participated in the Rockcastle Regional Hospital Future Docs program.

University of the Cumberlands congratulates these exemplary students on being chosen for such honorable awards and thanks them for their commitment to serving their communities and being such positive influences on Cumberlands campus. Well done, Patriots!, school officials said in a release.

Originally posted here:
University of the Cumberlands students recognized for scholarship, service - The News Journal

Cell Biology

Thwarting AAV-Neutralizing Antibodies Could Improve Gene Therapy – The Scientist

A little more than a decade ago, seven patients with hemophilia Ba disease caused by a mutation on the F9 gene that prevents patients from forming crucial clotting proteinsvolunteered to be the first humans to receive a gene therapy delivered using an adeno-associated virus as a vector. This particular treatment didnt move past the Phase 1/2 trial because, while it was deemed safe, the patients did not sustain expression of the gene. But two other gene therapies based on an adeno-associated virus (AAV), Luxturna for rare forms of blindness and Zolgensma for spinal muscular atrophy, have since been approved by the US Food and Drug Administration (FDA), and several pharmaceutical companies are now pursuing regulatory approval of AAV-carried gene therapies for hemophilia B.

Recently, scientists followed up with four of those original patients. In a study published in Molecular Therapy in September, they report that the men are still free of any worrisome toxicities related to the treatment. The study wasnt all good news, though. The team also found that after all these years, the men still had elevated levels of AAV-neutralizing antibodies. That means that if an AAV gene therapy is approved to treat their illness, they likely wont be able to benefit from itthe antibodies would chew up the vector before it could insert the corrective gene.

Administration of an AAV gene therapy is essentially a vaccine against AAV, says Lindsey George, a hematologist at the Childrens Hospital of Philadelphia who led the research. Hers was not the first study to identify antibodies as a problem for those receiving AAV gene therapies, but it is the first to show that elevated titers can last this long. This role of AAV neutralizing antibodies is huge, says George, as it stands to undermine the effectiveness of gene therapies.

Because AAVs are viruses, the human immune system creates antibodies upon exposure that recognize and neutralize them in subsequent encounters. Sometimes patients have neutralizing antibodies in their blood before ever having received a gene therapy because theyre exposed to AAVs in the environment.

The ability to effectively modulate the antibody-mediated immune response could make AAV gene therapies far more effective for far more patients than they are now.

Along with high levels of antibodies to the specific AAV vector that theyd receivedAAV2the patients Georges team evaluated also had neutralizing antibodies to several other commonly used AAV vectors, namely, AAV5 and AAV8, she tells The Scientist.

Andrew Davidoff, a pediatric surgeon at St. Jude Childrens Research Hospital who studies AAV gene therapies but was not involved in the study, says, This paper suggests that not only will they not be able to receive a second dose of vector of the same [type of AAV], but potentially even other [types].

If scientists can prevent antibodies from neutralizing the AAV, they would not only give patients like these another opportunity to receive a more effective dose of gene therapy, but it will expand the patients that we can treat with the therapy to include the 3050 percent of patients who have already been exposed to AAVs in the environment, says Giuseppe Ronzitti, who heads a lab focused on gene therapy research at Genethon.

But, Davidoff says, nobody has found a suitable solution yet that is likely to be accepted by patients. The body has evolved over millions of years, this immune system that helps fight off infections. So to overcome that, even temporarily, is not an easy task.

Some immunosuppressant drugs wont work if the body has already developed specific antibodies to a particular pathogen, such as AAV. Scientists are therefore testing combinations of different types of immunosuppressants they hope will prevent the body from attacking AAVs, but these are likely to come with major risks, chiefly, susceptibility to infection.

Another option is plasmapheresisa process in which a persons blood is removed from the body and the cells separated from the plasma so that they can be reinfused without the antibodies found in the plasmabut, like immunosuppressant drugs, the technique is nonspecific and comes with similar risks. Its a matter of risk-benefit with the continued immunosuppression, says Ronzitti.

So scientists have been looking for other ways to control the bodys response to these gene therapy vectors.

Ronzitti and his team recently proposed a solution in Nature Medicine. The scientists used the imlifidase (IdeS) protein, conditionally approved by the European Commission, to degrade immunoglobulin G (IgG) antibodies that are developed after the body encounters a specific antigen so that it can remember and target that antigen in the future, and thus might cause a patient to reject a transplanted kidney. IgG antibodies are responsible for the immune systems response to AAVs. Its a newer, less invasive alternative to plasmapheresis, Ronzitti tells The Scientist in an email.

The team injected monkeys with the IdeS protein before administering a dose of gene therapy targeting the liver. The treatment appeared safe, the monkeys levels of preexisting AAV antibodies went down, and the AAV vector successfully made its way to the liver. To model a scenario in which a patient would need more than one dose of gene therapy, the scientists administered an AAV gene therapy to another group of monkeys before giving them the IdeS protein to degrade the antibodies theyd developed in response, then readministered the gene therapy. Again, AAV antibodies diminished after the IdeS treatment and the second gene therapy dose was successfully delivered.

One drawback to the approach is that IgGs are the most prevalent type of antibody found in the blood, and destroying all of them may have undesirable side effects. In an attempt to develop a more targeted therapy, one group published a study in January demonstrating that a specialized version of plasmapheresis could reduce the levels of antibodies against human AAVs in mice to the point where a new gene therapy should be effective, without depleting all other immunoglobulins that formed in response to infections.

More recently, a team of researchers at the University of Pittsburgh Medical Center made use of CRISPR-Cas9 to increase the efficacy of AAV gene therapy in mice. Pathologist Samira Kiani and her team werent looking for ways to improve gene therapy, but instead were seeking to temporarily modulate immunity in hopes of changing the course of diseases such as septicemia, a precursor to sepsis that occurs when an infection makes its way to the blood. The researchers aimed to temporarily downregulate the Myeloid differentiation primary response 88(Myd88) gene, which would briefly dampen the immune response, and then remove the brakes.

The gene that we chose to target is known to a be a central gene for innate and adaptive immunity, says Kiani. It controls the production of IgG antibodies in response to AAV exposure, which provided a simple way to measure whether the strategy was effective. If the team administered an AAV to an animal shortly after it had received the CRISPR-Cas9 treatment, it should have a substantially lower antibody response to the virus.

First, they administered the CRISPR to tamp down Myd88 activity and measured a reduction in the expression of the Myd88 gene, as theyd expected. Then, the team used the technique to treat mice just before giving them a dose of AAV-based gene therapy that was designed to lower their cholesterol.

Weeks later, the researchers administered a second dose of the same AAV vector to determine if the temporary immunosuppression during the first dose had prevented the mice from making enough antibodies to thwart a second dose. The mice that were pretreated with the immune-modulating CRISPR showed lower levels of AAV-neutralizing antibodies and more dramatic responses to the cholesterol-lowering AAV treatment. The study was published in NatureCell Biologyin September.

If given prior to the administration of an AAV gene therapy, this approach would prevent the formation of new antibodies, so the patient could receive a second dose later, if needed, says Kiani. Given that the CRISPR treatment only prevents the development of antibodies temporarily, it shouldnt cause any long-term suppression of the rest of the immune system. On the flip side, because it doesnt clear existing antibodies, if the patients have already pre-existing antibodies [from natural exposure] this approach might not be the best approach.

All of the potential solutions have a long way to go, including still needing to be tested in human patients, but the ability to effectively modulate the antibody-mediated immune response could make AAV gene therapies far more effective for far more patients than they are now, says Ronzitti. The immune response to these vectors is quite a complex story, he says. But we are solving the issues one by one.

L. George et al., Long-term follow-up of the first in human intravascular delivery of AAV for gene transfer: AAV2-hFIX16 for severe hemophilia B,Molecular Therapy,doi:10.1016/j.ymthe.2020.06.001, 2020.

F. Moghadam et al., Synthetic immunomodulation with a CRISPR super-repressor in vivo,Nature Cell Biology,doi:10.1038/s41556-020-0563-3, 2020.

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Thwarting AAV-Neutralizing Antibodies Could Improve Gene Therapy - The Scientist

Physiology

Predictive Analytics Detects Breast Cancer Spread with 90% Accuracy – HealthITAnalytics.com

September 28, 2020 -A predictive analytics method was able to detect with 90 percent accuracy which stage 0 breast cancers are likely to spread and recur, according to a study published in the American Journal of Physiology-Cell Physiology.

Approximately one in five new breast cancers are caught at their earliest stages, the researchers noted, but physicians arent able to confidently predict which of these stage 0 breast cancers are likely to recur and spread after surgery, or which forms surgery is likely to cure.

Understanding which aggressive a stage 0 cancer is likely to be will help doctors and their patients decide on the best course of treatment, which consists of removal of the tumor and a small amount of tissue followed by radiation, or removal of the entire breast.

To help providers better forecast the aggressiveness of these cancers, researchers developed a predictive analytics tool using samples from 70 patients who had stage 0 breast cancer. These patients had all undergone a mastectomy, and each had at least ten additional years of medical records available. Twenty of the 70 patients experienced a recurrence of their cancer, while 50 did not.

The team stained these tissue samples so that the proteins of interest would fluoresce under the microscope. Then, using a computer vision application, researchers created a library of microscope images associated with either aggressive or non-aggressive ductal carcinoma in situ (DCIS) based on what had happened to that patient.

Researchers then showed the program roughly 100 micrographs it hadnt seen before, known as holdout images, to see how well it could accurately predict whether that patients cancer was likely to recur.

The computer is looking for patterns in the images that humans cant readily discern, from the level of individual pixels up to an entire image of a million pixels, said Howard Petty, PhD, a professor of ophthalmology and visual sciences, and of microbiology and immunology at Michigan Medicine, the University of Michigans academic medical center.

The program is now able to correctly identify aggressive and non-aggressive disease 96 percent of the time, the researchers noted.

Thats pretty impressive when you consider that a human looking at these images would get the answer right about 70 percent of the time, Petty said. And weve continued to work on reducing the level of false negatives.

The tool also reported false positives in four percent of cases, meaning it identified aggressive disease in patients who did not experience recurrence.

We believe many of these examples speak to the skill of the patients surgeon, who effectively cured them of more aggressive disease in the operating room, Petty said.

Researchers plan to continue to refine the approach using additional samples, and the team expects that with further validation the tool could be approved for clinical use by the FDA within the next few years. The approach could also help providers predict the aggressiveness of similar types of cancer.

We started with a hypothesis about the biochemical mechanisms that drive cancer recurrence, tested the role of the movement of key proteins to the cell membrane in cancer recurrence and then confirmed our understanding of the underlying biology by assessing how well our explanation predicted what we actually see in patients, Petty said.

This improved understanding of the biology of cancer recurrence could also inform the development of new anti-cancer drugs.

By determining that the location of key proteins can predict a cancers aggressiveness, researchers could enhance treatment of stage 0 breast cancers.

Scientists dont really understand what leads to cancer recurrence at the molecular level and that has made it impossible to accurately predict which patients will experience a recurrence and which wont, said Petty.

What we found is that certain key enzymes collect near the cell membrane in these early breast cancers that end up being aggressive, but they dont in the cancers that are non-aggressive.

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Predictive Analytics Detects Breast Cancer Spread with 90% Accuracy - HealthITAnalytics.com

Physiology

What happens to your body over months in isolation – 9News

Since the pandemic officially began in March, we've been told staying home is the best way to avoid catching COVID-19.

And it is. But life in confinement can cause physical ailments on its own.

Being homebound for so long contorts the body, weakens the heart and lungs and even impairs brain function. The effects of life in isolation may stay with us beyond the pandemic's end (whenever that may be).

This is what half a year of isolation, staying home and staying sedentary can do to your body.

A week homebound, whether you're working, eating or sleeping, may feel comforting and necessary. But all the inactivity can undo hard-won progress.

That's because it can take months to build muscle and just one week to lose it.

Humans, for all of our hardiness, also lose muscle more quickly the older we get, said Keith Baar, a professor of molecular exercise physiology at the University of California - Davis.

When you lose muscle, you're not necessarily losing bulk, but you are losing strength, which Baar said is one of the "strongest indicators" of how long you'll live.

"The stronger we stay, the easier it is for us to maintain our longevity."

Your heart and lungs get weaker

If you're not exercising, you're not raising your heart rate. And when your heart isn't pumping as hard, it gets weaker, Baar said.

The same thing happens to your lungs when you're inactive, said Dr Panagis Galiatsatos, a pulmonologist from Johns Hopkins Bayview Medical Centre.

He said many of his patients have felt their breathing function deteriorate because they're no longer conditioned to exercise.

People with poor lung health are already considered more susceptible to coronavirus because it's a respiratory illness, so they're likely staying home to reduce their risk of infection.

But if they're not moving and increasing blood flow to their lungs, then their preexisting condition might harm them anyway.

Exercise is the only key to improve both heart and lung function.

"Not a single medication can do that," Galiatsatos said.

If it's not safe to leave the house, Baar recommends dancing or finding household objects for home strength training - think milk jug deadlifts.

If you're home all day, every day, you're likely feet away from your pantry.

Depending on your perspective, that's either convenient or dangerous.

With such easy access, your "feeding" window, or the period of time during which you eat most of your meals, might widen from 10 or 12 hours every day to 15 hours a day- more than half the day, which could cause your insulin levels to spike.

Insulin encourages fat storage and converting other fat molecules to fat, said Giles Duffield, an associate professor of anatomy and physiology at the University of Notre Dame who studies circadian rhythms and metabolism, among other subjects.

Excessive eating is also an issue because, at the beginning of the pandemic, many people stocked up on nonperishable foods in case of supply shortages, Duffield said.

Many nonperishable foods are highly processed and rich in sugars and starches.

Weight gain during periods of intense stress is normal, and 2020 has been unrelentingly stressful. Weight gain becomes dangerous, though, when it turns into obesity.

Then, your body might start to resist insulin, and chronic health issues like metabolic illness or diabetes may develop, Duffield said.

We all have a seated position we subconsciously sink into - slumped forward, shoulders hunched; spine curled, neck bent; on your chest, elbows up.

But sitting and lying down all day can seriously affect your posture and strain your back, neck, shoulders, hips and eyes, said Brandon Brown, an epidemiologist and associate professor in the Center for Healthy Communities at the University of California - Riverside.

Brown suggests getting up from your seat once an hour, walking around and stretching for a moment.

You might even lie on the floor and "let your back readjust," he said.

At least half of all Americans are skimping on vitamin D, which sustains bone density and keeps fatigue at bay.

You're definitely one of them if you spend most of your day at home, curtains drawn, Duffield said.

Getting enough sunlight in the morning helps synchronize your body's circadian rhythm, Duffield said.

So if you're shut in all week or working in the dark, your sleep might suffer, too.

Brown said as long as you're going on walks or exercising, doing yard work or other activities that drag you outside for a bit, you won't need to worry about getting enough sunlight.

If you're unable to get out of the house or the weather won't permit you to, an artificial bright light can help your body retune in the morning, Duffield said, as can avoiding blue lights at night.

A sedentary lifestyle can slow your brain, too.

Exercise produces certain chemicals in the brain that break down toxins in the blood and even prevent them from going to the brain, where they can kill brain cells, Baar said.

Not exercising means you won't as efficiently break down amino acid byproducts that wind up as neurotoxins in the brain.

The effects of isolation are insidious - like the pandemic, the physical symptoms after months of seclusion often aren't obvious until they become harmful or extreme.

It's possible, too, to stave off those symptoms before they set in for good.

Prioritising your mental and physical health while staying home requires some work, but it's a healthier coping mechanism for uncertainty than staying stationary until COVID-19 is no longer a threat, health experts say.

GALLERY: One last look at Melbourne's deserted streets

And when it's safe to live fully again, you'll be prepared.

Excerpt from:
What happens to your body over months in isolation - 9News

Physiology

This is what happens to your body over months in isolation – WXII The Triad

Since the pandemic officially began in March, we've been told staying home is the best way to avoid catching COVID-19. And it is. But life in confinement can cause physical ailments on its own.Being homebound for so long contorts the body, weakens the heart and lungs and even impairs brain function. The effects of life in isolation may stay with us beyond the pandemic's end whenever that may be.This is what half a year of isolation, staying home and staying sedentary can do to your body.You start losing muscleA week homebound, whether you're working, eating or sleeping, may feel comforting and necessary. But all the inactivity can undo hard-won progress.That's because it can take months to build muscle and just one week to lose it. Humans, for all of our hardiness, also lose muscle more quickly the older we get, said Keith Baar, a professor of molecular exercise physiology at the University of California-Davis.When you lose muscle, you're not necessarily losing bulk, but you are losing strength, which Baar said is one of the "strongest indicators" of how long you'll live."The stronger we stay, the easier it is for us to maintain our longevity."Your heart and lungs get weakerIf you're not exercising, you're not raising your heart rate. And when your heart isn't pumping as hard, it gets weaker, Baar said.The same thing happens to your lungs when you're inactive, said Dr. Panagis Galiatsatos, a pulmonologist from Johns Hopkins Bayview Medical Center. He said many of his patients have felt their breathing function deteriorate because they're no longer conditioned to exercise.People with poor lung health are already considered more susceptible to coronavirus because it's a respiratory illness, so they're likely staying home to reduce their risk of infection. But if they're not moving and increasing blood flow to their lungs, then their preexisting condition might harm them anyway.Exercise is the only key to improve both heart and lung function "Not a single medication can do that," Galiatsatos said. If it's not safe to leave the house, Baar recommends dancing or finding household objects for home strength training think milk jug deadlifts.You gain fatIf you're home all day, every day, you're likely feet away from your pantry. Depending on your perspective, that's either convenient or dangerous.With such easy access, your "feeding" window, or the period of time during which you eat most of your meals, might widen from 10 or 12 hours every day to 15 hours a day more than half the day, which could cause your insulin levels to spike. Insulin encourages fat storage and converting other fat molecules to fat, said Giles Duffield, an associate professor of anatomy and physiology at the University of Notre Dame who studies circadian rhythms and metabolism, among other subjects.Excessive eating is also an issue because, at the beginning of the pandemic, many people stocked up on nonperishable foods in case of supply shortages, Duffield said. Many nonperishable foods are highly processed and rich in sugars and starches.Weight gain during periods of intense stress is normal, and 2020 has been unrelentingly stressful. Weight gain becomes dangerous, though, when it turns into obesity. Then, your body might start to resist insulin, and chronic health issues like metabolic illness or diabetes may develop, Duffield said.Your posture is affectedWe all have a seated position we subconsciously sink into slumped forward, shoulders hunched; spine curled, neck bent; on your chest, elbows up.But sitting and lying down all day can seriously affect your posture and strain your back, neck, shoulders, hips and eyes, said Brandon Brown, an epidemiologist and associate professor in the Center for Healthy Communities at the University of California-Riverside.Brown suggests getting up from your seat once an hour, walking around and stretching for a moment. You might even lie on the floor and "let your back readjust," he said.Your sleep suffersAt least half of all Americans are skimping on vitamin D, which sustains bone density and keeps fatigue at bay. You're definitely one of them if you spend most of your day at home, curtains drawn, Duffield said.Getting enough sunlight in the morning helps synchronize your body's circadian rhythm, Duffield said. So if you're shut in all week or working in the dark, your sleep might suffer, too.Brown said as long as you're going on walks or exercising, doing yard work or other activities that drag you outside for a bit, you won't need to worry about getting enough sunlight. If you're unable to get out of the house or the weather won't permit you to, an artificial bright light can help your body retune in the morning, Duffield said, as can avoiding blue lights at night.Your brain slowsA sedentary lifestyle can slow your brain, too.Exercise produces certain chemicals in the brain that break down toxins in the blood and even prevent them from going to the brain, where they can kill brain cells, Baar said.Not exercising means you won't as efficiently break down amino acid byproducts that wind up as neurotoxins in the brain.The effects of isolation are insidious like the pandemic, the physical symptoms after months of seclusion often aren't obvious until they become harmful or extreme.It's possible, too, to stave off those symptoms before they set in for good.Prioritizing your mental and physical health while staying home requires some work, but it's a healthier coping mechanism for uncertainty than staying stationary until COVID-19 is no longer a threat, health experts say. And when it's safe to live fully again, you'll be prepared.

Since the pandemic officially began in March, we've been told staying home is the best way to avoid catching COVID-19. And it is. But life in confinement can cause physical ailments on its own.

Being homebound for so long contorts the body, weakens the heart and lungs and even impairs brain function. The effects of life in isolation may stay with us beyond the pandemic's end whenever that may be.

This is what half a year of isolation, staying home and staying sedentary can do to your body.

A week homebound, whether you're working, eating or sleeping, may feel comforting and necessary. But all the inactivity can undo hard-won progress.

That's because it can take months to build muscle and just one week to lose it. Humans, for all of our hardiness, also lose muscle more quickly the older we get, said Keith Baar, a professor of molecular exercise physiology at the University of California-Davis.

When you lose muscle, you're not necessarily losing bulk, but you are losing strength, which Baar said is one of the "strongest indicators" of how long you'll live.

"The stronger we stay, the easier it is for us to maintain our longevity."

If you're not exercising, you're not raising your heart rate. And when your heart isn't pumping as hard, it gets weaker, Baar said.

The same thing happens to your lungs when you're inactive, said Dr. Panagis Galiatsatos, a pulmonologist from Johns Hopkins Bayview Medical Center. He said many of his patients have felt their breathing function deteriorate because they're no longer conditioned to exercise.

People with poor lung health are already considered more susceptible to coronavirus because it's a respiratory illness, so they're likely staying home to reduce their risk of infection. But if they're not moving and increasing blood flow to their lungs, then their preexisting condition might harm them anyway.

Exercise is the only key to improve both heart and lung function "Not a single medication can do that," Galiatsatos said. If it's not safe to leave the house, Baar recommends dancing or finding household objects for home strength training think milk jug deadlifts.

If you're home all day, every day, you're likely feet away from your pantry. Depending on your perspective, that's either convenient or dangerous.

With such easy access, your "feeding" window, or the period of time during which you eat most of your meals, might widen from 10 or 12 hours every day to 15 hours a day more than half the day, which could cause your insulin levels to spike. Insulin encourages fat storage and converting other fat molecules to fat, said Giles Duffield, an associate professor of anatomy and physiology at the University of Notre Dame who studies circadian rhythms and metabolism, among other subjects.

Excessive eating is also an issue because, at the beginning of the pandemic, many people stocked up on nonperishable foods in case of supply shortages, Duffield said. Many nonperishable foods are highly processed and rich in sugars and starches.

Weight gain during periods of intense stress is normal, and 2020 has been unrelentingly stressful. Weight gain becomes dangerous, though, when it turns into obesity. Then, your body might start to resist insulin, and chronic health issues like metabolic illness or diabetes may develop, Duffield said.

We all have a seated position we subconsciously sink into slumped forward, shoulders hunched; spine curled, neck bent; on your chest, elbows up.

But sitting and lying down all day can seriously affect your posture and strain your back, neck, shoulders, hips and eyes, said Brandon Brown, an epidemiologist and associate professor in the Center for Healthy Communities at the University of California-Riverside.

Brown suggests getting up from your seat once an hour, walking around and stretching for a moment. You might even lie on the floor and "let your back readjust," he said.

At least half of all Americans are skimping on vitamin D, which sustains bone density and keeps fatigue at bay. You're definitely one of them if you spend most of your day at home, curtains drawn, Duffield said.

Getting enough sunlight in the morning helps synchronize your body's circadian rhythm, Duffield said. So if you're shut in all week or working in the dark, your sleep might suffer, too.

Brown said as long as you're going on walks or exercising, doing yard work or other activities that drag you outside for a bit, you won't need to worry about getting enough sunlight. If you're unable to get out of the house or the weather won't permit you to, an artificial bright light can help your body retune in the morning, Duffield said, as can avoiding blue lights at night.

A sedentary lifestyle can slow your brain, too.

Exercise produces certain chemicals in the brain that break down toxins in the blood and even prevent them from going to the brain, where they can kill brain cells, Baar said.

Not exercising means you won't as efficiently break down amino acid byproducts that wind up as neurotoxins in the brain.

The effects of isolation are insidious like the pandemic, the physical symptoms after months of seclusion often aren't obvious until they become harmful or extreme.

It's possible, too, to stave off those symptoms before they set in for good.

Prioritizing your mental and physical health while staying home requires some work, but it's a healthier coping mechanism for uncertainty than staying stationary until COVID-19 is no longer a threat, health experts say. And when it's safe to live fully again, you'll be prepared.

The rest is here:
This is what happens to your body over months in isolation - WXII The Triad

Physiology

AlzeCure Pharma provides a scientific update on Alzheimer’s disease and the Alzstatin project platform – BioSpace

STOCKHOLM, Sept. 28, 2020 /PRNewswire/ -- AlzeCure Pharma AB (publ) (FN STO: ALZCUR), a pharmaceutical company that develops a broad portfolio of drug candidates for diseases affecting the central nervous system, with projects in both Alzheimer's disease and pain, will hold a live business update focused on the company's Alzheimer's platform Alzstatin on Wednesday, September 30 at 10:00. The presentation will be followed by a Q&A session led by Vator Securities' analyst Felicia Rittemar.

CEO Martin Jnsson and CSO Johan Sandin will, among other things, present the pharmaceutical platform Alzstatin and the research behind it. Within the Alzstatin platform, AlzeCure develops disease-modifying and preventive drugs for Alzheimer's disease that focus on reducing the production of toxic amyloid beta (A) in the brain.

Henrik Zetterberg, chief physician and professor at the Department of Neuroscience and Physiology at Sahlgrenska Academy and professor at University College of London (UCL), will participate and provide a deeper review of disease development in Alzheimer's and the amyloid hypothesis, as well as provide an update on developments in biomarkers and diagnostics in Alzheimer's.

Watch the live broadcast on September 30 from 10:00am - 11:30am CET via: https://youtu.be/3QBa97Ue75o.

The business update will be held in English and will be available on the company's website afterwards.

The information was submitted for publication, through the agency of the contact person set out above at 10:00am CET on September 28, 2020.

About AlzeCure Pharma AB (publ)

AlzeCure is a Swedish pharmaceutical company that develops new innovative drug therapies for the treatment of severe diseases and conditions that affect the central nervous system, such as Alzheimer's disease and pain - indications for which currently available treatment is extremely limited. The company is listed on Nasdaq First North Premier Growth Market and is developing several parallel drug candidates based on three research platforms: NeuroRestore, Alzstatin and Painless.

NeuroRestore consists of three symptomatic drug candidates where the unique mechanism of action allows for multiple indications, including Alzheimer's disease, as well as cognitive disorders associated with traumatic brain injury, sleep apnea and Parkinson's disease. Alzstatin comprises two disease-modifying and preventive drug candidates for early treatment of Alzheimer's disease. Painless is the company's research platform in the field of pain and contains two projects: ACD440, which is a clinical candidate for the treatment of neuropathic pain, and TrkA-NAM, which targets severe pain in conditions such as osteoarthritis. AlzeCure aims to pursue its own projects through preclinical research and development to an early clinical phase and is continuously working with business development to find suitable out-licensing solutions with other pharmaceutical companies.

FNCA Sweden AB, +46(0)8 528 00 399 info@fnca.se, is the company's Certified Adviser. For more information, please visit http://www.alzecurepharma.se.

About Alzstatin

AlzeCure's disease-modifying research platform, Alzstatin, consisting of disease-modifying and preventive drug candidates, focuses on reducing the production of toxic amyloid beta (A) in the brain. A plays a key pathological role in Alzheimer's and begins to accumulate in the brain years before clear symptoms develop. The drug candidates in the Alzstatin platfrom modulate the function of the enzyme gamma secretase. Gamma secretase acts like a pair of scissors and cuts A42 out from a longer protein known as APP. The sticky A42 clumps together giving rise to the amyloid plaque so typical of Alzheimer's disease. The candidates in the Alzstatin platform affect enzyme function so that it instead cuts out shorter forms of the A peptide, A37 and A38, which in addition to them not being sticky and not forming aggregates, also have a restrictive effects on A42 aggregates already formed. This means the drug candidates in the Alzstatin platform have two separate but synergistic effects that together contribute to a stronger anti-amyloidogenic - and thus more potent - disease-modifyning effect.

About Alzheimer's disease

Alzheimer's disease is the most common form of dementia, affecting approximately 45 million people worldwide. Alzheimer's disease is a lethal disorder that also has a large impact on both relatives and the society. Today, preventive and disease modifying treatments are missing. The main risk factors to develop Alzheimer's are age and genetic causes. Even though the disease can start as early as between 40 and 65 years of age, it is most common after 65 years. Significant investments in Alzheimer research are being made because of the significant unmet medical need and the large cost of this disease for healthcare and society. The total global costs for dementia related diseases is estimated to about 1,000 billion USD globally in 2018. Given the lack of both effective symptomatic treatments and disease modifying treatments, the need for new effective therapies is acute.The few approved drugs on the market today have only a limited symptomatic effect and can produce dose limiting side effects. A disease modifying treatment for Alzheimer's disease is estimated to reach more than 10 billion USD in annual sales. In Sweden, approximately 100,000 people suffer from Alzheimer's disease with a healthcare cost of about 63 billion SEK yearly, which is more than for cancer and cardiovascular diseases combined.

For more information, please contactMartin JnssonCEOTel: +46-707-86-94-43martin.jonsson@alzecurepharma.com

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AlzeCure Pharma provides a scientific update on Alzheimer's disease and the Alzstatin project platform - BioSpace

Physiology

Animal Model Market research gain impetus due to the growing demand over (2020 2027) – The Daily Chronicle

Global Animal model market report provides geographic analysis covering regions such as North America, Europe, Asia Pacific, and Rest of World. The Animal model market for each region is further segmented for major countries including U.S., Canada, Germany, UK, France, Italy, China, India, Japan, Brazil, South Africa and others.

FYI, You will get latest updated report as per the COVID-19 Impact on this industry. Our updated reports will now feature detailed analysis that will help you make critical decisions.

Browse Full Report: https://www.marketresearchengine.com/animal-model-market

The Global Animal Model market is expected to grow at a CAGR of 8% during the forecast period. Scientist and research professionals perform biological and pathological experiments on animals, which is called animal model as animals and human beings share common biological structure. The model is chosen usually because it meets the determined taxonomic equivalency to a human for the research and investigation purpose so as to get the better understanding of the human disease.

The growing innovation in genetic engineering that helps in evaluating the drugs mechanisms of action is again boosting the demand for the drug discovery thereby raising the demand for the animal model.

Global Animal model market is segregated on the basis of application as toxicology, biomedical research, physiology, cancer research, genetic research, neurological research, xenotransplantation. Based on animal type, the global Animal model market is segmented in rabbits, dogs, cats, rats, mice and others. The report also bifurcates global Animal model market based on end user in research institutes, pharmaceutical companies, and educational institutes.

Competitive Rivalry

Envigo, SAGE Labs, Transgenic, Inc. are among the major players in the global Animal model market share. The companies are involved in several growth and expansion strategies to gain a competitive advantage. Industry participants also follow value chain integration with business operations in multiple stages of the value chain.

The Animal Model Market has been segmented as below:

Animal Model Market, by Application

Animal Model Market, by Animal Type

Animal Model Market, by End User

Animal Model Market, By Region

The report covers:

Report scope:

Global Animal model market report scope includes detailed study covering underlying factors influencing the industry trends.

The report covers analysis on regional and country level market dynamics. The scope also covers competitive overview providing company market shares along with company profiles for major revenue contributing companies.

The report scope includes detailed competitive outlook covering market shares and profiles key participants in the global Animal model market share. Major industry players with significant revenue share include SAGE Labs, Envigo, Transgenic, Inc., Charles River Laboratories etc.

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Animal Model Market research gain impetus due to the growing demand over (2020 2027) - The Daily Chronicle

Physiology

Proper funding for women’s health research could save lives during pandemic – Policy Options

Womens health research is chronically underfunded, and womens health receives little attention across the spectrum of health research, from funding to academic opportunities. Although steps have been taken to incorporate sex and gender-based analysis (SGBA) into research in Canada, there is a continued lack of analyses of sex and gender across health research areas. This lack of attention paid to SGBA and to womens health research has led to misdiagnoses, minimized symptoms and poorly targeted treatment in women.

Indeed, if we had provided more funding and resources to womens health research, one could make the argument that we would be closer in our search for a treatment and cure for COVID-19. Why?

Mortality from COVID-19 follows from attacks on the immune and vascular system, and both systems have striking sex differences. Yet, there is little research on how female-specific factors affect immune and vascular systems. If we knew more about how these systems work in women, we would be in a better position to understand why female physiology offers some protection against COVID-19-related mortality as shown in higher mortality rates in males. We would also be further ahead in our quest for an effective COVID-19 treatment for both men and women.

A sex and gender-focused approach and targeted consideration of womens health issues in health science research, policy and practice will ensure we do not deepen sex and gender disparities in COVID-19 research and outcomes and promote an inclusive and balanced path for the future health of all Canadians. And it will save lives, faster.

Sex differences matter in health research

Womens health research may seem like a niche research area; however, many diseases disproportionately affect women compared to men. For instance: depression and anxiety-related diseases are more prevalent in women than in men; heart attack symptoms manifest differently between the sexes; and treatments for certain diseases are more effective in one sex versus the other.

It is essential to understand these sex differences and how female-specific factors, such as contraceptive use, pregnancy and menopause, may contribute to disease susceptibility, symptoms and treatment. These unique aspects of womens health are compounded by a range of intersectional factors such as gendered societal norms, race and socioeconomic status, which can accumulate to negatively affect womens health, and are often ignored in health literature.

Womens health research is chronically underfunded. In a 2019 report commissioned by B.C. Womens Health Foundation, we found that over the past ten years, one percent of salary awards went to womens health researchers in Canada, and in B.C., womens health grants made up only eight percent of Canadian Institutes for Health Research (CIHR) grants. Given that women make up over 50 percent of the population, these percentages are dishearteningly low.

Furthermore, the amount of funding per grant was $50,000 lower per year for womens health grants compared to others. Perhaps unsurprisingly, more women than men researchers study womens health and conduct research analysing sex and gender. Women, on average, have lower funding success rates at CIHR, and receive less money (over $100,000 less per CIHR grant).

Inequities exacerbated by COVID-19

COVID-19 has amplified these inequities in womens health research affecting funding, authorship, data acquisition and analysis. Health research suffered a serious blow when CIHR cancelled their 2020 spring competition one month after grants were submitted. Thankfully, the decision was reversed; however, the subsequent delay and resulting interim funding gap will have a cascading negative impact on health researchers, disproportionately affecting those with less funding, including womens health researchers. Unpredictability of funding opportunities and low funding levels greatly impede research progress according to a survey of Canadian health researchers.

Emerging data indicates that women researchers are being surpassed by their male counterparts in COVID-19 scientific outputs, likely linked to the increased volume of caregiving and domestic responsibilities falling on women during the pandemic. Females are conducting less research on COVID-19, as depicted by publications, registered reports and awarded grants.

Furthermore, fewer female researchers as first authors are submitting and publishing during the pandemic compared to the year prior and these trends appear to be getting worse as time goes on. From the CIHR funding decisions database, of the initial 99 grants awarded for the CIHR Novel Coronavirus (COVID-19) Rapid Research Funding Opportunity, only 23 percent of the grant awardees had a woman as the nominated principal investigator.

In the latest round of CIHR COVID-19 grants, which included grants on mental health, clinical management and social policy, the percentage of grants lead by a woman as principal investigator increased to 40 percent.

Yet the general picture is still worrying. Studies indicate that diversity breeds discovery. We need more minds with diverse interests and multidisciplinary research to solve the many health, economic and societal issues related to the pandemic. If women are missing from the equation, diversity is compromised, and we will continue to lag in our efforts to solve the pandemic crisis for all.

Worse yet, commitment to SGBA for COVID-19 research grants is not evident. Only four percent of awarded grants met SGBA criteria, and only two percent went specifically to studying womens health. Two months after the funding announcements, a supplement to understand the effect of sex as a biological variable (SABV) was awarded and currently 11 percent of the COVID-19 grants consider SGBA.

This is still not enough. If we ignore sex and gender as a variable in COVID-19 research, we miss crucial information to propel the research forward.

Disaggregated data is a critical tool

Additionally, despite the Canadian governments commitment to applying a GBA+ policy lens in its decisions, it is difficult to find Canadian data on COVID-19 infections, hospitalizations and deaths disaggregated by sex and age.

Canada is one of the countries now providing the Global Health 50/50 program with sex-disaggregated data. However, the troubling lack of commitment to SGBA in the CIHR COVID-19 funding decisions, makes it evident that little work in Canada is underway to investigate the known sex and gender differences of this disease.

To rectify these biases and inequities, first and foremost, funding for womens health research needs to increase by creating dedicated funding sources specifically for womens health research, both for COVID-19 and for womens health research in general.

Second, Canada needs to create a national open repository where all federally funded research must be submitted with mandatory recording of sex, gender and age data. Doing so will enable secondary analyses of sex and gender and allow for new health initiatives that benefit women, men and gender diverse peoples.

Third, while federal funding agencies such as CIHR are to be applauded for making gender metrics public, granting bodies must consistently demonstrate a commitment to gender equity in funding awards, terms and amounts. One method is to employ modular budgets, which have eliminated sex differences in funding amounts for the National Institute of Health in the United States and reduced sex differences in funded grant amounts to less than $5000 under the Natural Sciences and Engineering Research Council of Canada system.

These steps will improve health research both in response to this pandemic and more widely. It will also help us better respond to future pandemics. The solution is simple: fund more womens health research.

This article is part of theTackling inequality as part of Canadas post-pandemic recoveryspecial feature.

Photo: Shutterstock/By Gorodenkoff

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Proper funding for women's health research could save lives during pandemic - Policy Options

Physiology

ONLINE: The Future of Medicine – Isthmus

Watch here: https://www.youtube.com/watch?feature=youtu.be&v=VVkQU91KbEs

press release: The UW has a long history of pioneering medical advancements that have transformed the world. From performing the first bone marrow transplant in the United States to cultivating the first laboratory-derived human embryonic stem cells. Now, where will UW medical research go next?

On the next Wisconsin Medicine Livestream, meet trailblazing doctors, researchers, and medical leaders who are charting a bold course to completely alter the health care landscape. During this insightful panel discussion, well explore how gene therapy and cell replacements could hold the keys to treating inherited and acquired blindness. Youll also discover the remarkable potential in xenotransplantation where nonhuman animal source organs are transplanted into human recipients. In addition, you will learn about UW Healths journey to build a multidisciplinary program to serve the community. These, and other, fascinating developments in treatment and care are happening right now at the UW and are the future of medicine. The presentation will be moderated by Robert Golden, the dean of the University of WisconsinMadisons School of Medicine and Public Health.

Our Guests:

David Gamm, professor, Department of Ophthalmology and Visual Sciences; Emmett A. Humble Distinguished Director, McPherson Eye Research Institute; Sandra Lemke Trout Chair in Eye Research

Dr. Gamms lab is at the forefront in developing cell-based therapies to combat retinal degenerative diseases (RDDs). As the director of the McPherson Eye Research Institute and a member of the Waisman Center Stem Cell Research Program, the UW Stem Cell and Regenerative Medicine Center, and the American Society for Clinical Investigation, his efforts are directed toward basic and translational retinal stem cell research. The Gamm Lab uses induced pluripotent stem cells to create retinal tissues composed of authentic human photoreceptor cells rods and cones that can detect light and initiate visual signals in a dish. The aims of his laboratory are to investigate the cellular and molecular events that occur during human retinal development and to generate cells for use in retinal disease modeling and cell replacement therapies. In collaboration with other researchers at UWMadison and around the world, the lab is developing methods to produce and transplant photoreceptors and/or retinal pigment epithelium (RPE) in preparation for future clinical trials. At the same time, the Gamm Lab uses lab-grown photoreceptor and RPE cells to test and advance a host of other experimental treatments, including gene therapies. In so doing, the lab seeks to delay or reverse the effects of blinding disorders, such as retinitis pigmentosa and age-related macular degeneration, and to develop or codevelop effective interventions for these RDDs at all stages of disease.

Dhanansayan Shanmuganayagam, assistant professor, Department of Surgery, School of Medicine and Public Health; Department of Animal and Dairy Sciences, UWMadison; director, Biomedical, and Genomic Research Group

Dr. Shanmuganayagams research focuses on the development and utilization of pigs as homologous models to close the translational gap in human disease research, taking advantage of the overwhelming similarities between pigs and humans in terms of genetics, anatomy, physiology, and immunology. He and his colleagues created the human-sized Wisconsin Miniature Swine breed that is unique to the university. The breed exhibits greater physiological similarity to humans, particularly in vascular biology and in modeling metabolic disorders and obesity. He currently leads genetic engineering of swine at the UW. His team has created more than 15 genetic porcine models including several of pediatric genetic cancer-predisposition disorders such as neurofibromatosis type 1 (NF1). In the context of NF1, his lab is studying the role of alternative splicing of the nf1 gene on the tissue-specific function of neurofibromin and whether gene therapy to modulate the regulation of this splicing can be used as a viable treatment strategy for children with the disorder.

Dr. Shanmuganayagam is also currently leading the efforts to establish the University of Wisconsin Center for Biomedical Swine Research and Innovation (CBSRI) that will leverage the translatability of research in pig models and UWMadisons unique swine and biomedical research infrastructure, resources, and expertise to conduct innovative basic and translational research on human diseases. The central mission of CBSRI is to innovate and accelerate the discovery and development of clinically relevant therapies and technologies. The center will also serve to innovate graduate and medical training. As the only center of its kind in the United States, CBSRI will make UWMadison a hub of translational research and industry-partnered biomedical innovation.

Petros Anagnostopoulos, surgeon in chief, American Family Childrens Hospital; chief, Section of Pediatric Cardiothoracic Surgery; professor, Department of Surgery, Division of Cardiothoracic Surgery

Dr. Anagnostopoulos is certified by the American Board of Thoracic Surgery and the American Board of Surgery. He completed two fellowships, one in cardiothoracic surgery at the University of Pittsburgh School of Medicine and a second in pediatric cardiac surgery at the University of California, San Francisco School of Medicine. He completed his general surgery residency at Henry Ford Hospital in Detroit. Dr. Anagnostopoulos received his MD from the University of Athens Medical School, Greece. His clinical interests include pediatric congenital heart surgery and minimally invasive heart surgery.

Dr. Anagnostopoulos specializes in complex neonatal and infant cardiac reconstructive surgery, pediatric heart surgery, adult congenital cardiac surgery, single ventricle palliation, extracorporeal life support, extracorporeal membrane oxygenation, ventricular assist devices, minimally invasive cardiac surgery, hybrid surgical-catheterization cardiac surgery, off-pump cardiac surgery, complex mitral and tricuspid valve repair, aortic root surgery, tetralogy of Fallot, coronary artery anomalies, Ross operations, obstructive cardiomyopathy, and heart transplantation.

When: Tuesday, Sept. 29, at 7 p.m. CDT

Where: Wisconsin Medicine Livestream: wiscmedicine.org/programs/ending-alzheimers

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ONLINE: The Future of Medicine - Isthmus