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The Lexus GS350: longevity for a bargain – News from southeastern Connecticut – theday.com

September 13th, 2020 2:52 am

2020 Lexus GS350: Does GS stand for Grandpa's Sedan?

Price: $58,335 as tested. The All-Weather Package added $290; 19-inch wheels, $660; power trunk, $400; park assist, $500; heated steering wheel and open-pore trim, $800. More mentioned throughout.

Conventional wisdom: Car and Driver liked the "refined driving dynamics, huge trunk, extensive range of standard features," but not that "fuel economy trails that of several rivals; Apple CarPlay and Android Auto aren't offered; underwhelming cabin design."

Marketer's pitch: "Experience amazing."

Reality: It's a Grandpa Sedan, but maybe he knows a thing or two, right?

What's new: I've never been convinced that the latest thing is always the best. I take the long-term approach to life and tend not to be an early adopter. Best to stick with simple and familiar.

Well, the GS may not be so simple, but it's certainly familiar. The latest generation of GS was introduced for the 2016 model year, and its age is really starting to show. And while the 2020 is the end of the GS line, don't write it off your list just yet.

Up to speed: The 3.5-liter V-6 engine creates 311 horsepower, plenty of oomph for a standard sedan. The translates into nice acceleration, with a 0 to 60 of 5.8 seconds, according to Car and Driver.

On the road: I had a rare opportunity (these days) to take the GS350 out on a longish trip, to visit Sturgis Grandma 1.0 while she recuperates from a broken hip.

The all-wheel-drive test model handled the turnpike smoothly, but without giving any real reason to get excited. It's a four-door sedan from Toy er, Lexus, and it actually felt a lot like last generation's Avalon, a real road sailor of the old Ford LTD variety. I thought it would feel better out on the open road, somehow smoother and ready to cruise, but I found the GS350 liked to wander and waver.

The GS350 really shone, though, closer to home. No, it didn't make winding country roads a delight, but it sure felt smooth and sure-footed on the more gentle bends, and hill-climbing is a real strength. Sport mode makes the handling tighter, but the acceleration turns a little too wild.

Shifty: The pricey luxury sedan does it all with last generation's gearbox. That's a six-speed automatic driving the wheels.

The vehicle seemed to rely on downshifting for a lot of braking and often seemed to get "stuck" in a lower gear in a variety of situations. For instance, say you were coming upon a state trooper parked by the side of the road, so you needed to let off the gas in a hurry because, lo, the car just got away from you there. So while suddenly scooting back toward the high 60 mph range, the vehicle chose fourth gear. And stayed there. An unwelcome phenomenon, indeed both the gear selection and the, uh, roadside reminder.

Driver's Seat: Like most Lexii, the GS350 certainly offers drivers a comfortable saddle. The Premium Package ($1,760) turns the leather seats warm or cold at the touch of a button (and also offers rain sensing wipers and rear sunshade). It's roomy and spacious with a lot of dashboard in view, like Grandpa's old LTD as well.

Friends and stuff: The rear seat provides a comfortable space, but not nearly as roomy as the bulky exterior of the sedan would have you believe. Though legroom invites stretching, a low front seat nibbles away foot room while a low roof tightens headroom.

Cargo space is cavernous 18.4 cubic feet.

Play some tunes: The Mark Levinson stereo system ($1,180) features 17 speakers, 835 watts, and premium surround. Sound quality is about an A-, great at high volumes but not much in a more normal range.

Lexus gives this vehicle last generation's infotainment controls, though, and that's a good thing. Today's standard-issue touchpad can be a challenge to direct, but the GS350 gets the old joystick control. Bump up, down, left, or right to move around the screen. Better than a touchpad, but it still requires too much attention to be effective. Our eyes are supposed to be on the road, right, Lexus?

Night shift: The interior lights cast a friendly, subtle glow. LED headlights shine clearly and in the right places, a feature not often standard with the LEDs.

Fuel economy: I averaged 23 mpg in a long highway test and a couple of short runs near home. Feed the GS350 premium, natch.

Where it's built: Aichi, Japan.

How it's built: Consumer Reports predicts the GS350 reliability to be a 5 out of 5.

In the end: If you're in the market for a luxury sedan with comfort, some decent handling, and a good chance at longevity, the end of the GS line may give you a shot at a bargain and a Lexus without a stereo touchpad control.

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Fast-Tracking Covid Vaccine ‘Is Not That Straightforward’ – TheStreet

September 13th, 2020 2:52 am

Creating a vaccine that would be injected into the arms of millions of people is a usually a years-long endeavor. Not only is the process slowed by trial and error and first-time failures, it's also traditionally restricted by rigorous clinical trials that in their final stages can give public health authorities a reasonable idea of whether a vaccine is safe and effective.

But not even a full year after the first infection from the novel coronavirus in China was documented, the White House is now saying a vaccine could be fast-trackedas soon as early November.

A safe, effective shot produced so rapidly would be unprecedented. It could also save tens of millions of Americans from falling ill with Covid-19 and prevent countless deaths. And the U.S. could desperately use a shot in the arm in its losing fight against the outbreak: Nearly 6.5 million Americans have been diagnosed with the virus -- with some severely sickened-- and nearly 200,000 have been killed.

But what if a hastily rolled out vaccine that skips the final stages of study turns out to have unforeseen problems -- either with safety or efficacy? What happens, for example, if millions of vials are distributed of a prematurely OK'd vaccine and then it turns out to be inferior to a better one that completes all trials months later? What if fading antibodies mean a vaccine's protection wears off after only a short time -- a possibility that can't be known with trials only carried out over several months? Would your own physician even recommend a fast-tracked vaccine if it lacked key data that would be typically expected for review?

To sort through these questions, we asked Dr. Otto O. Yang, a veteraninfectious disease expert and medical doctor at the David Geffen School of Medicine at UCLA. Yang specializes in clinical infectious diseases, and his laboratory focuses on T-cell immunology in HIV infection, as it relates to developing immune therapies and vaccines for HIV and other diseases and infections.

While it would be impossible to predict which of the dozens of vaccine candidates might be most likely to see early approval, said Yang, the two leading candidates could be themRNA nanoparticle vaccine byModerna (MRNA) - Get Reportand therecombinant adenovirus one byOxford University and AstraZeneca (AZN) - Get Report.

"From the limited amount of data Ive seen" that's publicly available, said Yang, "it looks like both vaccine candidates generate the right types of antibodies that we would expect to be effective at preventing infection. And, they both generate T-cell responses, which could be effective in more than one way."

But there are many other factors at play in creating a Covid shot -- and there could be unexpected consequences of speeding through vaccine approvals or just running with the first one that looks acceptable.

Yang was reached by phone this week by TheStreetto discuss these vaccine projects, the possibility for a fast-track OK and potential pitfalls. The following is an edited version of the interview.

TheStreet: Specifically, looking at the vaccine project by Oxford University and AstraZeneca, Ive heard some concern that it might prevent the development of full-blown disease in patients, but might not prevent the spread of the virus from one person to another. What are your thoughts?

Yang: Its a theoretical possibility. So, if a vaccine doesnt fully protect somebody from getting infected, its possible they could get a milder infection. Even with the flu vaccine that we get annually, in some cases it appears to make infection milder, even if it doesnt protect you from getting infected. But I think its most likely that even if somebody did get infected, the immune responses that would be put in place by the vaccine would probably reduce symptoms and reduce severity. If so, it would most likely reduce the degree to which somebody is contagious. Its a theoretical concern, but not something that I would be that worried about.

TheStreet: In a general sense, weve seen reports about, and youve researched, the potential for fading of antibodies. Is there a concern that there could be a vaccine that is safe and it seems to work and then, say six months down the road, somebody gets infected, though they were vaccinated?

Yang: Its definitely a possible scenario. Potentially dropping antibodies might mean that immunity will wane, but its not entirely clear that thats true. The fact is that immunology is kind of a black box and we dont know for sure that antibodies are the whole story for protecting somebody from infection. The data are worrisome that protection will be short-lived for natural infection. And there recently have been increasing news reports of people getting reinfected. That does raise concerns for the longevity of protection from a vaccine, and, of course, short-term vaccine trials are not going to be able to tell us about longevity.

That does raise concerns for the longevity of protection from a vaccine, and, of course, short-term vaccine trials are not going to be able to tell us about longevity.

But one of the big unknowns is whether the vaccine could actually do a better job at making antibodies or T-cell responses than natural infection itself. The study that we did on dropping antibodies was on people who were naturally infected and had fairly mild disease. It is clear that people with more severe infection have fairly high antibody levels, so a vaccine could look more like that like a person who has a more severe infection and fairly high levels of antibodies.

The other thing is, we dont know if the virus actually has mechanisms to interfere with immune response. Many viruses have evolved to have ways to blunt the immune response to enhance their survival. From an evolutionary standpoint, if the immune system is trying to do something to reduce the virus, then the virus can evolve to counter that. If thats the case with this virus if immune response is short-lived because the virus is actively doing something to the immune system to cause that a vaccine could theoretically do better, because the vaccine is not the whole live virus. It might not have that negative impact on the immune system. Well have to just wait and see.

TheStreet: Do you think fast-tracking a vaccine by, say, skipping or shortening the final clinical trials, would be warranted? Hong Kong, Taiwan, New Zealand, China and many other countries have proven that the spread of Covid-19 can be mostly controlled with public health measures.

Yang: So, theres the ideal, theoretical answer, and theres the practical answer. Unfortunately, we are much less like Taiwan or New Zealand, than we are like Brazil. From the standpoint that this country has been unable to implement effective public health measures, for whatever reason, that makes the urgency for a vaccine higher. Ideally, we would be able to get the pandemic under control to an acceptable level and take our time with the vaccine. But theres added urgency, because, for various reasons, were unable to do that theres not enough public buy-in, theres not enough political leadership. Whatever the reasons, were unable to contain it, and the pandemic is just burning on and lives are being lost, so that adds greater urgency for a vaccine

TheStreet: Would you take a fast-tracked vaccine would you recommend it to friends or family?

Yang: It would really depend on what data were available ... safety data being No. 1., and, of course efficacy. I would say that I would certainly be cautious and hesitant, because I feel that the Food and Drug Administration has lost a lot of its credibility, because of its bowing to political pressures. Its already made major fumbles during this pandemic. So I would go with what experts say, and if there is not enough available data to make me feel comfortable to recommend it, then I would say dont take it. Because, as you pointed out, with the right measures, you can prevent spread and you can(potentially)protect yourself from getting infected. So, until its clear that a vaccine is safe and effective, we can each protect ourselves.

TheStreet:That brings up another question. Lets say a vaccine is fast-tracked and millions of doses are produced, and, then, say, several months later, a problem is discovered with the vaccine. At the same, lets say, another vaccine that finishes all its trials comes along and it looks great. Would that pose a logistical problem for distributing the latter, better vaccine could it cause a vaccine production traffic jam?

Yang: Yes, in more ways than one. Lets, for argument, say one vaccine is 50% effective and the other is 75% effective, what do you do? What do you do with all these 50% effective vaccine vials you have sitting around? Is there going to be motivation to get them out and get them used? It raises all sorts of questions about what would happen. What would be the threshold for saying you just throw out the first vaccine which would be at a huge cost? Another point to raise is potentially the first vaccine could interfere with the second. The first vaccine might steer your immune responses in ways that are less effective than the second would have. To some extent, the immune system tends to be trained in a certain way, and once its trained, its hard to get it to change. Theoretically, there could be interference.

Potentially the first vaccine could interfere with the second.

Theres a concept in immunology called original antigenic sin. The concept is that the immune system tends to want to react to something the same way every time, so if you challenge it with something that looks very similar, but is not exactly the same, it will still stick to the original way that it responded. That is the explanation for Dengue fever. Dengue fever is a disease where you get very mild illness the first time you are exposed, and if you get exposed again, to a second strain, then you can get hemorrhagic Dengue fever, which is a very severe, life-threatening infection, and that is because the immune system is still stuck on the first strain and unable to adapt to the second strain. So, you can see something like that happening, as well. Its not that straightforward.

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Fast-Tracking Covid Vaccine 'Is Not That Straightforward' - TheStreet

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$3.7 million grant awarded to UAB to study antiviral therapies and accelerated aging – The Mix

September 13th, 2020 2:52 am

A new grant will look at the effects of aging caused by antiviral therapies in individuals with HIV.

People living with HIV are fortunate that effective therapies are now available that dramatically reduce mortality for those infected with that virus. Despite the effects of antiviral therapy on longevity, people living with HIV are showing signs of accelerated aging.

University of Alabama at Birmingham College of Arts and Sciences Department of Biology Chair Steve Austad, Ph.D., received a National Institutes of Health five-year grant for $3.7 million to study the intersection of HIV and aging.

People with HIV using antiviral therapy are experiencing earlier onset of age-related diseases including heart disease, cancer and dementia. The grant through a collaboration of multiple institutions led by UAB, the University of Washington and Wake Forest University is designed to provide interdisciplinary training to researchers and clinicians in both HIV and aging biology. Investigators will use the knowledge gained from research working at the junction of aging and HIV biology to improve clinical treatment and care of people living with HIV.

Further, the grant will provide pilot grant support for projects involving molecular links between HIV infection and aging. Researchers will collaborate with the UAB Center for AIDS Research and the McKnight Brain Institute.

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Fauci says it may take more than a year to return to ‘a degree of normality’ | TheHill – The Hill

September 13th, 2020 2:52 am

White House coronavirus advisor Anthony Fauci on Friday said life may not get back to normal in the U.S. until late 2021 when a COVID-19 vaccine could be widely distributed.

During an interview with MSNBCs Andrea Mitchell Reports, the nations top infectious diseases expert said hes confident a vaccine could receive emergency use authorization from the U.S. Food and Drug Administration by the end of this year or early 2021, but it will take some time before it becomes widely available.

Our country is in a historic fight against the Coronavirus. Add Changing America to your Facebook or Twitter feed to stay on top of the news.

By the time you mobilize the distribution of the vaccinations, and you get the majority, or more, of the population vaccinated and protected, thats likely not going to happen to the mid or end of 2021, Fauci told MSNBCs Andrea Mitchell.

If you're talking about getting back to a degree of normality which resembles where we were prior to COVID[-19], it's going to be well into 2021, maybe even towards the end of 2021, he said.

Movie theaters, gyms and other public spaces are reopening in some states, and New York Gov. Andrew Cuomo this week announced New York City would resume indoor dining with limited capacity on Sept. 30. New York has managed to keep its coronavirus infections rate under 1 percent for more than 30 days.

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Fauci said he had some concerns about restaurants reopening.

If you go indoors in a restaurant, whatever capacity, 25, 50 percent or what have you, indoors absolutely increases the risk, Fauci said. I am concerned when I see things starting to move indoors, and that becomes more compelling when you get into the fall into winter season when you essentially have to be indoors.

He said areas that want to get back to being able to sit inside a restaurant should get the community level of infection to the lowest level possible.

Coronavirus cases in the U.S. have plateaued around 40,000 daily new cases and 1,000 deaths a day. Fauci during a panel discussion with doctors from Harvard Medical School Friday said that number is still an unacceptable baseline and hed like to see the number of daily cases fall to 10,000 or less.

As of Friday, more than 6.4 million people in the U.S. have been infected with COVID-19 and more than 192,000 have died, according to Johns Hopkins University data.

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Fauci says it may take more than a year to return to 'a degree of normality' | TheHill - The Hill

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More than 500,000 children in the U.S. have tested positive for coronavirus since pandemic began, report finds | TheHill – The Hill

September 13th, 2020 2:52 am

More than500,000 children in the U.S. have tested positive for the coronavirus since the pandemic began, according to a report from the American Academy of Pediatrics (AAP).

The AAP report found children represent about 9.8 percent of the more than 6.3 million coronavirus cases recorded in the U.S. The report includes data from 49 states, New York City, Washington, D.C., Puerto Rico and Guam.

Our country is in a historic fight against the Coronavirus. Add Changing America to your Facebook or Twitter feed to stay on top of the news.

More than 70,000 coronavirus infections were recorded among children in the two weeks between Aug. 20 and Sept. 3, bringing the total number of cases in kids to more than 513,000. Puerto Rico, as well as Montana, North Dakota, South Dakota, Missouri, Kentucky and Indiana showed the highest increases.

Nine states tallied more than 15,000 cases in children while half of states reported 7,000 child cases.

The AAP said data from 42 states and New York City showed 103 children died from COVID-19 between May 21 and Sept. 3, making up just 0.07 percent of total coronavirus deaths in the U.S. Only 0.02 percent of child coronavirus cases resulted in death.

At this time, it appears that severe illness due to COVID-19 is rare among children, the AAP report said. However, states should continue to provide detailed reports on COVID-19 cases, testing, hospitalizations, and mortality by age and race/ethnicity so that the effects of COVID-19 on childrens health can be documented and monitored.

Evidence suggests children who contract the virus are less likely to experience serious illness than adults. There have been several instances in which children who tested positive for the coronavirus also developed a rare inflammatory illness.

The report from the AAP was released as millions of kids made their way back to school this week for the fall semester.

WHAT YOU NEED TO KNOW ABOUT CORONAVIRUS RIGHT NOW

MAJORITY OF AMERICANS FEAR POLITICAL PRESSURE WILL RUSH CORONAVIRUS VACCINE

HALF OF US HOUSEHOLDS IN THE FOUR LARGEST CITIES STRUGGLE TO PAY BILLS AMID PANDEMIC

FAUCI SAYS US HIT HARD BY CORONAVIRUS BECAUSE IT NEVER REALLY SHUT DOWN

HERD IMMUNITY EXPLAINED

FAUCI: WHY THE PUBLIC WASNT TOLD TO WEAR MASKS WHEN THE PANDEMIC BEGAN

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More than 500,000 children in the U.S. have tested positive for coronavirus since pandemic began, report finds | TheHill - The Hill

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Vaping by US teenagers saw steep drop this year: survey | TheHill – The Hill

September 13th, 2020 2:52 am

E-cigarette use among U.S. youth fell this year for the first time in three years following last years outbreak of vaping-related illnesses and deaths. But officials warn rates still remain unacceptably high, according to a federal report released Wednesday.

A national survey foundless than 20 percent of high school students and 4.7 percent of middle school students recently used e-cigarettes and other vaping products. Thats a decline from the 27.5 percent of high schoolers and 10.5 percent of middle school students who said they vaped in 2019.

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The National Youth Tobacco Survey conducted in partnership with the U.S. Food and Drug Administration (FDA) found about 3.6 million youth in the U.S. reported using e-cigarettes this year, a drop from 5.4 million last year.

Teen rates fell between 2015 and 2016 before spiking.

Expertsbelieve media reports about vaping-related illnesses likely contributed to the decline in use among teens, as well as flavor bans and higher age limits.

A series of cases were reported last year in which teens fell ill and even died due to vaping injuries.

Although the decline in e-cigarette use among our Nations youth is a notable public health achievement, our work is far from over, the Centers for Disease Control and Prevention (CDC) Director Robert Redfield said in a statement. Youth e-cigarette use remains an epidemic, and CDC is committed to supporting efforts to protect youth from this preventable health risk."

Officials found that pre-filled cartridges remained the most commonly used product, but disposable e-cigarette use increased 1,000 percent among high school students and 400 percent among middle school students since last year. Most users reported using flavored e-cigarettes, and the use of menthol flavor was prominent.

The FDA earlier this year prohibited flavors such as candy, fruit and mint from small vaping devices like Juul. The policy, however, exempted disposable e-cigarettes that often contain fruity flavors.

Health advocates said the Trump administration missed the opportunity to make greater progress against youth vaping when it failed to clear the market of all e-cigarettes.

The evidence couldnt be clearer: As long as any flavored e-cigarettes are left on the market, kids will get their hands on them and we will not solve this public health crisis, Matthew Myers, president of Campaign for Tobacco-Free Kids, said in a statement.

The annual survey includes more than 20,000 middle and high school students. This years survey was shortened due to the coronavirus pandemic, but researchers said they gathered enough information to be comparable to past years. They said it is unclear how the COVID-19 outbreak is affecting youth vaping.

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How to live longer – the very best exercise to add years onto your lifespan – Express

September 13th, 2020 2:52 am

Maintaining a healthy lifestyle, including a well-rounded diet is crucial to prolonging your lifespan.

You could also boost your lifespan by doing regular exercise. Its the miracle cure weve all been waiting for, according to the NHS.

Making some small diet or lifestyle changes could help to increase your life expectancy and avoid an early death.

One of the best ways to make sure that you live longer is to regularly play tennis, it's been revealed.

READ MORE: How to live longer - flowers to boost longevity

But playing any team-based sport could also have a lasting effect on your lifespan, they added.

The social aspect to these types of activities may be the key to increasing the length of your life.

For both mental and physical well-being and longevity, were understanding that our social connections are probably the single-most important feature of living a long, healthy, happy life, says study cardiologist, Dr James OKeefe.

If youre interested in exercising for health and longevity and well-being, perhaps the most important feature of your exercise regimen is that it should involve a playdate.

Meanwhile, you could also make sure that you live longer by making just a few changes to your daily diet.

Olive oil is one of the best cooking oils to use, as it forms part of a heart-healthy diet, according to medical website WebMD.

All non-tropical vegetable oils, including olive, corn, peanut and safflower oils, have added benefits for your heart.

A heart-healthy diet could also help patients to lose weight, if they're overweight.

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Patenting Stem Cell Inventions in India- What to Expect? – Lexology

September 13th, 2020 2:51 am

Stem cells offer hope as a promising treatment option for various diseases and are the future of medicine. Embryonic stem cells, have been at the heart of many debates globally, in view of the embryonic destruction or manipulation that their generation may require. Converging between research and law, patent law and policy grant yet throw their own challenges to obtaining exclusivity.

In India, in addition to satisfying the criteria of novelty and inventive step, inventions need to fall outside the realm of Section 3 of the Patents Act, to be patentable. Presenting an additional bar to patentability, Section 3 enlists inventions which are not patentable. Owing to this section it is oftentimes the case that the claim scope granted in India is quite different from that granted in other jurisdictions.

Public order and morality

Over the years, the Indian Patent Offices perspective on the issue of patentability of inventions involving embryonic stem cells, appears to have changed. This change in stance is apparent from the changes in the Manual of Patent Office Practice and Procedure. The 2005 draft of said guidelines treated the use of human or animal embryos for any purpose against public order and morality and prohibited the same from patentability. This restriction however, was removed from the subsequent draft of the guidelines and has not reappeared ever since.

Inspite of this change in the guidelines, the Patent Office till date raises the public order and morality objection under section 3(b) of the Patents Act, on stem cell related inventions (both methods and stem cell products). The concern most frequently expressed is the possibility of destruction of human embryos. The prosecution history of several cases shows that an objection on public order and morality has been raised even if the claims do not call out embryonic stem cells but the specification mentions the possibility of use of embryonic stem cells. The objection is frequently overcome by excluding any reference to embryonic stem cells from the claims and by disclaiming the use of embryonic stem cells in the operation of the invention.

However, the approach of treating stem cell research against public order and morality appears to be in contrast to public policy in India. The National Guidelines for Stem Cell Research (published by ICMR and DBT under the Ministry of Science and Technology) prescribe conditions subject to which research on stem cells should be conducted. The conditions include verification that the blastocysts used are spare embryos. The guidelines also permit establishment of new human embryonic stem cell lines from spare embryos subject to the approval of certain committees. Clearly, these government guidelines permit safe and responsible stem cell research, including research on embryonic stem cells.

Moreover, it is a well-known fact that not every invention involving embryonic stem cells would necessitate destruction of human embryos and a lot of research is based on embryonic stem cell lines. Therefore, the indiscriminate imposition of objections under Section 3(b) requires change.

Parts of Plants or Animals and Products of Nature

While claims relating to methods of isolation and propagation of stem cells are frequently granted, the Indian Patent Office appears to have never granted even a single application with claims directed to stem cells per se.

This brings us to another common objection frequently encountered in stem cell applications, namely, Section 3(j) which prohibits from patentability plants and animals in whole or any part thereof other than micro-organisms but including seeds, varieties and species and essentially biological processes for production or propagation of plants and animals. Another commonly encountered objection is of Section 3(c) which bars the patentability of any living thing or non-living substance occurring in nature.

There is no judicial precedent that could throw light on what exactly constitutes parts of plants and animals under Section 3(j). The Patent Office considers any cell or tissue derived from plants or animals as parts of plants or animals leading to refusal of cell claims under this ground. Claims related to compositions comprising stem cells are also frequently refused as the compositions are treated as indirectly claiming stem cells. There have been some exceptions though, such as patent number 333231, where a composition comprising stem cells was granted.

A moot issue here is whether cells are actually parts of animals/plants or whether they can be treated as microorganisms. While the Patents Act permits the patentability of microorganisms (that do not occur in nature), the term microorganism has not been defined in either the Act or the manuals that the Patent Office has issued so far. In fact, even the TRIPS agreement which mandates member states to grant patents in relation to microorganisms does not define the term. The European Patent Office recognizes all generally unicellular organisms with dimensions beneath the limits of vision which can be propagated and manipulated in a laboratory. (T 0356/93) as microorganisms.

Since the Patents Act does not limit the scope of the term microorganism and if one were to accept the literary or dictionary meaning of the term microorganism, it would appear that the Patents Act does not prohibit from the scope of patentability cells, which are not visible to the naked eye or which are so small that they require a microscope for viewing.

Moreover, stem cells like induced pluripotent stem cell and human parthenogenetic stem cells, which are somatic cells or oocytes that have been induced to develop the characteristics of unrestrained propagation and ability to develop into any cell type, are markedly distinct from the parent cell from which they are derived and are new cell types altogether. Such cells are indeed creations of man and cannot qualify as an animal part. They are also not living substances that occur in nature and being purely man made fall outside the prohibitory restraint of Section 3(c).

In the absence of judicial precedents and well defined guidelines, the law in India in relation to patentability of stem cell research is at a nascent stage. The Indian Patent Office has been following an unwritten code in the examination of these applications but the approach currently adopted is debatable. It is important to offer robust patent protection to encourage innovation in all fields. While there has been some change in the Patent Offices approach to patentability of stem cells and claims related to methods of producing, culturing and isolation of stem cells, culture media for stem cells, etc., are commonly granted, there is still a lot that can be patented but is currently not. Hopefully, India will see some judicial precedents in the future that will clarify the patentability issues that this field is struggling with.

This article was first published by Legal Era

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Global Stem Cell Banking Market Is Projected To Witness Vigorous Expansion By 2026 – Kewaskum Statesman News Journal

September 13th, 2020 2:51 am

DBMR has added a new report titled Global Stem Cell Banking Market with data Tables for historical and forecast years represented with Chats & Graphs spread through Pages with easy to understand detailed analysis. this report provides exact information about market trends, industrial changes, and consumer behaviour etc. The report assists in outlining brand awareness, market landscape, possible future issues, industry trends and customer behaviour about industry which eventually leads to advanced business strategies. Being a verified and reliable source of information, this market research report offers a telescopic view of the existing market trends, emerging products, situations and opportunities that drives the business in the right direction of success. The report has been framed with the proper use of tools like SWOT analysis and Porters Five Forces analysis methods.

Global stem cell banking market is set to witness a substantial CAGR of 11.03% in the forecast period of 2019- 2026. The report contains data of the base year 2018 and historic year 2017. The increased market growth can be identified by the increasing procedures of hematopoietic stem cell transplantation (HSCT), emerging technologies for stem cell processing, storage and preservation. Increasing birth rates, awareness of stem cell therapies and higher treatment done viva stem cell technology.

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Competitive Analysis:

Global stem cell banking market is highly fragmented and the major players have used various strategies such as new product launches, expansions, agreements, joint ventures, partnerships, acquisitions, and others to increase their footprints in this market. The report includes market shares of inflammatory disease drug delivery market for Global, Europe, North America, Asia-Pacific, South America and Middle East & Africa.

Key Market Competitors:

Few of the major competitors currently working in global inflammatory disease drug delivery market are: NSPERITE N.V, Caladrius, ViaCord, CBR Systems, Inc, SMART CELLS PLUS, LifeCell International, Global Cord Blood Corporation, Cryo-Cell International, Inc., StemCyte India Therapeutics Pvt. Ltd, Cordvida, ViaCord, Cryoviva India, Vita34 AG, CryoHoldco, PromoCell GmbH, Celgene Corporation, BIOTIME, Inc., BrainStorm Cell Therapeutics and others

Market Definition:Global Stem Cell Banking Market

Stem cells are cells which have self-renewing abilities and segregation into numerous cell lineages. Stem cells are found in all human beings from an early stage to the end stage. The stem cell banking process includes the storage of stem cells from different sources and they are being used for research and clinical purposes. The goal of stem cell banking is that if any persons tissue is badly damaged the stem cell therapy is the cure for that. Skin transplants, brain cell transplantations are some of the treatments which are cured by stem cell technique.

Cord Stem Cell Banking MarketDevelopment and Acquisitions in 2019

In September 2019, a notable acquisition was witnessed between CBR and Natera. This merger will develop the new chances of growth in the cord stem blood banking by empowering the Nateras Evercord branch for storing and preserving cord blood. The advancement will focus upon research and development of the therapeutic outcomes, biogenetics experiment, and their commercialization among the global pharma and health sector.

Cord Stem Cell Banking MarketScope

Cord Stem Cell Banking Marketis segmented on the basis of countries into U.S., Canada and Mexico in North America, Germany, France, U.K., Netherlands, Switzerland, Belgium, Russia, Italy, Spain, Turkey, Rest of Europe in Europe, China, Japan, India, South Korea, Singapore, Malaysia, Australia, Thailand, Indonesia, Philippines, Rest of Asia-Pacific (APAC) in the Asia-Pacific (APAC), Saudi Arabia, U.A.E, South Africa, Egypt, Israel, Rest of Middle East and Africa (MEA) as a part of Middle East and Africa (MEA), Brazil, Argentina and Rest of South America as part of South America.

All country based analysis of the cord stem cell banking marketis further analyzed based on maximum granularity into further segmentation. On the basis of storage type, the market is segmented into private banking, public banking. On the basis of product type, the market is bifurcated into cord blood, cord blood & cord tissue. On the basis of services type, the market is segmented into collection & transportation, processing, analysis, storage. On the basis of source, market is bifurcated into umbilical cord blood, bone marrow, peripheral blood stem, menstrual blood. On the basis of indication, the market is fragmented into cerebral palsy, thalassemia, leukemia, diabetes, autism.

Cord stem cell trading is nothing but the banking of the vinculum plasma cell enclosed in the placenta and umbilical muscle of an infant. This ligament plasma comprises the stem blocks which can be employed in the forthcoming time to tackle illnesses such as autoimmune diseases, leukemia, inherited metabolic disorders, and thalassemia and many others.

Market Drivers

Increasing rate of diseases such as cancers, skin diseases and othersPublic awareness associated to the therapeutic prospective of stem cellsGrowing number of hematopoietic stem cell transplantations (HSCTs)Increasing birth rate worldwide

Market Restraint

High operating cost for the therapy is one reason which hinders the marketIntense competition among the stem cell companiesSometimes the changes are made from government such as legal regulations

Key Pointers Covered in the Cord Stem CellBanking MarketIndustry Trends and Forecast to 2026

Market SizeMarket New Sales VolumesMarket Replacement Sales VolumesMarket Installed BaseMarket By BrandsMarket Procedure VolumesMarket Product Price AnalysisMarket Healthcare OutcomesMarket Cost of Care AnalysisMarket Regulatory Framework and ChangesMarket Prices and Reimbursement AnalysisMarket Shares in Different RegionsRecent Developments for Market CompetitorsMarket Upcoming ApplicationsMarket Innovators Study

Key Developments in the Market:

In August, 2019, Bayer bought BlueRock for USD 600 million to become the leader in stem cell therapies. Bayer is paying USD 600 million for getting full control of cell therapy developer BlueRock Therapeutics, promising new medical area to revive its drug development pipeline and evolving engineered cell therapies in the fields of immunology, cardiology and neurology, using a registered induced pluripotent stem cell (iPSC) platform.In August 2018, LifeCell acquired Fetomed Laboratories, a provider of clinical diagnostics services. The acquisition is for enhancement in mother & baby diagnostic services that strongly complements stem cell banking business. This acquisition was funded by the internal accruals which is aimed to be the Indias largest mother & baby preventive healthcare organization.

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Research objectives

To perceive the most influencing pivoting and hindering forces in Cord Stem Cell Banking Market and its footprint in the international market.Learn about the market policies that are being endorsed by ruling respective organizations.To gain a perceptive survey of the market and have an extensive interpretation of the Cord Stem Cell Banking Market and its materialistic landscape.To understand the structure of Cord Stem Cell Banking Market by identifying its various sub segments.Focuses on the key global Cord Stem Cell Banking Market players, to define, describe and analyze the sales volume, value, market share, market competition landscape, SWOT analysis and development plans in next few years.To analyze competitive developments such as expansions, agreements, new product launches, and acquisitions in the market.To share detailed information about the key factors influencing the growth of the market (growth potential, opportunities, drivers, industry-specific challenges and risks).To project the consumption of Cord Stem Cell Banking Market submarkets, with respect to key regions (along with their respective key countries).To strategically profile the key players and comprehensively analyze their growth strategiesTo analyze the Cord Stem Cell Banking Market with respect to individual growth trends, future prospects, and their contribution to the total market.

Customization of the Report:

All segmentation provided above in this report is represented at country levelAll products covered in the market, product volume and average selling prices will be included as customizable options which may incur no or minimal additional cost (depends on customization)

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Global Stem Cell Banking Market Is Projected To Witness Vigorous Expansion By 2026 - Kewaskum Statesman News Journal

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What Is Covid-19 Doing to Our Hearts? – The New Republic

September 11th, 2020 3:56 pm

Brady Feeney hadnt even taken any classes at Indiana University when he fell ill with Covid-19. Three weeks after he moved to Bloomington, the incoming freshman was in the emergency room, struggling to breathe. Before his illness, Feeney had been a perfectly healthy teenager, with no preexisting conditions. In high school, he was a three-time all-state football player and won two state titles in Missouri. But after two weeks of hell fighting the virus, his mother said, his bloodwork indicated possible heart problems.

When SARS-CoV-2 first struck the United States, the medical community had two working assumptions: First, this was primarily a respiratory disease, and second, it seemed to hit older people much harder than younger people, with eight out of 10 confirmed Covid-19 deaths in the U.S. happening in adults 65 or older. But now, new research is challenging both of these assumptions.

Growing evidence suggests that SARS-CoV-2 doesnt only infect the lungs. It also affects the brain, kidneys, and heart. At first, doctors and researchers wondered if these issues beyond the lungs came just from the stress of having Covid-19 and being on a ventilator or life support. But increasingly, research indicates that the virus may be attacking other organs in the body directlyand this may be more common than previously thought, even among those who arent sick enough to be hospitalized. Some have suggested that Covid-19 is actually a blood vessel disease; the lungs are merely the way the virus enters the body, but from there it gets into the bloodstream and takes up residence in major organs, leaving patients with complex, long-lasting symptoms. Moreover, experts now believe, healthy young people can get mild cases of the coronaviruseven not knowing they were sickthat could leave them with lasting cardiovascular damage. Even those who seem to have recovered from the deadly respiratory illness are not free of its complications.

Heart failure could be the next chapter of the coronavirus illness, Dr. Gregg C. Fonarow, interim chief of UCLAs Division of Cardiology, recently argued in a co-authored editorial in the journal JAMA Cardiology. Even if in younger adults Covid-19 may not be fatal, there still may be important health consequences, he told me.

Myocarditis, or inflammation of the heart, is usually a rare condition that can occur with viral infections, including the flu. But from the start of the pandemic, doctors were seeing heart inflammation among patients hospitalized with serious cases of Covid-19, Fonarow said: Early research showed that 20 to 30 percent of those hospitalized had heart issues. Left untreated, myocarditis can damage the heart and lead to heart attacks and arrhythmias, among other complications.

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What Is Covid-19 Doing to Our Hearts? - The New Republic

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‘Mini organs’ offer treatment hope for children with intestinal failure study – The Northern Farmer

September 11th, 2020 3:56 pm

Mini organs grown using stem cells from a patients tissue could offer hope for children with intestinal failure, a study suggests.

Scientists at the Francis Crick Institute, Great Ormond Street Hospital (GOSH) and UCL Great Ormond Street Institute of Child Health (ICH) have grown human intestinal grafts using stem cells from patient tissue.

The team hope the findings could one day lead to personalised transplants for children with intestinal failure.

Dr Vivian Li, senior author and group leader of the Stem Cell and Cancer Biology Laboratory at the Crick, said: Its urgent that we find new ways to care for children without a working intestine because, as they grow older, complications from parental nutrition can arise.

Weve set out a process to grow one layer of intestine in the laboratory, moving us a step closer to being able to offer these patients a form of regenerative medicine, which uses materials created from their own tissue.

This would reduce some of the risks that transplant patients face, such as their immune system attacking the transplant.

Children with intestinal failure cannot absorb the nutrients essential for their overall health and development, researchers said.

While they can be fed intravenously, via a process called parenteral nutrition, this is associated with severe complications such as line infections and liver failure, they added.

If complications arise, or in severe cases the children need a transplant, researchers said there is a shortage of suitable donor organs and problems can arise after surgery such as the body rejecting the transplant.

The proof-of-concept study, published in Nature Medicine on Monday, showed how intestinal stem cells and small intestinal or colonic tissue taken from patients can be used to grow the inner layer of small intestine in the laboratory with the capacity to digest and absorb peptides and digest sucrose in food.

The researchers took small biopsies of intestine from 12 children who either had intestinal failure or were at risk of developing the condition.

In the lab they then stimulated the biopsy cells to grow into mini-guts, also known as intestinal organoids, generating over 10 million intestinal stem cells from each patient over the course of four weeks.

The researchers also collected small intestine and colon tissue that would have been discarded from other children undergoing essential surgery to remove parts of their gut.

Using laboratory techniques cells were removed from these tissues leaving behind a skeleton structure which formed scaffolds.

The researchers placed the mini-guts onto these scaffolds where they grew on this structure to form a living graft.

Due to specific culture conditions, the stem cells changed into many of the different types of cells that exist in the small intestine and the grafts were able to digest and absorb peptides, the building blocks of proteins, as well as digest sucrose into glucose sugars.

The authors said research was the first step in efforts to engineer all the layers of the intestine for transplantation in the hope that laboratory-grown organs could offer a safe and longer-lasting alternative to traditional donor transplants.

Senior author Professor Paolo De Coppi, consultant paediatric surgeon at GOSH, said the research was an important step forward in regenerative medicine.

He added: Although this research is in the lab right now, were concentrating on making this a realistic and safe treatment option.

Whats significant here is weve shown that scaffolds can be created using tissue from the colon, not only tissue from the small intestine.

Its an important step forward in regenerative medicine and were optimistic about what this means for patients, but more research lies ahead before we can safely and effectively translate this approach to treatment.

As well as proving that biopsies taken from children could be used to grow functioning intestinal grafts, the researchers said that the grafts can survive and mature when transplanted into mice.

Researchers said the next step was to start growing the other layers of the intestine such as muscle and blood vessels.

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'Mini organs' offer treatment hope for children with intestinal failure study - The Northern Farmer

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Tweet Chat Recap: Evaluating Treatment Approaches for Relapsed/Refractory DLBCL – Targeted Oncology

September 11th, 2020 3:56 pm

Targeted Oncology was joined by Kami J. Maddocks, MD, associate professor of clinical internal medicine, Division of Hematology, The Ohio State University Comprehensive Cancer CenterJames, for the discussion of a 76-year-old man with relapsed/refractory diffuse large B-cell lymphoma (DLBCL) in a recent tweet chat. In this case scenario, the patient presented with stage IV high-risk disease and received R-CHOP (Rituximab [Rituxan], cyclophosphamide, doxorubicin, vincristine, prednisone), and radiotherapy.

Although the treatment appeared well-tolerated, the patient presented with similar symptoms as at diagnosis after completing 6 cycles with complete response to the therapy. According to the work-up, the patient is ineligible for transplant.

The patient was ineligible for stem cell transplantation (SCT), which Maddocks speculates may be due to the patients age, although other considerations could include comorbidities or intolerance to R-CHOP. Eligibility is the first thing she considers for her patients as it is currently the standard of care and the only curative approach for patients to receive salvage chemotherapy followed by consolidation with autologous SCT.

Maddocks told Targeted Oncology, In some patient cases, [the reason for ineligibility] is age even though there's no specific age cutoff, but we know that it's harder on the marrow as patients get older to collect stem cells and get that aggressive salvage chemotherapy. Patient comorbidities [can also impact eligibility], so heart conditions, lung conditions, renal insufficiency can be a problem. Performance status and then lastly, just if the patient had trouble getting to their initial chemotherapy with R-CHOP or had a lot of complications, then it's probably going to be harder for them to tolerate even more aggressive or intensive therapy.

In a twitter poll ahead of the chat, Targeted Oncology asked what the next best line of therapy for this patient might be, with 4 potential different treatment options. The option that drew the most attention, however, was the recently approved regimen of tafasitamab (Monjuvi) and lenalidomide (Revlimid).

Maddocks tweeted, All these options are potential therapeutic choices for this patient, but the combination of tafasitamab/lenalidomide is the only option approved in this setting. The treatment has a promising ORR [overall response rate], and CR [complete response], and the remissions for patients who respond are durable!

During the tweet chat, Maddocks reviewed each of the different treatment options in the poll, and why she selected this combination regimen as the next best line of therapy for this particular patient. Following the chat, she spoke with Targeted Oncology to share further insights on each of these therapeutic approaches and the importance of the FDAs approval of tafasitamab plus lenalidomide in this setting.

The combination of tafasitamab plus lenalidomide held the majority vote, which Maddocks agreed would be the next best line of therapy for this patient.

For patients who are not candidates or considered eligible for a salvage chemotherapy followed by autologous SCT, the tafasitamab/lenalidomide combination was recently approved in the setting of first relapse, and it's the only approved therapy in this setting, Maddocks said. Historically, we would give some sort of palliative chemotherapy approach if patients were candidates and interested in pursuing therapy, or consideration of clinical trial, but this is the only therapy approved in this setting.

The approval of tafasitamab in combination with lenalidomide includes an indication for patients who are not eligible for autologous SCT, as describes the patient in our case. This regimen was approved on the basis of the phase 2 L-MIND (NCT02399085) clinical trial, which explored this use of this regimen in 81 patients with relapsed/refractory DLBCL. Two-year follow-up demonstrated an ORR of 58.5%, which included CRs in 41.3% of patients and partial responses (PRs) in 17.5% of patients. In addition, 15.0% achieved stable disease, and the median duration of response was 34.6 months (95% CI, 26.1-34.6).1

I think this patient case is the perfect example of where this can fit into the treatment landscape, Maddocks explained. For patients who first relapse from the standard R-CHOP therapy, the toxicities were generally manageable, and with the response rate, this is a great option for patients at first relapse who are not going to be candidates for a transplant. I think maybe patients who go on to get palliative chemotherapy or maybe patients who get treatment with plans to go to transplant but just don't tolerate it and dont look like they're going to [undergo] aggressive therapy, this may be an option for those patients too, understanding that there is some role for CAR T in a set of those patients.

This study, which was presented during the 25th Congress of the European Hematology Association (EHA), demonstrated that the majority of toxicities were hematologic, and most were reversible. The most common grade 3 hematologic treatment-emergent adverse events (TEAEs) were neutropenia in 49.4% of patients, thrombocytopenia in 17.3%, and febrile neutropenia in 13.2%.1

These were able to be managed by holding the dose growth factor, and there was a population of patients who had to be dose-reduced on the lenalidomide. The starting dose was 25 mg, so the majority were able to maintain 20 mg if they were dose-reduced, although a few had to be reduced more than once, Maddocks said. The most common grade 3/4 or serious AEs were infection, probably not surprisingly, and overall, that's probably similar to what you see with other options in this setting. There was a small number of infusion reactions, but these were all grade 1 in the trial and were easily managed.

Non-hematologic TEAEs of grade 3 included pneumonia in 8.6% of patients and hypokalemia in 6.2%. Serious AEs reported included pneumonia in 8.6%, febrile neutropenia in 6.2%, and pulmonary embolism in 3.7%, as well as bronchitis, lower respiratory tract infection, atrial fibrillation, and congestive cardiac failure in 2.5% each.1

Given the safety profile of this combination of tafasitamab plus lenalidomide, this regimen is particularly suitable for a large proportion of patients with DLBCL, Gilles Salles, MD, PhD, lead author of L-MIND, toldTargeted Oncology. We do know that the median age of occurrence of DLBCL is in the late 60s, and there are many, many patients that are over 70 and that are not usually transplant eligible. Clearly this is a great opportunity for patients to receive this non-cytotoxic regimen.

Although this regimen is an exciting opportunity for patients with DLBCL and relapsed/refractory disease, 1 challenge that needs to be addressed is the potential use of tafasitamab plus lenalidomide in sequence with CAR T-cell therapy. There is very little experience, if any, of patients receiving the combination regimen after receiving CAR T-cell therapy. The combination and CAR T cells both target the same antigen, CD19, which can be problematic. As its known that some patients will lose CD19 expression on CAR T-cell therapy, the regimen may no longer be an effective treatment option.

For those patients that had failed CAR T-cell therapy, substantial proportions, about 30% of them, may have lost CD19 expression and then may not be eligible anymore for this regimen. There is, however, a substantial proportion of patients that retains CD19 and in whom tafasitamab/lenalidomide can be used as a treatment option, Salles commented.

A large proportion of patients will maintain CD19 expression following CAR T-cell therapy, so tafasitamab plus lenalidomide may still be effective in a percentage of patients.

Its hard to say because we dont have a lot of data, but we do know there are other CD19-directed therapies outside of CAR T cell development, Maddocks told Targeted Oncology. I think in the next few years, were going to see patients treated both pre- and post-CAR T with other CD19-directed therapies, and well have more information on this.

The combination of polatuzumab vedotin (Polivy) plus bendamustine (Bendeka) and rituximab (BR) was approved by the FDA as treatment of patients with relapsed/refractory DLBCL after 2 prior lines of therapy in June 2019 based on the findings from the phase 1b/2 GO29365 (NCT02257567) clinical trial. Although this option is also not FDA-approved for the treatment of patients after first relapse, Maddocks noted that this was the only treatment evaluated in a randomized trial. The study had included patients who were ineligible for transplant.

Significant improvements were observed with polatuzumab vedotin plus BR compared with BR alone in an international, multicenter, open-label study, particularly in regard to the ORR, CRs, progression-free survival (PFS), and overall survival (OS). CRs were observed in 40.0% of the patients with the combination versus 17.5% with BR alone. Survival rates favored the combination as well, with a median PFS of 9.5 months with the combination versus 3.7 months with BR alone (HR, 0.36; 95% CI, 0.21-0.63; P <.001) and a median OS of 12.4 months versus 4.7 months (HR, 0.42; 95% CI, 0.24-0.75; P =.002), respectively.2

The addition of polatuzumab did increase toxicity from the standpoint of cytopenias, but that didn't really translate to increased serious infections. It did add neuropathy as a side effect, but most of that was reversible, so I think this was a regimen that, by the addition of polatuzumab, was something that you could offer patients that did give them somewhat of a better overall response and was more durable than just giving them a palliative chemotherapy alone, Maddocks added. This is also a regimen that's been used in patients who were not able to achieve a remission to bridge them to CAR T or in some patients after CAR T, and so I can understand why this was definitely one of the more favorable choices.

In the study, grade 3/4 neutropenia was observed more frequently in the combination arm (42.6%) compared with the BR alone arm (33.3%), but the occurrence of grade 3/4 infections was comparable between the 2 groups (23.1% vs. 20.5%, respectively). In addition, the study authors noted that although many of the fatal AEs occurred after disease progression, 11 patients in the BR arm experienced fatal AEs compared with 9 in the combination arm, infection being the most common, which was the cause in 4 patients in each arm.2

Although the regimen appeared tolerable in this setting, Maddocks tweeted, it is more attractive than chemotherapy alone and understandable why it was chosen [as the second-best option in the Twitter poll].

Among the treatment options considered in our twitter poll ahead of the tweet chat, selinexor (Xpovio) only caught the attention of 16.7% of voters, similar to CAR T-cell therapy. However, both of these options are currently only approved in patients who have received at least 2 prior lines of therapy, which this case did not.

In regard to selinexor in particular, Maddocks tweeted, Looking at the single arm phase 2 data, it also has the lowest overall response rates of all the options listed with an ORR of 28%.

Selinexor received its approval from the FDA in June 2020, which is indicated for the treatment of adult patients with relapsed/refractory DLBCL, not otherwise specified, who have received at least 2 prior systemic therapies. This is the only oral single-agent therapy approved in this setting, and it is also the only nuclear export inhibitor approved by the FDA for use in hematologic malignancies.

The agent was approved on the basis of the phase 2b SADAL clinical trial, which demonstrated an ORR of 29% with 13% CRs and 16% PRs. The responses achieved in the study were durable, which led to a median duration of response of 9.2 months in the overall population (95% CI, 4.8-23.0) and 13.5 months in those who had achieved a CR (95% CI, 9.3-23.0).3

The most common treatment-related AEs were cytopenias and gastrointestinal/constitutional symptoms, which were generally reversible and manageable with dose modifications and/or standard supportive care approaches. The most common on-hematologic AEs, which were mostly grade 1/2, were nausea (52.8%), fatigue (37.8%), and anorexia (34.6%). The most common grade 3/4 AEs included thrombocytopenia (39.4%), neutropenia (20.5%), and anemia (13.4%). No treatment-related grade 5 AEs were observed.

CAR T-cell therapy, on the other hand, offers a unique option to this patient case even though it is still only approved in patients who have progressed or relapsed after 2 prior therapies or SCT. The TRANSCEND-PILOT-017006 (NCT03483103) study is evaluating the potential for CAR T-cell therapy lisocabtagene maraleucel (liso-cel) as treatment of patients with relapsed/refractory aggressive B-cell non-Hodgkin lymphoma who have received at least 1 prior therapy and are ineligible for SCT. While this does appear promising for introducing CAR T-cell therapy earlier on for patients with DLBCL, the treatment is not available off trial and is not a standard approach.

Maddocks told Targeted Oncology, It's very clear who's eligible for autologous transplant by age and comorbidities, but with CAR T, it's not so clear all the time who is going to be a candidate. There's not as great of data or information on who is going to be a candidate for that or not. Probably more patients are going to be a candidate for transplant, but there is still going to be patients that are comorbidities that they're not going to be a candidate for CAR T cells, and while they're approved in this setting and they can be very effective, there's also logistical issues, including that right now there's only certain centers, most often transplant centers, that are able to administer CAR T cells, so the patient has to have access to a center, they have to be able to get through the time that their leukapheresis cells are sent out and then sent back, and there's still barriers to cost and insurance in some patients, too.

This particular patient case does represent a challenge, Maddocks said. Historically, this is not a patient that's going to be a candidate for an autologous SCT, and that's going to be the only curative approach. CAR T is not approved in this setting, which is the other curative approach we know outside of patients who are unable to get to autologous STC, or at least appears to be likely curative for a percentage of patients.

Overall, CAR T-cell therapy is not a viable treatment option for the patient depicted in our tweet chat discussion, although it can still offer curative opportunities to a select group of patients with DLBCL who are ineligible for transplant.

In conclusion, tafasitamab plus lenalidomide helps fulfill the unmet need of patients who are in first relapse but are ineligible for transplant, which is the only curative option for patients with relapsed/refractory DLBCL. Although CAR T cells appear hopeful in this space, more research needs to be done to further determine their role in the treatment paradigm.

When you look at relapsed DLBCL, in general, and have these options, it's exciting for our patients to be able to have these. All of these have come up in the last 1 to 2 years, CAR T being a little bit longer than the other 3 regimens, but they all have offered patients tolerable therapy in the setting of previously not having these options.

Reference

1. Salles G, Duell J, Gonzlez-Barca E, et al. Long-term outcomes from the phase II L-MIND study of Tafasitamab (MOR208) plus lenalidomide in patients with relapsed or refractory diffuse large B-cell lymphoma. Presented at: Presented at: EHA25 Virtual; June 11-21, 2020. Abstract EP1201.

2. Sehn LH, Herrera AF, Flowers CR, et al. Polatuzumab Vedotin in Relapsed or Refractory Diffuse Large B-Cell Lymphoma.J Clin Oncol. 2019;38(2):155-165. doi: 10.1200/JCO.19.00172

3. Kalakonda N, Cavallo F, Follows G, et al. A phase 2b study of selinexor in patients with relapsed/refractory (r/r) diffuse large B-cell lymphoma (DLBCL).Hematol Oncol. 2019;37(S2). doi: 10.1002/hon.31_2629

Continued here:
Tweet Chat Recap: Evaluating Treatment Approaches for Relapsed/Refractory DLBCL - Targeted Oncology

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Roche receives FDA clearance for BK virus quantitative test on cobas 6800/8800 Systems to support better care for transplant patients – Yahoo Finance

September 11th, 2020 3:56 pm

Basel, 8 September 2020 - Roche (SIX: RO, ROG; OTCQX: RHHBY) today announced U.S. Food and Drug Administration (FDA) 510k clearance for the cobas BKV Test on the cobas 6800 and 8800 Systems. The test was previously granted FDA Breakthrough Device designation demonstrating the improved treatment or diagnosis of life-threatening diseases or conditions for transplant patients. The test provides standardised, high-quality results that can help healthcare professionals better assess the risk of complications caused by the BK virus in transplant patients and identify effective treatment options.

BK virus (BKV) is a member of the polyomavirus family that can cause severe transplant-associated complications. Infection can occur without symptoms and happen early in life. After primary infection, the virus can remain inactive, only to possibly reactivate in immunocompromised individuals such as transplant recipients.

Our diagnostic tests can help clinicians greatly improve patient treatment plans and make quick adjustments for personalised healthcare, said Thomas Schinecker, CEO Roche Diagnostics. This FDA clearance allows Roche to offer healthcare professionals a transplant testing portfolio that includes Cytomegalovirus, Epstein-Barr virus and BK virus so they can simultaneously monitor and improve care for transplant patients who are at risk for these common infections or viral reactivations which can cause further illness or death.

The cobas BKV Test is a polymerase chain reaction (PCR) viral load test that runs on the fully automated and widely available cobas 6800 and cobas 8800 Systems. Along with the previously approved cobas EBV and CMV Tests, the cobas BKV Test has been calibrated to the World Health Organization (WHO) International Standard. This means that test results are reported in international units, making it possible for laboratories anywhere in the U.S. to obtain comparable results when measuring levels of BKV DNA.

About the cobas BKV TestThe cobas BKV Test was previously granted Breakthrough Device Designation by the FDA, together with the cobas EBV Test.

The cobas BKV Test is a real-time polymerase chain reaction (PCR) test with dual-target technology that provides quantitative accuracy and guards against the risk of sequence variations that may be present in the BK virus. The cobas BKV Test has robust coverage with a limit of detection of 21.5 IU/mL and an expanded linear range from 21.5 IU/mL to 1E+08 IU/mL in EDTA plasma.

The test offers an alternative to lab-developed tests (LDTs) or Analyte Specific Reagent (ASR) combinations, potentially minimising variability and complexity in testing, reducing workload and alleviating risk for laboratories. The test supports the goal of result standardisation across institutions by providing reproducible, high-quality results for clinical decision-making.

The fully automated cobas BKV Test and the cobas CMV and cobas EBV Tests can run on the cobas 6800/8800 Systems simultaneously, providing absolute automation with proven performance and flexibility, leading to time savings and increased efficiency.

About BK polyomavirus BK polyomavirus (BKV) is a member of the polyomavirus family that can cause transplant-associated complications including nephropathy in kidney transplantation and hemorrhagic cystitis in hematopoietic stem cell transplantation. Infection can occur early in life, often with no symptoms. After primary infection, the virus can remain inactive throughout life, only to possibly reactivate in immunocompromised individuals, such as patients who receive solid-organ transplants. For kidney transplant patients, BKV infection is considered the most common viral complication, causing polyomavirus nephropathy (PVN) in up to 10 percent of kidney transplant recipients, and about 50 percent of PVN-affected patients will experience transplant graft failure.1 BKV is also associated with hemorrhagic cystitis after allogeneic hematopoietic stem cell transplantation.2

About the cobas 6800/8800 SystemsWhen every moment matters, the fully automated cobas 6800/8800 Systems offer the fastest time to results with the highest throughput and the longest walk-away time available among automated molecular platforms. The systems provide up to 96 results in about three hours and 384 results for the cobas 6800 System and 1,056 results for the cobas 8800 System in an eight hour shift.*

Both systems make it possible for labs to perform up to three tests in the same run with no pre-sorting required. The systems also enable up to eight hours (cobas 6800 System) and four hours (cobas 8800 System) of walk-away time with minimal user interaction.*

These real-time PCR systems serve the areas of infectious disease, donor screening, sexual health, transplant, respiratory and antimicrobial stewardship.

Through an ever-increasing worldwide install base of cobas 6800/8800 Systems, labs are quickly and easily processing millions of tests per month to meet the changing demands of their communities, their customers, and the patients relying on the results of each assay. Globally, labs know and trust that a Roche assay guarantees high precision, accuracy, and traceability to World Health Organization standards.

Today, rapid advancements in healthcare technology, a shortage of skilled workers, industry-wide consolidation, and the proven need to be ready for the next outbreak have health systems looking to lay a reliable foundation for the future. With proven performance, absolute automation, and unmatched flexibility delivering unparalleled throughput 24/7cobas 6800/8800 Systems are designed to ensure a labs long-term sustainability and success now, more than ever.

Learn more now: http://www.cobas68008800.com or http://diagnostics.roche.com.*May vary based on workflow demands

About RocheRoche is a global pioneer in pharmaceuticals and diagnostics focused on advancing science to improve peoples lives. The combined strengths of pharmaceuticals and diagnostics under one roof have made Roche the leader in personalised healthcare a strategy that aims to fit the right treatment to each patient in the best way possible.

Roche is the worlds largest biotech company, with truly differentiated medicines in oncology, immunology, infectious diseases, ophthalmology and diseases of the central nervous system. Roche is also the world leader in in vitro diagnostics and tissue-based cancer diagnostics, and a frontrunner in diabetes management.

Founded in 1896, Roche continues to search for better ways to prevent, diagnose and treat diseases and make a sustainable contribution to society. The company also aims to improve patient access to medical innovations by working with all relevant stakeholders. More than thirty medicines developed by Roche are included in the World Health Organization Model Lists of Essential Medicines, among them life-saving antibiotics, antimalarials and cancer medicines. Moreover, for the eleventh consecutive year, Roche has been recognised as one of the most sustainable companies in the Pharmaceuticals Industry by the Dow Jones Sustainability Indices (DJSI).

The Roche Group, headquartered in Basel, Switzerland, is active in over 100 countries and in 2019 employed about 98,000 people worldwide. In 2019, Roche invested CHF 11.7 billion in R&D and posted sales of CHF 61.5 billion. Genentech, in the United States, is a wholly owned member of the Roche Group. Roche is the majority shareholder in Chugai Pharmaceutical, Japan. For more information, please visit http://www.roche.com.

All trademarks used or mentioned in this release are protected by law.

References[1] Jamboti, J. S. (2016) BK virus nephropathy in renal transplant recipients. Nephrology, 21: 647 654. doi: 10.1111/nep.12728. [2] Hirsch HH, Randhawa PS; AST Infectious Diseases Community of Practice. BK polyomavirus in solid organ transplantation-Guidelines from the American Society of Transplantation Infectious Diseases Community of Practice. Clin Transplant. 2019;33(9):e13528. doi:10.1111/ctr.13528

Roche Group Media RelationsPhone: +41 61 688 8888 / e-mail: media.relations@roche.com

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Coronavirus, Charity, and the Trolley Problem – Crooked

September 11th, 2020 3:56 pm

I signed up to be a bone marrow donor in 2016, after an anonymous strangers marrow saved my father. It started out easy enough: The registry mailed me a kit to swab my cheeks, I mailed it back, and then I heard nothing for years. This wasnt unusual. Marrow transplantation requires finding complex and rare genetic matches; according to Be The Match, only about one out of every 430 people who sign up will ever go on to donate. I expected it would be a while before I got to pay my dads transplant forward. It did not occur to me that my opportunity might arise at the height of a global coronavirus pandemic.

The coronavirus created a tangle of moral dilemmas that most Americans never expected to face. At the extremes, weve resolved these dilemmas easily. Weve designated whole categories of labormostly underpaid, perennially underappreciatedessential because we accept that even with a plague lurking, people must eat and medicate and have working showers in which to cry. On the opposite end of the spectrum, weve trained our online shaming apparatus on the most reckless and selfish offendersthe wealthy New Yorkers who fled to the Hamptons, the house parties posted to Instagram with weak defensive captions (we only took our masks off for the body shots).

The longer we live in the shadow of an uncontained virus, the more agonizing the in-between dilemmas become. How long should people be expected to remain isolated from their loved ones? Is there a point at which the negative effects of physical distancing begin to outweigh the toll of the disease itself? On the one hand, we should do everything in our power to protect the most vulnerable in our communities. On the other hand, what should we tell the vulnerable seniors who feel they dont have endless spare months to let pass without embracing their grandchildren? Are our individual mitigation responsibilities lessened by the fact that we all made sacrifices to buy an incompetent president time to get this under control, and he squandered it? Are we that much more obligated to pick up the slack?

In some sort of sick philosophical joke, the moral waters get even murkier when you throw altruism into the mix. For all of the guidance reminding us of the impact of our selfish choices on strangersyou might not kill your own grandmother by going to that dive bar, but think of the bartenders roommates grandmothermoral experts have had far less to say about the boundaries around charitable acts. How should we think about helping strangers when doing so requires a dangerous level of social interaction? How should we measure the suffering of the people we want to help against the harm we risk causing to unseen others in the process? That quandary leads to another awful question that most people should never have to confront: When does human life become too risky to save?

Be The Match first notified me that it had identified me as a potential match in June, when coronavirus cases in Los Angeles, where I live, had just begun to spike. By the time I was confirmed as the patients best match and asked to proceed with a donation several weeks later, the city had become a full-blown hotspot. The idea of navigating the whole process in plague conditions made me nervous, but underneath the anxiety was a distinct whiff of relief. Like a lot of people, Id spent the last few months in a horrified daze, helpless to do anything but stay home, donate money, and cyberbully the mayor. Here, finally, was a task that felt equal to the urgency of the moment. Here was somethingsomeonereal. I just wasnt allowed to know who.

Be The Match will put donor and recipient in contact one year after the transplant, if both have consented; until then, everything is completely anonymous. I was told that my recipient was a man in the United States, along with his age (surprisingly young), and diagnosis (a type of blood cancer). Because matches are typically found within shared ancestries, I assume that he is, like me, an Ashkenazi Jew, and because he needed a bone marrow transplant, his situation must have been dire.

Fortunately, helping people like him has become simpler. When most people think of donating for a bone marrow transplant, they imagine general anesthesia; a very big needle; a painful recovery. This is one of the two ways to donate, but its grown much less common. Ninety percent of donors (including me) are instead asked to donate peripheral blood stem cells (PBSC), through a process called apheresis. While a donor is awake and watching Party Down, their blood flows through a tube attached to one arm, gets spun around in a centrifuge that separates out the extra blood-forming stem cells, and is returned through a tube into the other arm. This can take several hours, but its painless, and neednt even happen at a hospital. Usually.

(Sarah Lazarus)

On August 13, two nurses met me at the San Bernardino blood bank where I was scheduled to donate later that month. We were all there for an assessment, to make sure my arm veins could handle the apheresis needles. It was a weird little ritual. The two women bent on either side of me, intently tapping along my upturned arms in total silence as if waiting for something to tap back. They then switched sides, tapped the opposite arm, and issued their verdict: Too small. I would need to donate through a central line placed in one of my larger veins, and that could only happen at a hospital. I would probably be sent to a medical center two hours south in La Jolla, they told me.

This was a complication, but not necessarily a big deal. Be The Match footed the bill for all of my donation-related expenses, including the fancy car service that seemed safer, COVID-wise, than using Lyft. (I am a genius who moved to Los Angeles without a drivers license. A worse essay for another time.) Donating at the La Jolla hospital would mean a longer commute, maybe even one night in a hotel, but that was about it.

Later that morning I was waiting for my next appointment at an urgent care center when Heather, my donor coordinator, called to tell me that La Jolla didnt have an opening on the right day. Neither did the next-closest option, she told me as I paced around the parking lot, and the patients team couldnt shift his treatment schedule.

So my question for you is, would you feel comfortable flying to Boise, Idaho?

I went back inside to the busy waiting room and reclaimed my seat. Across the room, a man in a UPS uniform freed his nose to rest obscenely on top of his mask. I hunched over my phone and googled, Boise coronavirus. My phone informed me that it was dying. The UPS man coughed. On a TV in the corner, the president admitted he was sabotaging the post office to steal the election. I googled, airports coronavirus. At last, a nurse called me back and started checking my vitals.

Your heart rate is really elevated, she said, frowning at the reading. Any idea why?

As of this writing, Be The Matchs COVID-19 FAQ page was last updated on April 6. Heres part of the section on air travel:

Q: Are there alternatives to donors traveling for donation?A: Possibly. If you feel uncomfortable traveling, we respect your decision. However, it is extremely important that you tell us right away so we can look for alternatives. Donation is time-sensitive, and any delay can have a negative impact on the recipients wellbeing. It may be possible to arrange for donation to occur somewhere within driving distance.

There was an alternative to Boise, it turned out, if I felt uncomfortable. I could donate at the La Jolla hospital a day later than originally planned. My cells would be cryogenically frozen and given to the patient a week or two later, instead of immediately. Heather told me that the patients team preferred me to stick with the original date, that a delayed transplant would be riskier for him, but, for confidentiality reasons, they couldnt tell me how much riskier.

We dont want you to feel pressured, Heather emphasized. You should only agree to travel if you feel comfortable.

Did I feel comfortable? It depended on the circumstances, which I wasnt allowed to know. The window of risks were willing to take expands as the stakes get higher; anyone who showed up to a Black Lives Matter protest this summer or signed up to be a poll worker this fall can attest to that. I wouldnt feel at all comfortable flying for the heck of it, but I would certainly do it to save a life. This fell somewhere on the vast spectrum in between, but I had no idea where.

How do you make a call about your personal risk tolerance when its also a choice about the course of a strangers cancer treatment? If the pandemic had taught us all a valuable lesson about the interconnectedness of our fates, I was now being beaten over the head with it. Stuck without enough facts to make an informed decision, I thought about my dads old hospital room in Baltimore, the airlock separating his ward from the rest of the building because any mundane microbe could kill the patients on the other side. I imagined a somber-looking doctor walking through those doors to give my vulnerable recipient the news.

Im afraid theres been a change of plans, he would say, removing his glasses. It seems your donor is a pussy-ass bitch.

I called Heather back and told her to arrange my donation in Boise.

In most respects, my pre-donation medical screening was extremely, almost ludicrously thorough. I submitted vials and vials of blood to check for a host of diseases and disorders. I peed in a cup to make sure I wasnt pregnant. I had more blood drawn, to make sure I really wasnt pregnant. After the second pregnancy test confirmed the results of the first pregnancy test, I got the following email from Heather:

The result of your repeat pregnancy test on 8/13 was negative, but we are still required to complete our pregnancy assessment with you today. The assessment consists of a single question Is there any chance you could be pregnant? Please respond via email when convenient.

I have not touched another person in five months, I wrote back.

Thank you for completing the pregnancy assessment, Heather replied.

In one respect, my pre-donation medical screening seemed oddly lax. I wasnt tested for coronavirus until the day before my flight, and only then because I panicked.

(Sarah Lazarus)

The PBSC donation process begins in earnest a few days before the stem cells are actually collected, with five rounds of filgrastim injections. Its a drug normally given to cancer patients to bring up low white-blood cell counts after chemo or radiation. In my case, it would send my healthy bone marrow into overdrive, to produce enough cells for the donation. The injections have a few side effects: bone pain, fatigue, headaches, nausea. Essentially, filgrastim makes you feel like you have the flua particularly special feeling in the year of our lord 2020. My side effects were mild and I knew to expect them, and I was managing them fine until an extra one showed up.

The night after receiving my second round of shots, I went for a walk around my neighborhood. It was a hot night, and I was tired and achy from the medication; this was not a fast walk. And yet within a few blocks I noticed that my breathing was quick and shallow, and my heart was pounding as if Id just run a sprint. When I tried to take a deep breath, it felt like there was an elastic band cinched around my chest.

Shortness of breath was not on my list of filgrastim side effects. Neither were the heart palpitations, which continued long after I went home and collapsed on my bed.

I put an empty Gatorade bottle on my stomach and watched it pulse up and down as I considered how fucked I was. I had assumed my fatigue and body aches were side effects; what if those were symptoms, too? I mentally tallied up my appointments from over the past week. I had been to five different medical facilities, been a passenger in three different cars. Of course I had caught it. How stupid to think I wouldnt catch it.

The timing was a nightmare. At some point while I was receiving the filgrastim injections, the patient began a course of high-dose chemo to kill off his own blood-forming stem cells in preparation for the transplant. If I had to back out of donating after that treatment began, the patient would die quickly.

For a few desperate minutes, I thought about keeping these symptoms to myself. I didnt have a fever. As long as I didnt develop one, maybe I could get to Boise and finish the donation leaving no one the wiser. What was the moral math, I wondered, of proceeding with travel plans that might seed multiple new outbreaks (but also might not) and lead to numerous deaths (but maybe none), knowing that if I didnt, one person would certainly die? Had anyone solved that particular trolley problem? My heart palpitations got worse. This was insane. I texted Heather everything and asked if she could arrange for a rapid coronavirus test the next day.

It was nearly 11 p.m. by this point, later in Heathers time zone. She made sure my shortness of breath wasnt an emergency, then said shed see how I was feeling in the morning to assess whether a test was necessary.

I went to bed and thought about what they would tell the patient. Would his doctors be allowed to explain why I couldnt donate? Would he think I had just bailed? Would he and his family hate me? What did it say about my motivations that I was fixated on this? Probably nothing good. I drifted off into a stress dream, and then it was dawn.

My breathing was still labored in the morning, and now, compounding my dread, I had a definite tickle in my throat that verged on a cough. Heather and the medical team decided this did indeed warrant a coronavirus test, and went about setting one up. In the meantime, Heather told me, I should proceed with my third day of filgrastim.

When my home nurse Maria arrived at 8 a.m. to do the honors, I stopped her outside to inform her that I might be a vector of death. She was unimpressed. (Ok, sweetie. Can I come in and wash my hands?) Soon afterwards, Heather called to let me know she had found a doctors office that would send someone to test me at my apartment, and deliver results within 24 hoursjust fast enough that I could still make my flight if I tested negative. Be The Match picked up the tab for this, too, but the receipt came to my email. The cost of a rapid PCR test, antibody test, and home visit came out to a cool $900.

The unaffordable testing nurse arrived an hour later cloaked in full PPE. She coached me on how to swab my own mouth and throat for the diagnostic test, then we made small talk while waiting for the little white antibody tray, which looked for all the world like yet another pregnancy test, to reveal either one or two lines. She had been doing these home visits for two weeks, she told me, and none of her patients had yet tested positive for an infection. For no good reason at all, this made me feel better. The antibody test came up negative. The nurse wished me luck with my other results and headed off to her next appointment, leaving me alone with my wonderful thoughts.

I had nothing to do for the rest of the day but wait. By late afternoon my throat felt better, and my breathing had become less conspicuous. At one point I started to pack a bag, wondered if I was jinxing it, and unpacked the bag. At 10 p.m., less than 12 hours after my throat swab, the results arrived in my inbox. NOT DETECTED. I texted Heather a screenshot and lay down on the floor, awash with relief.

(Sarah Lazarus)

The travel and donation themselves were mercifully uneventful. My parents, who were very pleased that I was donating and terrified that I was flying, had shipped me a steady stream of hand sanitizer, KN95 masks, surgical masks, disinfectant wipes, face shields, safety glasses, and gloves. I wore only some of this to the airport, unless you are my parents, in which case I wore all of it. In any event, I felt protected. My terminal at LAX was deserted, and Heather had booked me a first class seat on Delta, which limits capacity to 50 percent. After barely leaving my immediate neighborhood for half a year, the feeling of takeoff, even for a two-day trip to Boise, was sensational.

The next day I arrived at the hospital at 7:15 a.m. By 8:30 Id had a central line inserted above my collarbone, in a painless 15-minute procedure under local anesthesia. The song We Are Young was playing, and the doctors threading a tube into my neck were chatting quietly about a patient whod given them trouble over the weekend. (Im just saying, if youre cussing people out and trying to beat me up, you probably didnt have too bad of a stroke.) Ive had much less pleasant mornings.

By 9:30 I was in bed and hooked up to the apheresis machine, where I would remain for the next seven hours. At one point my calcium levels dropped too low and I threw up; this was the excitement peak of the day. I spent the rest of the time comfortably reading or watching Netflix, keeping an eye on the stem cells slowly collecting in the bag above my head, and carefully avoiding any RNC coverage that might cause the nausea to recur. At around 4:30 I was loosed from the machine, and after waiting a couple more hours while the lab made sure I had forked over enough cells, the nurse removed my central line and I was officially done.

I was exhausted that evening, but the next day felt well enough to go for a walk along the Boise River, where I took 50 terrible photos of a great blue heron. My shortness of breath, whatever it had been, was gone. The day after that I was just a little more fatigued than usual, and by day three I was back to my 2020-adjusted tiredness baseline.

Coronavirus complications aside, the actual donation process was remarkably easy; shockingly easy, when you consider the scale of what it means for the recipient. It was a time commitment for a few weeksIm lucky to have employers who were happy to give me the necessary leaveand involved some mild discomfort, but as a baby about both pain and scheduling, I would not hesitate to do this again.

I also came away with a clearer sense of how to approach the kind of altruistic acts that standard social-distancing guidelines say we shouldnt engage in. The people and organizations that facilitate charity, particularly sensitive medical charity, have existing support systems that theyve retrofitted to help mitigate the extra risks. Those systems may be imperfect and require some self-advocacy, but when combined with ones own diligence and added layers of protection (and, if one is lucky, a concerned Jewish mother), its possible to get help to the people who need it with risk levels not much higher than we tolerate in normal times. There is a way to be selfless without being self-sacrificing, or worse, becoming an inadvertent menace.

Even so, pandemic experiences like this one wont be universally feasible. One might live with immunosuppressed family members or roommates, or have care-taking responsibilities, or lack the spare emotional bandwidth, or have any number of circumstances more complex than my own. And thats finethere will still be people in need of a lifeline on the other side of this crisis, and that lifeline will be no less appreciated.

I asked my dad, Mitchell Lazarus, what he thought potential donors should know about the recipient experience. He sent me this:

The diagnosis is, literally, a death sentence: you will soon die. Word of a matching donor who has agreed to participate is a reprieve the only possible reprieve. I have felt relief many times in my life, but except possibly for the safe birth of my children, nothing like that. I was in a chemo chair when they came by and told me. I called my wife and said, I have a donor, and I started to cry.

Patients in the transplant ward talk a lot about our donors, despite not knowing who they are. Everybody everybody! tears up when talking about their donors.

True story: I was in the hallway on the transplant floor, talking with the woman in the room next to mine. A nurse walking by stopped and said, Mr. Lazarus, are you having trouble with allergies? (which would require attention). I said no, I was talking about my donor. No other explanation needed. She patted my arm and walked on.

I am a chimera. The rest of me has my own DNA, but my blood cells carry my donors DNA, not mine. Somebody elses blood pumps through my body, keeping me alive, not just through treatment, but every second of every day for the rest of my life. How can you not be grateful to someone who literally gave you the rest of your life?

At some point during the 24 hours after I was unhooked from the machine, a volunteer courier arrived at the hospital in Boise. He or she or they retrieved the bag of my donated cells, flew with it to wherever the recipient is located, and hand-delivered it to his hospital. The patient almost certainly received the transplant before I made it back to Los Angeles. If all goes well, my stem cells will navigate their way into his bone marrow, where theyll settle in, multiply, and start producing healthy blood cells. If all goes well, this perfect stranger will eventually have my blood type, and potentially even my childhood immunitieshe might soon, in other words, have my immune system. If all goes well, may that sucker protect us both.

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Coronavirus, Charity, and the Trolley Problem - Crooked

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Global Induced Pluripotent Market By 2026 Emerging Technology, Opportunities, Analysis And Future Threats With Key Players Like Thermo Fisher…

September 11th, 2020 3:56 pm

Induced Pluripotent MarketIs Expected To Rise To An Estimated Value Of Usd 2.33 Billion By 2026, Registering A Substantial Cagr In The Forecast Period Of 2019-2026. This Rise In Market Value Can Be Attributed To The Increasing Prevalence Of Chronic Diseases And Ailments Requiring The Development Of Modern Technologically Advanced Therapeutic Options.

The strategies encompassed in the Induced Pluripotent report mainly include new product launches, expansions, agreements, joint ventures, partnerships, acquisitions, and others that boost their footprints in this market. This gives more accurate understanding of the market landscape, issues that may affect the industry in the future, and how to best position specific brands. The base year for calculation in the report is taken as 2017 whereas the historic year is 2016 which will tell you how the Induced Pluripotent market is going to perform in the forecast years by informing you what the market definition, classifications, applications, and engagements are.

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Few of the major competitors currently working in the induced pluripotent market are Bristol-Myers Squibb Company; CELGENE CORPORATION; Astellas Pharma Inc.; Thermo Fisher Scientific; Cell Applications, Inc.; Axol Bioscience Ltd.; Organogenesis Holdings; Merck KGaA; FUJIFILM Holdings Corporation; Fate Therapeutics; KCI Licensing, Inc.; Japan Tissue Engineering Co., Ltd.; Vericel; ViaCyte, Inc.; STEMCELL Technologies Inc.; Horizon Discovery Group plc; Lonza; Takara Bio Inc.; Promega Corporation and QIAGEN.

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Market Restraints

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Segmentation: Global Induced Pluripotent Market

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Headaches, confusion and delirium with COVID-19: How SARS-CoV-2 attacks the brain – Firstpost

September 11th, 2020 3:56 pm

The ACE2 receptor that the virus targets is rare in the brain. But new research shows that the virus could enter brain cells via this method too.

The coronavirus targets the lungs foremost, but also the kidneys, liver and blood vessels. Still, about half of patients report neurological symptoms, including headaches, confusion and delirium, suggesting the virus may also attack the brain.

A new study offers the first clear evidence that in some people, the coronavirus invades brain cells, hijacking them to make copies of itself. The virus also seems to suck up all of the oxygen nearby, starving neighboring cells to death.

Its unclear how the virus gets to the brain or how often it sets off this trail of destruction. Infection of the brain is likely to be rare, but some people may be susceptible because of their genetic backgrounds, a high viral load or for other reasons.

If the brain does become infected, it could have a lethal consequence, said Akiko Iwasaki, an immunologist at Yale University who led the work.

The study was posted online Wednesday and has not yet been vetted by experts for publication. But several researchers said it was careful and elegant, showing in multiple ways that the virus can infect brain cells.

Scientists have had to rely on brain imaging and patient symptoms to infer effects on the brain, but we hadnt really seen much evidence that the virus can infect the brain, even though we knew it was a potential possibility, said Dr. Michael Zandi, consultant neurologist at the National Hospital for Neurology and Neurosurgery in Britain. This data just provides a little bit more evidence that it certainly can.

Zandi and his colleagues published research in July showing that some patients with COVID-19, the illness caused by the coronavirus, develop serious neurological complications, including nerve damage.

In the new study, Iwasaki and her colleagues documented brain infection in three ways: in brain tissue from a person who died of COVID-19, in a mouse model, and in organoids clusters of brain cells in a lab dish meant to mimic the brains three-dimensional structure.

Brain scans of coronavirus patients from a study published in July. The new study offers the first clear evidence that in some people, the coronavirus invades brain cells, hijacking them to make copies of itself, and the virus also seems to suck up all of the oxygen nearby, starving neighbouring cells to death. By [Apoorva Mandavilli/Ross W. Paterson, Rachel L. Brown, et al./Brain, Oxford University Press] 2020 The New York Times

The coronavirus is much stealthier: It exploits the brain cells machinery to multiply, but doesnt destroy them. Instead, it chokes off oxygen to adjacent cells, causing them to wither and die.

The researchers didnt find any evidence of an immune response to remedy this problem. Its kind of a silent infection, Iwasaki said. This virus has a lot of evasion mechanisms.

These findings are consistent with other observations in organoids infected with the coronavirus, said Alysson Muotri, a neuroscientist at the University of California, San Diego, who has also studied the Zika virus.

The coronavirus seems to rapidly decrease the number of synapses, the connections between neurons.

Days after infection, and we already see a dramatic reduction in the amount of synapses, Muotri said. We dont know yet if that is reversible or not.

The virus infects a cell via a protein on its surface called ACE2. That protein appears throughout the body and especially in the lungs, explaining why they are favoured targets of the virus.

Previous studies have suggested, based on a proxy for protein levels, that the brain has very little ACE2 and is likely to be spared. But Iwasaki and her colleagues looked more closely and found that the virus could indeed enter brain cells using this doorway.

Its pretty clear that it is expressed in the neurons and its required for entry, Iwasaki said.

Her team then looked at two sets of mice one with the ACE2 receptor expressed only in the brain, and the other with the receptor only in the lungs. When they introduced the virus into these mice, the brain-infected mice rapidly lost weight and died within six days. The lung-infected mice did neither.

The structure and cross-sectional view of the novel coronavirus SARS-CoV-2. Image: Wikimedia

Despite the caveats attached to mouse studies, the results still suggest that virus infection in the brain may be more lethal than respiratory infection, Iwasaki said.

The virus may get to the brain through the olfactory bulb which regulates smell through the eyes or even from the bloodstream. Its unclear which route the pathogen is taking, and whether it does so often enough to explain the symptoms seen in people.

I think this is a case where the scientific data is ahead of the clinical evidence, Muotri said.

Researchers will need to analyse many autopsy samples to estimate how common brain infection is and whether it is present in people with milder disease or in so-called long-haulers, many of whom have a host of neurological symptoms.

Forty percent to 60% of COVID-19 patients experience neurological and psychiatric symptoms, said Dr. Robert Stevens, a neurologist at Johns Hopkins University. But the symptoms may not all stem from the virus invading brain cells. They may be the result of pervasive inflammation throughout the body.

For example, inflammation in the lungs can release molecules that make the blood sticky and clog up blood vessels, leading to strokes. Theres no need for the brain cells themselves to be infected for that to occur, Zandi said.

But in some people, he added, it may be low blood oxygen from infected brain cells that triggers strokes: Different groups of patients may be affected in different ways, he said. Its quite possible that youll see a combination of both.

Some cognitive symptoms, like brain fog and delirium, might be harder to pick up in patients who are sedated and on ventilators. Doctors should plan to dial down sedatives once a day, if possible, in order to assess COVID-19 patients, Stevens said.

Apoorva Mandavilli. c.2020 The New York Times Company

Link:
Headaches, confusion and delirium with COVID-19: How SARS-CoV-2 attacks the brain - Firstpost

Read More...

Post-COVID heart damage alarms researchers: ‘There was a black hole’ in infected cells – Yahoo Movies UK

September 11th, 2020 3:56 pm

Shelby Hedgecock contracted the coronavirus in April and thought she had fought through the worst of it the intense headaches, severe gastrointestinal distress and debilitating fatigue but early last month she started experiencing chest pain and a pounding heartbeat. Her doctor put her on a cardiac monitor and ordered blood tests, which indicated that the previously healthy 29-year-old had sustained heart damage, likely from her bout with COVID-19.

I never thought I would have to worry about a heart attack at 29 years old, Hedgecock told Yahoo News in an interview. I didnt have any complications before COVID-19 no preexisting conditions, no heart issues. I can deal with my taste and smell being dull, I can fight through the debilitating fatigue, but your heart has to last you a really long time.

Hedgecocks primary-care physician has referred her to a cardiologist she will see this week; the heart monitor revealed that Hedgecocks pulse rate is wildly irregular, ranging from 49 to 189 beats per minute, and she has elevated inflammatory markers and platelet counts. She was told to go to the emergency room if her chest pain intensifies before she can see the specialist. A former personal trainer who is now out of breath just from walking around the room, Hedgecock is worried about what the future holds.

She is far from alone in her struggle. Dr. Ossama Samuel is a cardiologist at New Yorks Mount Sinai Hospital, where he routinely sees coronavirus survivors who are contending with cardiac complications. Samuel said his team has treated three young and otherwise healthy coronavirus patients who have developed myocarditis an inflammation of the heart muscle weeks to months after recovering from the virus.

Shelby Hedgecock in a hospital bed. (Shelby Hedgecock)

Myocarditis can affect how the heart pumps blood and trigger rapid or abnormal heart rhythms. It is particularly dangerous for athletes, doctors say, because it can go undetected and can result in a heart attack during strenuous exercise. In recent weeks, some collegiate athletes have reported cardiac complications from the coronavirus, underscoring the seriousness of the condition.

Last month, former Florida State basketball center Michael Ojo died from a heart attack in Serbia; Ojo had recovered from the coronavirus before he collapsed on the basketball court. An Ohio State University cardiologist found that between 10 and 13 percent of university athletes who had recovered from COVID-19 had myocarditis.When the Big Ten athletic conference announced the cancellation of its season last month, Commissioner Kevin Warren cited the risk of heart failure in athletes. Researchers have estimated that up to 20 percent of people who get the coronavirus sustain heart damage.

Samuel said he feels an obligation to warn people, particularly since some of the patients he and Mount Sinai colleagues have seen with myocarditis had only mild cases of the coronavirus months ago.

We are now seeing people three months after COVID who have pericarditis [inflammation of the sac around the heart] or myocarditis, Samuel said. He said he believes a small fraction of coronavirus survivors are sustaining heart damage, but when a disease is so widespread it is concerning that a tiny fraction is still sizable.

Samuel said he worries particularly about athletes participating in team sports, since many live together and spend time in close quarters. Teammates may all get the coronavirus and recover together, Samuel said, but the one who really gets that crazy myocarditis could be at risk of dying through exercise or training.

Story continues

Its a concern about what do you do: Should we do sports in general, should we do it in schools, should we do it in college, should we just do it for professionals who understand the risk and they're getting paid? Samuel asked. I hope we dont scare the public, but we should make people aware.

Samuel is recommending that patients recovering from COVID-19 with myocarditis avoid workouts for three to six months.

Todd McDevitt, who runs a stem-cell lab at Gladstone Institutes, which is affiliated with the University of California at San Francisco, recently published images that show how the coronavirus can directly invade the heart muscle. McDevitt said he was so alarmed when he saw a sample of heart muscle cells in a petri dish get diced by the coronavirus that he had trouble sleeping for nights afterward.

Todd McDevitt. (Facebook)

McDevitt said his teams research was spurred by their desire to understand if the coronavirus is entering heart cells and how it is affecting them. He was surprised to see the heart muscle samples he was studying react to a very small amount of the coronavirus, usually within 24 to 48 hours. He said the virus decimated the heart cells in his petri dishes.

Cell nuclei the hubs of all the genetic information, all of the nuclear DNA in many of the cells were gone, McDevitt said. There was a black hole literally where we would normally see the nuclear DNA. Thats also pretty bizarre.

While McDevitts study has not yet been peer-reviewed it is still in pre-print he said he felt compelled to share the findings as soon as possible. He said his team also sampled tissues from three COVID-19 patient autopsies and found similar damage in the heart muscles of those patients, none of whom had been flagged for myocarditis or heart problems while they were alive.

This is probably not the whole story yet, but we think we have insights into the beginning of when the virus would get into some of these people and what it might be doing that is concerning enough that we should probably let people know, because clinicians need to be thinking about this, McDevitt said in an interview. We dont have any means of bringing heart muscle back. ... This virus is [causing] a very different type of injury, and one we haven't seen before.

McDevitt said the chopped-up heart muscles he and his colleagues saw are so concerning because when the microfibers in the muscle are damaged, the heart cant properly contract.

If heart muscle cells are damaged and they cant regenerate themselves, then what youre looking at is someone who could prematurely have heart failure or heart disease due to the virus, McDevitt said. This could be a warning sign for a potential wave of heart disease that we could see in the future, and its in the survivors thats the concern.

McDevitt said he believes the risk of heart disease is serious and one people should consider as they assess their own risk of getting the coronavirus.

I am more scared today of contracting the virus, by far, than I was four months ago, he said.

In lab experiments, infection of heart muscle cells with SARS-CoV-2 caused long fibers to break apart into small pieces, shown above. (Gladstone)

The medical journal the Lancet recently reported that an 11-year-old child had died of myocarditis and heart failure after a bout of COVID-induced multisystem inflammatory syndrome (MIS-C). An autopsy showed coronavirus embedded in the childs cardiac tissue.

A recent study from Germany found that 78 percent of patients who had recovered from the coronavirus and who had only mild to moderate symptoms while ill with the disease had indications of cardiac involvement on MRIs conducted more than two months after their initial infection.Lead investigator Eike Nagel said it is concerning to see such widespread cardiac impact; six in 10 of the patients Nagels team studied experienced ongoing myocardial inflammation.

We found an astonishingly high level of cardiac involvement approximately two months after COVID infection, Nagel said in an email. These changes are much milder than observed in patients with severe acute myocarditis.

The scale of the cardiac impact on relatively healthy, young patients surprised many doctors. Nagel said the findings are significant on a population basis, and that the impact of COVID-19 on the heart must be studied more.

Dr. Gregg Fonarow. (UCLA)

Dr. Gregg Fonarow, chief of UCLAs Division of Cardiology and director of the Ahmanson-UCLA Cardiomyopathy Center, said the picture is evolving, but the new studies showing cardiac impact in even young people with mild cases of COVID-19 have raised troubling new questions.

We really do need to take seriously individuals that have had the infection and are having continued symptoms, [and] not just dismiss those symptoms, Fonarow said. There could be, in those who had milder or even asymptomatic cases, the potential for cardiac risk.

Fonarow said it is important to understand whether a more proactive screening and treatment approach is needed to better address the needs of patients who have recovered from the coronavirus and who may still have weakened heart function. Fonarow said he found McDevitts research to be potentially significant because it proves from a mechanistic standpoint that there can be direct cardiac injury from the virus itself.

Even if it were going to impact, say, 2 percent of the people that had COVID-19, when you think of the millions that have been infected, that ends up in absolute terms being a very large number of individuals, Fonarow said in an interview. You dont want people to be unduly alarmed, but on the other hand you dont want individuals to be complacent about, Oh, the mortality rate is so low with COVID-19, I dont really care if Im infected because the chances that it will immediately or in the next few weeks kill me is small enough, I dont need to be concerned. There are other consequences.

_____

Read more from Yahoo News:

See the original post here:
Post-COVID heart damage alarms researchers: 'There was a black hole' in infected cells - Yahoo Movies UK

Read More...

‘There was a black hole’ in infected cells – Sports Grind Entertainment

September 11th, 2020 3:56 pm

Shelby Hedgecock contracted the coronavirus in April and thought she had fought through the worst of it the intense headaches, severe gastrointestinal distress, and debilitating fatigue but early last month she started experiencing intense chest pain and a pounding heartbeat. Her doctor put her on a cardiac monitor and ordered blood tests, which indicate the previously healthy 29-year-old had sustained heart damage, likely from her bout with COVID-19.

I never thought I would have to worry about a heart attack at 29 years old, Hedgecock told Yahoo News in an interview. I didnt have any complications before COVID-19 no pre-existing conditions, no heart issues. I can deal with my taste and smell being dull; I can fight through the debilitating fatigue, but your heart has to last you a really long time.

Hedgecocks primary care physician has referred her to a cardiologist she will see this week; the heart monitor revealed Hedgecocks pulse rate is wildly irregular, ranging from 49 to 189 beats per minute, and she has elevated inflammatory markers and platelet counts. Hedgecock was told to go to the emergency room if her chest pain intensifies before she can see the specialist. A former personal trainer who is now out of breath just from walking around the room, Hedgecock is worried about what the future holds.

Hedgecock is far from alone in her struggle. Dr. Ossama Samuel is a cardiologist at New Yorks Mount Sinai Hospital, where he routinely sees coronavirus survivors who are contending with cardiac complications. Samuel said his team has treated three young and otherwise healthy coronavirus patients who have developed myocarditis an inflammation of the heart muscle weeks to months after recovering from the virus.

Myocarditis can affect how the heart pumps blood and trigger rapid or abnormal heart rhythms. It is particularly dangerous for athletes, doctors say, because it can go undetected and can result in a heart attack during strenuous exercise. In recent weeks, some collegiate athletes have reported cardiac complications from coronavirus, underscoring the seriousness of the condition.

Story continues

Last month, former Florida State basketball center Michael Ojo died from a heart attack in Serbia; Ojo had recovered from coronavirus before he collapsed on the basketball court. An Ohio State University cardiologist found that between 10 and 13 percent of university athletes who had recovered from COVID-19 had myocarditis. When the Big Ten athletic conference announced the cancellation of its season last month, Commissioner Kevin Warren cited the risk of heart failure in athletes. Researchers have estimated that up to 20 percent of people who get coronavirus sustain heart damage.

Samuel said he feels an obligation to warn people, particularly since some of the patients he and other Mount Sinai colleagues have seen with myocarditis had only mild cases of coronavirus months ago.

We are now seeing people three months after COVID who have pericarditis [inflammation of the sac around the heart] or myocarditis, Samuel said. He said he believes a small fraction of coronavirus survivors are sustaining heart damage, but when a disease is so widespread it is concerning that a tiny fraction is still sizable.

Samuel said he worries particularly about athletes participating in team sports since many live together and spend time in close quarters. Teammates may all get coronavirus and recover together, Samuel said, but the one who really gets that crazy myocarditis could be at risk of dying through exercise or training.

Its a concern about what do you do: Should we do sports in general, should we do it in schools, should we do it in college, should we just do it for professionals who understand the risk and theyre getting paid? Samuel asked. I hope we dont scare the public, but we should make people aware.

Samuel is recommending patients recovering from COVID-19 with myocarditis avoid workouts for three to six months.

Todd McDevitt, who runs a stem-cell lab at the University of California at San Francisco-affiliated Gladstone Institutes, recently published images that show how coronavirus can directly invade the heart muscle. McDevitt said he was so alarmed when he saw a sample of heart muscle cells in a petri dish get diced by the coronavirus that he had trouble sleeping for nights afterward.

McDevitt said his teams research was spurred by their desire to understand if the coronavirus is entering heart cells and how it is affecting them. McDevitt was surprised to see the heart muscle samples he was studying react to a very small amount of coronavirus, usually within 24-48 hours. He said the virus decimated the heart cells in his petri dishes.

Cell nuclei the hubs of all the genetic information, all of the nuclear DNA in many of the cells were gone, McDevitt said. There was a black hole literally where we would normally see the nuclear DNA. Thats also pretty bizarre.

While McDevitts study has not yet been peer-reviewed it is still in pre-print he said he felt compelled to share the findings as soon as possible. He said his team also sampled tissues from three COVID-19 patient autopsies and found similar damage in the heart muscles of those patients, none of whom had been flagged for myocarditis or heart problems while they were alive.

This is probably not the whole story yet, but we think we have insights into the beginning of when the virus would get into some of these people and what it might be doing that is concerning enough that we should probably let people know because clinicians need to be thinking about this, McDevitt said in an interview. We dont have any means of bringing heart muscle back. This virus is [causing] a very different type of injury and one we havent seen before.

McDevitt said that the chopped up heart muscles he and his colleagues saw is so concerning because when the microfibers in the muscle are damaged, the heart cant properly contract.

If heart muscle cells are damaged and they cant regenerate themselves, then what youre looking at is someone who could prematurely have heart failure or heart disease due to the virus, McDevitt said. This could be a warning sign for a potential wave of heart disease that we could see in the future, and its in the survivors thats the concern.

McDevitt said that he believes the risk of heart disease is serious and one people should consider as they assess their own risk of getting the coronavirus.

I am more scared today of contracting the virus, by far, than I was four months ago, McDevitt said.

The Lancet recently reported an 11-year-old child had died of myocarditis and heart failure after a bout of COVID-induced multi-system inflammatory syndrome (MIS-C). An autopsy showed coronavirus embedded in the childs cardiac tissue.

A recent study from Germany found that 78 percent of patients who had recovered from coronavirus and who had only mild to moderate symptoms while ill with the disease had indications of cardiac involvement on MRIs conducted more than two months after their initial infection.Lead investigator Eike Nagel said it is concerning to see such widespread cardiac impact; six in 10 of the patients Nagels team studied experienced ongoing myocardial inflammation.

We found an astonishingly high level of cardiac involvement approximately two months after COVID infection, Nagel said in an email. These changes are much milder than observed in patients with severe acute myocarditis.

The scale of the cardiac impact on relatively healthy, young patients surprised many doctors. Nagel said the findings are significant on a population basis, and that the impact of COVID-19 on the heart must be studied more.

Gregg Fonarow, chief of UCLAs Division of Cardiology and director of the Ahmanson-UCLA Cardiomyopathy Center, said the picture is evolving, but the new studies showing cardiac impact in even young people with mild cases of COVID have raised troubling new questions.

We really do need to take seriously individuals that have had the infection and are having continued symptoms [and] not just dismiss those symptoms, Fonarow said. There could be, in those who had milder or even asymptomatic cases, the potential for cardiac risk.

Fonarow said it is important to understand whether a more proactive screening and treatment approach is needed to better address the needs of patients who have recovered from coronavirus and who may still have weakened heart function. Fonarow said he found McDevitts research to be potentially significant because it proves from a mechanistic standpoint that there can be direct cardiac injury from the virus itself.

Even if it were going to impact, say, 2 percent of the people that had COVID 19, when you think of the millions that have been infected that ends up in absolute terms being a very large number of individuals, Fonarow said in an interview. You dont want people to be unduly alarmed, but on the other hand you dont want individuals to be complacent about, Oh, the mortality rate is so low with COVID-19, I dont really care if Im infected because the chances that it will immediately or in the next few weeks kill me is small enough, I dont need to be concerned. There are other consequences.

_____

Read more from Yahoo News:

Read more:
'There was a black hole' in infected cells - Sports Grind Entertainment

Read More...

The reason your face mask might be causing dry eye – The List

September 11th, 2020 3:55 pm

Eye doctors say MADE, like maskne orfogged-up glasses, are not reasons to skip a mask. "The real reason for bringing this to people's attention is to say, 'Hey, if you notice this, this is why it's happening and let's help you manage your dry eye while you continue to wear your mask," Lyndon Jones, the director of the Center for Ocular Research and Education at Canada's University of Waterloo tells The Washington Post.

To keep MADE at bay, doctors suggest you find a face mask that fits properly, so that air has less of a chance of escaping from the top. Also, step away from the computer every 20 minutes to give your eyes a break. And speak to an eye specialist when you feel an early onset of MADE, which includes discomfort and blurred vision.

Much as we hate all the associated problems that come with wearing face masks, there is a compelling reason you need to keep them on. The CDC says clinical studies have shown that face masks are an important ally in the pandemic, because they catch potentially infectious droplets before they spread through coughing, sneezing, talking, or raising your voice. This means masks, along with social distancing, are still the best way to keep the virus from spreading.

See original here:
The reason your face mask might be causing dry eye - The List

Read More...

Can we stand together and overcome adversity and genetics? – Laurel Outlook

September 11th, 2020 3:53 pm

I would like to refer to the excellent article by Barbara Karst in the Outlook September 3rd edition. I take exception to one statement.

Racism is not an inherent attitude. It has to be taught by someone - parents, grandparents, and others who are racist/ bigoted. This statement brings into play the continuing discussion; does man learn through nurture or nature? Do we only learn from the experiences encountered from the time of conception on, or is there residual knowledge passed on to us via genetics?

I would like to refer you to the works of Dr. E. O. Wilson, major proponent of sociobiology, Robert Ardrey and his four book series, The Nature of Man, and to the work of Dr Raymond Dart after his 1924 discovery of the Australopithecus Africanus. Their assertion is we learn by both nurture AND nature. Dr. Darts bold, blunt and controversial statement is both man and animals retain knowledge through instinct. The strongest instinct being the instinct to survive.

There are many facets to the act of survival. Currently most common is the discussion of the herd instinct, or the social need for community. This need for community is so strong, we use the deprivation of community as a form of punishment. We imprison, or remove from society our criminals. Solitary confinement is not only considered a punishment but has proven to be a form of torture. Religions shun or excommunicate controversial individuals. We instinctually repel or fear that which is new or not understood for it may threaten our survival.

To be succinct, we are all bigots. Strength in numbers, or the herd can provide security. We look alike. We talk alike. We think alike. I will be safe. I will survive and in times of stress, we revert to that which we presume will again protect us.

Ironically, the study of genetics has shown us the necessity for diversity. We have learned the inbreeding of animals and humans can cause numerous physical and mental deficiencies. We can also inbreed our society intellectually. The art of learning is augmented through the nurturing of our young and the continued exploration of creation throughout our lives.

In this time of social and economic uncertainty, will we revert to the herd? Retreat to our embattlements and separate into isolated communities fearful of the unknown? Or do we have the courage and strength of character to stand together in an ever expanding herd and face the unknown? Strength of numbers, nature, expansion of knowledge, nurture, they can work together.

Jim Tikalsky of Laurel

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Can we stand together and overcome adversity and genetics? - Laurel Outlook

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