The Cancer Custodians Hidden Truths

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Part of Dennis Plenker’s daily job is growing cancer. And a variety of different ones, too. Depending on the day and the project, different tumors may burgeon in the petri dishes stocked in the Cold Spring Harbor Laboratory where Plenker works as a research investigator. They might be aggressive breast cancers.

They might be glioblastomas, one of the deadliest brain tumors that rob patients of their ability to speak or read as they crowd out normal cells. Or they might be pancreatic cancers, the fast and vicious slayers that can overtake a healthy person within weeks or even days.

These tiny tumor chunks are transparent and bland—they look like little droplets of hair gel that accidentally plopped into a plastic dish and took hold. But their unassuming appearance is deceptive. If they were still in the human bodies they came from, they would be sucking up nutrients, rapidly growing and dodging the immune system defenses.

But in Plenker’s hands—or rather in the CSHL’s unique facility—these notorious killers don’t kill anyone. Instead, scientists let them grow to devise the most potent ways to kill them. These tumor chunks are called organoids. They are three-dimensional assemblages of malignant growths used to study cancer behavior and vulnerability to chemotherapy and the so-called “targeted drugs”—the next generation therapies.

Scientists used to study tumors at a single-cell level, but because tumors grow as cell clusters in the body, it proved to be inefficient. The three-dimensional structures make a difference. For example, chemo might destroy the tumor’s outer cell layer, but the inner ones can develop resistance, so where single cells may die, a 3D mass will bounce back. Organoids can provide a window into these little-known mechanisms of drug resistance.

They can reveal how normal tissues turn malignant and where the cellular machinery goes off-track to allow that to happen. As their name suggests, organoids are scientists’ windows into organs, whether healthy or stricken with disease. You need to know your enemy to beat it, Plenker says, and cancer organoids offer that opportunity.

Taken from patients currently undergoing cancer treatments, these tumor chunks will reveal their weaknesses so scientists can find the cancers’ Achilles’ heel and devise personalized treatments. “Organoids are essentially patients in a dish,” Plenker says. Only unlike real patients, the organoids can be subjected to all sorts of harsh experiments to zero in on the precise chemo cocktails that destroy them in the best possible way.

And they will likely provide a more realistic scenario than drug tests in mice or rats, as animal models aren’t perfect proxies for humans.

These notorious killers don’t kill anyone. Instead, scientists devise the most potent ways to kill them.

The way that cancer proliferates in the body is hard to reproduce in the lab. Stem-cell research made it possible. After scientists spent a decade understanding how various cells multiply and differentiate into other cell types based on molecular cues and nourishment, they were able to make cells grow and fuse into tissues.

To stick together like bricks in a nicely laid wall, cells need a biological scaffold that scientists call an extracellular matrix or ECM, which in the body is made from collagen and other materials. Today, the same collagen scaffolds can be mimicked with a gooey substance called Matrigel—and then seeded with specific cells, which take root and begin to multiply.

Some tissue types were easy to grow—Columbia University scientists grew viable bones as early as 2010.1 Others, like kidney cells, were trickier. They would grow into immature tissues incapable of performing their job of cleaning and filtering blood. It took scientists time to realize that these cells wanted more than scaffolding and food—they needed to “feel at home,” or be in their natural habitat. Kidney cells needed the feeling of liquid being washed over them, the Harvard University group found, when they first managed to grow functioning kidney tissue in 2018.2

Cancers have their own growth requirements. In the body, they manage to co-opt the organism’s resources, but keeping them happy in a dish means catering to their dietary preferences. Different cancers need different types of molecular chow—growth factors, hormones, oxygen and pH levels, and other nutrients. Pancreatic adenocarcinoma thrives in low-oxygen conditions with poor nutrients.3 Glioblastomas feed on fatty acids.4 These nutrients are delivered to organoids via a specific solution called growth medium, which the lab personnel regularly doles out into the dishes.

Plenker is charged with keeping this murderous menagerie alive and well. He is the one who designs the cancers’ dietary menu, a specific protocol for each type. And while his official title is facility manager and research investigator who works closely with David Tuveson, director of the CSHL’s Cancer Center, he is essentially a cancer custodian, a curator of a unique collection that aims to change the paradigm of cancer treatment.

Plenker’s research area is pancreatic cancer—one of the most notorious killers known. Often diagnosed late and resistant to treatment, it is essentially a death sentence—only 8 to 10 percent of patients remain alive five years after diagnosis. The chemo drugs used to treat it haven’t changed in 40 years, Plenker says. In the past decade, physicians tried combining multiple drugs together with relative success. Identifying winning combos can save lives, or at least prolong them—and that’s what the organoids will help clinicians do better.

In a groundbreaking clinical trial called PASS-01 (for Pancreatic Adenocarcinoma Signature Stratification for Treatment), Plenker’s team collaborates with other American and Canadian colleagues to identify the most effective chemo cocktails and to understand the individual patients’ tumor behaviors, which would lead to more personalized treatments.5

Scientists know the same cancer types behave differently in different patients. Typically, all malignancies have the so-called “driver mutation”— the cancer’s main trigger caused by a mutated gene. But tumors also often have “passenger mutations” that happen in nearby genes. These additional mutated genes can generate various proteins, which may interfere with treatment.

Or not. Scientists call these mutated gene combinations tumor mutational signatures, which can vary from one patient to the next. With some cancers, doctors already know what mutations signatures they may have, but with pancreatic cancer they don’t have good tale-telling signs, or biomarkers. “There aren’t many biomarkers to help clinicians decide which chemo may be better for which patient,” explains oncologist Grainne O’Kane, who treats pancreatic cancer patients at the Princess Margaret Hospital in Toronto, Canada.

That’s the reason O’Kane participates in the PASS-01 trial—it will give doctors a better view into the exact specifics of their patients’ malignancies. As they take their patients’ biopsies, they are sending little cancer snippets to the CSHL to be grown into organoids, which will be subjected to chemo cocktails of various combinations to design more personalized regiments for them.

The hospital treats all patients with the so-called standard of care chemotherapy, which is more of a one-size-fits-all approach. Some patients will respond to it but others won’t, so the goal is to define the second line of chemo defense in a more personalized fashion. “That’s where the biopsies we send to Tuveson’s lab might be useful,” O’Kane says. “They can help us find something to benefit patients after the first line of chemo stopped working.”

Organoids are patients in a dish. Unlike real patients, organoids can be subjected to experiments.

Scientists can try all kinds of combos on the tumorous organoids, which they can’t do in living people. “You can treat 100 organoids with 100 different compounds and see which one works, or which compound does a good job and which ones don’t work at all,” Plenker says. That would also allow scientists to define the precise amount of chemo, so doctors wouldn’t have to over-treat patients with harsh drugs that create sickening side effects. Ultimately, organoids should take a lot of guesswork out of the process.

With about 150 patients’ adenocarcinomas already collected, the team hopes to come up with some answers. O’Kane says her team already has three patients for which they were able to design the more personalized second line of defense chemo, based on what their organoids revealed. They haven’t yet tried it, because the trial has only started recently, but this would be the next step.

“Being able to piece all this information together in real time as patients are moving through their therapies can really improve the outcomes,” O’Kane says. And while they may not be able to save all of those who graciously donated their biopsy snippets to science, it will help build better treatments in the future. “Even if we won’t be able to help these specific patients we’re hoping to use this info in the future clinical trials,” O’Kane says.

Organoids can also help understand how cancer develops. This is particularly true for breast cancers, says Camilla dos Santos, associate professor and a member of the CSHL Cancer Center. She studies the inner life of human mammary glands, more commonly referred to as breasts, and is also part of the cancer custodian crew. The hormonal changes that women go through during pregnancy subsequently modify breast cancer risk, sometimes lowering it and sometimes increasing—a complex interplay of the body’s chemicals.

“We know that women who get pregnant for the first time before they turn 25 years old, have a 30 percent decrease in breast cancer incidents later in life,” dos Santos says. “When they turn 60 or 70, 30 percent of them will not develop cancer.” On the contrary, those who are pregnant past 38 have a 30 to 50 percent increase in developing aggressive breast cancer types. Clearly, some molecular switches are involved, but they are very hard to study within the body. That’s where organoids can provide a window into the surreptitious process.

Using breast organoids, scientists can model the complex life of mammary glands at various stages of a woman’s life. And while most women wouldn’t want their breasts poked and pierced when they are pregnant or breastfeeding, many donate their tissues after breast reduction surgery or prophylactic mastectomy due to high-risk mutations like the BRCA gene.

That’s where organoids shine because scientists can not only grow them, but also give them the pregnancy hormonal cues, which will make cells generate milk, stop lactating, or do it again—and study the complex cellular interactions that take place in real life.

There’s a lot to study. At birth, mammary glands are similar in both genders—just little patches of the mammary epithelium tissue. But when puberty hits, the female glands fill up with the so-called mammary tree—a system of ducts for future milk production, which fully “blooms” in pregnancy.

“When a woman becomes pregnant, the duct tree expands, growing two types of cells—luminal and myoepithelial ones,” explains Zuzana Koledova, assistant professor of Masaryk University in Czech Republic who also uses organoids in her work. When the baby is born, the luminal cells, which line the inside of the ducts, produce the proteins that comprise milk.

The myoepithelial cells reside outside the ducts and work as muscles that squeeze the ducts to push milk out. Dos Santos likens this pregnancy mammary gland growth to the changes of the seasons. The images of sprouting ducts look like blossoming trees in the spring while later they shrivel like plants do in the fall.

The body governs these processes via the molecular machinery of hormones, which stimulate breast cells growth during pregnancy, and later cause them to die out. The two pregnancy-related hormones, prolactin and oxytocin, are responsible for milk production. Prolactin induces the luminal cells to make milk while oxytocin makes the myoepithelial cells contract. Once the baby is weaned, the levels of these hormones drop, causing cells to shrink back to their non-pregnant state.

With organoids scientists can observe these cellular dynamics at work. Koledova’s team had watched breast organoids secrete milk based on biological cues. They even recorded movies of cells pumping tiny milk droplets in the dish they were growing in. Using tiny snippets of donated breast tissue, the team grew the organoids inside the Matrigel matrix in the growth media and then added the two pregnancy hormones into the mix, explains Jakub Sumbal, a mammary gland researcher in Koledova’s group.

As they began to secret proteins that compose milk, the organoids, which looked like little domes inside the dish, changed from translucent to opaque. “At first, you can see through them, but then as they produce these proteins, they kind of darken,” Sumbal says. “And you can see them pushing out these little droplets.”

Cancer patients would no longer have to undergo chemotherapy by trial and error.

Dos Santos’s team, who also did similar work, outlined molecular changes that follow such dish-based hormonal cues in their recent study.6 In response to hormonal messages, cells produce proteins, which they display on their surfaces, like status symbols. During pregnancy the burgeoning cells prepping for milk production display the “proteins flags” that make them look important, attracting nourishment. When it’s time to die, they commit a cellular suicide.

They signal to the bypassing macrophages—immune system cleanup crew—to devour them. “They essentially say ‘come eat me!’ to the macrophages,” dos Santos says. “Because I’m no longer needed.”

The ability to mimic these processes in a dish, allows scientists to study the molecular switches that trigger breast cancer development—or minimize it. Scientists know that cancerous cells can hide from the immune system and even co-opt it into protecting themselves. They do it by displaying their own “do not eat me” protein flags on the surface and avoid destruction.

“Sometimes cancer cells can recruit specific types of immune cells to protect them,” dos Santos says. “They can not only say ‘do not eat me,’ but say ‘come hang out with me’ to the macrophages, and the macrophages will send suppressive signals to the B-cells or T-cells, the body defenders.” It is as if the cancer requests protection—a crew of guardians around it to defend against other cells that would otherwise wipe it out.

Scientists can’t telescope into the body to peek at these interactions, but they now can watch these stealth battles unfolding in a dish. “Right now we are looking at the proteins that are secreted by the organoids—the proteins that go on the surface of the organoids’ cells and what they would communicate to the immune system,” dos Santos says.

“Even when there’s no immune system surrounding them, they would still be doing that.” There’s a way to mimic the immune system, too. Scientists can add B-cells, T-cells, macrophages, and other players into the growth medium and watch the full-blown cellular warfare in action. “That’s the next step in our research,” dos Santos says.

Understanding what hormonal fluxes trigger breast cancer, and how it recruits other cells for safekeeping, can give scientists ideas for pharmaceutical intervention. “We can find drugs that pharmacologically turn off the switches that trigger cancer or interrupt its signaling for protection,” dos Santos says. “That opens novel ways to treat people.”

Can organoid research lead to a new standard of care for cancer patients? That’s the ultimate goal, researchers say. That’s why Plenker works at keeping his collection of cancer glops alive and well and thriving—he calls it a living biobank. And he keeps a stash in the cryogenic freezer, too.

He is also developing protocols that would allow commercial companies to grow organoids the same way chemical industries make reagents or mice suppliers grow rodents for research. A benefit of organoid experiments is they don’t involve animals at all.

Hospitals may one day start growing organoids from their patients’ biopsies to design and test personalized chemo cocktails for them. Once science crosses over to that reality, the entire treatment paradigm will change. Cancer patients won’t have to undergo chemotherapy by trial and error.

Instead their cancer organoids will be subjected to this process—knocked out by a gamut of drug combinations to find the winning one to use in the actual treatment. Plenker notes that once enough data is gathered about the tumors’ mutational signatures, scientists may create a database of tumor “mugshots” matching them to the chemo cocktails that beat them best.

And then just sequencing a biopsy sample would immediately inform oncologists what drug combo the patient needs. “We may be about 10 years away from that,” Plenker says, but for now there’s a lot more research to do. And a lot more cancers to grow.

By: Lina Zeldovich

Lina Zeldovich grew up in a family of Russian scientists, listening to bedtime stories about volcanoes, black holes, and intrepid explorers. She has written for The New York Times, Scientific American, Reader’s Digest, and Audubon Magazine, among other publications, and won four awards for covering the science of poop. Her book, The Other Dark Matter: The Science and Business of Turning Waste into Wealth, will be released in October 2021 by Chicago University Press. You can find her at LinaZeldovich.com and @LinaZeldovich.

Source: The Cancer Custodians – Issue 102: Hidden Truths – Nautilus

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Critics:

Cancer is a group of diseases involving abnormal cell growth with the potential to invade or spread to other parts of the body. These contrast with benign tumors, which do not spread. Possible signs and symptoms include a lump, abnormal bleeding, prolonged cough, unexplained weight loss, and a change in bowel movements. While these symptoms may indicate cancer, they can also have other causes. Over 100 types of cancers affect humans.

Tobacco use is the cause of about 22% of cancer deaths. Another 10% are due to obesity, poor diet, lack of physical activity or excessive drinking of alcohol. Other factors include certain infections, exposure to ionizing radiation, and environmental pollutants. In the developing world, 15% of cancers are due to infections such as Helicobacter pylori, hepatitis B, hepatitis C, human papillomavirus infection, Epstein–Barr virus and human immunodeficiency virus (HIV).

These factors act, at least partly, by changing the genes of a cell. Typically, many genetic changes are required before cancer develops. Approximately 5–10% of cancers are due to inherited genetic defects. Cancer can be detected by certain signs and symptoms or screening tests. It is then typically further investigated by medical imaging and confirmed by biopsy.

Most cancers are initially recognized either because of the appearance of signs or symptoms or through screening. Neither of these leads to a definitive diagnosis, which requires the examination of a tissue sample by a pathologist. People with suspected cancer are investigated with medical tests. These commonly include blood tests, X-rays, (contrast) CT scans and endoscopy.

The tissue diagnosis from the biopsy indicates the type of cell that is proliferating, its histological grade, genetic abnormalities and other features. Together, this information is useful to evaluate the prognosis and to choose the best treatment.

Further reading

How To Harness The Pain Blocking Effects of Exercise

Athletes have a very complicated relationship with pain. For endurance athletes in particular, pain is an absolutely non-negotiable element of their competitive experience. You fear it, but you also embrace it. And then you try to understand it.

But pain isn’t like heart rate or lactate levels—things you can measure and meaningfully compare from one session to the next. Every painful experience is different, and the factors that contribute to those differences seem to be endless. A recent study in the Journal of Sports Sciences, from researchers in Iraq, Australia, and Britain, adds a new one to the list: viewing images of athletes in pain right before a cycling test led to higher pain ratings and worse performance than viewing images of athletes enjoying themselves.

That finding is reminiscent of a result I wrote about last year, in which subjects who were told that exercise increases pain perception experienced greater pain, while those told that exercise decreases pain perception experienced less pain. In that case, the researchers were studying pain perception after exercise rather than during it, trying to understand a phenomenon called exercise-induced hypoalgesia (which just means that you experience less pain after exercise).

This phenomenon has been studied for more than 40 years: one of the first attempts to unravel it was published in 1979 under the title “The Painlessness of the Long Distance Runner,” in which an Australian researcher named Garry Egger did a series of 15 runs over six months after being injected with either an opioid blocker called naloxone or a placebo. Running did indeed increase his pain threshold, but naloxone didn’t seem to make any difference, suggesting that endorphins—the body’s own opioids—weren’t responsible for the effect. (Subsequent research has been plentiful but not very conclusive, and it’s currently thought that both opioid and other mechanisms are responsible.)

But the very nature of pain—the fact that seeing an image of pain or being told that something will be painful can alter the pain you feel—makes it extremely tricky to study. If you put someone through a painful experiment twice, their experience the first time will inevitably color their perceptions the second time.

As a result, according to the authors of another new study, the only results you can really trust are from randomized trials in which the effects of exercise on pain are compared to the results of the same sequence of tests with no exercise—a standard that excludes much of the existing research.

The new study, published in the Journal of Pain by Michael Wewege and Matthew Jones of the University of New South Wales, is a meta-analysis that sets out to determine whether exercise-induced hypoalgesia is a real thing, and if so, what sorts of exercise induce it, and in whom. While there have been several previous meta-analyses on this topic, this one was restricted to randomized controlled trials, which meant that just 13 studies from the initial pool of 350 were included.

The good news is that, in healthy subjects, aerobic exercise did indeed seem to cause a large increase in pain threshold. Here’s a forest plot, in which dots to the left of the line indicate that an individual study saw increased pain tolerance after aerobic exercise, while dots to the right indicate that pain tolerance worsened. 

The big diamond at the bottom is the overall combination of the data from those studies. It’s interesting to look at a few of the individual studies. The first dot at the top, for example, saw basically no change from a six-minute walk. The second and third dots, with the most positive results, involved 30 minutes of cycling and 40 minutes of treadmill running, respectively. The dosage probably matters, but there’s not enough data to draw definitive conclusions.

After that, things get a little tricker. Dynamic resistance exercise (standard weight-room stuff, for the most part) seems to have a small positive effect, but that’s based on just two studies. Isometric exercises (i.e. pushing or pulling without moving, or holding a static position), based on three studies, have no clear effect.

There are also three studies that look at subjects with chronic pain. This is where researchers are really hoping to see effects, because it’s very challenging to find ways of managing ongoing pain, especially now that the downsides of long-term opioid use are better understood. In this case, the subjects had knee osteoarthritis, plantar fasciitis, or tennis elbow, and neither dynamic nor isometric exercises seemed to help. There were no studies—or at least none that met the criteria for this analysis—that tried aerobic exercise for patients with chronic pain.

The main takeaway, for me, is how little we really know for sure about the relationship between exercise and pain perception. It seems likely that the feeling of dulled pain that follows a good run is real (and thus that you shouldn’t conclude that your minor injury has really been healed just because it feels okay when you finish).

Exactly why this happens, what’s required to trigger it, and who can benefit from it remains unclear. But if you’ve got a race or a big workout coming up, based on the study with pain imagery, I’d suggest not thinking about it too much. Hat tip to Chris Yates for additional research. For more Sweat Science, join me on Twitter and Facebook, sign up for the email newsletter, and check out my book Endure: Mind, Body, and the Curiously Elastic Limits of Human Performance.

By: Alex Hutchinson

Source: How to Harness the Pain-Blocking Effects of Exercise | Outside Online

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Critics:

Exercise-associated muscle cramps (EAMC) are defined as cramping (painful muscle spasms) during or immediately following exercise. Muscle cramps during exercise are very common, even in elite athletes. EAMC are a common condition that occurs during or after exercise, often during endurance events such as a triathlon or marathon.

Although EAMC are extremely common among athletes, the cause is still not fully understood because muscle cramping can occur as a result of many underlying conditions. Elite athletes experience cramping due to paces at higher intensities.The cause of exercise-associated muscle cramps is hypothesized to be due to altered neuromuscular control, dehydration, or electrolyte depletion.

It is widely believed that excessive sweating due to strenuous exercise can lead to muscle cramps. Deficiency of sodium and other electrolytes may lead to contracted interstitial fluid compartments, which may exacerbate the muscle cramping. According to this theory, the increased blood plasma osmolality from sweating sodium losses causes a fluid shift from the interstitial space to the intervascular space, which causes the interstitial fluid compartment to deform and contributes to muscle hyperexcitability and risk of spontaneous muscle activity.

The second hypothesis is altered neuromuscular control. In this hypothesis, it is suggested that cramping is due to altered neuromuscular activity. The proposed underlying cause of the altered neuromuscular control is due to fatigue. There are several disturbances, at various levels of the central and peripheral nervous system, and the skeletal muscle that contribute to cramping.

These disturbances can be described by a series of several key events. First and foremost, repetitive muscle exercise can lead to the development of fatigue due to one or more of the following: inadequate conditioning, hot and or humid environments, increased intensity, increased duration, and decreased supply of energy. Muscle fatigue itself causes increased excitatory afferent activity within the muscle spindles and decreased inhibitory afferent activity within the Golgi tendon.

The coupling of these events leads to altered neuromuscular control from the spinal cord. A cascade of events follow the altered neuromuscular control; this includes increased alpha-motor neuron activity in the spinal cord, which overloads the lower motor neurons, and increased muscle cell membrane activity. Thus, the resultant of this cascade is a muscle cramp.

See also

Sage Modelling Warns of Risk of ‘Substantial’ Covid Third Wave

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New modelling for the government’s Sage committee of experts has highlighted the risk of a “substantial third wave” of infections and hospitalizations, casting doubt on whether the next stage of Boris Johnson’s Covid roadmap can go ahead as planned on 21 June.

Government sources suggested the outlook was now more pessimistic but stressed that a decision would be taken after assessing a few more days’ worth of data on the effect that rising infections are having on hospitalizations.

The prime minister is due to announce on Monday whether the lifting of the remaining restrictions – nicknamed “freedom day” by anti-lockdown Tory MPs – will have to be delayed.

Johnson is understood to be personally frustrated at the prospect of delaying the reopening, but a No 10 source said there were now clearly signs for concern in the data.

Key ministers and officials are expected to discuss a range of options on Sunday, when Johnson will still be hosting the G7, including a two- to four-week delay, as well as the possibility of a watered-down reopening that keeps some rules in place.

A Whitehall source said it was “broadly correct” that the outlook was now more pessimistic. “Cases are obviously higher and they are growing quickly,” the source said.

Prof Neil Ferguson, of Imperial College London, said modelling updated this week suggested there was a risk of a surge in infections and hospitalizations that could rival the second wave in January.

Johnson sounded markedly less confident than in recent days when he was asked about the case for a delay as he visited a wind farm in Cornwall on Wednesday as part of the buildup to the G7 summit.

“What everyone can see very clearly is that cases are going up and in some cases hospitalizations are going up,” he said. “I think what we need to assess is the extent to which the vaccine rollout, which has been phenomenal, has built up enough protection in the population in order for us to go ahead to the next stage.

“And so that’s what we’ll be looking at. And there are arguments being made one way or the other, but that will be driven by the data. We’ll be looking at that and we’ll be setting it out on Monday.”

The prime minister had previously repeatedly said he had seen nothing in the data to justify a delay.

Ferguson said the cases of the Delta variant were now doubling in less than a week, close to what was seen before Christmas when the Alpha variant took hold and sent infections soaring in January to a daily peak of 68,000. What is unclear is how long the doubling will continue with so many adults vaccinated, and what proportion of new cases will turn into hospitalizations and deaths.

“There is a risk of a substantial third wave,” Ferguson said. “It could be substantially lower than the second wave or it could be of the same order of magnitude, and that critically depends on how effective the vaccines are at protecting people against hospitalization and death.”

He suggested there may be a case for postponing the reopening to get more shots into arms and reduce the size of any summer surge. “Clearly you have to be more cautious if you want measures to be irreversibly changed and relaxed,” he said. “Having a delay does make a difference. It allows more people to get second doses.”

Ministers have been encouraged by the enthusiasm with which younger people are taking up the opportunity to get their jab. The NHS announced that 1 million people had booked appointments through its website on Tuesday as eligibility was extended to 25- to 29-year-olds.

The next two to three weeks will be crucial for scientists on Sage to work out what the rise in hospitalizations – and potentially deaths – might look like in the months ahead.

Ferguson said: “One of the key things we want to resolve in the next few weeks is do we see an uptick in hospitalizations – we are seeing it in some areas – matching the cases, and what is the ratio between the two, because vaccination has substantially changed that.”

Evidence is firming up around the Delta variant being 60% more transmissible than the Alpha variant, with estimates ranging from 40% and 80%. The variant is somewhat resistant to vaccines, particularly after one dose.

While Ferguson believes we may see fewer deaths in the third wave compared with in January, the latest modelling does not rule out what he called a “disastrous” third wave if transmission and vaccine resistance are at the higher end of the best estimates.

The latest official data showed 7,540 new confirmed cases of the virus in England. Hospitalizations are not yet rising sharply nationwide, though they are surging in hotspot areas including Greater Manchester.

Chris Hopson, the chief executive of NHS Providers, said trusts in hard-hit areas were confirming that the vaccines provide good protection against the virus.

“There is a growing sense that thanks to the vaccine, the chain seen in previous waves between rising infections and high rates of hospital admissions and deaths has been broken. That feels very significant,” he wrote in a blogpost for the British Medical Journal.

But Hopson warned that the NHS was already “running hot” in many areas, and an increase in Covid admissions would set back efforts to tackle the long backlog of treatment for other health problems that has been caused by the crisis.

By:, and

Source: Sage modelling warns of risk of ‘substantial’ Covid third wave | Health policy | The Guardian

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Critics:

Recommended preventive measures include social distancing, wearing face masks in public, ventilation and air-filtering, hand washing, covering one’s mouth when sneezing or coughing, disinfecting surfaces, and monitoring and self-isolation for people exposed or symptomatic. Several vaccines have been developed and widely distributed since December 2020.

Current treatments focus on addressing symptoms, but work is underway to develop medications that inhibit the virus. Authorities worldwide have responded by implementing travel restrictions, lockdowns and quarantines, workplace hazard controls, and business closures. Numerous jurisdictions have also worked to increase testing capacity and trace contacts of the infected.

The pandemic has resulted in significant global social and economic disruption, including the largest global recession since the Great Depression of the 1930s. It has led to widespread supply shortages exacerbated by panic buying, agricultural disruption, and food shortages. However, there have also been decreased emissions of pollutants and greenhouse gases.

Numerous educational institutions and public areas have been partially or fully closed, and many events have been cancelled or postponed. Misinformation has circulated through social media and mass media, and political tensions have been exacerbated. The pandemic has raised issues of racial and geographic discrimination, health equity, and the balance between public health imperatives and individual rights.

The COVID-19 pandemic has resulted in misinformation and conspiracy theories about the scale of the pandemic and the origin, prevention, diagnosis, and treatment of the disease. False information, including intentional disinformation, has been spread through social media, text messaging, and mass media. Journalists have been arrested for allegedly spreading fake news about the pandemic. False information has also been propagated by celebrities, politicians, and other prominent public figures. The spread of COVID-19 misinformation by governments has also been significant.

Commercial scams have claimed to offer at-home tests, supposed preventives, and “miracle” cures. Several religious groups have claimed their faith will protect them from the virus. Without evidence, some people have claimed the virus is a bioweapon accidentally or deliberately leaked from a laboratory, a population control scheme, the result of a spy operation, or the side effect of 5G upgrades to cellular networks.

The World Health Organization (WHO) declared an “infodemic” of incorrect information about the virus that poses risks to global health. While belief in conspiracy theories is not a new phenomenon, in the context of the COVID-19 pandemic, this can lead to adverse health effects. Cognitive biases, such as jumping to conclusions and confirmation bias, may be linked to the occurrence of conspiracy beliefs.

See also

References

Show Your Immune System Some Love

If the immune system ran its own version of The Bachelor, antibodies would, hands down, get this season’s final rose. These Y-shaped molecules have acquired some star-caliber celebrity in the past year, due in no small part to COVID-19. For months, their potentially protective powers have made headlines around the globe; we test for them with abandon, and anxiously await the results.

Many people have come to equate antibodies, perhaps not entirely accurately, with near imperviousness to the coronavirus and its effects. Antibodies are, in many ways, the heartthrobs of the immune system—and some 15 months deep into immunological infatuation, the world is still swooning hard. Frankly, it’s all getting to be a little too much.

Don’t get me wrong: Antibodies have served me well, and thanks to my recent dalliance with the Pfizer vaccine, the anti-coronavirus variety will be receiving an extra dose of my admiration for a good while yet. I am, above all else, eager for the rest of the global population to nab the safeguards they offer, ideally for keeps.

But antibodies are simply not the only immune-system singles worthy of our love. A multitude of cells and molecules are crucial to building a protective immune response against this virus and many others. It’s time we took a break from antibodies, and embarked on a brief Rumspringa with the rest of the body’s great defenders.

What follows isn’t even close to a comprehensive overview of the immune system, because I am not a masochist, and because no one wants to read a 75,000-word story. Instead, I asked a few immunologists to chat with me about some of their favorite immune cells and molecules, and imagine what these disease fighters might be like if they truly were single and ready to mingle. As it were, everyone needs someone to be their starter bae.

Some good candidates might be found among the members of the innate immune system, a fast-acting fleet of cells that are the first to contend with an infection. (Antibodies belong to another branch, called the adaptive immune system; more on that later.) They’re a lot like adolescent lovers: dogged and earnest, but impulsive and, on occasion, woefully imprecise. Unlike antibodies, which can zero in on specific pathogens, innate immune cells are built to clobber just about anything that doesn’t resemble their human host. Perhaps it’s no surprise that these underdog cells are often forgotten or outright snubbed in conversations about immune protection.

But the all-purpose approach of innate immune cells has its charms. They’ll try anything at least once, and they’re admirably selfless. When pathogens come knocking, innate cells are the first to volunteer to fight, and often the first to die (RIP, neutrophils). Some ambush invading microbes directly, snarfing them down or bathing them with deadly toxins, while others blow up infected cells—tactics reminiscent of guerrilla warfare. Although antibodies take many days to appear, innate cells will immediately be “by your side when you have a problem,” Ashton Trotman-Grant, an immunologist at the University of Toronto, told me.

These acts of martyrdom buy the rest of the immune system time to prepare a more targeted attack. And in many cases, innate immune cells act so quickly and decisively that they can subdue an invasive microbe on their own—a level of self-sufficiency that most other defenders can’t match.

Some innate immune cells are also just plain adorable. Among the fan favorites are macrophages (“big eaters” in Greek), aptly named for their round-boi physique and insatiable appetite. Their goal in life is to chow down for the greater good. “They’ll never make you feel like you’re eating too much, and they’re open to trying new foods,” Juliet Morrison, a virologist and immunologist at UC Riverside, told me. They’re also endearingly unselfish: If a microbe crosses their path, they’ll gobble it up, then belch up bits to wave at adaptive immune cells as a warning of potential danger. It’s a great gift-giving strategy, Morrison said, especially if weird microscopic puke is what makes your heart go pitter-patter.

Dendritic cells have a similar modus operandi. Like macrophages, they specialize in regurgitating gunk for other immune cells. But they are much more social than macrophages, which prefer to gorge and digest in solitude. Dendritic cells are sentinels and gregarious gossips; their primary imperative is to “talk and hang out with other cells,” and they’ll flit from tissue to tissue to do it, David Martinez, an immunologist at the University of North Carolina at Chapel Hill, told me. If you’ve recently caught word of a new and dangerous infection, you probably heard about it from a dendritic cell.

A few weeks ago, Trotman-Grant put together a March Madness–style bracket to choose the “best” immune cell; after a couple of grueling weeks of voting, dendritic cells won. They’re almost certainly the cells you’d want to take to prom. But Trotman-Grant warned that their social-butterfly tendencies could be a double-edged sword: Dendritic cells just aren’t the type to settle down. Innate immune cells might be convenient dates, for a time. But while they’re great at first impressions, they can also be commitment-phobes, as likely to ghost you as they are to come on strong. (Besides, who wants to date someone who’s always arriving on the early side?)

The real keepers belong to the adaptive branch of the immune system: B cells—the makers of antibodies—and T cells, which, among many other tasks, kill virus-infected cells. Adaptives are slow-moving specialists. They take down microbial invaders that innate cells can’t handle on their own, relying heavily on intel from macrophages, dendritic cells, and other early defenders. They won’t be the first to make a move, but they’re sharp and sophisticated, capable of singling out individual pathogens and zapping them with precision.

B and T cells are self-assured enough to know what they want. Unlike innate cells, they’re also capable of remembering the things they’ve encountered before, ensuring that most pathogens can’t trouble the same person twice; that capacity is the conceptual basis of vaccines. “They do a great job at committing things to memory,” Ryan McNamara, a virologist at UNC Chapel Hill, told me. That also means no missed birthdays or anniversaries—and no chance they’ll ever forget that time you were wrong.

If you’re a fan of antibodies, you have B cells to thank: They are the glorious wellsprings whence these molecules hail. (On Mother’s Day, antibodies call their B cells.) Unfortunately, B cells are often overlooked; as living, dividing cells that hide away in tissues, they’re harder to isolate and study than the proteins they produce. But the antibodies they deploy can be powerful enough to quash microbes before they break into cells, potentially halting infections in their tracks. And even after antibodies disappear, B cells persist, ready to produce more.

Martinez stans the B cells he studies. But he’s wary of their romantic potential. B cells, he said, are almost too good at their job, and will compete aggressively among themselves. Their crime-fighting careers consume them, leaving little room for a fulfilling personal life. “I would say B cells are selfish,” he told me. In the cold light of morning, it turns out a lot of them are just self-involved snobs.

T cells play a far more subtle game. Their career choices range from demolishing virus-killed cells to corralling and coordinating other immune cells. As several researchers have pointed out, T cells might be some of the most underappreciated cells in the war against COVID-19, especially when it comes to vaccines. Some evidence even suggests that, in the absence of decent antibodies, T cells can clean up the coronavirus mostly on their own.

Certain T cells are killers. As their name suggests, they operate with devilish flair: When they happen upon virus-infected cells, they force them to self-destruct. Killers’ excellent memories also give them a predilection for grudges—enemies that trouble them twice should expect to be trounced with extra gusto. Thrill seekers might be drawn to killers, but Avery August, an immunologist at Cornell University, points out that these cells, also called cytotoxic T cells, might be all take and no give. Scientifically, they’re full of intrigue; romantically, he told me, “not so much”—at least for him.

Then there are the helpers—the benign Jekyll to the killers’ bellicose Hyde. Helper Ts are some of the most loyal partners you’ll find in the immune system, nurturing almost to a fault and versatile to boot. They coax B cells into maturing into antibody factories. They cheer killers along their murderous paths. They even goad innate immune cells into becoming the most ferocious fighters (and feeders) they can be. Effectively, helpers are “badass multitaskers that coordinate every level of immunity,” Marion Pepper, an immunologist at the University of Washington, told me. They’re about as supportive as they come—as long as you don’t mind being micromanaged from time to time.

It’s easy to see the appeal of antibodies. They’re among the few immune-system soldiers that can annihilate viruses before they enter cells, and they’re thought to be crucial to most vaccines. They can also be team players, throwing up red flags around microbes in order to alert other defenders to their presence. Transferred from animal to animal, or human to human, antibodies can confer protection against COVID-19; synthetic versions of the molecules are also relatively straightforward to manufacture en masse. Scoring a date with an antibody is a bit like finally getting together with the most popular person in school.

But counting on antibodies, and only antibodies, for protection is like shacking up with the first eligible suitor you meet—a risky and perhaps close-minded gamble. In the same way that our immune systems can guard against multiple pathogens at once, we could stand to be a bit less monogamous with our affections.

Besides, the choice might not ultimately be ours to make. Love is a two-way street, and antibodies are incorrigibly picky. Their sole mission is to glom on to a very specific microbe and cling to it, ignoring everything else along the way; it’s largely them doing the picking and choosing. And if you’re not the soul mate they imagined, there’s little you can do to change their minds—they’re proteins, and they don’t have one. Really, it’s not them. It’s you.

By: Katherine J. Wu

Source: Show Your Immune System Some Love – The Atlantic

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This Remote Patient Monitoring Startup Just Landed A $70 Million Series C

Health Recovery Solutions in action

hen Covid-19 cases began to soar around Ann Arbor in April, the University of Michigan Hospital reached 100% capacity. Like most hospitals, University of Michigan Hospital was not ready for the pandemic surge, but they did have a leg up.

That same month they’d coincidentally implemented Health Recovery Solutions’ remote patient monitoring, a patented technology system that records patient vitals via Bluetooth and connects them with their clinicians through video or instant messaging. This enabled the resource-strapped hospital to care for over 400 patients remotely throughout 2020.

Today, HRS announced it closed a $70 million series C led by LLR Partners with participation from existing investor Edison Partners, bringing the Hoboken, New Jersey-based startup’s total funding to $86 million. The news comes on the heels of a year of massive growth, which saw their head count balloon 258% to 155 employees and revenue grow by 188% to $23.5 million.

“People are choosing the proven remote-monitoring solution right now,” says Jarrett Bauer, HRS’ Forbes 30 Under 30 cofounder and CEO. “That’s one of the reasons why we’re doing so well—people are looking for the company that’s best.”

Bauer, now 34, was inspired to start by HRS by his grandma. Battling a heart condition, Bauer’s grandma was admitted to the hospital three times, resulting in over $14,000 of medical bills. While pursuing his M.B.A. at Johns Hopkins in 2012, Bauer began constructing an at-home hospital alternative that would eventually become HRS. “We didn’t know where to start,” Bauer told Forbes in 2019 when the company raised its $10 million series B. “We just knew it was a problem, and the best companies solve problems.”

With Covid-19, telehealth doctor appointments have become just doctor appointments, increasing 154% from March to October of 2020, according to the Centers for Disease Control. Rather than cut into HRS’ margins, the telehealth boom has helped HRS soar. The healthcare company has deals with over 220 U.S. healthcare systems—74 of which signed on as clients of HRS during the pandemic—with over 20,000 nurses checking HRS logs every day.

“We consider Health Recovery Solutions the Cadillac model,” says Brandy Knudson, Michigan Medicine’s Telehealth Project Manager. “It fills a huge gap for us because we want to reduce readmissions and reduce unnecessary trips to the hospital.”

The company makes money by billing clinical institutions on subscription to integrate their solutions in treatment, coming at no additional cost to patients. HRS recognizes the varying levels of sickness and technological ability of patients, so the company’s products range from a pulse oximeter for the sickest, while near-recovered patients can manually enter symptoms on HRS’ smartphone app.

All of this patient data is stored in a cloud for clinicians, making it easier to recognize prognosis patterns and health trends. By implementing HRS, major healthcare systems like Penn Medicine have reduced 30-day readmission by over 50% for all heart failure patients, while FirstHealth of the Carolinas says the technology has saved patients more than $1.9 million since its implementation in 2016.

“Patients are looking to stay in their homes longer, get care in their homes longer, and there’s an increasing prevalence of chronic conditions,” says Sasank Aleti, a partner at Philadelphia-based private equity firm LLR Partners. “HRS met our criteria of taking costs out of the system, driving better outcomes and a better patient experience.”

For Bauer, the future of HRS lies in universalizing hospital-from-home treatment. With the $70 million round, the company plans to more than double head count in 2021 to 250 employees with the goal of being able to treat over a million patients by adding new healthcare providers and upping their disease module count (they currently treat 90 diseases). “Why aren’t we like Google? Why aren’t we like Apple?” asks Bauer. “We’re playing to win—to be that.”

I’m the Under 30 Editorial Community Lead at Forbes. Previously, I directed marketing at a mobile app startup. I’ve also worked at The New York Times and New York Observer. I attended the University of Pennsylvania where I studied English and creative writing. Follow me on Instagram and Twitter at @iamsternlicht.

Source: This Remote Patient Monitoring Startup Just Landed A $70 Million Series C

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The coronavirus pandemic has overwhelmed hospitals, physicians and the medical community. That’s pushed telemedicine into the hands of providers and patients as the first response for primary care. Telemedicine isn’t new to the medical community, however it hasn’t been embraced due to insurance coverage, mindset and stigma. Here’s how it works and what it means for the future of health care. » Subscribe to CNBC: https://cnb.cx/SubscribeCNBC » Subscribe to CNBC TV: https://cnb.cx/SubscribeCNBCtelevision » Subscribe to CNBC Classic: https://cnb.cx/SubscribeCNBCclassic
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What’s The Difference Between Covid-19 Coronavirus Vaccines

Coronavirus COVID-19 single dose small vials and multi dose in scientist hands concept. Research for new novel corona virus immunization drug.

The world can’t return to normal without safe and effective vaccines against the SARS-CoV-2 coronavirus along with a coordinated global vaccination programme.

Researchers have been racing to develop potential drugs that could help end the ongoing Covid-19 pandemic. There are currently around 200 vaccine candidates and about a quarter passed preclinical tests and are now undergoing clinical trials.

What’s the difference between the various candidate vaccines?

A pie chart of candidates can be cut several ways. One is to slice it into six uneven pieces according to the technology (or ‘platform’) that’s used to produce the drug. Those six technologies can be grouped into three broader categories: dead or disabled viruses, artificial vectors, and viral components.

Dead or disabled viruses

Traditional vaccines contain a dead or disabled virus, designed to be incapable of causing severe disease while also provoking an immune response that provides protection against the live virus.

1. Live-attenuated viruses

Attenuated means ‘weakened’. Weakening a live virus typically involves reducing its virulence — capacity to cause disease — or ability to replicate through genetic engineering. The virus still infects cells and causes mild symptoms.

For a live-attenuated virus, an obvious safety concern is that the virus might gain genetic changes that enable it to revert back to the more virulent strain. Another worry is that a mistake during manufacturing could produce a defective vaccine and cause a disease outbreak, which once happened with a polio vaccine. MORE FOR YOUJapan Has Opened Hayabusa2’s Capsule, Confirming It Contains Samples From Asteroid RyuguDonald Trump’s Presidency Will End On The Day Of A Comet, A Meteor Shower And A Total Eclipse Of The SunIn A New Epidemiological Study, Daily Doses Of Glucosamine/Chondroitin Are Linked To Lower All-Cause Mortality

But using a live-attenuated virus has one huge benefit: vaccination resembles natural infection, which usually leads to robust immune responses and a memory of the virus’ antigens that can last for many years.

Live-attenuated vaccines based on SARS-CoV-2 are still undergoing preclinical testing, developed by start-up Codagenix and the Serum Institute of India.

2. Inactivated viruses

Inactivated means ‘dead’ (‘inactivated’ is used because some scientists don’t consider viruses to be alive). The virus will be the one you want to create a vaccine against, such as SARS-CoV-2, which is usually killed with chemicals.

Two Chinese firms have developed vaccines that are being tested for safety and effectiveness in large-scale Phase III clinical trials: ‘CoronaVac’ (previously ‘PiCoVacc’) from Sinovac Biotech and ‘New Crown COVID-19’ from Sinopharm. Both drugs contain inactivated virus, didn’t cause serious adverse side-effects and prompted the immune system to produce antibodies against SARS-CoV-2.

Sinopharm’s experimental vaccine has reportedly been administered to hundreds of thousands of people in China, and both drugs are now being trialled in countries across Asia, South America and the Middle East.

COVID-19 vaccine landscape (left) and platforms for SARS-CoV-2 vaccine development (right)
The global COVID-19 vaccine landscape (left) and Vaccine platforms used for SARS-CoV-2 vaccine … [+] Springer

Artificial vectors

Another conventional approach in vaccine design is to artificially create a vehicle or ‘vector’ that can deliver specific parts of a virus to the adaptive immune system, which then learns to target those parts and provides protection.

That immunity is achieved by exposing your body to a molecule that prompts the system to generate antibodies, an antigen, which becomes the target of an immune response. SARS-CoV-2 vaccines aim to target the spike protein on the surface of coronavirus particles — the proteins that allows the virus to invade a cell.

3. Recombinant viruses

A recombinant virus is a vector that combines the target antigen from one virus with the ‘backbone’ from another — unrelated — virus. For SARS-CoV-2, the most common strategy is to put coronavirus spike proteins on an adenovirus backbone.

Recombinant viruses are a double-edged sword: they behave like live-attenuated viruses, so a recombinant vaccine comes with the potential benefits of provoking a robust response from the immune system but also potential costs from causing an artificial infection that might lead to severe symptoms.

A recombinant vaccine might not provoke an adequate immune response in people who have previously been exposed to adenoviruses that infect humans (some cause the common cold), which includes one candidate developed by CanSino Biologics in China and ‘Sputnik V’ from Russia’s Gamaleya National Research Centre — both of which are in Phase III clinical trials and are licensed for use in the military.

To maximize the chance of provoking immune responses, some vaccines are built upon viruses from other species, so humans will have no pre-existing immunity. The most high-profile candidate is ‘AZD1222’, better known as ‘ChAdOx1 nCoV-19’ or simply ‘the Oxford vaccine’ because it was designed by scientists at Oxford University, which will be manufactured by AstraZeneca. AZD1222 is based on a chimpanzee adenovirus and seems to be 70% effective at preventing Covid-19.

Some recombinant viruses can replicate in cells, others cannot — known as being ‘replication-competent’ or ‘replication-incompetent’. One vaccine candidate that contains a replicating virus, developed by pharmaceutical giant Merck, is based on Vesicular Stomatitis Virus (VSV), which infects guinea pigs and other pets.

4. Virus-like particles

A virus-like particle, or VLP, is a structure assembled from viral proteins. It resembles a virus but doesn’t contain the genetic material that would allow the VLP to replicate. For SARS-CoV-2, the VLP obviously includes the spike protein.

One coronavirus-like particle (Co-VLP) vaccine from Medicago has passed Phase I trials to test it’s safe and has entered Phase II to test that it’s effective.

While there are currently few VLPs being developed for Covid-19, the technology is well-established and has been used to produce commercial vaccines against human papillomavirus (HPV) and hepatitis B.

Viral components

All vaccines are ultimately designed to expose the immune system to parts of a virus, not the whole thing, so why not deliver just those parts? That’s the reasoning behind vaccines that only contain spike proteins or spike genes.

5. Proteins

Protein-based vaccines can consist of the full-length spike protein or the key part, the tip of the spike that binds the ACE2 receptor on the surface of a cell — ACE2 is the lock that a coronavirus picks in order to break into the cell.

Manufacturing vaccines containing the protein alone has a practical advantage: researchers don’t have to deal with live coronaviruses, which should be grown inside cells within a biosafety level-3 lab.

A vaccine against only part of the protein — a ‘subunit’ — will be more vulnerable to being rendered useless if random mutations alter the protein, known as ‘antigenic drift‘, but full-length proteins are harder to manufacture. The immune system can recognize either as an antigen.

One candidate vaccine based on protein subunits is ‘NVX-CoV2373’ from Novavax, where the spike subunits are arranged as a rosette structure. It’s similar to a vaccine that’s already been licensed for use, FluBlok, which contains rosettes of protein subunits from the influenza virus.

6. Nucleic acids

Nucleic-acid vaccines contain genetic material, either deoxyribonucleic acid or ribonucleic acid — DNA or RNA. In a coronavirus vaccine, the DNA or RNA carries genetic instructions for producing a spike protein, which is made within cells.

Those spike genes can be carried on rings of DNA called ‘plasmids’, which are easy to manufacture by growing them in bacteria. DNA provokes a relatively weak immune response, however, and can’t simply be injected inside the body — the vaccine must be administered using a special device to force DNA into cells. Four DNA-based candidates are in Phase I or II trials.

The two most famous nucleic-acid vaccines are the drugs being developed by pharmaceutical giant Pfizer, partnered with BioNTech, and Moderna. Pfizer’s ‘BNT162b2’ and Moderna’s ‘mRNA-1273’ both use ‘messenger RNA’ — mRNA — to carry the spike genes and are delivered into cells via a lipid nanoparticle (LNP). The two mRNA vaccines have completed Phase III trials and preliminary results suggests they’re over 90% effective at preventing Covid-19.

As the above examples show, not only there are many potential vaccines but also various approaches. And while some technologies have already provided promising results, it remains to be seen which will actually be able to defeat the virus.

Full coverage and live updates on the CoronavirusFollow me on Twitter or LinkedIn. Check out my website or some of my other work here

JV Chamary

JV Chamary

I’m a science communicator specialising in public engagement and outreach through entertainment, focusing on popular culture. I have a PhD in evolutionary biology and…

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TODAY

Dr. Ashish Jha, dean of Brown University’s School of Public Health, joins the 3rd hour of TODAY to break down the differences between Moderna’s and Pfizer’s coronavirus vaccine candidates. He also comments on speculation of another national shutdown and whether families should still get together over Thanksgiving. » Subscribe to TODAY: http://on.today.com/SubscribeToTODAY » Watch the latest from TODAY: http://bit.ly/LatestTODAY About: TODAY brings you the latest headlines and expert tips on money, health and parenting. We wake up every morning to give you and your family all you need to start your day. If it matters to you, it matters to us. We are in the people business. Subscribe to our channel for exclusive TODAY archival footage & our original web series. Connect with TODAY Online! Visit TODAY’s Website: http://on.today.com/ReadTODAY Find TODAY on Facebook: http://on.today.com/LikeTODAY Follow TODAY on Twitter: http://on.today.com/FollowTODAY Follow TODAY on Instagram: http://on.today.com/InstaTODAY Follow TODAY on Pinterest: http://on.today.com/PinTODAY#COVID19Vaccines#AshishJha#TodayShow

Can We Claim Medical Expenses on Our Taxes

Extensive series of several doctors with various patients in a medical exam room.

Medical expenses can take a bite out of your budget, especially if you have unforeseen emergencies that are not fully covered by your insurance. The Internal Revenue Service allows taxpayers some relief, making some of these expenses partly tax-deductible. To take advantage of this tax deduction, you need to know what counts as a medical expense and how to claim the deduction.

Deduction value for medical expenses

In 2020, the IRS allows all taxpayers to deduct the total qualified unreimbursed medical care expenses for the year that exceeds 7.5% of their adjusted gross income.

Your adjusted gross income (AGI) is your taxable income minus any adjustments to income such as contributions to a traditional IRA and student loan interest.Your resource on tax filingTax season is here! Check out the Tax Center on AOL Finance for all the tips and tools you need to maximize your return.Go Now

For example, if you have an adjusted gross income of $45,000 and $5,475 of medical expenses, you would multiply $45,000 by 0.1 (10 percent) to find that only expenses exceeding $4,500 can be deducted. This leaves you with a medical expense deduction of $975 (5,475 – 4,500).

Which medical expenses are deductible?

The IRS allows you to deduct preventative care, treatment, surgeries and dental and vision care as qualifying medical expenses. You can also deduct visits to psychologists and psychiatrists. Prescription medications and appliances such as glasses, contacts, false teeth and hearing aids are also deductible.

The IRS also lets you deduct the expenses that you pay to travel for medical care such as mileage on your car, bus fare and parking fees.

What’s not deductible?

Any medical expenses for which you are reimbursed, such as by your insurance or employer, cannot be deducted. In addition, the IRS generally disallows expenses for cosmetic procedures. You cannot deduct the cost of non-prescription drugs (except insulin) or other purchases for general health such as toothpaste, health club dues, vitamins or diet food, non-prescription nicotine products or medical expenses paid in a different year.

Claiming the medical expenses deduction

To claim the medical expenses deduction, you must itemize your deductions. Itemizing requires that you not take the standard deduction, so you should only claim the medical expenses deduction if your itemized deductions are greater than your standard deduction (TurboTax will do this calculation for you).

If you elect to itemize, you must use IRS Form 1040 to file your taxes and attach Schedule A.

  • On Schedule A, report the total medical expenses you paid during the year on line 1 and your adjusted gross income (from your Form 1040) on line 2.
  • Enter 7.5% of your adjusted gross income on line 3.
  • Enter the difference between your expenses and 7.5% of your adjusted gross income on line 4.
  • The resulting amount on line 4 will be subtracted from your adjusted gross income to reduce your taxable income for the year.
  • If this amount, plus any other itemized deductions you claim, is less than your standard deduction, you should not itemize.

Remember, TurboTax will ask you simple questions about your expenses, tell you which deductions you qualify for, and fill in all the right forms for you.

For more tax tips in 5 minutes or less, subscribe to the Turbo Tips podcast on Apple Podcasts, Spotify and iHeartRadio

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Great Ways to Get Charitable Tax DeductionsGenerally, when you give money to a charity, you can use the amount of that donation as an itemized deduction on your tax return. However, not all charities qualify as tax-deductible organizations. While there are many types of charities, they must all meet certain criteria to be classified by the IRS as tax-deductible organizations. There are legitimate tax-deductible organizations in many popular categories, such as those listed below.Read MoreBrought to you byTurboTax.com

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Debi Peverill

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Why Scientists & Public Health Officials Need To Address Vaccine Mistrust Instead of Dismissing it

Recent polls indicate that more than a third of the country has concerns about a vaccine that in all likelihood will be the only reliable way to end to the COVID-19 pandemic.

These results reflect a similar public sentiment in the U.S. in the 1950s when a polio vaccine was introduced. There are likely multiple reasons for this suspicion, including safety concerns, lack of transparency from the scientific community, lack of trust in the government and the desire to wait until a longer track record of safety can be established.

We are experts in media literacy, health and political communication and biostatistics and biomedical research for future health care providers, from Washington State University’s Edward R. Murrow Center for Media & Health Promotion Research and the Elson S. Floyd College of Medicine. We also live in the communities we hope to serve with our science.

Based on our research, we believe that officials need to use this testing period to build trust, not to create reasons for diminishing it. Respect and forthrightness can turn the tone from adversarial to collaborative, and from a provider-directed practice to a shared decision-making process. Scientists and public health officials must anticipate and address people’s concerns and not brush aside concerns, a process that has become commonplace across other areas of the provider-patient relationship, but vaccine decisions remain a notable exception.

Vaccines and complications

Vaccines are among the safest, most transformative drugs on Earth, with adverse events so low that very nearly universal vaccination is a reasonable expectation. With such a safety record, and with so much at risk with diseases like COVID-19, measles and influenza, vaccine advocates have good reason to stress the overwhelmingly positive safety record.

History has included some vaccines of questionable quality as well as vaccination tactics of even more concern. Certain minority groups have been targeted with egregious coercion. This included cases of forced vaccination for smallpox of African Americans at gunpoint in the southern United States in the early 1900s. At a tenement house in Manhattan’s Little Italy, over 200 men in 1901 in essence performed a smallpox vaccination raid in the middle of the night, trying to vaccinate as many people as they could.

When the miracle vaccine for polio was widely distributed in 1955, speed took precedent over safety, and many doses were distributed that contained live polio virus. As a result, 70,000 children developed muscle weakness, 164 were paralyzed permanently and 10 children died. This led to direct government intervention that has led to thousands of required tests in order to ensure safety and effectiveness.

Why can’t vaccines bounce back from mistakes?

As medical and public health researchers, we have found it interesting that corporations that have been lax and dishonest have bounced back without lasting damage to their reputations. For example, Volkswagen was caught in 2014 for outright lying to the public about their emissions. By 2019, the company topped its prescandal sales record of 2014.

We accept these occasionally fatal flaws and ethical missteps because cars are essential to our lives. The documented safety record of vaccines is staggering, not unlike the impressive safety record boasted by most automobiles on the road today.

Why do vaccines get special scrutiny? Have scientists and health care providers engaged in scientific snobbery by assuming people should do what we advise, without question or any decision-making process? Can scientists and health care providers communicate the good and positive (and bad) background of vaccines better? Has social media sown doubt in an authority that can be perceived to be overconfident? Personal health care decisions have a lasting impact on our kids and our families, so let’s rise to the occasion and utilize this unique opportunity to reframe the conversation about vaccines.

Embrace shared decision-making

The existence of a little-known but critical government office both acknowledges past problems with some vaccines and also provides a method of recourse for those injured by vaccines. The National Vaccine Injury Compensation Program, launched in the 1980s, is a powerful tool for transparency and accountability that should help shape this important, shared decision-making process. For example, between 2006 and 2018 over 3.7 billion doses of covered vaccines were distributed in the U.S. During this same period, 5,233 filed petitions to this office were compensated out of a total of 7,482 petitions. This means that for every 1 million vaccine doses distributed, one individual received compensation.

Rather than brushing off concerns among parents and others who are concerned about safety, experts should listen. When they do talk, they should explain safety issues and should use metaphors such as the safety of vehicles and other medical breakthroughs (e.g., insulin, heart valve surgery) so often relied upon in an effort to work toward the same goal together as a country, and as health care provider and patient.

Experts should acknowledge that the practice of medicine and public health research is a relatively new field of science to drive public health, medical practice advancement and policies when compared to other, far more established scientific disciplines such as physics or chemistry. Building public support requires more than citing solid evidence in the peer-reviewed scientific literature. Owning up to setbacks in vaccine development that the current administration may be on the brink of repeating – and then making the necessary repairs to move forward again, as the auto manufacturers do – also builds confidence. AstraZeneca’s public announcement about a serious adverse event in one of their trials, which led to a pause of participant enrollment, was a great first step.

Let’s begin by acknowledging that all parties want to achieve the same end goal of a healthy, safe return to daily life. Despite the explosion of misinformation about COVID-19, a clear, consistent and respectful approach can reset the vaccine conversation.

[Deep knowledge, daily. Sign up for The Conversation’s newsletter.]

Next, let’s acknowledge that vaccines are not now and have not been 100% perfect (nor is any medicine or car). We should also note that the same science that produces vaccines also produces myriad breakthroughs in specialties such as cardiology and oncology, along with over-the-counter medications such as ibuprofen that mitigate minor ailments but also have limitations and warning labels.

Finally, invite skeptics to a conversation and acknowledge up front that, like any other scientific advancement of things that now work, there was a time when they didn’t work as well, or at all.

Instances like these undoubtedly fuel people’s concerns. Such occurrences should give us all pause, scientist or not, to do better next time and strive to never repeat such notable grievances.

By: Sterling M. McPherson/ Associate Professor, Director and Assistant Dean for Research, Washington State University

Erica Weintraub Austin/ Professor and Director, Edward R. Murrow Center for Media & Health Promotion Research, Washington State University

Porismita Borah/Associate Professor, health communication, Washington State University

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CBC News: The National

Misinformation about vaccines have public health officials in Canada looking for guidance on how to combat medical mistrust. As CBC’s Katie Nicholson reports, the answers they are looking for might be half a world away. »»» Subscribe to The National to watch more videos here: https://www.youtube.com/user/CBCTheNa… Voice Your Opinion & Connect With Us Online: The National Updates on Facebook: https://www.facebook.com/thenational The National Updates on Twitter: https://twitter.com/CBCTheNational »»» »»» »»» »»» »»» The National is CBC Television’s flagship news program. Airing six days a week, the show delivers news, feature documentaries and analysis from some of Canada’s leading journalists.

Anti-viral drug remdesivir effective against coronavirus, study finds

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Anti-viral drug remdesivir cuts recovery times in coronavirus patients, according to the full results of a trial published Friday night, three weeks after America’s top infectious diseases expert said the study showed the medication has “clear-cut” benefits.

Complete results from the research, which was carried out by US government agency the National Institute of Allergy and Infectious Diseases (NIAID), were published by leading medical periodical the New England Journal of Medicine.

The United States authorized the emergency use of remdesivir in hospitals on May 1, followed by Japan, while Europe is considering following suit.The study found that remdesivir, injected intravenously daily for 10 days, accelerated the recovery of hospitalized COVID-19 patients compared to a placebo in clinical tests on just over a thousand patients across 10 countries.

On April 29, NIAID director Anthony Fauci, who has become the US government’s trusted face on the coronavirus pandemic, said preliminary evidence indicated remdesivir had a “clear-cut, significant and in diminishing the time to recovery.”The National Institutes of Health, of which the NIAID is a part, said Friday in a statement online that investigators found “remdesivir was most beneficial for hospitalized patients with severe disease who required .”

But the authors of the trial wrote that the drug did not prevent all deaths.”Given high mortality despite the use of remdesivir, it is clear that treatment with an anti-viral drug alone is not likely to be sufficient,” they said.About 7.1 percent of patients given in the trial group died within 14 days—compared with 11.9 percent in the placebo group.

However, the result is just below the statistical reliability threshold, meaning it could be down to chance rather than the capability of the .

A total of 1063 patients underwent randomization. The data and safety monitoring board recommended early unblinding of the results on the basis of findings from an analysis that showed shortened time to recovery in the remdesivir group. Preliminary results from the 1059 patients (538 assigned to remdesivir and 521 to placebo) with data available after randomization indicated that those who received remdesivir had a median recovery time of 11 days (95% confidence interval [CI], 9 to 12).

As compared with 15 days (95% CI, 13 to 19) in those who received placebo (rate ratio for recovery, 1.32; 95% CI, 1.12 to 1.55; P<0.001). The Kaplan-Meier estimates of mortality by 14 days were 7.1% with remdesivir and 11.9% with placebo (hazard ratio for death, 0.70; 95% CI, 0.47 to 1.04). Serious adverse events were reported for 114 of the 541 patients in the remdesivir group who underwent randomization (21.1%) and 141 of the 522 patients in the placebo group who underwent randomization (27.0%).

Conclusions

Remdesivir was superior to placebo in shortening the time to recovery in adults hospitalized with Covid-19 and evidence of lower respiratory tract infection. (Funded by the National Institute of Allergy and Infectious Diseases and others; ACCT-1 ClinicalTrials.gov number, NCT04280705. opens in new tab.)

Source: https://medicalxpress.com

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Ford and GM launch battle to produce COVID-19 ventilators

Workers at GM and Ford are beginning to produce life-saving ventilators at Michigan plants that normally make cars and trucks.

While full production won’t begin until May, the many thousands of ventilators they make will be useful then and in later months should a COVID-19 resurgence occur in the fall or later in 2021 before a vaccine is ready and widely used.

The engineering feat of converting from making vehicles to ventilators is complex, not only because of the technology involved. Both cars and ventilators share electronics and metal and plastic parts that need to be assembled, but there are the added challenges of building thousands of medical devices rapidly with high accuracy and of keeping workers safe while they maintain personal distancing on an assembly line.

 “We’re used to building big automotive products but scaling to product a small ventilator requires different sourcing of components and capabilities,” Adrian Price, Ford’s director of global core engineering, said in an interview with CBS This Morning. 

“There’s quite a bit that goes into taking a design that is currently produced at the rate of two a day and scaling that to over 7,000 a week,” he added.

GM is bringing back hundreds of workers to produce ventilators next week and will be imposing safety guidelines that include distancing between workers, periodic taking of temperature and scrubbing down work areas between shifts, according to the CBS report.

The two companies together are enlisting up to 1,500 workers to make ventilators, while Ford wants to produce 50,000 by July 4 and GM wants to build 200,000 overall, according to The Washington Post.

Getting fully functioning machines ready for use that are tested and reliable will be part of the process.  Some ventilators are built to operate only for short periods of time, pumping air or oxygen into a patient’s lungs, while others must pump for days.  There can be an array of electronics for controlling alarms and fail safes, as well as redundancy.

Testing of the machines will typically take a few minutes, looking at plastic and metal parts but also assessing how well a machine responds when in use, even when a patient coughs into a tube that is connected to the device, according to engineers that spoke to FierceElectronics.

RELATED: COVID-19 ramp-up marshals engineering army

Price told the Post that Ford is looking at ways to scale up more quickly, adding that “time is of the essence.”

Ford is partnering with Airon, which normally makes up to three ventilator machines a day, while GM is working with Ventec Life Systems.

Price told the Post that Ford asked thousands of auto suppliers to retool their manufacturing to create ventilator components and found that all but one component could be purchased inside the U.S.  Ford is developing ventilators in its Rawsonville, Michigan, plant with tradesmen from Local 898 of the United Auto Workers Union, according to the Post.

By: Matt Hamblen |

Source: Ford and GM launch battle to produce COVID-19 ventilators

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