‘Grey’s Anatomy’ Fans Are Applauding the Show’s Coronavirus Tribute Scene – Yahoo Lifestyle

Photo credit: ABC

From Harper's BAZAAR

[There are spoilers ahead for last night's episode of Grey's Anatomy. If you haven't watched the episode yet, return to this post at a later date!]

The doctors at Grey Sloan Memorial have been battling the coronavirus pandemic all season, but last night's episode dealt the fans the first really personal COVID-19 death of the year. Miranda Bailey's mom passed away from COVID-19 at the end of Thursday night's episode, in scene that can really only be described as a punch to the gut. After that, the show paid tribute to all the lives lost to COVID-19 this year, and fans are applauding that choice.

The assertion that those who have passed away during the coronavirus pandemic aren't just faceless statistics was present throughout the whole episode, and Bailey even talked about it in her voiceover. People should be remembered for the lives they lived and the people they loved, she said. So when the show transitioned into a scrolling list of names of those lost to the pandemic, fans were gutted, but appreciated the decision. It even made some Grey's fans angrier that there are still people in the real world that don't take coronavirus seriously. Here are some of their reactions.

Grey's has been handling the pandemic in a real (but tasteful) way all season. Last night's episode was a really good reminder of what's at stake right now. So stay home, mask up, and keep people safe! Miranda Bailey said so!

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'Grey's Anatomy' Fans Are Applauding the Show's Coronavirus Tribute Scene - Yahoo Lifestyle

Grey’s Anatomy star Chandra Wilson addresses her future on the show as Miranda Bailey – Digital Spy

Grey's Anatomy spoilers follow.

For the 17th season of Grey's Anatomy, the show has been tackling the coronavirus pandemic and showing the frontline workers battling and struggling to try and save lives.

In episode five, Miranda Bailey had a devastating loss when her mother was diagnosed with COVID-19 and brought to the hospital where she later died.

It was heartbreaking to watch, but the most emotional moment was when Bailey sang 'My Girl' to her mother as she passed away peacefully.

Chandra Wilson, who plays Bailey, said she isn't going anywhere soon and wants to keep playing the character "until the wheels come off".

"I always say until the wheels come off, I'll be there," she told Variety.

"I think there have been so many versions of when the show would end and how the show will end that there isn't a version at this point. I keep showing up when they call me and tell me that we're doing another one!"

Related: Grey's Anatomy star addresses "profound" reunion with Ellen Pompeo in surprise return

Chandra revealed that she would love to see her character have a complete life arc.

"I would love to see the end of her I would love to see the completion of that arc, not only as a character, but with the show, but everything is dictated by story, as always but what a great story to be able to tell that I was a starter and a finisher, that's a very cool story."

Grey's Anatomy season 17 airs on ABC in the US. It airs on Sky Witness in the UK with selected episodes also available on NOW TV.

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Grey's Anatomy star Chandra Wilson addresses her future on the show as Miranda Bailey - Digital Spy

Zoe Whittall: I started by rereading Melville; now I prefer reruns of Greys Anatomy which is good for self-care but bad for art – Toronto Star

The cherry tree in my front yard was bare when the pandemic began. It blossomed in May when it felt important to think it would all be over soon. I hosted near daily distanced visits with friends on my porch, sipping coffee under its defiantly vibrant pink and white flowers. My lover, an essential worker, made a plastic contraption so that we could hug.

When the blossoms fell later in summer, and the cherries grew Viva-Glam red, passersby filled their pockets. When they bruised purple and burst rotten, the COVID-19 numbers sunk to single digits. My lover and I got tests that we waited only twenty minutes in line for, with negative results in less than 12 hours. Then we went to the beach for a week.

While swimming in Sandy Lake, near Lakefield, the water glowed a type of turquoise Id only ever seen in the Caribbean Sea, an illusion from its shallow, sandy base. We bought roadside corn and cozied up in a rented cabin. We felt normal. The only issue was wed gotten so used to sleeping alone that we lay awake at night unsure how to handle the closeness of another person.

But I now think of August with a tender nostalgia normally reserved for college drug trips and poetic, pre-Internet love affairs. Because now the tree branches on my street are bare again, and it is just me for lockdown round two. I knew it was coming but knowing ahead of time isnt always as soothing as youd expect.

A few years ago, while promoting my last novel, I told a Macleans magazine journalist that my singular goal was to be able to spend every day writing in a room by myself. In the photo they used for the article I am sitting on my ex-partners red couch, looking out the window of our shared home. You can see a hole in my cardigan that I didnt realize was there. A shoddy, hack detail that nonetheless nails quite symbolically the state of my life at the time the photo was taken. But in 2020 I have an entire apartment in which to be alone, writing, every day of this sickly slog of a year. I know that I am extremely lucky. But perhaps I should have been more specific and ambitious with my aspirations.

I begin every pandemic day by playing phone Boggle with my friend Matt. I am terrible at it. I dont even scroll to the stats page to glimpse the tally of how many times he has beaten me anymore. One would think Boggle would be a suitable game for writers, but winning is less about being a wordsmith and more about spatial intelligence, of which I have very little. But accepting a small, insignificant daily loss while connecting to a friend has become a pleasant routine, and in keeping with the larger themes of 2020.

Like most people, Ive had several big losses in 2020, too depressing to write about, and I would prefer not to.

The act of rereading, rewatching, playing a repetitive game, or doing any activity that runs lightly over existing neural pathways, has in itself become routine for me. (I reread Herman Melvilles short story Bartleby: The Scrivener one day when I could not take in anything new. It still, as the kids say, slaps.) Now, I prefer reruns of shows like Greys Anatomy, whose predictable moralism and inane expository dialogue feels like a comforting hug when a real one is forbidden. Which is good for self-care, but bad for art.

What literature is going to come from this moment of pause? From this collective fear? Its a curious question to ponder in the semi-final stages of preparing a book manuscript, especially since everything I write about is, at its core, about anxiety. With this new book I found myself shifting the story to stagnant places. Why should my protagonist have an emotional arc, when that idea seems from the Before Times? Why are these crazy people I invented in 2018 allowed to kiss?

But Proust wrote In Search of Lost Time in bed, did he not? I ask my kitten, who responds by climbing me like a tree with his little knife hands.

To write well one must have a flourishing inner life, an ability to sink deep into an esthetic project and live in that pretend world. But for me it also helps to have real connections to the present moment. I palm handfuls of potting soil, trying to keep a geranium alive that my kitten insists on hollowing out every morning, because he knows it will rouse me, usually from a nightmare about standing in a crowd without a mask. (This dream has replaced the one about having to go back to high school naked.) My hands in the soil feels grounding, but sometimes I rarely speak for days, and connections to voice and spoken language fray, which can fracture a relationship with the present moment.

For example, the other day I blurted out something personal about my diet to my barista, because shed noticed Id changed my order. She is the one person I speak aloud to every day, so perhaps the misfire was appropriate. A comedy sketch aired that I wrote for The Baroness von Sketch Show about the daily emotional arithmetic of being an introvert. And while it did I texted a friend about how I longed to be dancing, sweaty, arms-raised and hair swinging loosely back and forth, bookended by strangers. Is COVID-19 going to make me over as a bubbly extrovert, ready to network my way back into an in-person career?

But there is something about this time that feels familiar. I grew up on a farm in the 70s and 80s, a time when childhood was largely unstructured, and my brother and I were encouraged to be imaginative and independent. Sometimes I catch myself staring out my window, watching my city-faced neighbours like a TV show, the way I used to watch the worms in our driveway, or the sheep in the pasture when I was a child, when the pace of life was slow and real TV was forbidden.

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I chat late into the night with my friend Dean in Iowa about our broken hearts and screenplay ideas. I make plans to meet a couple in Philadelphia Ive only met over Zoom, but who fill the interstitial moments of my work day with warmth and connection. My writer friend Jen in Vancouver sent me beautiful skin care products to soothe my broken heart. A friend from Instagram sent me brownies, another few sent flowers and cards when they knew I was grieving. No one is exactly OK, but we are finding what comfort we can this way, and for those of us who live alone, it feels life-saving.

So I encourage you to scroll your Netflix re-watch list or thumb through that well-worn paperback novel, play a losing game of Boggle, send some roses to your Instagram friend whose dog videos make you smile, send a hug emoji to the group text, and in the immortal words of the prophets vocal group Wilson Phillips, hold on for one more day.

Zoe Whittall is the author of The Best Kind of People. Her next novel, The Spectacular, will be out in August 2021.

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Zoe Whittall: I started by rereading Melville; now I prefer reruns of Greys Anatomy which is good for self-care but bad for art - Toronto Star

The Anatomy Lesson Swamp Thing – CBS Pittsburgh

SWAMP THING Tuesday, December 15, 2020, at 8pm on CW50

THE PRICE YOU PAY After being captured and taken to a Conclave facility, Swamp Thing (Derek Mears) is experimented upon by Jason Woodrue (guest star Kevin Durand), who makes an incredible discovery.

Meanwhile, Abby (Crystal Reed) and Liz (Maria Sten) track down the secret facility to free Swamp Thing.

Meanwhile, Daniel Cassidy (Ian Ziering) makes a fateful decision based on a possible future that the Phantom Stranger (guest star Macon Blair) shows him.

The episode was directed by Michael Goi and written by Noah Griffith & Daniel Stewart with teleplay by Mark Verheiden (#109).

The CW broadcast date airdate 12/15/2020.

Every episode of SWAMP THING will be available to stream on The CW App and CWTV.COM the day after broadcast for free and without a subscription, log in or authentication required.

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The Anatomy Lesson Swamp Thing - CBS Pittsburgh

‘Grey’s Anatomy’ Never Should Have Brought Teddy Back – Showbiz Cheat Sheet

Kim Raver debuted in the Greys Anatomy show in season 6 as a cardiothoracic and trauma surgeon. Later in season 8, she leaves indefinitely for Germany to work in the Army Medical Command.

Raver, who is referred to as Teddy Atman on the show, later returned on the show in season 14. However, her return displeases her fans, who are quite infuriated with her character when she returns. A fan commented on Reddit the following; Despite having other fascinating storylines, we only had to get Teddy back!

In Greys Anatomy, there is a lot of assumptions about Teddy and Owens relationship. The sparkle between the two is quite pronounced in season 14; Owen even follows Teddy to Germany. Their intimate relationship is almost predictable, but the accidental conceiving of a baby is something the fans didnt quite expect.

Although at first, the relationship seems healthy, things later turn sour on the two medics. Balancing between handling a toddler and an involving medical career becomes quite challenging for the two.

Later Teddy finds out that Amelia might have conceived Owens baby, which definitely wrecks her. In the strange turn of events, Teddy ends up confiding in her ex-boyfriend, Tom Koracick.

Teddy and Toms connection is obvious, and the two end up having an affair behinds Owens back. Later on, Teddy learns that the baby Amelia is carrying is not Owens, and she blames herself for having an affair.

RELATED: Greys Anatomy: What Would a Satisfying End to the Series Look Like?

In the episode Love of My Life, the Greys Anatomy show clearly reveals that Teddy is a peculiar woman. The back story on this episode portrays that Teddy was romantically involved with Allison, who later died in the terror attacks.

Coincidentally the love triangle between Allison and Teddy has some similarities to that of Teddy and Owen. In both relationships, three people are involved; in her first relationship, Claire was involved, while in the second, Tom is also involved.

In the same episode, we also learn that Teddy actually named her child after her lover, Allison. Fans think its weird and wrong naming her child after her allegedly best friend without informing Owen about the romantic involvement and attachment.

Fans can forgive Teddy for portraying impropriety in the show, but having an affair on the wedding eve is inexcusable. Making it worse, she accidentally recorded a voicemail during the intimate sessions for Owen. So, you can imagine the frustration Owen had to face before the proposed wedding on overhearing the encounter.

After having an affair, Teddy proceeded unapologetically and put on her wedding dress, awaiting her big moment, the wedding. The turn of events is ridiculous, and her character made fans displeased by her lack of empathy about Owens feelings.

In season 17, Owen confronts Teddy about the affair. In the uneasy conversation, Owen asks if there is anything she is hiding from him; he further professes that he trusts her and loves her. In this episode, we see that their relationship and friendship matters more to Owen, but Teddy is unbothered and continues to lie and have an affair.

As expected, Teddy denies hiding anything from Owen despite him probing for answers. Owen then takes out his phone and plays the sex voicemail Teddy accidentally left for him. Teddy is startled upon the revelation that Owen knows the truth.

She is confused about handling the situation, and the teary Owen leaves the room. Redeeming the dysfunctional relationship is almost impossible.

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'Grey's Anatomy' Never Should Have Brought Teddy Back - Showbiz Cheat Sheet

AstraZeneca to acquire Alexion, enhancing presence in immunology – BioPharma-Reporter.com

Boston-based biotech Alexion has been earmarked as a hot takeover target in the biotech sector: thanks to the significant market potential of ultra-rare disorder drugs with less competitive pressure than other sectors. Its leading medicine is soliris, which is approved for use against a range of rare immune disorders.

The value of the deal overtakes Gilead's acqusition of Immunomedics for $21bn in September; and marks AstraZeneca's largest ever acquisition.

AstraZeneca has recently been increasing its efforts in immunology research and the development of medicines for immune-mediated diseases.

As part of the acquisition, AstraZeneca will establish a dedicated rare disease unit in Boston and accelerate worldwide expansion of Alexions portfolio.Combining AstraZenecas capabilities in precision medicine and Alexions expertise in rare-disease development and commercialisation will enable the new company to develop a portfolio of medicines addressing the large unmet needs of patients suffering from rare diseases,says AstraZeneca.

Alexion was founded in 1992 and now employs more than 3,000 people. Led by what AstraZeneca terms its skilful commercial execution in building its blockbuster C5 franchise with soliris, Alexion now has five approved medicines (andexxa, kanuma, soliris, strensiq, and ultomiris) and a pipeline of 11 molecules in 20+ clinical development programs.

It serves patients in more than 50 countries and in 2019 generated a total revenue of $5bn and profit before tax of $2.2bn.

AstraZeneca predicts the combined company will deliver double-digit average annual revenue growth through 2025.

It says the two companies have been on converging paths: AstraZeneca expanding its presence from primary to speciality care, while Alexion has been progressing from ultra-orphan to orphan and speciality conditions.

And the British-Swedish giant also highlights rare diseases as a high-growth therapy area with rapid innovation and significant unmet medical need. Over 7,000 rare diseases are known today, yet only around 5% have US Food and Drug Administration-approved treatments.The global rare disease market is forecasted to grow by a low double-digit percentage in the future.

Alexion is focused in complement biology; with the complement cascade pivotal to the innate immune system. This plays a crucial role in many inflammatory and autoimmune diseases across multiple therapy areas: such as haematology, nephrology, neurology, metabolic disorders, cardiology, ophthalmology and acute care.

Meanwhile, AstraZeneca says its capabilities in genomics, precision medicine and oligonucleotides can be leveraged to develop medicines targeting less-frequent diseases.

AstraZeneca says the combined companies can bring together two rapidly converging, patient-centric models of care delivery with combined strengths in immunology, biologics, genomics and oligonucleotides to drive future medicine innovation.

The boards of directors of both companies have unanimously approved the acquisition. The acquisition is expected to close in Q3 2021, subject to receipt of regulatory clearances and approval by shareholders of both companies. Upon completion, Alexion shareholders will own around 15% of the combined company.

Alexion has pioneered complement inhibition for a broad spectrum of immune-mediated rare diseases caused by uncontrolled activation of the complement system, a vital part of the immune system.

Alexion's franchise includesSoliris(eculizumab), an anti-complement component 5 (C5) monoclonal antibody. The medicine is approved in many countries for the treatment of patients with paroxysmal nocturnal haemoglobinuria (PNH), atypical haemolytic uremic syndrome, generalized myasthenia gravis and neuromyelitis optica spectrum disorder.

More recently, Alexion launchedUltomiris(ravulizumab), a second-generation C5 monoclonal antibody with a more convenient dosing regimen.

Alexion's work in immunology extends to other targets in the complement cascade beyond C5 as well as additional modalities, with its deep pipeline including Factor D small-molecule inhibitors of the alternative pathway of the complement system, an antibody blocking neonatal Fc receptor (FcRn)-mediated recycling, and a bi-specific mini-body targeting C5, among others. The FcRn extends the half-life and hence the availability of pathogenic immunoglobulin G (IgG) antibodies.

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AstraZeneca to acquire Alexion, enhancing presence in immunology - BioPharma-Reporter.com

Frontier and AbbVie to develop therapies targeting ‘undruggable’ proteins – pharmaceutical-technology.com

Precision medicine-focused Frontier Medicines has signed a multi-year collaboration with AbbVie to discover, develop and commercialise multiple small molecule therapeutics against difficult-to-drug protein targets.

The collaboration will focus on developing an undisclosed number of therapeutics against validated, but previously inaccessible, E3 ligase, immunology and oncology targets.

In return for the use of its proprietary chemoproteomics platform, Frontier will be eligible for an upfront cash payment of $55m, as well as additional milestone payments that could exceed $1bn and royalty payments on any commercial sales. AbbVie will also reimburse Frontiers pre-clinical research and development costs.

Frontier co-founder, CEO and chairman Chris Varma explains the $55m upfront payment will support the independent advancement of the companys own pipeline of high-value targets. These internal programmes are not part of this latest collaboration with AbbVie.

Varma notes that

Approximately 90% of human proteins could not be targeted by small-molecule drugs because there was no known or accessible binding site on the surface of the protein, adds Varma. However, proteins are dynamic and when they function in a cellular context and interact with other cellular members, the movement and bending creates temporary pockets to which a drug can bind.

Frontiers chemoproteomics approach allows the company to exploit these binding pockets using covalent drug discovery and by leveraging a curated and diverse chemical library, a proprietary hotspot database and machine learning approaches, according to Varma.

Varma argues that Frontiers platform enables a paradigm shift in drug discovery by allowing previously undruggable proteins to now be accessible to therapeutic intervention. It allows for a precision medicine discovery approach that can identify unique, even disease-specific pockets for a given protein, with laser precision, pointing our teams to the highest quality sites for ligandability and to increase the probability of success.

In a release, AbbVie vice-president of discovery Jose-Carlos Gutirrez-Ramos commented: AbbVie is focused on making investments in promising new technologies that assist us in our mission to develop innovative medicines.

One of our key strategic focus areas is targeted protein degradation and chemoproteomics, and this collaboration with Frontier will be highly synergistic and complementary to our ongoing efforts.

Varma echoes this sentiment, stating: AbbVies commitment to explore clinically meaningful yet extremely challenging targets is aligned with Frontiers focus and expertise.

They are embracing innovative approaches to discovering new therapies such as with our chemoproteomics platform which ensures that these programs will be appropriately prioritised.

In addition, Varma notes that AbbVie has significant useful expertise in global research, development and commercialisation of drugs, and it can provide the necessary know-how and resources to maximise on the potential of transforming these promising targets into therapies benefiting patients.

Importantly, by partnering with AbbVie, Frontier is able to advance more targets than it could on its own. Some of the immunology and oncology targets that the pair are focused on are exciting, but not part of Frontiers internal focus.

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Frontier and AbbVie to develop therapies targeting 'undruggable' proteins - pharmaceutical-technology.com

Autoantibody Problems | In the Pipeline – Science Magazine

Heres a preprint from a large team at Yale with a close look at a less-studied aspect of coronavirus infection. Its been well established by now that a feature of severe cases is a misfiring immune response (the cytokine storm, etc.), and one reason that fatality rates have been going down for hospitalized cases is better management of this problem. But the details are still being worked out and since were talking immunology, there are a lot of details.

And it looks like one of those details, potentially a very important one, is a striking correlation with autoantibodies. Those are antibodies to a persons own proteins the sort of friendly fire that you see in autoimmune diseases of all sorts (acute and chronic). This work features a new assay (Rapid Extracellular Antigen Profiling, REAP) against a displayed library of 2,770 extracellular (secreted) human proteins displayed via yeast cells, providing a high-throughput method to check a patients own serum for antibodies to these. 194 subjects (Yale patients and healthcare workers) were screened, with a wide range of disease severity, as compared to 30 uninfected controls. The new assay showed good correlation with standard ELISA assays as a reality check.

It appears that the more severe a coronavirus infection a patient has, the better the chances that they show a wide variety of autoantibodies towards their own cell-surface and secreted proteins (see the figures above). I wrote here about a study that showed that patients with antibodies towards some of their own interferons have a harder clinical course of the disease, and this new paper confirms that work and extends it. A set of patients were examined over time, and it appears that at least 50% of these reactivities were observed early enough in the course of the disease that they may well have been pre-existing. Around 10% of them were seen to increase over time, though, suggesting that the coronavirus infection was bringing on such autoimmune problems. Interestingly, about 15% of the antibody titers seemed to decrease over time, and Im not sure what to make of that.

The paper goes on to make connections between specific autoantibodies and immune function for example, some of the ones that target specific proteins on the surfaces of immune cells are associated in patients with decreased numbers of those cells. The team also looked for correlations between antibodies to specific targets (or those associated with specific tissues) and clinical outcomes. Its a complex thing to untangle, though. If you think about some specific circulating cytokine protein, antibodies to it could help to clear it from the bloodstream more quickly, or to bind to it in a way that keeps it from working (either partially or completely, which seems to be the case for the interferon autoantibodies), or at the other end of the scale, to bind to it in a way that doesnt interfere so much with its function and could even stabilize its levels in the blood.

But overall, there was no well-defined set of COVID-19 antibodies that showed up in infected patients but not in controls, and no obvious ways to match up antibody profiles to specific outcomes. Some of that difficulty, though, may be due to the wide variety of responses seen. Instead of broadly obvious trends, what shows up are a great number of individual responses that can add up to real outcomes, but which are very hard to untangle. Immunology!

One of the things that needs to be done, then, is more extensive profiling in the population. I would assume that ideally youd want to get a good-sized sample of healthy people, profile them for autoantibodies, and then watch over time to see what happens. This isnt just a coronavirus story at that point. Are there people who have greater susceptibility to various diseases, or to worse outcomes, if they have particular autoimmune fingerprints? Or will it still be a big tangled ball of yarn if you try to track these things down? At the least, I would expect that if there is indeed a population who have some sort of partial failure of immune tolerance and thus show existing high levels of auto-antibodies, they they would be at greater risk of severe coronavirus infection. How many such people are there, and how many of them are currently unrecognized?

Beyond that, theres the possibility that some of the autoimmune effects are being actually brought on by the infection. We already know about some of the larger, more obvious examples of this sort of thing (such as Guillain-Barr and others), but profiling via an assay like REAP could help to shed more light. There are already several mechanisms known for such tolerance failures, but its for sure that theres a lot more to learn, and I would think that a good-sized longitudinal study might have a lot to tell us. (Of course, Im not the person who has to go out and get funding for it, so thats easy for me to say!)

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Autoantibody Problems | In the Pipeline - Science Magazine

Research Could Offer Novel Way to Restore Lung Function to COVID-19 Patients – Stony Brook News

December 14, 2020 3 minutes

Targeting endothelial cells cells that comprise the blood vessel wall which regulate oxygen exchange between airways and the bloodstream may be a novel approach restoring normal lung function to Covid-19 patients with serious lung disease.

This hypothesis stems from a study by researchers in the Department of Microbiology and Immunology in the Renaissance School of Medicine at Stony Brook University and published inmBio, the leading journal for the American Society for Microbiology.

SARS-CoV-2 causes Covid-19, characterized by pulmonary edema, viral pneumonia, coagulopathy, inflammation and other physiological abnormalities. SARS-CoV-2 uses angiotensin-converting enzyme 2 (ACE2) receptors to infect and damage ciliated epithelial vascular cells in the upper respiratory tract. Yet how SARS2 dysregulates vascular functions causing an acute respiratory distress syndrome (ARDS) in Covid-19 patients remains an enigma.

Led byErich Mackow, PhD, a Professor of Microbiology and Immunology, the team of scientists sought to unravel this mechanism by investigating SARS-CoV-2 infection of human endothelial cells from the lung, brain, heart and kidney that are impacted in COVID-19 patients.

Claims that endothelial cells are infectedby SARS-CoV-2 through ACE2 receptors have never been assessed directly, Mackow said. Our research revealed that endothelial cellslack ACE2 receptors and that endothelial cells were only SARS-CoV-2 infected after expressing ACE2 receptors in them. Since endothelial cell functions are dysregualted by SARS-CoV-2, these findings suggest a novel mechanism of regulation that does not require viral infection. Instead it suggests the indirect activation of the endothelium, potentially resulting from surrounding tissue damage, that could be the basis for further research to therapeutically target and restore normal endothelial cell responses.

Mackow adds that their work centers on both endothelial cells and ACE2 functions in Covid-19 disease to identify mechanisms of capillary inflammation and aberrant clotting within vessels. He explains that the research reveals a novel mechanism of clotting and endothelial inflammation observed in the lung and heart of COVID-19 patients.

A transformative change in the mechanism of endothelial cell dysfunction, not the infection of the cells themselves, changes the way in which disease is initiated and rationales for therapeutic targeting. If endothelial cells are not infected or directly damaged, they can still direct inflammation and clotting by just being activated, he concludes from the research findings.

The team is working on how endothelial cells can be activated by the virus or in response to other SARS-CoV-2 infected lung cells that express ACE2.

The research suggests the potential to therapeutically target activation, rather than infection of the endothelium, as a strategy for resolving coagulation and inflammatory Covid-19 symptoms.

Mackow emphasizes that additional research of endothelial cells and down-regulated ACE2 functions following SARS-CoV-2 infection are necessary to determine targets that could lead to a reduction in respiratory distress and symptoms of Covid-19 patients.

Read story "Research Could Offer Novel Way to Restore Lung Function to COVID-19 Patients" on SBU News

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Research Could Offer Novel Way to Restore Lung Function to COVID-19 Patients - Stony Brook News

SIMON The Machine Learning Platform Paving the Future of Vaccine Development – News-Medical.Net

This article was written in correspondence with Adriana Tomic, Ph.D., of the Oxford Vaccine Group.

The Oxford Vaccine Group is in high demand at the moment as they make huge progress in their goal to finalize a vaccine for COVID-19. However, elsewhere in the group, other work is going on that also has wide implications for COVID-19 and the future of vaccine development.

Adriana Tomic, co-developer of SIMON, an open-source platform for applying machine learning to biomedical data, has given News-Medical insight into this groundbreaking research on flu vaccine responses.

Image Credit: People Image Studio / Shutterstock.com

Millions of people are infected with the influenza virus, commonly known as flu, every year, and whilst for most, suffering is short-term, what many do not realize is that for some people, it can be fatal. It is estimated that every year flu kills up to 0.5 million people worldwide, and especially vulnerable are elderly and young children.

Due to a high mutational rate, new flu strains appear regularly, making the development of a vaccine particularly challenging. Each year, we have to develop flu vaccines to provide protection against the circulating viral strains otherwise there is a risk of a global pandemic. Therefore, to prevent future pandemics, it is of critical importance to understand how seasonal vaccines provide protection against flu.

Tomic describes SIMON, or Sequential Iterative Modeling OverNight, as an open-source software for the application of machine learning to biomedical data.

The Oxford Vaccine Group set about with the goal of improving the vaccines effectiveness by determining who was likely to respond positively to it.

The major aims of our project are to understand why some individuals who receive the vaccine are protected against flu while others get infected and to predict if an individual will respond appropriately to the vaccine.

Adriana Tomic, Ph.D., Oxford Vaccine Group

Using SIMON to understand these challenges involved a lot of time-consuming work, processing and standardizing all the clinical data before the analysis. However, the results have proved it was worth it.

SIMON was able to identify immune cell subsets that were present in those who would respond well to the vaccine, described in one of the most-read publications of 2019 and 2020 as rated by the American Association of Immunologists. These results came from FluPRINT, a project in collaboration with Stanford University that analyzed five flu clinical studies from 2007-2015.

SIMON can be used to predict if the individual can respond appropriately to a vaccine based on a set of immune system parameters. By using SIMON, we identified subsets of immune cells not previously described to provide protection against the virus.

These results are important for the development of the next generation of vaccines and have the capacity to fundamentally change vaccinology by application of computational discovery algorithms to speed up the discovery of the biomedical patterns.

Adriana Tomic, Ph.D., Oxford Vaccine Group

The theory behind this discovery for improving the flu vaccine is that the cell types that are responding well in some individuals could be ameliorated in those who are not responding well. This offers huge potential in improving the effectiveness of the flu vaccine.

SIMON - the open-source platform for applying machine learning to biomedical data. Image Credit: Adriana Tomic

SIMON was downloaded more than 3,000 times and it is widely used by immunology and vaccinology specialists across the University of Oxford, Stanford University, including also researchers at the Walter and Eliza Hall Institute for Medical Research in Melbourne. The software is open-source and free to download, as Tomic and the other developers believe it should be accessible to all in order to have the best impact.

Currently, SIMON is being used to investigate the flu vaccine which is given to children and understand whether re-immunization reduces protection. If this is proved true, it will greatly affect when flu vaccines should be given.

Vaccines for other diseases are also being examined. The Oxford Vaccine Group is also looking into meningococcal vaccine given to infants and vaccines against Salmonella typhi.

Adriana Tomic is part of the team developing a potential vaccine for COVID-19, which is well on its way to approval.

Our work with SIMON and systems immunology approach might be crucial for understanding SARS-CoV2 and the development of the vaccine to stop COVID-19 pandemics.

Adriana Tomic, Ph.D., Oxford Vaccine Group

SIMON could be a key factor in supporting this vaccine by applying machine learning to the immunological data being gathered around the world. It may help to develop more targeted and efficient therapies for COVID-19.

Another important aspect is an open-access FluPRINT database which we generated from multiple clinical trials on flu vaccines performed at the Stanford University, Tomic writes. Generating similar datasets from ongoing clinical trials on SARS-CoV2 will be critical for understanding this virus and generating an efficient vaccine.

Beyond the current vaccine, this research could have larger implications, as it may be used in vaccine development for all sorts of diseases. This is a promising prospect, given the likelihood of increasing numbers of new diseases in our future and hence the potential for pandemics to become more common.

To view the SIMON website, click here (genular.org).

The entire FluPRINT project is described in detail on the following website: http://www.fluprint.com

The publication on SIMON is available at:https://www.jimmunol.org/content/jimmunol/early/2019/06/13/jimmunol.1900033.full.pdf

Access Adriana Tomics review of how the dataset was generated here: https://researchdata.springernature.com/channels/1455-behind-the-paper/posts/53950-unifying-clinical-data-to-reveal-influenza-imprint-on-immune-system.

The publication for the open-access FluPRINT database is available at: https://www.nature.com/articles/s41597-019-0213-4.

Adriana Tomic, Ph.D. is a Marie Curie Fellow working at the Oxford Vaccine Group where she leads a systems immunology research aimed at applying machine learning to understand how vaccines work. During her postdoctoral training with Dr. Mark M. Davis at Stanford University she developed a computational tool for the application of machine learning to clinical datasets.

As a Ph.D. student at the Hannover Medical School, Germany, Adriana generated a novel cytomegalovirus vaccine and for this work, she received the award for the best Ph.D. work.

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