Immunology

The Role of the Host Immune Response in COVID-19: Friend or Foe? – Technology Networks

One of the biggest mysteries of the current pandemic is why outcomes from SARS-CoV-2 infection vary so widely between different people. Researchers are searching for clues in the host immune response to the virus.Most people who are infected with SARS-CoV-2 will clear the virus with few or no symptoms, whereas others will develop a severe illness that can lead to hospitalization and death.As with any virus, its your immune system that protects you against the deleterious consequences of an infection, says Arne Akbar, professor of immunology at University College London. But theres something about the immune system that isnt quite right in combating SARS-CoV-2 that gives these very bad outcomes in some individuals.But exactly what this immune dysfunction looks like is poorly understood and is likely to differ between patients with severe disease.It appears that if the infection isnt cleared straight away, some of the disease pathologies might be caused by the immune system rushing to try and fight it, describes Deborah Dunn-Walters, professor of immunology at the University of Surrey and chair of the British Society of Immunology COVID-19 taskforce. So its important to try and understand the balance of the immune response whats good and whats not.Unraveling the complex interactions between SARS-CoV-2 and the immune system is challenging, but hugely important in shaping our response to the virus. Our knowledge of the host immune response is already helping to identify existing drugs for treating critically ill patients. It is also underpinning work to develop novel vaccines that offer our best hope of escaping the devastating impact of the current pandemic.

The next stage is the adaptive immune response, which takes longer to get up and running but generates a highly specific response against the virus. The immune system has B cells that can produce neutralizing antibodies against the virus and T cells that can recognize and kill virus-infected cells, continues Akbar. During the lag phase, as B and T cells become activated, innate immune cells can offer some protection, but theyre not as specialized in what they do.

During the early stages of the pandemic, some people expressed concern that the host immune response to SARS-CoV-2 might deviate from the normal pattern.Its been really positive to see the data accumulate, says Lucy Walker, professor of immune regulation at University College London. Its panned out pretty much as we would expect, with most people generating antibodies and nice T-cell responses.

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But like any army, it needs to be tightly controlled, says Akbar. If its not, this can lead to autoimmune conditions, like rheumatoid arthritis or type 1 diabetes, where the immune system starts to attack a persons body tissues.

Researchers are exploring what happens when the balance starts to shift the wrong way in COVID-19, leading to the immune system turning on the host.

Its rather like autoimmunity, says Walker. Most people clear the virus with few problems and switch off the immune response but some end up with a prolonged response and immune-mediated damage.

Researchers have uncovered a variety of factors that are known to increase the risk of severe COVID-19, including age and certain pre-existing health conditions which could provide clues as to what might be going wrong.

Theres a phenomenon called inflamm-aging where people have more background inflammation as they get older, says Akbar. Interestingly, some of the pre-existing health conditions that predispose to severe COVID-19 are associated with higher levels of these inflammatory mediators.

Researchers are exploring the hypothesis that background inflammation could interfere with the bodys ability to get rid of the virus quickly without inducing tissue damage.

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This immune memory should trigger a faster and bigger response if you encounter the virus again, explains Walker. That means you should clear the infection with far fewer symptoms compared to the first time and hopefully none at all.A recent study showed that healthcare workers who have previously had COVID-19 are provided with 83% protection for at least 5 months. Another study showed that immunity may last up to eight months, indicated by the presence of neutralizing antibodies, memory B cells and T cells in the bloodstream.For the vast majority of people, once youve had it you dont tend to get it again, says Akbar. A few anecdotal cases have generated a lot of attention, but its actually only a small number of people who get reinfected.

Understanding how long protection lasts will be important for informing future vaccination strategies. Some researchers predict that immunization against SARS-CoV-2 may even generate a better immune memory compared to a natural infection.

Viruses often have ways to evade the immune response, explains Walker. Thats one of the things that SARS-CoV-2 is quite good at delaying or suppressing the initial immune response very early on in an infection, whereas vaccines dont have those characteristics.

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Weve needed to draw on pre-existing knowledge about the normal immune response and the types of immune response you want to elicit with vaccines, says Walker. And weve also relied on the availability of immunological assays to measure these effects.

Every vaccine candidate must first undergo extensive pre-clinical testing to find out whether they offer protection against the infection and the disease.

You need the immunology to assess the safety and efficacy of a candidate vaccine before taking it into clinical trials, explains Dunn-Walters. You need to monitor for the presence of neutralizing antibodies and T-cell responses that are specific to the virus.Defining whats known as the correlates of protection is key, providing scientists with the ability to assess a vaccines efficacy by measuring the immune response rather than through clinical outcomes.It gives you the tools to then look at different populations without having to challenge thousands of people with the virus, says Dunn-Walters. Once a vaccine is proven to work, it may even become unethical for people to take part in randomized placebo-controlled trials.

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Every pandemic is going to be different so you cant necessarily write a complete rule book, reflects Dunn-Walters. But we can learn lessons that will help us to be better prepared to deal with future threats.

Others emphasize the importance of investing in a breadth of basic science, which has underpinned so much of what has been achieved.

We dont know where the next problem for humanity is going to come from and what were going to need to tackle it, says Walker. But having up-to-date textbooks about the basic principles will certainly put us in the best position to succeed.

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The Role of the Host Immune Response in COVID-19: Friend or Foe? - Technology Networks

Immunology

Screening, Within and Without | In the Pipeline – Science Magazine

So Im a small-molecule drug discovery person at heart, since I started out as a synthetic organic chemist. Talking about vaccines and antibodies nonstop is a bit of a strain, then, because immunology is full of stuff thats rather far removed from good ol small-molecule ligands. Actually immunology eventually wears out everyone. Even immunologists. It just keeps on going: detail on top of detail, layer upon layer of complex, interconnected, rococo feedback loops and backup systems, repurposed evolutionary holdovers, insanely subdivided cell lineages, all the rest of it.

But in the end, even a medicinal chemist starts to feel at home in some parts of it. Because one of the key events in the adaptive immune system is exactly like one of the key events in so many small-molecule drug research programs: high-throughput screening. I know that I have a lot of people reading this who have never done any such thing, so its worth some explanation. Now, in traditional med-chem and its allied fields, HTS has been a way of life for around 30 years now (before that it was low-throughput screening!) Its had a lot of refinements and extensions, but the fundamental process has not changed one bit: round up some of your biological target (an enzyme, a receptor, an interaction between two proteins, whatever youve got), and find some setup where you can get a signal when a compound does what you want to it. Do you want to set off a signal from a receptor? Keep two proteins from coming together? Gum up the works of some enzyme? Work up some assay system where when that desired event happens, you get a signal that come up out of the noise.

It could be (and often is) a flash of fluorescence at a particular wavelength. That idea has had plenty of changes rung on it maybe youre looking at two wavelengths at the same time and checking the ratio between them. Or you can set things up where its the polarization of that fluorescent light thats telling you something. Maybe youre running things in a way where the fluorescence is already going on and your desired stuff will shut it off. You can have fluorescent probe compounds; there are whole careers involved with those things. Then there are of course fluorescent proteins (like the famous Green Fluorescent Protein), and listing the ways that those are used in assays would take us the rest of the week. Theres are physical phenomena that will allow fluorescence to be set off only when two suitable species are close enough together in space, and as you can imagine, these have been turned into workhorse assays.

Luminescence can be used in similar ways. The enzyme luciferase has been exploited six ways from Sunday, with a long list of variations. Any good screening lab has a list of their compounds that have been shown to directly interfere with the enzyme (and can thus hose up your data). We love luciferase so much that we use both the firefly kind and one from a deep-sea critter called a sea pansy because they come in both green and red versions (and sometimes you use both of those at the same time, too). That same sort of only when they come close together trick can be worked with luminescence, too. No. there are all sorts of tricks you can play with funny wavelengths of colorful light, and all sorts of interesting ways you can set up assays to emit them.

But it doesnt have to be light. A classic way to do receptor assays (and others) is to have a radioactive compound already stuck to your target. You add some of your test substance and see if it kicks any of the hot stuff off, which you read off after a filtration step: the more radioactive your filtrate, the better your compound bound to the target. You can mix radioactivity and a light-driven readout, with a scintillation proximity assay: a radioligand that gives off a beta-particle lights things up only when its next to your target, and not under other conditions.

No matter how you run any of these, the idea is to get such an assay set up so that theres a high signal-to-noise, low chances for false positives and false negatives, no need for too many picky dispensing or mixing steps to get it running, and (especially) the ability to run at the smallest scale you can handle. I well recall when doing such things in assay plates with 8 wells by 12 (96 total) was considered kind of high-tech, but for a long time now any assay that cant be shrunk down to 384 wells (1624) or 1536 (3248) has been greeted with a weary sigh and a roll of the eyes. There are legions of commercial assay kits and associated dispensers, plate-handling robots, and plate-reading machines that will assist you in getting all this going.

You want this miniaturization, of course, because you want to put the HT in the HTS. A full-deck screen at a big drug company can be a few million compounds if you pull out all the stops (which we dont so often any more, to be honest), and doing that 96 wells at a time will take you a while. Especially when you consider controls and duplicates, and youd better if you dont want to seriously waste your time. No, if youre going to screen a really impressive set of compounds, youre going to need all the help you can get. The latter 1990s and early 2000s in the drug business was a period when the high-throughput screeners and the combinatorial chemists tried to outdo each other

And heres where we get back to coronaviruses, antibodies, and vaccines. Because high-throughput screening is what goes on in your bloodstream constantly, as your adaptive immune system watches for pathogens. Everyone carries around a huge variety of different antibodies, all of which fit into some basic structural templates. No one is quite sure just how many different antibodies a person has, actually, because a real count is just an overwhelming task: the usual guesses are in the tens of billions, hundreds of billions, maybe a trillion different ones, which is a hard number to grasp. Imagine a company with a million compounds in its screening deck (OK), and then try to picture a million such companies (nope, not happening). And it might be a lot more incomprehensible than that the first link in this paragraph will take you to a paper that estimates that the available diversity for circulating antibodies is on the order of 10 to the 18th, and whats yet another factor of a million between friends? Given the combinatorial possibilities, it is beyond certain that no two humans have ever had the same repertoire of antibodies, and that no two humans ever will.

These things are floating around in your blood and being displayed on the surface of your various B cells (a mere hundred thousand or so per B cell), just waiting to see if there might someday be something that they bind to. Theyre just like a compound collection in a drug company, actually, except theyre not being stored in separate vials or wells, but are rather dumped all together in your bloodstream. And the assay conditions have been long worked out by evolution, with a huge signal/noise: activation of complement or of the various types of effector cells that respond so dramatically to the presence of antibodies bound to an antigen target.

Theres actually a screening method used in drug discovery thats broadly similar to this: DNA-encoded libraries. Thats where you build up a huge set of small molecules, each of which has its own DNA bar code attached to it. You screen these all at once, too you can hold up a small plastic Eppendorf vial that has (easily) tens of millions of different compounds in it, each with its own DNA identifier. You run the assay in a way that you pan for the potent binders, washing the less potent ones out of the system. Then after you finally knock the strong binders off with stronger conditions, you amplify and sequence their DNA barcode regions and get a reading of what small-molecule structures they must have been. That makes it sound relatively straightforward, but doing this right takes a good deal of care and a lot of data analysis of the hits at the end.

But you can see how it works in a roughly similar fashion to the way native antibodies work in our own bloodstreams. You start with a large variety of compounds, all mixed together, and you try them against a given target. When one of them binds strongly, you use some sort of amplification to pick out this rare event which is present in extremely small concentration. With DNA-encoded libraries, its getting rid of all the weaker binders by washing them off, and using PCR to make far more copies of the DNA sequences you have left. In the immune system, the amplification is built into the cellular responses, which propagate strongly through the immune system and set off further responses in turn.

The immune system is a lot more impressive, of course. Its had a long time to get better, under constant whole-organism threats of illness and death and subsequent inability to reproduce. The screening collection in any single humans bloodstream is far larger than any human efforts have ever reached, so the amplification of any given binding signal has to be a lot more robust. Thats been under serious selection pressure as well, of course: if we pick the wrong compound in a screening effort we will waste time and money, but if the immune system picks the wrong antigen to go off on, it can start attacking your own bodys tissues and kill you. The amount of infrastructure thats been built up over the millennia to avoid that is pretty intimidating all by itself.

Note that we wouldnt even be able to do the DEL trick without piggybacking on all that evolutionary work, either. The ligase enzymes that allow us to build up the DNA barcodes and the PCR that lets us amplify the DNA at the end yeah, we stole all that and repurposed it, and theres no way that you could ever get things to work without them. But its just like the fluorescent proteins mentioned above molecular biology and chemical biology depend on being able to repurpose the amazing array of tools found in living cells. Weve added plenty of our own technologies as well. No living organism does anything like electrospray mass spectrometry, Frster resonance energy transfer, NMR, surface plasmon resonance or the like. But combining what weve learned of chemistry and physics with what evolution has developed, you can run some pretty fancy systems, which are getting fancier all the time.

But for sheer library size and ability to pick out hits, nothing we humans have been able to put together rivals the adaptive immune system. Perhaps thats been one minor side effect of the pandemic: people who have taken the time to learn a bit about immunology can only come away with a sense of awe when they start to see the huge panorama of whats been going on inside their bodies for every second of their lives.

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Screening, Within and Without | In the Pipeline - Science Magazine

Immunology

Efficacy of Tezepelumab in Patients with Severe, Uncontrolled Asthma w | JAA – Dove Medical Press

Claire Emson,1 Jonathan Corren,2 Kinga Saapa,3 sa Hellqvist,4 Jane R Parnes,5 Gene Colice6

1Translational Science and Experimental Medicine, Research and Early Development, Respiratory and Immunology, BioPharmaceuticals R&D, AstraZeneca, Gaithersburg, MD, USA; 2David Geffen School of Medicine, University of California, Los Angeles (UCLA), Los Angeles, CA, USA; 3Biometrics, Late-Stage Development, Respiratory and Immunology, BioPharmaceuticals R&D, AstraZeneca, Warsaw, Poland; 4Biometrics, Late-Stage Development, Respiratory and Immunology, AstraZeneca, Gothenburg, Sweden; 5Amgen, Thousand Oaks, CA, USA; 6Late-Stage Development Respiratory and Immunology, BioPharmaceuticals R&D, AstraZeneca, Gaithersburg, MD, USA

Correspondence: Claire EmsonAstraZeneca, One MedImmune Way, Gaithersburg, MD, 20878, USATel +13013980304Email Claire.emson@astrazeneca.com

Background: Tezepelumab is a human monoclonal antibody that blocks thymic stromal lymphopoietin, an epithelial cytokine implicated in asthma pathogenesis, from binding to its heterodimeric receptor. In the phase 2b PATHWAY study, tezepelumab significantly reduced annualized asthma exacerbation rates (AAERs) versus placebo, irrespective of baseline disease characteristics, and improved lung function and symptom control, in adults with severe, uncontrolled asthma. This post hoc analysis assessed the efficacy of tezepelumab in adults with severe, uncontrolled asthma with and without nasal polyposis (NP).Methods: In this post hoc analysis of the PATHWAY study (NCT02054130), participants (N=550) were randomized 1:1:1:1 to receive subcutaneous tezepelumab 70 mg every 4 weeks (Q4W), 210 mg Q4W or 280 mg every 2 weeks (Q2W), or placebo Q2W, for 52 weeks. The AAER over 52 weeks and the change from baseline to week 52 in blood eosinophil count, fractional exhaled nitric oxide (FeNO) levels and serum levels of interleukin (IL)-5 and IL-13 with tezepelumab 210 mg (the phase 3 dose) and placebo were analyzed in patients grouped by self-reported presence (NP+) or absence (NP) of NP at screening.Results: At baseline, NP+ patients had higher blood eosinophil counts, higher FeNO levels and higher serum IL-5 and IL-13 levels than NP patients. Tezepelumab 210 mg reduced the AAER versus placebo to a similar extent in both NP+ and NP patients (NP+, 75% [95% confidence interval (CI): 15, 93], n=23; NP, 73% [95% CI: 47, 86], n=112). Patients treated with tezepelumab 210 mg demonstrated greater reductions in blood eosinophil count and levels of FeNO, IL-5 and IL-13 than placebo-treated patients, irrespective of NP status.Discussion: Tezepelumab reduced exacerbations and reduced type 2 inflammatory biomarkers in patients with and those without NP, supporting its efficacy in a broad population of patients with severe asthma.

Keywords: asthma, biomarkers, nasal polyps, sinusitis, tezepelumab, thymic stromal lymphopoietin

This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution - Non Commercial (unported, v3.0) License.By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms.

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Efficacy of Tezepelumab in Patients with Severe, Uncontrolled Asthma w | JAA - Dove Medical Press

Immunology

Scientists fear COVID-19 variant is taking the edge off vaccines – Sydney Morning Herald

Based on early studies, Pfizer has said it does not expect a significant reduction in the effectiveness of its vaccine. The company says it can quickly adjust its vaccine if necessary.

However, that is based on laboratory studies, not human data. And all four vaccines use different technologies but have an identical core component a piece of the virus spike protein they try to generate an immune response to.

Nurse Novita Sirait gives a COVID-19 vaccine to a colleague at a community health centre in Medan, North Sumatra, Indonesia.Credit:AP

Pfizers vaccine was approved for use in Australia in January, and 53.8 million doses of AstraZenecas vaccine have been bought and will be distributed over coming months.

The South African variant of the virus has been picked up eight times in Australia.

It is hard to say for sure, but you would think there is the potential they would also be reduced, said Associate Professor Corey Smith, head of translational and human immunology at the QIMR Berghofer Medical Research Institute.

He said the results suggested the virus could mutate in ways that made antibodies and vaccines less effective. But I dont think thats a real surprise, he said. Viruses always mutate.

The South African variant, known as N501Y.V2, has several mutations that in lab tests appear to change the shape of the virus spike in a way that reduces the ability of some antibodies generated from infection with the original Wuhan variant of COVID-19 from binding.

That raises concerns about reinfection, and about how well COVID-19 vaccines based on the original variant will protect against the South African variant.

Professor David Tscharke, head of the department of immunology and infectious diseases at the Australian National University, said it was always likely that we will have to chase variants by changing our vaccines.

However, he said it was not clear cut that AstraZeneca and Pfizers vaccines faced the same problems as Novavax and Johnson & Johnson.

You might guess that but the extent of that is going to be varied, he said. Although they have the same antigens, they are presented in a different way.

Virus-killing T-cells also played a role in immunity, he said, and they might allow Pfizer and AstraZenecas jabs to still offer strong protection against the variant.

Early lab evidence suggested Pfizers vaccine would be less effective against the South African variant, but would still cover the virus.

But those studies were carried out using pseudoviruses viruses manipulated to look like N501Y.V2 and were done on cells in a lab. Such studies do not always translate to humans.

Science and health explained and analysed with a rigorous focus on the evidence. Examine is a weekly newsletter by science reporter Liam Mannix. Sign up to receive it every Tuesday.

Novavax and Johnson & Johnson are the first vaccine developers to report human data on the variants.

Novavaxs trial of more than 4400 patients in South Africa reported efficacy of 49.4 per cent (excluding HIV-positive patients, efficacy rose to 60 per cent). Nearly all the cases of infection among vaccinated subjects were from the South African variant.

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Johnson & Johnsons trial of 6576 people in South Africa reported efficacy of 57 per cent; 95 per cent of infections in people vaccinated were from the South African variant.

These trials were small and the results were preliminary, experts said. South Africa also presents a unique environment to test vaccines: a runaway epidemic means people may be exposed to unusually high levels of virus.

But even with all that in mind, said Associate Professor Stuart Turville, a virologist at the Kirby Institute, the data early on, looks like the edge has been taken off by the South African variant.

What were seeing in the real world is this thing has the potential to take the edge off vaccines. Which may mean we need to update the formulation.

It is anticipated that the Pfizer and AstraZeneca vaccines will have significant efficacy against the newer strains of COVID-19, a spokesman for the Therapeutic Goods Administration said.

The vaccines work by inducing what is known as a polyclonal response a collection of immunological responses to many different parts of the COVID spike protein. In the new variants, only a limited part of the spike protein is changed, and much is unchanged. So the vaccines should still work against the main, unchanged parts to the COVID-19 spike protein.

The results from the Novavax and Johnson & Johnson vaccines cannot be directly extrapolated to the other COVID-19 vaccines, such as the Pfizer BioNTech or Oxford AZ vaccine as each vaccine produces differing immune responses in vaccinated individuals.

The experts emphasised it was important to wait for real-world data from Pfizer and AstraZeneca. It may be the vaccines different designs work better against the variant.

These vaccines also stimulate T-cell immunity although it is not clear what role that plays in protection from COVID-19.

And even a vaccine with reduced effectiveness was much better than no vaccine at all.

To put this into context, were still getting significant protection, said Professor Tscharke. We could be living in a world where all these vaccines were giving numbers like that all around the world and we would still be pretty happy.

Get our Coronavirus Update newsletter for the day's crucial developments at a glance, the numbers you need to know and what our readers are saying. Sign up to The Sydney Morning Herald's newsletter here and The Age's here.

Liam is The Age and Sydney Morning Herald's science reporter

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Scientists fear COVID-19 variant is taking the edge off vaccines - Sydney Morning Herald

Embryology

Black History Month: Monumental moments at the WSU School of Medicine – The South End

Jaila Campbell, seen here as part of the Warrior Strong campaign, is a Wayne State University medical student and a graduate of the Post-Baccalaureate Program.

February is Black History Month through the United States. The Wayne State University School of Medicine has a storied history of African Americans of its own that dates back to a mere year after the medical school was founded. Joseph Ferguson, M.D., graduated from what was then Detroit Medical College, in 1869. He became the first Black man in Detroit and most likely in Michigan to earn a medical degree.

Fast forward more than 150 years, and the school hit another milestone in 2019 the 50th anniversary of the Post-Baccalaureate Program, founded in 1969 to ensure that qualified minorities continued to have the opportunity to enter medical school. It was the first of its kind in the nation. Initially launched to address the dearth of Black students entering medical schools, the free program now immerses first-generationstudents into a year-long education in biochemistry, embryology, gross anatomy, histology and physiology. Many who graduated from the program were accepted into the WSU School of Medicine, but the program also served for several years as a major pipeline for Black students into medical schools across the nation. Today, the program accepts students from a category deemed underrepresented in medicine, which includes African Americans, Hispanic/Latino, Native American and students from socio-economically disadvantaged backgrounds.

In between, the school continued to play a major role in addressing the physician workforce in America and bridging the gap in health disparities and health outcomes.

The WSU School of Medicine was founded in 1868 by four Civil War veteran physicians. At the same time, the first medical school in the county that was open to all people, Howard University Medical Department, opened in Washington, D.C., under the direction of Civil War veteran and Commissioner of the Freedmens Bureau, Gen. Oliver Howard. One year later, in 1869, the Detroit College of Medicine and Howard University graduated their first Black physicians.

Albert Henry Johnson, M.D., became the third Black graduate of the Detroit College of Medicine, in 1893. Dr. Johnson was one of the founders of Dunbar Hospital, the first Black non-profit hospital in Detroit.

In 1926, Chester Cole Ames, M.D., graduated from the Detroit College of Medicine and Surgery. He was the first Black physician to obtain an internship in Urology at a white hospital in Detroit, but he was never allowed to join staff. Dr. Ames was Detroit's first Black intern, resident and member of the Wayne University medical faculty. He cofounded three Black hospitals in Detroit, but was never granted privileges to practice his specialty in white hospitals.

Some 17 years later, Marjorie Peebles-Meyers, M.D., graduated from the Wayne University College of Medicine, the schools first Black female graduate. She was also the first Black female resident at Detroit Receiving Hospital, the first Black chief resident at Detroit Receiving Hospital, the first Black female appointed to the WSU medical faculty and the first Black female to join a private white medical practice in Detroit. After retiring, she began a second career as the first Black female medical officer at Ford Motor Co. World Headquarters. Dr. Peebles-Meyers received many awards and honors, including induction into the Michigan Womens Hall of Fame.

The same amount of time elapsed before Black physicians Thomas Flake Sr., M.D., Class of 1951; Addison Prince, M.D.; William Gibson, M.D.; and James Collins, M.D., were appointed to the staff at Harper Hospital, thereby integrating the Detroit Medical Center hospital staff.

Only five years later, Charles Whitten, M.D.,became the first Black physician to head a department in a Detroit hospital when he was selected clinical director of Pediatrics at Detroit Receiving Hospital. He was also a founder of the aforementioned Post-Baccalaureate Program.

In 1981, Alexa Canady, M.D., became the first Black neurosurgeon in the United States. Dr. Canady went on to serve as professor in the WSU Department of Neurosurgery. She was named one of the countrys most outstanding doctors by Child magazine in 2001.

Around 1988, two School of Medicine students Don Tynes, M.D. 95, and Carolyn King, M.D. 93, -- established Reach Out to Youth to introduce children 7 to 11 in underrepresented populations to the possibility of careers in science and medicine. Since then, the hands-on, workshop- and activity-focused program has been presented annually by the School of Medicines Black Medical Association, a chapter of the Student National Medical Association.

In 1995, Professor of Pediatrics and Sickle Cell Detection and Information Center Founder Charles Vincent, M.D., was appointed to the Membership Committee of the American Medical Association, making him the first Black doctor appointed to the committee in the AMAs 147-year history.

In 2017, Cheryl Gibson Fountain, M.D., F.A.C.O.G., a 1987 graduate, was named the president of the Michigan State Medical Society. The obstetrician/gynecologist served a one-year term as the societys first Black female president.

Last November, an anti-racism educational effort led by School of Medicine Class of 2024 medical student Cedric Mutebi and third-year Internal Medicine-Pediatrics resident Selena Rodriguez, M.D., aimed at stopping racial disparities through reimagined medical education won a $10,000 grant from the Association of American Medical Colleges. The grant allowed the team to develop Healing Between the Lines, a sub-curriculum targeting upstream structural inequities that drive downstream disparities.

Today, the push for more diversity, more inclusion and the elimination of health disparities continue to shape the future of the School of Medicine, from student-led efforts to longitudinal research projects dedicated to the health of Black Americans.

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Black History Month: Monumental moments at the WSU School of Medicine - The South End

Embryology

Barbara Kay: Following the science in the controversy over when you became you – National Post

Article content continued

I sympathize with their mission. Not because I am ideologically pro-life (Im not). Only that I favour informed consent in all ethics-related decisions. And deplore any systemic dumbing down of such decisions gravity through pedagogical misdirection.

In an email exchange with the authors, they told me their organization is active on social media, where they have discovered that many young people believe an embryo is just a clump of cells. They have never heard, for example, of the 23 Carnegie Stages of embryology, the gold standard for accurate scientific facts in the sexual reproduction cycle of life, which in rudimentary form provide the plot line of When You Became You.

I favour informed consent in all ethics-related decisions

The book did not strike me as in any way controversial on a first, casual reading, but during a more focused re-read, the charged word human jumped out at me: It does not matter what you look like Or even if you arent born yet. You are a human being; And from the moment your life begins, you are the same human being throughout your entire life; Just like you used to be a toddler and an infant, before that, you used to be a fetus, and before that, you were an embryo; A human fetus is simply a special name that scientists call a pre-born human being from nine weeks until birth. Well, you can see why this book has ruffled some progressive feathers.

Stanton and West worked with their China-based, best-selling illustrator over a period of months, with her name on the cover throughout their collaboration. But when the author/publisher of her previous books got wind of the project, her American representatives told the authors they had to pull the illustrators name, as it was too controversial. Since they couldnt acquire the high-resolution images they needed otherwise, Stanton and West agreed. A shame because, as noted, the illustrations are magnificent.

The book launched in November. The first printing has sold out and a number of schools in the U.S. are using it. West informs me that only 34 per cent of Canadians believe life begins at conception. Hopefully, When You Became You will find its way to many Canadian homes (maybe even schools?) and help to nudge those numbers upward.

Email: kaybarb@gmail.com | Twitter: BarbaraRKay

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Barbara Kay: Following the science in the controversy over when you became you - National Post

Neuroscience

Nerd Knowledge: The neuroscience of religion – Sapulpa Times

From a cognitive and neurobiological perspective, the scientific study of the human brains interaction with religion is fascinating. There is now a new branch of neuroscience called neurotheology. This discipline attempts to explain religious experience and behavior in neuroscientific terms.

Dr. Andrew Newberg, director of the Research Marcus Institute of Integrative Health at the Thomas Jefferson University and Hospital in Villanova, PA, has written a book, Principles of Neurotheology, which provides a novel approach to scientific and theological dialogue.

According to Newberg, neurotheology applies science and the scientific method to spirituality through brain imaging studies.

His studies show that both meditating Buddhists and praying Catholic nuns have increased activity in the frontal lobes of the brain. These areas are linked with increased focus and attention, planning skills, the ability to project into the future, and the ability to construct complex arguments.

Interestingly, nuns who pray with words, rather than relying on visualization techniques used in meditation, show increased activity in the language-processing brain areas of the subparietal lobes. Both prayer and meditation correlate with decreased activity in the parietal lobes, which are responsible for processing temporal and spatial orientation.

However, other religious exercises can have the opposite effect on the same areas of the brain.

Dr. Newberg co-authored studies which show that intense Islamic prayer, which has, as its most fundamental concept, the surrendering of ones self to God, reduces the neural activity in the prefrontal cortex, the frontal lobes, as well as the activity in the parietal lobes.

It is thought that the prefrontal cortex is involved in executive control, or willful behavior, as well as decision-making. Therefore scientists postulate it is logical that a practice that focuses on abdicating control would result in reduced activity in this brain area.

Dr. Jeff Anderson, Ph.D., a neuroradiologist from the University of Utah School of Medicine in Salt Lake City, along with his research team, examined the brains of 19 young Mormons using a functional MRI scanner.

The participants were asked to what degree they were feeling the spirit. Those who reported the most intense spiritual feelings displayed increased activity in the bilateral nucleus accumbens, the frontal attentional, and ventromedial prefrontal cortical loci.

These brain areas are associated with pleasure and reward processing and are also active when we engage in sexual activities, gamble, listen to music, or drug use. The subjects also reported feelings of physical warmth and peace.

Michael Ferguson, who was a bioengineering graduate student at the time, was the author of the first study, said: When our study participants were instructed to think about a savior, about being with their families for eternity, about their heavenly rewards, their brains and bodies physically responded.

Previous studies showed that spiritual practices raise levels of serotonin and endorphins which are neurotransmitters that are associated with a sense of happiness and well-being. Endorphins work on the opiate receptors in the brain. Thus, Such neurochemical responses to religion lend credence to that dictum, Religion is the opium of the people.

Dr. Andersn stated brain imaging technologies have matured in ways that are letting us approach questions that have been around for millennia, such as What causes the feeling that someone else is present in the room, or that we are outside of our bodies?

Prof. James Giordano, from the Georgetown University Medical Center in Washington, D.C., explained that activity in the superior parietal cortex, (which is a region in the upper part of the parietal lobe) or the prefrontal cortex increases or decreases, our bodily boundaries change.

These parts of the brain control our sense of self in relation to other objects in the world, as well as our bodily integrity; hence the out of body and extended self sensations and perceptions many people who have had mystical experiences confess to.

It is noteworthy that a study of Vietnam veterans shows that those who had suffered injuries to the brains dorsolateral prefrontal cortex were more likely to report mystical experiences and religious fundamentalism.

in the 1990s, Dr. Michael Persinger, Director of the Neuroscience Department at Laurentian University in Ontario, Canada, designed what came to be known as the God Helmet. It was a

device that was designed to simulate religious experiences by stimulating an individuals tempoparietal lobes using magnetic fields.

Out of the 2,000 participants, only one percent reported feeling, 81 percent felt a presence of some sort, and the remaining subjects felt no presence.

Newberg stresses that although neurotheology wont prove the existence of a higher power, it can provide a better understanding of what it means for a person to be religious.Neurotheology can explore how religion and spirituality affect physical and mental health in terms of beliefs and practices.

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Nerd Knowledge: The neuroscience of religion - Sapulpa Times

Neuroscience

McDermott to head Division of Neuroscience | HWCOM News – FIU News

Dr. Michael McDermott, an internationally renowned neurosurgeon, has been named chief of the Division of Neuroscience at the Herbert Wertheim College of Medicine. In this role, he will oversee and lead all curricular and clinical activities of the Division.

McDermott is widely known for advancing neurosurgical techniques and pioneering the surgical management of meningioma, a slow-growing tumor that affects the brain. He is an expert in the treatment of a wide variety of neurological disorders including skull base tumors, brain metastases, gliomas, hydrocephalus, central nervous system infections and complex tumors of the skull base and spinal cord.

He also serves as chief medical executive of Miami Neuroscience Institute at Baptist Health.

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McDermott to head Division of Neuroscience | HWCOM News - FIU News

Neuroscience

The Neuroscience Market to rest on innovations in the next decade NeighborWebSJ – NeighborWebSJ

Market Report Summary

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With healthy CAGR of 6.4%, theglobalneuroscience marketis likely to grow from US$ 301.6 Mn in 2016 to US$ 520.8 Mn by 2025 end. This growth is mainly fuelled by advancement in neuroimaging and increasing R & D in neuroinformatics. Neuroscience Market: Global Industry Analysis (2012-2016)and Forecast (2017-2025),is the new publication of Persistence Market Research that focuses on merger and acquisition, strategic collaborations and technology, and technology transfer agreements, which play a vital role in the global neuroscience market.

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North America and Europe are expected to dominate the global neuroscience market in the assessed period of 8-years that is between 2017 and 2025.

Global Neuroscience Market: Relevance and Impact of Factors

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Global Neuroscience Market: Forecast by Component Type

On the basis of component type, the global neuroscience market is segmented into instrument, software and services. Instrument segmented is sub-segmented into MRI imaging systems and neuromicroscopy, while services segmented divided into consulting services, installation services and maintenance services.

Instrument segment dominated the global neuroscience market in revenue terms in 2016 and is projected to continue to do so throughout the forecast period. Instrument segment is the most attractive segment, with attractiveness index of 2.6 over the forecast period.

Instrument segment was valued atUS$ 221.6 Mnin 2016 and is projected to be valued atUS$ 408.1 Mn in 2025growing at aCAGR of 7.2%during the forecast period. This segment is expected to accounts for high revenue contribution to the global neuroscience market as compared to software and services segments over the forecast period.

Software segment is expected to be the second most lucrative segment in the global neuroscience market, with attractiveness index of0.3 duringthe forecast period. This segment was accounted for 15.4% value share in 2017 which is expected to drop down to 12.9 % revenue share in 2025.

Global Neuroscience Market: Forecast by End User

On the basis of end user, global neuroscience market is segmented into hospitals, diagnostic laboratories, research institutes, and academic institutes.

Diagnostics laboratory segment is expected to be the second most lucrative segment in the global neuroscience market by 2025 end. However, in terms of CAGR and revenue share, hospitals segment is expected to lead he market throughout the estimated period. In 2025, hospital segment is likely to grab 40.2% market share in 2025, expanding at a robustCAGR of 7.3%during the estimated period.

Research institutes segment is expected to be the least attractive segment in the global neuroscience market, with attractiveness index of 0.7 during the forecast period.

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Global Neuroscience Market: Forecast by Region

On the basis of region, global neuroscience market is segmented into North America, Latin America, Europe, APAC and MEA. North America dominated the global neuroscience market in revenue terms in 2016 and is projected to continue to do so throughout the forecast period.

North America is projected to be the most attractive market with attractiveness index of 2.3 during the forecast period. Europe is expected to be the second most lucrative market, with attractiveness index of 1.1 respectively during the forecast period.

Europe Neuroscience market accounted for 23.9% share in 2017 and is projected to account for 23.1% share by 2025 end.

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The Neuroscience Market to rest on innovations in the next decade NeighborWebSJ - NeighborWebSJ

Neuroscience

OnlyFans Model And Neuroscience Student Is Giving Back To The Troops – BroBible

Cami Strella gives back to the troops in her own incredible way. The Instagram model utilizes her OnlyFans account to provide much-needed support to military members who are struggling.

The 27-year-old OnlyFans star is the daughter of immigrant parents, including one who is a veteran. Thats part of the reason that Cami has a special appreciation of the military. Her first viral post was a somber TikTok video posted on Veterans Day where she explains the tragic story of her Army officer friend who committed suicide after surviving a traumatic brain injury following three military deployments.

The suicide was what compelled Strella to go to school for neurological rehabilitation, so she could help other troops who were suicidal. She is attending graduate school where she is studying traumatic brain injuries (TBI) and spinal cord injuries (SCI) to hopefully save more lives.

To pay for her graduate school, Cami worked at strip clubs and in the adult industry. But following the COVID-19 lockdowns, shes now working for herself on OnlyFans. And she is succeeding, where she is in the top .3% of entertainers.

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I worked in a gentlemens club previously, and I became increasingly worried about paying for my graduate school tuition as my program started in May 2020, so I joined the site as a creator, Cami told Military Times.

Cami is also giving back to the troops on her OnlyFans.

If anything, I just want service members to know that I care, and that although it may be in an unusual way, Im fighting to help them, Strella said. I also donate 10 percent of my monthly earnings to a military charity and I typically have subscribers vote for which one they want me to donate to.

Cami said a lot of my more public content is geared towards the military community. I was raised in an area with a large concentration of service members of all branches, as well as federal government and contract workers, so I always felt embedded with the culture from a young age, Cami explained.

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When asked about how much she makes from OnlyFans, Cami reveals that it wasnt always easy.

I started in February 2020 and made $11.18, she said. Now, I rank in the top 0.88 percent of all creators worldwide.

She dispels the myth that everyone makes money on OnlyFans.

People seem to think that you just create an account and you instantly make money, and thats not how it works at all, she said. If you truly want to be successful with OnlyFans, you need to be ready to invest a significant amount of time, money, and energy, just like any business.

Cami points out, OnlyFans, unlike other social media platforms, does not have a built-in algorithm where others who dont know about you can find you. Its a direct-to-consumer type of model in which a creator has to do all of their own marketing outside of the platform.

Strella says she tries to make a name for herself by giving her fans a personal and intimate experience.

I truly love talking to my subscribers, she said. I have a few that I exchange letters with and it brings such a human touch in the digital age. Its helped me, too, to stay and feel connected during the pandemic.

You can read the entire interview with Cami over at Military Times.

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OnlyFans Model And Neuroscience Student Is Giving Back To The Troops - BroBible