Biochemistry

KGH, Andhra Medical College in Vizag to be revamped with Rs 500 crore – YoVizag

Age-old medical institutions in Vizag King George Hospital (KGH) and Andhra Medical College (AMC) are all set to receive a facelift under the Nadu-Nedu programme of the Andhra Pradesh state government. On Friday, during a meeting held at the AMC Principals office in Vizag, it was revealed that the infrastructure of the college, as well as the hospital, will be revived with a budget of Rs 500 crore.

Reportedly, the current Out-Patient, Cardiology, Cardiothoracic, Orthopaedic, Surgery, Radiology, and Obstetrics blocks at the hospital will be pulled down. Likewise, the existing buildings of Biochemistry and Pharmaceulogy departments at the AMC will be dismantled in order to make space for the new constructions. The officials are reportedly chalking out plans to build five new blocks to facilitate the aforementioned departments with state-of-the-art technology. While two of the blocks will be seven-storeyed buildings, the rest of them will be five-storeyed structures.

While the date of commencement of the project has not been announced, it was informed that the Obstetrics, Cardiology, Cardiothoracic, and Orthopaedic departments will be temporarily shifted to the VIMS Hospital after the construction activities begin at the KGH and Andhra Medical College in Vizag. As many as 500 beds from the KGH are likely to be shifted to the VIMS Vizag.

It is to be noted that the Surgery, Radiology, Biochemistry, and Pharmaceulogy departments will be temporarily operated from the newly built CSR Block at the KGH. The authorities have also decided to improve the green cover by planting saplings and developing gardens in place of the existing Outpatient and Medical blocks. However, the older buildings at the KGH and Andhra Medical College in Vizag, which were constructed during the colonial rule in Vizag, will not be modified under the Nadu-Nedu programme.

Andhra Pradesh state government launched Nadu-Nedu scheme to improve the basic infrastructure at schools and Anganwadis. Earlier in February, Andhra Pradesh Chief Minister, YS Jagan Mohan Reddy extended this initiative to modernise all the government hospitals within three years. Briefing the importance of the Nadu-Nedu programme in the health sector, Chief Minister mentioned that this scheme will be helpful in strengthening the public healthcare system in the state.

Original post:
KGH, Andhra Medical College in Vizag to be revamped with Rs 500 crore - YoVizag

Cell Biology

3 Questions: Phillip Sharp on the discoveries that enabled RNA vaccines for Covid-19 – MIT News

Some of the most promising vaccines developed to combat Covid-19 rely on messenger RNA (mRNA) a template cells use to carry genetic instructions for producing proteins. The mRNA vaccines take advantage of this cellular process to make proteins that then trigger an immune response that targets SARS-CoV-2, the virus that causes Covid-19.

Compared to other types of vaccines, recently developed technologies allow mRNA vaccines to be rapidly created and deployed on a large-scale crucial aspects in the fight against Covid-19. Within the year since the identification and sequencing of the SARS-CoV-2 virus, companies such as Pfizer and Moderna have developed mRNA vaccines and run large-scale trials in the race to have a vaccine approved by the U.S. Food and Drug Administration a feat unheard of with traditional vaccines using live attenuated or inactive viruses. These vaccines appear to have a greater than 90 percent efficacy in protecting against infection.

The fact that these vaccines could be rapidly developed within these last 10 months rests on more than four decades of study of mRNA. This success story begins with Institute Professor Phillip A. Sharps discovery of split genes and spliced RNA that took place at MIT in the 1970s a discovery that would earn him the 1993 Nobel Prize in Physiology or Medicine.

Sharp, a professor within the Department of Biology and member of the Koch Institute for Integrative Cancer Research at MIT, commented on the long arc of scientific research that has led to this groundbreaking, rapid vaccine development and looked ahead to what the future might hold for mRNA technology.

Q: Professor Sharp, take us back to the fifth floor of the MIT Center for Cancer Research in the 1970s. Were you and your colleagues thinking about vaccines when you studied viruses that caused cancer?

A: Not RNA vaccines! There was a hope in the 70s that viruses were the cause of many cancers and could possibly be treated by conventional vaccination with inactivated virus. This is not the case, except for a few cancers such as HPV causing cervical cancer.

Also, not all groups at the MIT Center for Cancer Research (CCR) focused directly on cancer. We knew so little about the causes of cancer that Professor Salvador Luria, director of the CCR, recruited faculty to study cells and cancer at the most fundamental level. The centers three focuses were virus and genetics, cell biology, and immunology. These were great choices.

Our research was initially funded by the American Cancer Society, and we later received federal funding from the National Cancer Institute, part of the National Institutes of Health and the National Science Foundation as well as support from MIT through the CCR, of course.

At Cold Spring Harbor Laboratory in collaboration with colleagues, we had mapped the parts of the adenovirus genome responsible for tumor development. While doing so, I became intrigued by the report that adenovirus RNA in the nucleus was longer than the RNA found outside the nucleus in the cytoplasm where the messenger RNA was being translated into proteins. Other scientists had also described longer-than-expected nuclear RNA from cellular genes, and this seemed to be a fundamental puzzle to solve.

Susan Berget, a postdoc in my lab, and Claire Moore, a technician who ran MITs electron microscopy facility for the cancer center and would later be a postdoc in my lab, were instrumental in designing the experiments that would lead to the iconic electron micrograph that was the key to unlocking the mystery of this heterogeneous nuclear RNA. Since those days, Sue and Claire have had successful careers as professors at Baylor College of Medicine and Tufts Medical School, respectively.

The micrograph showed loops that would later be called introns unnecessary extra material in between the relevant segments of mRNA, or exons. These exons would be joined together, or spliced, to create the final, shorter message for the translation to proteins in the cytoplasm of the cell.

This data was first presented at the Cancer Center fifth floor group meeting that included Bob Weinberg, David Baltimore, David Housman, and Nancy Hopkins. Their comments, particularly those of David Baltimore, were catalysts in our discovery. Our curiosity to understand this basic cellular mechanism drove us to learn more, to design the experiments that could elucidate the RNA splicing process. The collaborative environment of the MIT Cancer Center allowed us to share ideas and push each other to see problems in a new way.

Q: Your discovery of RNA splicing was a turning point, opening up new avenues that led to new applications. What did this foundation allow you to do that you couldnt do before?

A: Our discovery in 1977 occurred just as biotechnology appeared with the objective of introducing complex human proteins as therapeutic agents, for example interferons and antibodies. Engineering genes to express these proteins in industrial tanks was dependent on this discovery of gene structure. The same is true of the RNA vaccines for Covid-19: By harnessing new technology for synthesis of RNA, researchers have developed vaccines whose chemical structure mimics that of cytoplasmic mRNA.

In the early 1980s, following isolation of many human mutant disease genes, we recognized that about one-fifth of these were defective for accurate RNA splicing. Further, we also found that different isoforms of mRNAs encoding different proteins can be generated from a single gene. This is alternative RNA splicing and may explain the puzzle that humans have fewer genes 21,000 to 23,000 than many less complex organisms, but these genes are expressed in more complex protein isoforms. This is just speculation, but there are so many things about biology yet to be discovered.

I liken RNA splicing to discovering the Rosetta Stone. We understood how the same letters of the alphabet could be written and rewritten to form new words, new meaning, and new languages. The new language of mRNA vaccines can be developed in a laboratory using a DNA template and readily available materials. Knowing the genetic code of the SARS-CoV-2 is the first step in generating the mRNA vaccine. The effective delivery of vaccines into the body based on our fundamental understanding of mRNA took decades more work and ingenuity to figure out how to evade other cellular mechanisms perfected over hundreds of millions of years of evolution to destroy foreign genetic material.

Q: Looking ahead 40 more years, where do you think mRNA technology might be?

A: In the future, mRNA vaccine technology may allow for one vaccine to target multiple diseases. We could also create personalized vaccines based on individuals genomes.

Messenger RNA vaccines have several benefits compared to other types of vaccines, including the use of noninfectious elements and shorter manufacturing times. The process can scaled up, making vaccine development faster than traditional methods. RNA vaccines can also be moved rapidly into clinical trials, which is critical for the next pandemic.

It is impossible to predict the future of RNA therapies, such as the new vaccines, but there are some signs that new advancements could happen very quickly. A few years ago, the first RNA-based therapy was approved for treatment of lethal genetic disease. This treatment was designed through the discovery of RNA interference. Messenger RNA-based therapies will also likely be used to treat genetic diseases, vaccinate against cancer, and generate transplantable organs. It is another tool at the forefront of modern medical care.

But keep in mind that all mRNAs in human cells are encoded by only 2 percent of the total genome sequence. Most of the other 98 percent is transcribed into cellular RNAs whose activities remain to be discovered. There could be many future RNA-based therapies.

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3 Questions: Phillip Sharp on the discoveries that enabled RNA vaccines for Covid-19 - MIT News

Cell Biology

What Science Has Learned about the Coronavirus One Year On – Scientific American

Jeffery DelViscio: [00:00:00] This is a Science Talk podcast from Scientific American I'm Jeff DelViscio. Today's guest is Britt Glaunsinger, a virologist at the university of California, Berkeley, and the Howard Hughes Medical Institute. She's a specialist in infectious viruses, and she's been studying them with a focus on the herpesvirus in particular for the last 25 years. Welcome to science talk, Brit. Great to have you.

[00:00:26] Britt Glaunsinger: [00:00:26] Thank you, Jeff. It's great to be here.

[00:00:29] Jeffery DelViscio: [00:00:29] It's a really important moment to look back at our very different reality just 12 months ago. In December 2019, the first infections were just emerging inside of China. SARS-CoV-2, didn't have a name yet, and no one could imagine the global effects that the virus would have on us all. But it was also clear that this novel coronavirus lit a fire underneath the seat of science. So my question is how far has our scientific understanding about the biology and the behavior of the virus come since then?

[00:00:58] Britt Glaunsinger: [00:00:58] Yeah, we have learned some really critical things about how the virus works and also importantly about how our immune system responds to it and how this virus SARS-CoV-2, essentially causes our immune system to misfire in cases of severe COVID-19 and misfiring really centers on the very early immune responses that our body mounts, these are called innate immune responses. This innate immunity is a part of our body that really uses sensors that detect pieces of pathogens, like the CoV-2 virus that are not from our own body. And once these factors or sensors detect these viral bids they sound out an immediate alarm system that operates through molecules called cytokines and interferons. And these are important for activating those later immune responses like T-cells and antibodies that we hear about. And what we think is that it's likely that people who sound this innate immune alarm early upon exposure to the virus and induce early and high levels of that interferon alarm system go on to pretty rapidly and effectively clear the virus. So these might be the individuals with asymptomatic or moderate or mild disease.

[00:02:25] However, what scientists have learned is that people who go on to develop severe COVID do so probably because in them, the virus causes a misfiring of that immune response. So like the wrong sets of immune cells may be brought in and they might not induce that early interferon alarm system quickly or strongly. And then they can't control the viral load. The virus amplifies to really high levels in their body. So their body responds to this continued presence of the virus, basically by increasing production of factors that are involved in inflammation.

[00:03:02] This is an overexuberant inflammation or inflammatory response. And that's what leads to the lung tissue damage, which is really a hallmark of COVID pathology. So what we've discovered scientists over the past year is that there are biomarkers that can give clues about who ultimately goes on to get severe disease.

[00:03:24] Scientists have also discovered genetic differences or mutations that some people have in those innate immune genes that can contribute to poor initial control of the virus. I think that this understanding that there are essentially two phases of COVID-19 disease, that initial phase that's dominated by viral amplification. And a second phase that in severe cases is dominated by a misfiring of the immune response is really important. It's important because it illustrates that there are two types of therapies that are probably needed depending on the phase of the disease. So drugs that target the virus directly to stop its replication.

[00:04:07] These would be things like Remdesivir that we've heard a lot about in the news, or maybe treating with things like recombinant interferon. This is something that is used to treat other chronic viral infections. Those types of therapies are probably only going to be effective at stopping that first phase of the disease, um, but are not going to be very effective if they're given during that second phase, because, uh, it's then it's not the virus, but the immune system that's driving illness. And so conversely drugs that dampen that overexuberant inflammatory response, and dexamethazone is one of those these, might be dangerous of given during that first phase, when you really want a rapid and robust immune response, but could be helpful at dampening the damage that's caused by the immune system at later stages.

[00:04:59] Jeffery DelViscio: [00:04:59] One of the key parts of understanding the virus itself and how we fight it is scientifically really about timing, right?

[00:05:05] Britt Glaunsinger: [00:05:05] Exactly, timing is really key. A timing of figure out how your body responds very early and later. And you know, the timing and the dose of the virus that you might receive, understanding how sort of, you know, that timing or the kinetics of infection and response are essential. And we've made a lot of progress on that over the last year.

[00:05:27] Jeffery DelViscio: [00:05:27] So let's talk about some of that specific progress inside your own lab and within UC Berkeley. What kind of work have you been doing over the last year? And what kind of work is being done across the university itself?

[00:05:39] Britt Glaunsinger: [00:05:39] Yeah. So what my lab has been working on, uh, during this past year related to Coronavirus is understanding the viral side of things. So we know that this virus has a lot of strategies to try and dampen those early innate immune sensors. It is evolved to try and shut down that component of the immune response because that part of the immune response is so essential in essentially dampening down the ability of the virus to replicate very early on.

[00:06:12] And so what my lab and others at UC Berkeley have been doing is trying to figure out the strategies that the virus is using to fight that innate immune response--how it is lowering the levels of these innate immune sensor, proteins and genes that could be used by your body to counteract the virus. And so we study this at the molecular level, at the level of the individual RNAs that the virus is targeting and blocking from being expressed.

[00:06:45] But there's a wide variety of other research that's going on across campus. That sort of spans the scales of, uh, trying to solve the atomic structures of various viral components. Because with these, you can use that information to design specific inhibitors against viral enzymes, and also at the scale of designing diagnostic tests and setting up testing centers to, to do community-based surveillance and campus testing and things like that. So really, uh, you know, Spanning the understanding the fine molecular details of how the virus works and interacts with its host cell up through community-based surveillance work.

[00:07:27] Jeffery DelViscio: [00:07:27] So, can we step back a little bit, and just talk about the innate immune response. Maybe we can go from when the body first encounters it to post-infection. And could you talk a little bit about what we know about immunity post-infection and how long that might last given what you understand about the innate immune response? How can it be useful and effective or not, and helping them body to, to fight the virus?

[00:07:48] Britt Glaunsinger: [00:07:48] Yeah, well, it is known of course that the innate immune response plays really important roles in activating the adaptive immune response, those T cells and B cells that will either produce antibody in the case of B cells or T cells are components of the adaptive immune response that will come in and kill already infected cells and be able to recognize them.

[00:08:11] So there, these are two arms of the immunity the immune system, the innate and the adaptive, but there are clear links and crosstalk between them. We know that. A very important question, which you bring up is to what extent does our body have the capacity to remember this particular virus? If you encounter the virus naturally through an infection and mount long lasting. adaptive immunity to the virus. And this is a really important question, right? Because it will tell us, for example, if you've already been infected with SARS-CoV-2, are you protected against reinfection? And it's possible that you are, but it's also possible that you're not. We know from work that's been done with the cold causing Corona viruses.

[00:09:02] There are circulating Corona viruses. Of course, that caused about 30% of the common cold. Um, we know that individuals who are infected with these cold causing Corona viruses. Can get reinfected, um, as early as a year later, uh, with that same virus, which suggests that they don't have what we would call sterilizing immunity, meaning that your immunity is so good that your immune system blocks the virus from setting up any kind of infection.

[00:09:30] But the good news is is that these individuals, even if they get reinfected are generally protected against disease. And so that says that there is, uh, an immune response that can protect at least against disease and that's hopeful. And so we don't know yet what the situation is going to look like for SARS-CoV-2, because we're still barely a year into this pandemic. Um, although there are rare cases that have been reported already of reinfection with CoV-2 in individuals, um, from various parts of the world, including Hong Kong and the US and in Europe, et cetera, these are pretty rare examples, but they could be emblematic of the fact that natural infection with this virus, um, may not completely protect against re-infection, uh, within a short, relatively short period of time. Although it's possible that natural re-infection could protect against, um, severe disease. So the idea is that what we want to do is generate vaccines that could, um, in fact, improve that level of protection.

[00:10:36] So you could get a better, more long lasting immune response from a vaccine than you could from the virus in part, because we know that the virus itself has a lot of mechanisms built into dampen that innate immune response, and it may hide itself in ways that makes it difficult for our bodies to generate a robust, adaptive immune response.

[00:11:00] And by delivering pieces of virus, uh, through vaccines, we may actually get a better response. And I think that's the hope, but it is still too early for us to know whether that is going to bear out because you simply just have to wait the length of time and see, you know, one year out how many people are protected or from infection at all versus protected from disease two years out, five years out, uh, what happens there that unfortunately is just a long waiting game. There's no way to speed up getting an answer to that question.

[00:11:34] Jeffery DelViscio: [00:11:34] I'm glad you bring up vaccines because obviously there's a lot of focus on that right now. And that's because there are a few vaccine candidates who've done phase three trials by now, which is the last step before some kind of approval by the Food and Drug Administration. And that emergency approval may even come in the time between when we're recording this and when it goes live, that's how fast this process is moving.

[00:11:55] So two companies are reporting better than 90% efficacy. Those are Pfizer and Moderna. It should also somebody noted that there's another vaccine candidate from the University of Oxford and the drug company, AstraZeneca that's showing promise.

[00:12:08] But to go back to the Pfizer and maternal vaccines, they're both mRNA vaccines. Could you talk a little bit about what an mRNA vaccine actually is and how it works?

[00:12:18] Britt Glaunsinger: [00:12:18] Certainly, yeah, these two vaccines are... the data, first of all, are incredibly exciting to, to most, all of us in that the efficacy appears from these initial results that have been released to be very high. And, um, that's exceptionally great news. There are many unanswered questions, uh, related to these vaccines that we can certainly touch on. So it's not that that we have all of the information yet, but I think that's great news in part, because these messenger RNA vaccines. We don't have any track record with them.

[00:12:52] This is the first rollout or testing phase three testing of any mRNA vaccine. So we didn't know if this was going to work at all. Um, and the fact that they appear to be working so well is extremely exciting. So what is a messenger RNA vaccine compared to a traditional vaccine? Uh, to understand this, I need to just take a second to explain the concept of what an antigen is.

[00:13:15] An antigen is a bit of virus that you are, or a pathogen in general, but for our purposes, we're, we're talking about Cove too. So it's, it's a bit of virus that you're going to show to the immune system and tell the immune system essentially make. Antibodies against this, make an adaptive immune response against this and, you know, vaccine context, you are showing it an exact bit of virus that we know that if an antibody is made to that bit, that antibody can block or neutralize the virus.

[00:13:48] This is important because in the context of a natural infection, your immune system, doesn't a priori know which bit of the virus, if it makes an antibody to it is going to stop that virus. So it makes lots of antibodies to everything it sees and can. And many of those may bind the virus, but not bind it in a way that's actually gonna block it.

[00:14:10] And so the benefit of a vaccine for, um, developing immunity is that you're basically telling your immune system exactly what are the right kind of antibodies, hopefully for it to make. And so that's the benefit of that over a natural infection for acquiring immunity. And there are a couple of ways to give that antigen or that bit of the virus to an individual. The more traditional way would be to, uh, inject a person with a vaccine that, that has that protein already made.

[00:14:40] And so that the antigen of course, that all of the vaccines are targeting is the spike protein of the virus. That's that surface protein that is essential for allowing the viruses to bind cells and enter cells. And so if you can block spike protein binding, and the function, you essentially have stopped the virus in its tracks because it can't get into the cell.

[00:15:03] And a virus that can't get into a cell is for all practical purposes inert, and non-pathogenic. So traditional vaccines would deliver that protein directly. Either you grow up the protein, uh, you know, in a, in a big bio-reactor and injected itself, these are called subunit vaccines, or the protein is already present on the surface of an inactivated virus in some way.

[00:15:30] The thing that's different about the messenger RNA vaccines, and this is similar for DNA vaccines, similar for the, um, the, the adenovirus, the vector based vaccines, which is the weakened non-infectious, uh, vectors, all of the basic, you know, the front runners that we're going to hear about early on for the phase three trials is that they don't deliver the protein directly. They deliver the sequence, the gene coding sequence for that spike protein, uh, into your cells and use your own cells to then, uh, make the protein from that set of genetic instructions for spikes. So the messenger RNA is basically delivering the gene sequence for the spike protein, or maybe just the RNA, the receptor binding domain of the spike protein, uh, which is then, uh, used by your cells to produce protein in your own cells to then show the immune system.

[00:16:28] Do you think Mr. And a vaccines would have come so far so fast without the virus around? Is it a chicken, egg virus, vaccine situation?

[00:16:39] It certainly wouldn't have happened as quickly. And in fact, you know what we have here as a platform, unlike we've ever had before, where all of the possible types of vaccines are basically being generated and tested simultaneously. Both the sort of more classic tried and true, uh, strategies for vaccine making that have been used for other FDA approved vaccines and these newer platforms like the DNA based vaccines and the MRNs vaccines that have shown promise, but have never, um, been tested in these large scale clinical trials for vaccines before. So we'll be able to cross compare them. Uh, and of course the speed with which we're getting data for these is accelerated dramatically. We've never had a phase three trial results within less than. a year after a virus has emerged. The fastest and of course, with a four to five years, which was lightning fast compared to how long it takes to develop most vaccines.

[00:17:42] Jeffery DelViscio: [00:17:42] So it seems that SARS, cov two has remodeled the way science works.

[00:17:47] Britt Glaunsinger: [00:17:47] It is definitely remodeled the way that science works. Uh, I can't think of a time, um, in recent history or even maybe an older history where the entire scientific community and medical community has turned their expertise with laser-like focus onto one thing, in particular. We have a lot of big diseases, right? We've got cancer, we've got TB, we've got AIDS, we've got heart disease, all of which have a lot of effort dedicated towards them. But this virus has really brought the world to its knees in such a dramatic way that, um, that everybody is working, uh, together, uh, to use their expertise, whatever it may be to try and find ways to learn about and combat this virus and other viruses. And so the hope of course, is that, um, the, what comes out of, of this, uh, parallel approaches from many, many, many different angles and scientists and expertise can be extrapolated to other diseases as well, other viral diseases, other pathogens.

[00:18:54] So for example, the mRNA platform or the DNA platform for a vaccines, the benefit there is that you can do this plug and play of inserting the gene sequence, very easily, they can be very rapidly designed. And if they worked here that provides, uh, you know, a proof of principle, well, the next emerging pathogen that comes. We can use these as a starting point and have a good sense that, that, uh, they're going to be effective.

[00:19:23] Jeffery DelViscio: [00:19:23] As much damage as this virus has done to people's lives to the economy in a strange way, it sort of seems like a bit of a catalyst.

[00:19:30] Britt Glaunsinger: [00:19:30] Yeah, you could see it as a catalyst, a catalyst based on need.

[00:19:37] Jeffery DelViscio: [00:19:37] That's desperation in some ways, right?

[00:19:39] Britt Glaunsinger: [00:19:39] That's right. That's right.

[00:19:41] Jeffery DelViscio: [00:19:41] Let's talk about the future. Let's not try to project a year ahead. That seems unknowable. Given how much changed in the last year. So let's talk about the next few months. And maybe we can start in the White House. There's a change in the administration coming. How do you think the federal response to the virus might change in the coming month?

[00:19:59] Britt Glaunsinger: [00:19:59] I would say I don't have any insider information, but I can give you what is just my opinion from what I've read in the news and whatnot. Uh, and that's what, what I'm coming to expect is that there's going to be more of a coordinated federal response instead of, um, relying on sort of state to state. Uh, uh, responses, uh, you know, sort of figuring it out on their own and, and doing their own thing. My, my expectation is that there's going to be more coordination and more of a unified response that is led by the federal government, which I think will be very important, particularly for issues related to vaccine distribution and prioritization of course, of who gets the vaccine first and which factors do they get et cetera. And also in thinking about, you know, policy of should the federal government be the one, uh, eliciting perhaps mandates about, uh, distancing or mask wearing or shut downs instead of relying on States. And we may be seeing a more heavy hand there is, is my guess.

[00:21:06] Jeffery DelViscio: [00:21:06] And in terms of what happens with the virus, it's not waiting for anything, obviously. Can you talk to me about mutation? How important is it for the future of the virus? How might that change our approach to fighting it?

[00:21:17] Britt Glaunsinger: [00:21:17] Yeah. Mutation is something that we always think about in the context of pathogens and viruses in particular, because they randomly incorporate errors into their sequence every time they make a copy of themselves. Uh, and that's because for, for most viruses, they don't have the capacity of copying their genome sequence in a way that is error free. Our own cells have lots of ways of copying our own genome, um, and, and proofreading and checking and double checking it to make sure that errors are not made when we amplify, you know, our own genome and ourselves as cells, divide viruses by and larger many viruses, particularly viruses with them RNA genomes do not have that capacity.

[00:22:04] And this leads usually to, uh, for RNA viruses, very rapid mutation. And that mutation, uh, is something that can be really challenging in the context of developing antiviral drugs and in developing vaccines, because the concern is always that a very interim mutant version, a changed version of the virus will emerge that is resistant to, uh, an antibody or to a, um, an antiviral drug.

[00:22:38] Now there's good news on that front for the coronavirus, which is that yes, it mutates all viruses mutate, but that it is not mutating at the hyper speed rate that some other RNA viruses, mutate like influenza and HIV. Those are really tricky problems because of the rates that they, they, um, are undergoing mutation.

[00:23:04] Coronavirus has a special sort of feature that is very unusual for RNA viruses, um, in which it can actually correct errors that occur as it is copying its genome. It can proofread its own genome copying mechanism. And what that means is that the virus accumulates fewer errors than many other RNA viruses. Doesn't mean no errors. So of course people are constantly looking at how this virus is changing and they are identifying mutants that can arise. And in some cases, mutants that may help the virus bind to cells better or enter cells better. So called increase its uh, transmissibility or an infectability.

[00:23:55] And so those mutations, um, do exist and, but they are not arising at a super rapid clip. It's not like we're, we're seeing tons of escape mutations, particularly in the spike protein for where the receptor binding domain might be. It's relatively speaking stable, which I think is good news for the vaccine front, but it's definitely something that people are continuing to actively monitor. There are hundreds of thousands of coronavirus sequences that have been deposited into the database that, um, evolutionary biologists and genomic scientists are looking at exactly how these mutants are arising and what they mean for antibody escape and things like that.

[00:24:40] Jeffery DelViscio: [00:24:40] Well, in a seemingly unrelentingly bad year, that seems like a hint of at least a little good news. Am I being too hasty?

[00:24:48] Britt Glaunsinger: [00:24:48] I mean, that's it. What one might consider good news in this things. But I also think that it's important to keep in mind that as you mentioned, the virus is raging right now. Um, we're undergoing the third wave of infection here in the United States, the first being in April or may, and then we had a second wave in the summer and we're now encountering the third wave. We're seeing exponential growth of the virus pretty much across the nation. Um, and so there's a lot of concern that our darkest days may be ahead of us. We've got great news on the vaccine front potentially, but that's not going to materialize even in a best case scenario for several more months to come. And those several months, I think we're going to see a large number of deaths and severe infections and transmissions. And it's partly because we're entering the traditional respiratory illness season, right? This cold and flu season and coronavirus is one of those viruses that is a respiratory virus and tends to have seasonality to it.

[00:26:04] So I think that, you know, there's a real concern that, you know, part of it is exponential growth that is linked to people being indoors more and much of our lives are spent in doors and that's a, of course, much more so during the cold winter months.

[00:26:18] The problem with indoors and coldness is this tends to be environments where there's decreased humidity, uh, so low relative humidity, maybe, uh, 20 to 40%, uh, cold dry air. These are conditions where viruses tend to be more stable and easier to transmit through the airborne route. Um, dry air can also, uh, clear out some of the antiviral sort of mucus based clearing mechanisms that are in our airways that can impair that early innate immune response.

[00:26:53] And so, um, there are reasons to think that the, you know, the cold fall and winter air can exacerbate this problem, uh, of infection and that, uh, you know, so we've just got to be extra vigilant, even though we've got these great pieces of news from the vaccine that does not mean we can let down our guard, people need to be extremely careful during the wintertime about distancing and mask wearing and hand-washing and things like that. It's going to be up to all of us to, to prevent the spread as much as we can, as we wait for the vaccine distribution to happen and, you know, antiviral drugs to be discovered, et cetera. We all have pandemic fatigue, but you know, it's you get a time when boy, if we let our guard down, it's going to be a disaster over the next couple months.

[00:27:40] Jeffery DelViscio: [00:27:40] Well, it seems that science is not going to stop pushing on this. Finally, could you talk just a little bit about what it means to be you right now? Someone who's really been engaged with this kind of research for 25 years. What is it like to be working on this particular subject so closely given how important it is to really the whole world?

[00:27:59] Britt Glaunsinger: [00:27:59] It's a humbling experience on the one hand, because I, my perspective having worked on viruses so long helps me realize the magnitude of the problem and the magnitude of the challenge that, that faces us in a pandemic like this. And, and so, um, that's a very humbling, uh, experience, but also it's one that, that makes all of us who work on viruses and scientists in general, feel a sense of, of duty that we have something to contribute. We have a knowledge base. We have a skillset that can help us learn how this virus works and fight it. And, and that's a really motivating and invigorating feeling to, to know that that we have something to contribute and that my knowledge, you know, hopefully is useful in this context and as we go on in the future as well. And so, um, you know, if it continues to fuel my passion for virology, which has always been strong.

[00:29:00] Britt Glaunsinger is a virologist at the University of California, Berkeley, and the Howard Hughes Medical Institute. Thank you so much for joining us on Science Talk, Britt.

[00:29:08] Thank you so much for having me, Jeff.

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What Science Has Learned about the Coronavirus One Year On - Scientific American

Cell Biology

Alpine Immune Sciences Appoints Natasha Hernday to Board of Directors – Business Wire

SEATTLE--(BUSINESS WIRE)--Alpine Immune Sciences, Inc. (NASDAQ: ALPN), a leading clinical-stage immunotherapy company focused on developing innovative treatments for cancer and autoimmune/inflammatory diseases, today announced that Natasha A. Hernday has joined Alpines Board of Directors. Ms. Hernday brings more than 20 years of experience in corporate development and corporate strategy.

Im delighted to welcome Natasha to Alpine Immune Sciences Board at this important moment in our companys history, as we build on our strategic partnership with AbbVie and leverage Alpines financial strength to further advance our development pipeline, said Mitchell H. Gold, M.D., Executive Chairman and Chief Executive Officer of Alpine. I look forward to benefiting from Natashas extensive experience and acumen as we oversee the next stages of Alpines growth to the benefit of Alpiners, shareholders and patients alike.

Ms. Hernday currently serves as Executive Vice President, Corporate Development and as a member of the Executive Committee for the publicly traded biotechnology company Seagen, Inc. (NASDAQ: SGEN). Since joining Seagen in 2011, Ms. Hernday has built and led the business development team responsible for licensing deals, acquisitions and strategic alliances. From 1994 through 2010, after starting her career in molecular and mammalian cell biology, Ms. Hernday served in various roles of increasing responsibility at Amgen Inc., including as Director, Mergers & Acquisitions and as Director, Out-Partnering. She also serves on the board of directors of Xoma Corp. (NASDAQ: XOMA) and PDL BioPharma, Inc. (NASDAQ: PDLI), and on the Knight Campus External Advisory Board for the University of Oregon.

Ms. Hernday received her BA in microbiology from the University of California at Santa Barbara and MBA from Pepperdine University.

Concurrent with Ms. Hernday joining Alpines Board of Directors, the company also announced that Paul Sekhri will be stepping down as a director of the company. Mr. Sekhri has served on Alpines Board of Directors since February 2016.

Mitchell H. Gold commented, On behalf of the Board and Alpines executive team, I would like to thank Paul for the service he has provided to the company and wish him well in any and all future endeavors.

About Alpine Immune Sciences, Inc.

Alpine Immune Sciences, Inc. is committed to leading a new wave of immune therapeutics. With world-class research and development capabilities, a highly productive scientific platform, and a proven management team, Alpine is creating multifunctional immunotherapies via unique protein engineering technologies designed to improve patients lives. Alpine has entered into strategic collaborations with leading global biopharmaceutical companies and has a diverse pipeline of clinical and preclinical candidates in development. For more information, visit http://www.alpineimmunesciences.com. Follow @AlpineImmuneSci on Twitter and LinkedIn.

Forward-Looking Statements

This release contains forward-looking statements within the meaning of Section 27A of the Securities Act of 1933, Section 21E of the Securities Exchange Act of 1934 and the Private Securities Litigation Reform Act of 1995. These forward-looking statements are not based on historical fact and include statements regarding our platform technology and potential therapies, the future development plans and commercial potential of our product candidates, the progress and potential of our other ongoing development programs, and our ability to successfully develop and achieve milestones in our development programs. Forward-looking statements generally include statements that are predictive in nature and depend upon or refer to future events or conditions and include words such as may, will, should, would, expect, plan, intend, and other similar expressions, among others. These forward-looking statements are based on current assumptions that involve risks, uncertainties, and other factors that may cause actual results, events, or developments to be materially different from those expressed or implied by such forward-looking statements. These risks and uncertainties, many of which are beyond our control, include, but are not limited to: the impact of the COVID-19 pandemic on our business, research and clinical development plans and timelines and results of operations; our discovery-stage and preclinical programs may not advance into the clinic or result in approved products; any of our product candidates may fail in development, may not receive required regulatory approvals, or may be delayed to a point where they are not commercially viable; as well as the other risks identified in our filings with the Securities and Exchange Commission. These forward-looking statements speak only as of the date hereof and we undertake no obligation to update forward-looking statements, and readers are cautioned not to place undue reliance on such forward-looking statements.

Secreted Immunomodulatory Proteins, SIP, Transmembrane Immunomodulatory Protein, TIP, Variant Ig Domain, vIgD and the Alpine logo are registered trademarks or trademarks of Alpine Immune Sciences, Inc. in various jurisdictions.

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Cell Biology

Another Life: Moss growth this year has been exceptional – The Irish Times

In a rainy autumn, the moss grew thick as a rug on the concrete path to our door. A wavy white trail was worn down the middle by the postman, the SuperValu delivery man and a few fond and obliging friends in masks.

A bit ashamed, I took a spade to skim it off. Our daughter will come from Dublin at Christmas, the first time in almost a year, having quarantined for a fortnight with all her shopping done; we are hobbits enough already.

The moss growth has been quite exceptional, thriving in an atmosphere thickened hourly by the oceans exhalations. In dryer climes, its said that a boy scout lost in a wood could find north by seeing which side of the tree trunks the moss was on. Among our trees, hed be walking round and round.

Many beautiful mosses found in the woods are worth kneeling down to admire, but this isnt one of them. Its dark green fuzz has all the appeal of a worn and soggy rug.

Ask Google which moss grows on concrete in Connacht and the answers would sooner discuss power hoses and other stuff to spray. Actually, a lot of mosses love concrete, with its mix of ground limestone and minerals. As wild plant life I might prefer to let it grow but the supermarket delivery man could have a skid with his big basket.

Another ground-dwelling substance objected to by many readers is the blue-green alga called nostoc. Its frequent substrate is limestone gravel, used throughout Ireland on paths, drives and flat roofs. In dry spells it remains flaccid and unremarked, but rain swells it into a bubbly and slippery imitation of seaweed.

Found globally, it was one of those unconsidered, pioneering cellular forms that helped create oxygen for later humans to breathe. An American scientist, Malcolm Potts, traced its original naming to the 15th-century Swiss physician Paracelsus.

Familiar with the gelatinous colonies of the ubiquitous terrestrial cyanobacterium nostoc commune, Potts proposed, Paracelsus played on fables of excrement blown from the nostrils of some rheumatic planet. In nostoch first with an h he melded German and Old English words for the nose.

Star snot and star jelly have been among English folk names for sudden and puzzling lumps of transparent goo, deposited on grass or twigs of trees and sometimes reported to Eye on Nature. Much imagined in the past as the stellar debris of meteor showers, it has been assessed by the British Natural History Museum as the eggless spawn of female frogs, coughed up in mid-air from the gullets of predatory herons.

Which brings us to other, more complex and colourful blobs that have figured in recent inquiries. They belong to the slime moulds, the myxomycetes, a group of strange and shape-shifting micro-organisms that hover at the biological boundary between plant and animal life.

Readers have variously described Mucilago crustacea as dollops of scrambled egg or something the dog might have vomited. The largest species in Ireland is the tapioca slime mould, Brefeldia maxima, which may cover a square metre of fallen leaves or sheath a branch in a conifer forest.

Closely related to amoebae, slime moulds develop a giant cell with multiple nuclei, called the plasmodium. This can move about to find food (bacteria and fungi on fallen leaves or rotting wood), if not at a pace that catches the human eye. A one-centimetre plasmodium can crawl about 10cm a day, the bigger ones even further.

One species of slime mould propels itself up tree trunks to feed on bracket fungi. A plasmodium can also have amazing shape-shifting powers, feeding itself into a crevice one end of a rotting log and expanding again at the other.

Japanese research with the species Physarum polycephalum has even demonstrated an apparent cellular intelligence. An experiment reported in 2000 showed the mould finding the shortest route through a laboratory maze. Studies since then have shown it making decisions and learning habitual behaviour.

Revelations on Physarum, said the Journal of Physics this year, have triggered a surge of activity in numerous fields including physics, cell biology, genetics, behavioural ecology, computer science, natural computation and cognition among others, as well as philosophy of science and finally philosophy of mind.

At the latest count, Ireland has 228 myxomycete species, 142 of them in Co Wicklow. Very many of these have been described by Dr Roland McHugh of the Dublin Institute of Technology, now an authority on their kind.

Given the many mysteries of slime moulds, its a nice match to find that Dr McHughs other lifelong obsession has been with James Joyces Finnegans Wake, to which he has published a widely praised book of annotations. Its line-by-line notes are now considered a great aid to exploring a notoriously shape-shifting book.

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Another Life: Moss growth this year has been exceptional - The Irish Times

Cell Biology

Ginkgo Bioworks and Octant Partner to Expand COVID-19 Testing Capacity using Next-Generation Sequencing Technology – SynBioBeta

Partnership will bring large-scale test processing capacity to the San Francisco Bay Area as part of Ginkgos plans to expand testing nationwide

BOSTON,Dec. 10, 2020/PRNewswire/ Today,Ginkgo Bioworks, Inc. (Ginkgo) andOctant, Inc(Octant) announced a partnership to grow critical diagnostic testing capacity to address the COVID-19 pandemic, and build infrastructure to confront future health and biosecurity concerns. As part of this partnership, they will open a new processing facility in theSan Francisco Bay Areathat will deploy Octants SwabSeq sequencing platform and Next-Generation Sequencing (NGS) technology, initially capable of running up to 10,000 SARS-CoV-2 diagnostic tests per day, with potential to scale further. The lab will be established and run byConcentric by Ginkgo, Ginkgos end-to-end service for COVID-19 testing.

Though deployment of vaccines is on the horizon, testing remains a critical part of the larger public health strategy to combat COVID-19 and additional testing capacity is required to meet rising demand across the country. The nearly 22,000-square-foot Bay Area facility will support demand on the West Coast, and supplements the testing capacity Ginkgo has already built inBoston, which is designed to process tens of thousands of SARS-CoV-2 tests a day. The Bay Area lab will also serve as a replicable prototype for a processing center that could be easily repurposed and scaled across the country.

The infrastructure we are building in the Bay Area will expand testing access and further efforts on the West Coast to address the current pandemic, while also shoring up systems for early detection and pandemic response for the future, saidBarry Canton, PhD, CTO and co-founder of Ginkgo Bioworks. Were thrilled to collaborate with Octant to potentially develop a best-in-class high-sensitivity molecular diagnostic, and we look forward to developing a blueprint of a facility in the Bay Area that may be used as a template for additional locations across the country, extending access to diagnostic testing to more communities.

The lab will leverage Octants proprietary SwabSeq technology, a high-throughput sequencing platform. NGS technology can be used to detect the presence of the SARS-CoV-2 virus and significantly increase COVID-19 testing capacity. Octants SwabSeq platform optimized the NGS testing approach to be highly sensitive and cost-effective, while avoiding traditional bottlenecks in the testing process. This advanced technology, which is available for use through an open patent license, can also be further developed for broader testing efforts for other respiratory illnesses, including the common cold and flu.

SwabSeq is just one example of how high-throughput multiplexed biology will solve important problems in new ways. At Octant, we had built, optimized and scaled a high-throughput RNA-amplicon sequencing platform for our drug discovery programs. We were able to rapidly repurpose the technology for COVID-19 detection to aid in fighting the pandemic, saidSri Kosuri, PhD, CEO at Octant. We are proud to partner with Ginkgo and apply our platform to scale testing in this critical moment.

In the future, Ginkgo and Octant plan to collaborate to develop other diagnostic tests, and may also utilize the Bay Area facility to support future diagnostic projects.

Learnmoreabout Ginkgos COVID-19 response efforts.

About Ginkgo Bioworks:

Headquartered inBoston, Ginkgo Bioworks uses the most advanced technology on the planetbiologyto grow better products. The companys cell programming platform is enabling the growth of biotechnology across diverse markets, from food to fragrance to pharmaceuticals. For more information, visitwww.ginkgobioworks.com.

About Octant, Inc:

Octant is a synthetic biology drug discovery company designing multi-target drug leads for multifactorial diseases. Octant engineers biology using living cells to inform rational drug design by mapping, measuring and modeling compound reactions against GPCRs and ultimately, the entire universe of human receptors. For more information visitwww.octant.bio.

Ginkgo Bioworks Contact:Kelsey Donohueginkgobioworks@missionnorth.com

Octant Contacts:Susan Kinkead(415) 509-3610susan@waterhousebrands.com

Kim Kraemer(415) 939-9033kkraemer@waterhousebrands.com

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Ginkgo Bioworks and Octant Partner to Expand COVID-19 Testing Capacity using Next-Generation Sequencing Technology - SynBioBeta

Physiology

What dolphins can teach us about surviving COVID-19 – University of California

When Terrie Williams began hearing about the wide range of symptoms experienced by patients with COVID-19, she saw a connection between the various ways the disease is affecting people and the many physiological adaptations that have enabled marine mammals to tolerate low oxygen levels during dives.

Williams, a professor of ecology and evolutionary biology at UC Santa Cruz, has spent decades studying the physiology of marine mammals and their extraordinary ability to perform strenuous activities while holding their breath for long periods under water.

Diving marine mammals experience a lifetime of rapid physiological transitions between normal oxygenation and hypoxia [low oxygen levels], Williams said. Theyve got ways to protect themselves and allow their organs to keep functioning while holding their breath for hours at a time, but theres a whole suite of biological adaptations that had to happen for them to be able to do that.

Lacking those adaptations, humans are vulnerable to rapid damage in a wide range of tissues when oxygen levels drop due to the effects on the lungs and cardiovascular system of infection with the coronavirus SARS-CoV-2. In a review articlepublished December 3 inComparative Biochemistry and Physiology, Williams explores how the diving physiology of marine mammals can help us understand the effects of COVID-19.

It really highlights why it is so important for people to protect themselves from infection with this virus, she said. Damage to oxygen-deprived tissues happens fast and can be irreversible, which may account for the long-term effects we are beginning to see in people after coronavirus infections.

The heart and brain are especially sensitive to oxygen deprivation, and marine mammals have multiple mechanisms to protect these and other critical organs. In the first place, marine mammals have much higher oxygen carrying capacity than humans due to their greater blood volume and hemoglobin concentrations. In addition, some marine mammals contract their spleen during dives to release a store of oxygen-rich blood cells into the circulation. To avoid blood clots resulting from such high concentrations of red blood cells, many species lack a key clotting factor found in other mammals.

Other adaptations include greatly increased concentrations of oxygen-carrying proteins such as myoglobin in heart and skeletal muscles and neuroglobin and cytoglobin in the brain. In addition, numerous safety factors and biochemical buffers enable even the most oxygen-dependent tissues in marine mammals to withstand not only low oxygen but also the subsequent reperfusion of tissues with oxygenated blood. In humans, reperfusion after a heart attack or stroke often leads to additional tissue damage.

According to Williams, the solutions that marine mammals have evolved for tolerating hypoxia provide a natural template for understanding the potential for damage to oxygen-deprived tissues in humans.

Studying marine mammals allowed me to understand what it takes to protect the body when the availability of oxygen is low, she said. There are so many ramifications of shutting down the oxygen pathway, and I think thats what were seeing in these COVID patients.

Williams is particularly concerned about the so-called long-haulers who continue to have symptoms long after they were infected with the coronavirus.

You hear people say its just like the flu, but COVID scares the heck out of me because of the potential for long-term damage to the heart and brain, she said. When you think about oxygen deprivation and the tissue repair process, it makes sense that many people are having a hard time getting back to normal life, even after a mild infection.

Williams urges people to do all they can to avoid becoming infected. Our heart and brain cells are meant to last a lifetime, and we cannot replace them once they are damaged, she said. Dolphins and whales have natural protections that humans lack, so we are highly vulnerable to hypoxia.

Randall Davis, a marine biologist at Texas A&M University, coauthored the paper with Williams. This work was funded by the Office of Naval Research.

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What dolphins can teach us about surviving COVID-19 - University of California

Physiology

Unique wearable helps researchers study dementia patients and familial caregivers – Healthcare IT News

Couples with higher relationship satisfactions showed greater linkage in their physiological responses (for example, heart rate and skin conductance) during face-to-face interactions, which suggests a greater biological connection between the couples.

This is according to a variety of studies, including a recently published paper in the Journal of Personality and Social Psychology by Dr. Robert Levenson and Dr. Kuan-Hua Chen at the University of California, Berkeley.

In addition, there has been emerging evidence further suggesting that being physically linked with a partners physiological response may even have important implications to individuals mental and physical health.

HIMSS20 Digital

For example, findings from Levenson and Chens group suggested that a couples physiological linkage can predict their mental and physical health in both healthy married couples and couples in which one person is the spousal caregiver of the other who is diagnosed with a neurodegenerative disease.

Dr. Robert Levenson, University of California, Berkeley

Building upon this, researchers wanted to better understand whether synchronicity of objective physiology indicators between dementia patients and their caregivers also correlates to the influences between each other outside the laboratory, in real life.

In one recent study, Levenson and Chen had 22 patients, and their spousal caregivers wear a wrist-mounted actigraphy-monitor in their homes for seven days. They found that the more linked (particularly more synchronized) the patients and the caregivers activity was, the less anxiety the caregiver reported.

THE PROBLEM

In all of the above studies, the linkage and relationship/health data were collected around the same time, and therefore the researchers could not know whether greater linkage produced better relationship/health outcome, or vice versa, or both at the same time.

In addition, research participants in these previous studies were mostly living in the San Francisco/Northern California areas.Therefore the researchers could not know whether the effects that they found could be generalized to couples living in other, more rural areas in the United States.

PROPOSAL

To address these issues, Levenson and Chen launched a research project that recruited 300 patients and their familial caregivers (with the total number of participants at600) to study their activity linkage in their homes for six months.

Over the study period, both the patients and caregivers wear the Tracmo CareActive Watch continuously for thosesix months, and caregivers are monitored periodically for mental and physical health changes.

Researchers are eager to conduct studies in the field for example, in peoples homes and collect real-world behavioral data in complement to laboratory studies, said Levenson, director and principal investigator at the University of California, Berkeley.

In the past, our tools were limited to consumer wearable watches, which are typically expensive, need to be charged frequently, have restricted rules of data access, and do not provide accurate location data that are necessary for us to give a meaningful interpretation of the observed behaviors.

Compared with consumer wearable watches, the Tracmo CareActive solution is more affordable and overcomes the battery-life limitation, he added. It provides accurate room-to-room location information for research participants, and allows the team to access high-quality actigraphy data sampled with high temporal resolution (that is, in seconds), he explained.

MEETING THE CHALLENGE

The Berkeley research team provided two CareActive watches and three stations to each household, which included one participant with dementia or mild cognitive impairment and one familial caregiver. Participants install these devices at home through a CareActive App.

The CareActive watch can be worn for more than three months without battery replacement, said Chen, post-doctoral research fellow at the University of California, Berkeley. Our study is extremely benefited by CareActive watchs long battery life, because any single battery charging could interrupt our data collection.

Dr. Kuan-Hua Chen, University of California, Berkeley

More important,remembering to charge the watch routinely and put the watch back on after charging could be stressful and burdensome for research participants, particularly for those who are older and/or with age-related neurological conditions, he added.

Besides, unlike typical consumer watches that use GPS to localize the users, [and] therefore can only provide approximate user locations on a map, the CareActive system uses Bluetooth signal strength that allows precise room-to-room mapping of our research participants when they are in their homes, he said.

The room-to-room locations are important for us to better understand and interpret our participants daily behaviors, including behaviors occurring at both the individual level.For example, a person may stay in the bedroom when he feels sick, or the dyadic level, ... couples who feel happier with their relationships may spend more time being in the same room.

RESULTS

In the ongoing research project that started in mid-March 2020, the Berkeley team has successfully collected CareActive data from more than 90 homes, distributed across 33 states in the U.S. All participants self-installed the systems with minimal assistance from the research team.

ADVICE FOR OTHERS

All technology designed to be used in healthcare needs to consider the users backgrounds and needs, Levenson advised. When we study people with dementia and their familial caregivers, we put essential effort to simplify the steps for device installation, minimize the amount of work for maintenance, and maximize research participants motivation and benefit from using the device.

Social-contextual factors and individual differences need to be considered when interpreting any information collected from the users, he added.

For example, a fall-like behavior occurring in the bedroom may have different meanings than [one] occurring in the bathroom, he said. In addition, all homes have different sizes and layouts, [so] therefore we should be careful when generalizing patterns learned from one home to another.

The Berkeley team would recommend, if possible, collecting additional information from other sources to cross-validate and improve interpretation/prediction accuracyfor example, integrating motion sensor data with Bluetooth proximityhe concluded.

Twitter:@SiwickiHealthITEmail the writer:bsiwicki@himss.orgHealthcare IT News is a HIMSS Media publication.

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Unique wearable helps researchers study dementia patients and familial caregivers - Healthcare IT News

Physiology

Flavors added to vaping devices can damage the heart – Science Codex

TAMPA, Fla (Dec. 11, 2020) -- The appealing array of fruit and candy flavors that entice millions of young people take up vaping can harm their hearts, a preclinical study by University of South Florida Health (USF Health) researchers found.

Mounting studies indicate that the nicotine and other chemicals delivered by vaping, while generally less toxic than conventional cigarettes, can damage the lungs and heart. "But so far there has been no clear understanding about what happens when the vaporized flavoring molecules in flavored vaping products, after being inhaled, enter the bloodstream and reach the heart," said the study's principal investigator Sami Noujaim, PhD, an associate professor of molecular pharmacology and physiology at the USF Health Morsani College of Medicine.

In their study published Nov. 20 in the American Journal of Physiology- Heart and Circulatory Physiology, Dr. Noujaim and colleagues report on a series of experiments assessing the toxicity of vape flavorings in cardiac cells and in young mice.

"The flavored electronic nicotine delivery systems widely popular among teens and young adults are not harm-free," Dr. Noujaim said. "Altogether, our findings in the cells and mice indicate that vaping does interfere with the normal functioning of the heart and can potentially lead to cardiac rhythm disturbances."

Dr. Noujaim's laboratory is among the first beginning to investigate the potential cardiotoxic effects of the many flavoring chemicals added to the e-liquids in electronic nicotine delivery systems, or ENDS. He recently received a five-year, $2.2-million grant from the NIH's National Institute of Environmental Health Sciences to carry out this laboratory research. Commonly called e-cigarettes, ENDS include different products such as vape pens, mods, and pods.

Vaping involves inhaling an aerosol created by heating an e-liquid containing nicotine, solvents such as propylene glycol and vegetable glycerin, and flavorings. The vaping device's battery-powered heat converts this e-liquid into a smoke-like aerosolized mixture (e-vapor). Manufacturers tout e-cigarettes as a tool to help quit smoking, but evidence of their effectiveness for smoking cessation is limited, and they are not FDA approved for this use. E-cigarettes contain the same highly addictive nicotine found in tobacco products, yet many teens and young adults assume they are safe.

Among the USF Health study key findings:

-In mouse cardiac muscle cells (HL-1 cells), the researchers tested the toxicity of three different, popular flavors of e-liquid: fruit flavor, cinnamon, and vanilla custard. All three were toxic to HL-1 cells exposed to e-vapor bubbled into the laboratory dish where the cells were cultured.

-Cardiac cells derived from human pluripotent stem cells were exposed to three distinct e-vapors. The first e-vapor containing only solvent interfered with the electrical activity and beating rate of cardiac cells in the dish. A second e-vapor with nicotine added to the solvent increased the toxic effects on these cells. The third e-vapor comprised of nicotine, solvent, and vanilla custard flavoring (the flavor previously identified as most toxic) augmented damage to the spontaneously beating cells even more. "This experiment told us that the flavoring chemicals added to vaping devices can increase harm beyond what the nicotine alone can do," Dr. Noujaim said.

-Healthy young mice implanted with tiny electrocardiogram devices were exposed to 60 puffs of vanilla-flavored e-vapor five days a week, for 10 weeks. Heart rate variability (HRV) - that is, fluctuations in the time interval between successive heartbeats - decreased in these test mice compared to the control mice that inhaled only puffs of air under the same regimen. A sophisticated analysis by the USF Health researchers showed that vaping interfered with normal HRV in the mice by disrupting the autonomic nervous system's control of heart rate (the acceleration and slowing down of heartbeats), Dr. Noujaim said.

-Finally, mice exposed to vaping were more prone to an abnormal and dangerous heart rhythm disturbance known as ventricular tachycardia compared to control mice.

Whether the mouse findings will translate to people is unknown. Dr. Noujaim emphasizes that more preclinical and human studies are needed to further determine the safety profile of flavored ENDS and their long-term health effects.

A partial government ban on flavored e-cigarettes aimed at stopping young people from vaping focused on enforcement against flavored e-cigarettes with pre-filled cartridges, like those produced by industry leader JUUL. However, teens quickly switched to newer disposable e-cigarettes still sold in a staggering assortment of youth-appealing fruity and dessert-like flavors.

"Our research matters because regulation of the vaping industry is a work in progress," Dr. Noujaim said. "The FDA needs input from the scientific community about all the possible risks of vaping in order to effectively regulate electronic nicotine delivery systems and protect the public's health. At USF Health, in particular, we will continue to examine how vaping may adversely affect cardiac health."

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Flavors added to vaping devices can damage the heart - Science Codex

Physiology

With the Support of His Village, fall 2020 graduate Dr. Ray Jones Achieves Goal, is Ready to Help Others – Southern Miss Now

Fri, 12/11/2020 - 10:14am | By: David Tisdale

Even if he helps just one person in his career - through either his teaching or research - Dr. Ray Jones says all of his hard work in pursuit of his doctorate at The University of Southern Mississippi (USM) will have been worth it.

A newly minted Ph.D. in kinesiology from The University of Southern Mississippi (USM) School of Kinesiology and Nutrition, Dr. Jones is one of more than 1,000 USM students who earned degrees from the University this fall.

My time here at USM has molded me into an academician and researcher, said the Patterson, La. native. I was provided so many opportunities to grow as an independent thinker, researcher, and a person.

Under normal circumstances, a doctoral program is challenging. But as the COVID-19 pandemic continued throughout 2020, Dr. Jones had to adapt to new ways of living, working, and studying, along with fellow students.

Any Ph.D. program is going to be difficult, and this one was no different - juggling everything, including classes, research, teaching, and other activities. More recently, the most difficult thing I had to do was work on my dissertation - writing, data collection, defending - during the pandemic. That was hard.

What helped me overcome it all was a solid support system I call my village. This group of people faculty, staff, fellow students, family and friends - were there to keep pushing me and motivating me to be the best version of myself, to keep me moving forward on this journey, and for that I am so thankful.

Among those members of his village was his academic adviser, USM Assistant Professor Dr. Stephanie McCoy, who said Dr. Jones met and exceeded expectations as a student.

In his three years here, Ray showed a pointed interested in being more involved in scholarship and service to his field through publications, presentations, and involvement in our exercise physiology governing body, The American College of Sports Medicine, as well as the Southern Miss community, Dr. McCoy said.

Other than his many accomplishments as a student, Ray is also a joy to be around. He has an infectious laugh that brings a smile to everyones face. He will be truly missed by all of us, especially me.

Dr. Jones says he was drawn to kinesiology because the name looked cool and science-y. I went into my undergrad program knowing I wanted to go to physical therapy school, and kinesiology seemed like the most logical way to get there by combining my love for anatomy/physiology and exercise, Jones said. So I decided to stay in kinesiology, and it has been the most amazing experience.

However, I never thought I would be in research. I didnt get a taste of it until the end of my masters program. It was great because I learned new skills, but it was also extremely challenging, which I believe is what attracted me to it. Afterwards, I applied for jobs and Ph.D. programs, and the rest is history.

Dr. Joness research focuses on sedentary behavior and the cardiovascular contribution to brain health. Using noninvasive techniques such as Doppler ultrasound, he examines blood flow response during prolonged, uninterrupted sitting in minority populations, particularly African-Americans.

His work, recognized at the university, regional and national levels, includes accolades from the USM Susan A. Siltanen Graduate Research Symposium, the Southeast Region American College of Sports Medicine, and the American College of Sports Medicine. He is a recipient of the Robert Smith, MD Graduate Scholar designation through the Jackson Heart Study Graduate Training and Education Center at the University of Mississippi Medical Center [UMMC-GTEC] (2019-present), a highly competitive program enhancing the research skills in cardiovascular health epidemiology and health disparities of doctoral and health professions students. A 2020 inductee into the USM Graduate School Hall of Fame, he was a category winner and overall runner-up in the schools Three-Minute Thesis competition.

USM Graduate School Dean Dr. Karen Coats said she first became acquainted with Dr. Jones when he participated in the schools professional development program Professionals in Preparation during the 2018-19 academic year.

Ray was a leader in that group because he was so engaged and interactive, and contributed so much to all our discussions and activities, Dr. Coats said. He recognized the value in taking advantage of opportunities beyond the basic requirements for his degree program, and he excelled in all.

He is just a delightful, talented, and eager young scientist, and Im so glad I was able to interact with him during his studies at Southern Miss. He represents the best of USM, and I know he has a bright future ahead of him.

Dr. Jones now moves on to the University of Alabama at Birmingham School of Medicines Center for Exercise Medicine, where he has accepted an NIH-T32 Postdoctoral Fellowship.

I thoroughly enjoy the scientific process, and am motivated by the fact that there are so many questions in the field that are unanswered, he said. If I can just answer one question, thatll be one more thing that could, potentially, help someone else. On the other side of academia teaching - Im able to share my passions in exercise physiology and research with students, with the hope of shining some light on their own passion, and helping them achieve their goals.

That helping spirit was instilled in him early on, Dr. Jones said, because of the generosity that has been shown to me throughout my life.

The one thing that inspires me to continue is the prospect of helping others - even if its just one person.

The USM School of Kinesiology and Nutrition is housed in the Universitys College of Education and Human Sciences. Learn more about the School at https://www.usm.edu/kinesiology-nutrition/index.php.

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With the Support of His Village, fall 2020 graduate Dr. Ray Jones Achieves Goal, is Ready to Help Others - Southern Miss Now