Podcasts about asm podcast

¡Hola hola, confinados y confinadas! Bienvenidos a un nuevo episodio, pandemísticamente confinado, de ASM Podcast: tu podcast del molar. Un especial ASM, porque siempre es especial. Pero sobretodo hoy por: Nueva temporada, la octava. Y nueve años. Nuestro primer podcast es de febrero de 2011. Especial confinados, cada uno desde nuestras casas Y sí, quizá hayais […]

Catching up with the last few months of Conservative self owns, the end of Richard Spencer, and how women won't talk to Ben Shapiro. === Throw your spare change at me in the street, or via PAYPAL: https://www.paypal.me/AntiSocialMedia Ko-Fi (Buy me a coffee) : Coming soon Or donate via PATREON: https://www.patreon.com/AntiSocialMedia x ===== ANTI-SOCIAL MEDIA on Twitter: https://twitter.com/ASM_AntiSocial Listen to the ASM Podcast via; iTUNES: https://itunes.apple.com/gb/podcast/anti-social-media-podcast/id1076431995?mt=2 SPREAKER: https://www.spreaker.com/user/antisocialmedia LATEST EPISODES ONLY via SOUNDCLOUD: https://soundcloud.com/antisocial_media Stitcher: https://www.stitcher.com/podcast/antisocial-media-podcast Podbean: https://antisocialmediapodcast.podbean.com/ ASM on YouTube: https://www.youtube.com/c/AntiSocialMedia Xx

How are new diseases detected in a clinical microbiology lab? Melissa Miller talks about the time it takes to develop a test for a new disease (hint: it’s getting shorter). She also shares her definition of ‘point-of-care’ diagnostics and explains the major trends for clinical microbiology labs. Host: Julie Wolf  Subscribe (free) on iPhone, Android, RSS, or by email. You can also listen on your mobile device with the ASM Podcast app. Julie's biggest takeaways: Antibiograms are vital to understand the resistance characteristics of locally circulating disease strains. These help make empirical decisions for antibiotic therapy regimens before the susceptibility test results are available. New diseases require new diagnostic tests. How to determine how well new tests work once they’re developed? Clinical microbiologists look to the sensitivity (how well does a test detect if a patient has a disease) and specificity (how often is the test negative if the patients doesn’t have it) of the test. Having access to positive controls (that is, samples from a patient known to have the disease) can prove difficult in some settings, such as in North Carolina, where no Zika patients were admitted while the Zika virus test was being developed. When the HIV epidemic was beginning, it took several years after the HIV virus was identified to sequence its genome and use this for molecular testing. In 2002-2003, it took just over a month to get the SARS genome sequence for use in developing assays. It’s even quicker today; within a week, we can have sequences from viruses around the world. Defining ‘point-of-care’ testing took an entire hour at a recent American Academy of Microbiology colloquium! Melissa’s take: It’s a test that can be done at or near to where the patient is. Point-of-care tests are exciting but can also pose challenges. A recent example is false-positive pertussis tests that were shown to be due to pertussis vaccine being administered nearby. Ensuring the tests are used safely and accurately will best serve healthcare workers and patients alike. Molecular diagnostics have two trends: one trend simplifies existing technologies into point-of-care tests. The other trend adds complexity, by applying next-generation sequencing techniques in a reproducible manner. Featured Quotes (in order of appearance): “Laboratorians are often in the basement or in a setting where they aren’t visible to the healthcare team, but they’re very vital to taking care of the patient.”   “When you’re using laboratory-developed tests, the way it works in one laboratory may be very different from how it works in another laboratory.”   “The ultimate goal [of point-of-care testing] is to get a result that’s actionable. We don’t need to do tests that aren’t going to result in a clinically actionable decision.”   “In many ways, the technology is ahead of where our quality assurance protocols are.”   “I think it’s going to be very important in going ahead that we continue to have laboratorians involved in developing these point-of-care programs and consulting to these sites, helping to make sure that there are policies and procedures that ensure quality results for their patients.”   “It’s one thing to do it in a research setting; we’ve collaborated with a number of folks using next generation sequencing. But to then move it to the clinical lab and have it be reproducible and have the quality at the level you need for a clinical lab is a completely different challenge.” Links for this episode Melissa Miller University of North Carolina Website Division of Clinical Laboratory Science at University of North Carolina Searchable List of Clinical Laboratory Science Programs AAM Colloquium Report on Point-of-Care Testing CPEP Program Career Blog: Tips on becoming a clinical microbiology laboratory director HOM Tidbid: Papagrigorakis 2006 International Journal of Infectious Diseases report HOM Tidbit: Shapiro reply to Papagrigorakis report Send your stories about our guests and/or your comments to jwolf@asmusa.org.  

Dave Rasko uses comparative bacterial genomics to find DNA sequences that influence virulence or antibiotic resistance. Dave talks about his studies of E. coli, Acinetobacter baumanii, and B. anthracis, and the state of bacterial genomics past, present, and future. Host: Julie Wolf Subscribe (free) on iPhone, Android, RSS, or by email. You can also listen on your mobile device with the ASM Podcast app. Julie's biggest takeaways: Genome sequencing speed has significantly increased: The first bacterial genome sequenced, Haemophilus influenzae, took about 10 years to complete. The first organism with two sequenced genomes was Helicobacter pylori, published in 1999, and the first organism with three published genomes was Escherichia coli. Rasko’s initial project at TIGR to sequence 11 E. coli genomes took about 2 years. Today, Rasko’s lab can sequence 500 genomes in about five days.   In E. coli, up to half of the genome can differ between two strains. The core genome is the collection of genes that will be shared among all isolates of a particular species. Core gene conservation varies among species and is important to consider in analyses for one’s species of interest.   Working on the Amerithrax investigation was unlike many other scientific inquiries for many reasons, including that the Federal Bureau of Investigation only gave the scientists involved the information pieces necessary to conduct their studies. Rasko and collaborators sequenced the genomes of spores within the samples, and found that the morphology of the colonies that grew were associated with genetic differences between the spores within the sample, linking phenotype and genotype.   While comparative genomics can provide a lot of information, there are some phenomena that will always require further study. For example, Rasko is researching isolates of A. baumanii and Klebiella pneumoniae that quickly develop drug resistance when grown in sub-inhibitory drug concentrations. The genomic sequences of resistant or susceptible strains show no difference in DNA sequence, suggesting the phenotype is due to transcriptional changes. Featured Quotes (in order of appearance) “Genomics is fun in that we can hypothesize all day long, every day. It’s really the start of a lot of very very hard work figuring out why.” “There’s a lot of DNA pieces that we don’t fully understand how they moved, where they moved, where they came from. In some cases, there’s evidence to say where they came from; in terms of G-C content and coding biases, we can make some assumptions, but in the grand scheme of things, we have no idea where they’re coming from! In some cases, we’ll see them dominant throughout a lineage, and in some cases we’ll see them in sporadic isolates around the entire phylogenetic tree. . .We all thought genomics was going to solve so many problems, and it’s really just made it more difficult!” “Plasmids tend to be mobile and exchangeable, and the pieces tend to be - I tend to think of them as legos, in the fact that you can put a plasmid together in a bunch of different ways.” “I think a lot of conventional PCR fails and people assume that it’s because it’s negative, and not necessarily that it fails because of diversity.” “Many microbiologists think of that colony on a plate as a clone. I force the people in my group to think about it a little differently, because it’s really what I like to call ‘genome space’. They’re not all the same; bacteria are constantly evolving. There’s changes all the time, some of them are positive, some of the are negative, the negative ones get lost, the positive ones unusually become dominant - and then there’s lots of neutral changes that just kind of hang out.” “Genomes really normalized everything. Before that, there were certain labs that could clone and there were certain labs that could sequence, and it was a little bit restrictive to the elite labs who had those resources. Now with the genome sequences out there, everyone was starting from the same place.” “You really have to understand your organism to make the bioinformatics work.” Links for this episode Rasko lab at the University of Maryland FBI summary of Amerithrax investigation 2011 PNAS report on B. anthracis comparative genomics Bugs N the ‘hood HOM Tidbit: Stanley Falkow gives both video history and written history of plasmid biology Save on Microbe 2018, use code: asmpod Send your stories about our guests and/or your comments to jwolf@asmusa.org.

Bill Jacobs talks about developing mycobacterial genetic tools and using them to discover ways to shorten TB treatment. He also talks about the SEA-PHAGES program that allows high-school students to participate in phage discovery. Host: Julie Wolf Subscribe (free) on iPhone, Android, RSS, or by email. You can also listen on your mobile device with the ASM Podcast app. Julie's biggest takeaways: The challenges of working with an easily aerosolized bacterium are aided by complementary studies on a noninfectious relative. M. smegmatus doesn’t colonize mammals and grows slower, giving researchers the opportunity to acclimate themselves to working with mycobacterial cultures. Jacobs was the first scientist to introduce DNA into M. tuberculosis using a phasmid - part plasmid, part mycobacterial phage. The first phage came from Jacobs’ dirt yard in the Bronx, so he named it BxB1 for the Bronx Bomber. Another phage, TM4, became the workhorse phasmid when Jacobs cloned an E. coli cosmid sequence into a nonessential part of the phage genome. It replicates in E. coli as a plasmid but becomes a phage inside Mycobacteria, facilitating manipulation. The shuttle phasmids allowed transposon delivery to make transposon libraries, and the creation of gene knockouts. To this day, we use Ziehl-Neelsen staining to differentiate acid-fast mycobacteria from gram-positive or gram-negative bacteria - the mycolic acids on the outer part of the envelope make up some of the longest microbial lipid chains. But mycobacteria can regulate its acid-fast positive or negative status; the acid-fast negative organisms are a persistent population that are often ignored inside of patients. 99.99% of M. tuberculosis bacteria are not persistent, but the last 0.1% have entered into a persistent state expressing many stress proteins that help them become refractory to killing. A normal course of antibiotic chemotherapy for patients is six months. If infected with a strain resistant to the two frontline drugs, that time goes up to two years. The problem is even greater in extremely multidrug resistant (XDR) strains. What we really need is a way to understand persistence and a way to shorten chemotherapy. That’s why were were absolutely amazed when we discovered that cysteine with isoniazid completely sterilizes Mtb cultures in vitro and in vivo! The culture is sterilized because the bacteria can’t form persisters. Vitamin C co-treatment with antibiotics may lead to a shortened course of therapy for TB treatment. Neutralizing antibodies to the herpesvirus glycoprotein have been the dogma for protecting from herpes. Jacobs and his colleagues discovered that a vaccine based on a glycoprotein-knockout virus confers sterilizing immunity not through neutralizing antibodies but through antibody-dependent cell cytoxicity (ADCC). This ADCC response may also be important to develop a more effective TB vaccine.   Featured Quotes (in order of appearance): “You’ll never know how bad your aseptic technique is until you start working with tuberculosis!” “I think part of the reason I had the opportunity to develop genetics for TB - it’s not like it wasn’t important to do - but a lot of people were disappointed when working with the organism.” “We’re about to take TB genetics to where yeast genetics is.” “One of the tubicle bacilli’s greatest powers or one of its most important phenotypes is that it has the ability to persist, which means it has the ability to tolerate killing effectors, either killing by the immune system or killing by bactericidal drugs.” “I took students to the Bronx Zoo, and over by the zebra pen, I sniffed and said ‘I smell a phage!’ In fact, that’s not crazy - anyone who plants flowers knows what good soil smells like, and in the good soil, you’re smelling the bacteria that live in the soil, the Streptomyces and Mycobacteria. I reached down and grabbed that dirt, and when we went back to work we isolated BxE1.” “I’ve never met a phage I wasn’t excited about!” “I now believe that most pathogens do not ‘want’ ADCC antibodies to be made, and they have immune evasion strategies where they skew the immune response to get the wrong antibodies. Since the time we published our first paper, numerous groups have shown that correlates of protection for HIV, for influenza, and for Zika, turn out to be ADCC antibodies.” “Genetics is the mathematics of biology!”   Links for this episode Bill Jacobs lab site NYTimes story on 1993 rapid diagnostic test using luciferase AACJournal: Vitamin C potentiates the killing of Mycobacterium tuberculosis by the first-line tuberculosis drugs isoniazid and rifampicin in mice Cell: Origins of highly mosaic mycobacteriophage genomes SEA-PHAGES program eLife: Whole genome comparison of a large collection of mycobacteriophages reveals a continuum of phage genetic diversity mBio: Dual-reported mycobacteriophages (Φ2DRMs) reveal preexisting Mycobacterium tuberculosis persistent cells in human sputum Tuberculosis - Its cause, cure and prevention [1914] (pdf)   Send your stories about our guests and/or your comments to jwolf@asmusa.org.  

Dave Rubin may be the stupidest person online, closely followed by Piers Morgan and Toby Young. ANTI-SOCIAL MEDIA on Twitter: https://twitter.com/ASM_AntiSocial ASM on Youtube: Buy me a beer via PAYPAL: https://www.paypal.me/AntiSocialMedia Or donate $1 (or more) a month via PATREON: https://www.patreon.com/AntiSocialMedia You can also listen to the podcast via these links: Listen to the ASM PODCAST via; iTUNES: https://itunes.apple.com/gb/podcast/anti-social-media-podcast/id1076431995?mt=2 LATEST EPISODES ONLY via SOUNDCLOUD: https://soundcloud.com/antisocial_media Music Tracklisting coming soon...

Most bacteria live a sedentary lifestyle in community structures called biofilms. Vaughn Cooper tells us what bacterial biofilms are, why biofilms differ from test tube environments, and how long-term evolution experiments combined with population genomics are teaching us how bacteria really work. He also discusses using hands-on bacterial evolution activities to introduce high schoolers to future STEM possibilities. Host: Julie Wolf Subscribe (free) on iPhone, Android, RSS, or by email. You can also listen on your mobile device with the ASM Podcast app. Julie's biggest takeaways: Cells in a biofilm shift to dedicate their resources to protection rather than reproduction. This allows biofilms to be innately more resistant to antibiotics than those growing in planktonic culture. One of the least-understood parts of a biofilm cycle is the dispersal stage. What cues or signals influence some biofilm-embedded cells to leave? This is a vital part of biofilm formation, since these dispersal cells can eventually attach to a new surface and restart the process of forming a biofilm. The bead system of biofilm propagation allows Vaughn and his colleagues to study the long-term evolution of biofilms. This system, combined with population genomics, allows the study of all the different genetic changes within the population. Traditional genetic screens compare libraries of mutants to see which survive under different conditions. Rather than on libraries of mutant strains, evolution works on random mutants that arise naturally. The accessibility of sequencing technologies has changed the way scientists study evolution, as now the mutations can be found as they form, rather than being seeded into the initial mutant library screen. High schoolers using nonpathogenic bacteria can study evolution in action by developing new colony morphologies. Work with high schoolers and their teachers has shown students who do hands-on learning do better on standardized tests and that girls, especially, express higher interest in technology and an interest in STEM careers after a 1-2 week project. Featured Quotes (in order of appearance) “From a perspective of an ecologist and evolutionary biologist, this is what captivated me about biofilms: that instantly in the process of forming a biofilm, the environment becomes heterogeneous. Different cells that are clone mates are experiencing different selective pressures.” “The hypothesis that we’ve been testing for the last 15 years or so is that biofilms in and of themselves may generate ecological and heritable evolutionary diversity in really short periods of time.” "In describing the wrinkled Pseudomonas colonies that can stem from biofilm cells: “I think they look like hydrangeas, and some look more like doilies. I think they’re captivating and pretty charismatic as far as microbes go.” “The average bacteria picked from any environment does an unbelieveably good job of protecting its genetic material. The per-cell mutation rate, per-genome, per-generation rate is about 1 in 1000 cells. So a bacterial cell needs to divide about 1000 times to create a single mutant. That means that mutations are actually relatively scarce, but bacterial populations are extraordinarily immense. If you grow a single cell to 108 cells, you’ve got about 105 new mutations. That’s a pretty large number. Some of them, maybe a handful, maybe 1/100 of those 105 mutations, which would be about 1000, would be beneficial. Then selection will act on them, and the better ones will rise more quickly because they make more progeny. And that’s evolution in action!” “Increasingly, we’re using evolution to teach us about how the organism works.” “I’m not saving lives with any of our studies on microbes in biofilm-associated infections just yet. We are seeing how they change in these infection and how they become more drug resistant. That’s great, and I think that’s a valuable contribution. But when we can encourage hundreds of high schoolers to really consider careers in the life sciences or mathematics or engineering, we’re changing lives.” Links for this episode Vaughn Cooper University of Pittsburgh website Rich Lenski Long-Term Evolution Experiment ASM video Journal of Bacteriology cover featuring Pseudomonas colonies Journal of Bacteriology report on the evolution of Pseudomonas biofilm diversity Journal of Bacteriology tribute to Bill Costerton Bill Costerton YouTube interview Send your stories about our guests and/or your comments to jwolf@asmusa.org.  

Marylynn Yates discusses how the urban water cycle and its importance in eliminating waterborne pathogens. She describes the types of microbes that can survive in water and how testing for different microbial types can affect interpretation of contamination levels. Host: Julie Wolf Subscribe (free) on iPhone, Android, RSS, or by email. You can also listen on your mobile device with the ASM Podcast app. Julie's biggest takeaways: Worldwide, water is a large source of infectious disease. Billions of people have no access to safe water and this culminates in 1.5 billion cases of diarrhea and 1.5 million deaths from contaminated water annually. The urban water cycle takes water from lakes or the ground for its first treatment before delivery to our homes. Water leaving our homes as waste water goes to a second facility where water is given a different set of treatments to eliminate disease-causing microbes before the water is returned to lakes or rivers. Different treatment facilities are needed because the concentration of contaminants is different in water before and after use in our homes. Crystal clear spring water can be deceiving, but can carry disease-causing microbes. Animals can carry protozoans such as Giardia and Cryptosporidium, which also cause disease in people. This is why treating water, even with a simple boiling procedure, is important when backpacking or camping. Bacterial sentinels such as Escherichia coli can be used to measure potential bacterial pathogen presence, but they don’t measure pathogenic protozoans or viruses. This is in part because the treatment necessary to eliminate bacteria is different than that necessary to eliminate protozoans and viruses. Some scientists argue that bacteriophage are a better measure of potential pathogenic virus present, though no regulations require phage monitoring. Others argue that detection of a spore-forming bacteria, such as Clostridium perfringens, would better predict protozoan presence.   Featured Quotes (in order of appearance): “Because there is no new water on Earth, we need to make sure that after we use water that we treat it in a way so that when it’s used again as drinking water, it’s as clean as it can possibly be.” “Some viruses are very hardy and can survive for a long time (outside their host cell). They don’t need nutrients like bacteria do, so they just sit there - almost like a chemical contaminant.” “Some of these viruses, such as hepatitis A virus or norovirus, can survive for a long time in the environment. When I say ‘quite a long time’, I mean for weeks or months, or in the case of hepatitis A, there was one report that it lasted up to a couple of years.” “It’s that real-world application that has kept me going for all these years, knowing that I can have an impact on public health in my own, tiny way.”   Links for this episode Marylynn Yates website at UCR Marylynn Yate interview with UCR mBiosphere blog post on developing water safety testing with the EPA mBiosphere blog post on developing new technologies for water safety testing Milwaukee Wisconsin Journal Sentinel 20th Anniversary of Cryptosporidiosis Outbreak Monsters Inside Me: Cryptosporidiosis   Send your stories about our guests and/or your comments to jwolf@asmusa.org.

Colleen Kraft talks about treating Americans who became sick with Ebola during the west African outbreak and were evacuated to her hospital for treatment. In the second half, Kraft talks about her experience performing fecal transfers, and explains why she sees the gut microflora like a garden. Host: Julie Wolf Subscribe (free) on iPhone, Android, RSS, or by email. You can also listen on your mobile device with the ASM Podcast app. Julie's biggest takeaways: The patient conditions couldn’t be more different between the Liberian care centers and Emory University. The nursing ratio, access to both basic and experimental medicines, and even environmental conditions such as air conditioning created drastically different healthcare experiences between the two. While Ebola is a deadly disease, the symptoms such as headache, fever, and diarrhea are much more common than the bloody hemorrhaging often described. Patients can lose up to 10 liters of fluid each day! Fecal microbiota transfer is a more appropriate name than transplant; new microbes overlaid on top of the dysbiotic flora will reshape the microbiota already present. While FMT is currently used only to treat C. difficile (aka C. diff), forthcoming studies will determine if FMT can decrease risk of an antibiotic-resistant infection by displacing resistant bacteria. Featured Quotes(in order of appearance) “Ebola virus disease is much more mundane than all of the novels you might read. It’s really a sepsis syndrome with a spectrum of that sepsis. Part of sepsis can be abnormal coagulation factors and low platelets, and so those bleeding complications go along with that sepsis syndrome.” “It sounds really mundane, but supportive care is really the most important thing for these patients. When that can occur, people can recover.” “The body doesn’t really like Ebola. One patient was encephalopathic, had kidney failure, liver failure, had some bleeding. Once the viral load was gone, all those things uprighted! It was like a capsized ship that uprighted.” “I really view our guts like gardens. There are good fruits and vegetables when our gardens are in homeostasis. Once we use antibiotics, it kills the good fruits and vegetables of the garden and C. diff grows up like a weed. All we’re doing [when we treat C. diff] is giving weed killer but we’re not replanting that garden.” “I’m somebody who thinks after every antibiotic treatment for anything that we do, we should be giving people some sort of item to enrich or restore their microbiome.” “The most exciting thing I can think of is to bring cutting-edge research and contributing to people being cured by these methods.”   Links for this episode Colleen Kraft Emory website And the Band played on Virus Hunters of the CDC The Hot Zone NETEC Clinical Virology Symposium Send your stories about our guests and/or your comments to jwolf@asmusa.org.  

Sabra Klein addresses the question: how does biological sex influence influenza infection and vaccination? She explains her findings on inflammation differences between males and females, and how these differences can affect the outcome of disease. Klein also discusses her advocacy for inclusion of biological sex in method reporting as a means to improve scientific rigor. Host: Julie Wolf Subscribe (free) on iPhone, Android, RSS, or by email. You can also listen on your mobile device with the ASM Podcast app. Julie's biggest takeaways: Information from the 1918 influenza pandemic suggested males died at a higher rate than females, which could be due to a gender fator or a biological factor. In 1918, men lived in close quarters of military barracks while women didn’t, representing a cultural difference of gender norms (women were exempted from military duty). But males are more susceptible to secondary bacterial infections that often accompany flu, which may represent a biological difference in infection outcome. In Klein’s studies, female mice suffer influenza more severely than males. Women who contracted the H1N1 flu epidemic in 2009 were more likely to be hospitalized with severe influenza than men. These data have yet to be aligned and leave many variables yet to explore! Influenza infection disrupts the female menstrual cycle, causing lowered estrogen and progesterone levels. Providing exogenous progesterone can dampen inflammation and stimulate repair mechanisms needed to fix the damaged lung tissue. This type of host treatment is less likely to lead to the evolution of resistance than using antiviral compounds. Females and males respond differently to vaccination; females mount a higher antibody response and have greater cross-protection than males. Many diseases in addition to influenza show these sex-specific differences. The sex differences observed are specific to age; with older age, the differences are lost. In several other countries, epidemiological and clinical data are analyzed for differences between sexes. With greater awareness, the United States may incorporate this practice too.   Featured Quotes (in order of appearance): “Both genes as well as the hormones define the biological construct of sex.” “There’s an ample amount of data that suggest men are less likely to wash their hands than women. We all know handwashing is probably one of the best ways to avoid contact with viruses - really anything infectious. We always have to question if we do things that influence our exposure; but in our mice studies, we can control their exposure.” “We really have a love-hate relationship with inflammation. We need it to recognize the presence of the virus, but then we need it to dissipate. Our data suggest hormones are integral to regulating inflammation and the repair following inflammation.” “The immune responses to the influenza vaccine - and this extends to many vaccines - are often higher in females as compared with males. This has been shown in humans as well as animal models.” “I don’t know that I think that man flu is real. I think a lot can depend on both your age as well as your vaccine status that can influence whether you’re going to land in the hospital with severe influenza. Much like we were talking about with individuals who don’t have a vaccine, such as during a pandemic, females may be suffering a bit more, but once vaccinated females seem to do better than males. There are some nuances we shouldn’t lose sight of.”   Links for this episode Sabra Klein website Klein speaking on heart disease differences in men and women Klein editorial in mBio: Sex reporting in microbiological and immunological research Smithsonian exhibit notification HOM Tidbit: Smithsonian article: How the horrific 1918 flu spread across America HOM Tidbit: Aeon article: Who names diseases? Send your stories about our guests and/or your comments to jwolf@asmusa.org.

Jennifer Martiny describes the incredible microbial biodiversity of natural ecosystems such as soils and waterways. She explains how to add a bit of control in experiments with so many variables, and why categorizing microbial types is important for quantifying patterns. Host: Julie Wolf Subscribe (free) on iPhone, Android, RSS, or by email. You can also listen on your mobile device with the ASM Podcast app. Julie's biggest takeaways: Studying microbial community functions in their natural environment are harder to understand, but help us to parse the complexity of the natural world, in part because these experiments also include local flora and fauna that are often omitted in the controlled lab environment. Microbial cages - an actual physical barrier that contains a soil-based community - can help to disentangle the effects of the microbial community from those of the surrounding environment by adding a level of control by limiting interaction of microbes inside the nylon mesh cage with those outside of it. Are microbial functions redundant? It depends on what function you look at - respiration is a very common function, so it’s less likely to be affected by a change in microbiome composition. Other functions, such as degrading particular compounds, may have a stronger relationship between the microbes present and those functions. Microbes are hugely diverse! Jennifer’s comparison of all the diversity of the birds on Earth to a single bacterial taxon is mind-blowing! Microbial categorization may be hard, but the ability to group similar organisms is necessary to formulate hypotheses and conduct experiments. It’s important to remember the groupings are manmade and sometimes have to be reconstructed!   Featured Quotes (in order of appearance) “One of the hardest things we study is not on the microbiology side but is on the ecosystem side, measuring those biochemical functions in the environment.” (10:05) “It’s not as if we are ever going to be able to study every particular organism out there and build a model with thousands of equations; instead what we really need to do is go after trade-offs and overall relationships that may hold across large groups, and in that way have some simple rules under different conditions like drought or temperature.” (16:45) "Modern birds evolved about 100, 125 million years ago. Two sequences that share the 16S gene, if it’s roughly 97% identical, probably diverged 150 million years ago. That means we are lumping in all the diversity within the bacteria group within one taxon, calling it a species, which is the equivalent of lumping all birds together!" (18:47) “It’s a bit overwhelming to imagine that for each 16S rRNA taxon, you could have as much functional, morphological, and behavioral diversity as what we see in all of birds!” (19:39) “In biology, we’re always using an operational definition but we don’t want to get too hung up on the definition and miss all the interesting patterns going on!” (20:49) “If you can start to quantify patterns, then you can start to ask ecological and even evolutionary questions about why we see those patterns.” (33:04)   Links for this episode Jennifer Martiny Lab Home Page University of California Irvine Microbiome Initiative HOM Tidbit: TWIM 50: These things aren’t even bacteria! Carl Woese Obituary (New York Times) Carl Woese 1996 Feature (New York Times) Send your stories about our guests and/or your comments to jwolf@asmusa.org.

Vincent and Elio discuss the reason for poor efficacy of one of the influenza virus vaccines, and using a hyperthermophilic anaerobe to produce hydrogen from fruit and vegetable wastes in seawater. Hosts:  Vincent Racaniello and Elio Schaechter. Subscribe to TWiM (free) on iPhone, Android, RSS, or by email. You can also listen on your mobile device with the ASM Podcast app. Become a patron of TWiM. Links for this episode Glycosylation site on influenza H3N2 viruses (PNAS) Biohydrogen production by Thermotoga (Waste Man) Image credit Letters read on TWiM 166 Send your microbiology questions and comments (email or recorded audio) to twim@microbe.tv

Peter Hotez talks about neglected tropical diseases: what are they, where are they found, and where did the term “neglected tropical disease” come from, anyway? Hotez discusses some of the strategies his and other groups are using for vaccine development, and his work as an advocate for childhood vaccines and global health. Host: Julie Wolf Subscribe (free) on iPhone, Android, RSS, or by email. You can also listen on your mobile device with the ASM Podcast app. Julie's biggest takeaways: Renaming “other diseases” - a large collection of disparate diseases such as schistosomiasis, leishmaniasis, and onchocerciasis (also called river blindness) - as “neglected tropical diseases” by Hotez and colleagues was integral to bringing attention to the diseases of the bottom billion, people that live on less than one U.S. Dollar per day. Neglected tropical diseases are often chronic and debilitating without high mortality. These diseases trap people in poverty due to their long-term effects. The NTDs are often associated with terrible stigma that can lead to additional challenges for affected populations. Neglected tropical diseases are found worldwide, in rich and poor countries. The poorest peoples living in the G20 countries (and Nigeria) now account for most of the world’s NTDs. Parasitic infections present challenges for vaccine design, but reverse vaccinology may be a useful strategy. Reverse vaccinology mines genomes to identify promising vaccine candidates in silico, which are then narrowed sequentially for those that are expressed on the bacterial surface, immunogenic, and ultimately protective against disease. This strategy has worked for Neisseria meningitidis, and Hotez is hopeful that it will produce effective vaccines for the parasitic infections he studies. The tradition of individual fields and departments, combined with the old-fashioned notion that scientists needn’t spend their time engaging with the public, has led to flatlined budgets and the rise of anti-science movements. Scientists need to engage the public to ensure the future of science and science-based policy.   Featured Quotes (in order of appearance): “The concept of ‘neglected tropical diseases’ was very much born out of the Millennium Development Goals launched in the year 2000.”   “Treating NTDs in rich countries “is not a resource problem; it’s an awareness problem.”   “If you want to enter global health, we need as many people with a scientific background to go into business and law and international relations as we need to go into traditional scientific pathways”   “Many involved in the antivaccine movement disproportionately involve either parents who are affluent or educated, or both: those who know just enough to do a google search but without the background to separate the garbage from the important stuff. And of course the anti-vaccine groups are deliberately misleading.”   “Research America found that 81% of Americans can’t name a living scientist. That’s our fault. We’re so inward looking that we aren’t taking the time to do public engagement.”   Links for this episode Peter Hotez at Baylor College of Medicine Peter Hotez website Millennium Development Goals published by the World Health Organization in 2000 WHO list of Neglected Tropical Diseases Forgotten People, Forgotten Diseases by Peter Hotez Blue Marble Health by Peter Hotez Public Health United episode featuring Hotez HOM Tidbit: Oncocerciasis now: 1986 British Medical Journal report Send your stories about our guests and/or your comments to jwolf@asmusa.org.

Stacey Schultz-Cherry explains the selection process to choose the influenza virus strains to include in the annual influenza vaccine. Schultz-Cherry also discusses her research on the influence of obesity on the course of disease and vaccine efficacy. Host: Julie Wolf Subscribe (free) on iPhone, Android, RSS, or by email. You can also listen on your mobile device with the ASM Podcast app. Julie's biggest takeaways: The WHO Collaborating Centers and National Influenza Centers around the world work with a humongous network of physicians, public health workers, and veterinarians to identify strains most likely to become part of the circulating influenza viruses. An influenza strain that makes birds very sick is not necessarily a strain that will make people sick. Predicting phenotype from genotype remains a challenge. Receptor binding to mammalian receptors, signatures in the genome that allow it to replicate in mammalian cells, and transmission between ferrets are the marks of potentially bad strains. Genetics can also tell you a little bit about the antiviral resistance characteristics of a strain. Why can’t we incorporate all known influenza strains into a vaccine? It’s an issue of immunodominance - having enough antibodies against an infectious agent that it will be neutralized should it cause infection. Researchers don’t know how many HAs you can incorporate to generate proper immunity to each molecular version, and this is one area of influenza vaccine research. Obesity appears to decrease the immune response to influenza, potentially affecting the ability to form memory response. This means the vaccine is less effective, the course of disease when infected is worse, and the likelihood of secondary bacterial infection is higher. Featured Quotes (in order of appearance) “People don’t appreciate how much work goes into this. The importance of surveillance - if we lose our surveillance, it’s going to be very difficult to know which strains to select for the vaccine, as well as diagnostics.”   “Part of the trick is not just predicting which viral strain to use but understanding which of those strains will grow to the highest efficiency without changing when we grow it in eggs to make the vaccine.”   “My bet is, whatever we find, it’s going to end up being 10 times more complicated...which is great for my post-docs, because there’s plenty of opportunities for them to find new things and build new labs, which is ultimately the most important thing you can do as a P.I.”   “I did wound repair during my Ph.D. . . . with my background in wound repair, I said ‘what is a virus but a great big wound”    “When I was changing fields, my thesis committee asked me, ‘what are you doing? I was told it would take five years just to read the literature. You can’t change fields!’ And I said, ‘Yeah, I can.’” And I did!   “Whatever your decision is, you go for it you don’t have regrets, but you put 110% into whatever you decide to do.”   Links for this episode Stacey Schultz-Cherry St. Jude Graduate School of Biomedical Sciences CDC Flu Activity Map HOM Tidbit: Vaccination against Influenza (review) Send your stories about our guests and/or your comments to jwolf@asmusa.org.

Jack Gilbert talks about his studies on microbiomes of all sorts. He describes the origin of the Earth Microbiome Project, which has ambitions to characterize all microbial life on the planet, and talks more specifically about the built microbiome of manmade ecosystems such as hospitals. Gilbert explains how advances in scientific techniques have driven past microbiome-related discoveries and will continue to do so in the future. Host: Julie Wolf Subscribe (free) on iPhone, Android, RSS, or by email. You can also listen on your mobile device with the ASM Podcast app. Julie's biggest takeaways: Insect-pathogenic fungi living in plant roots can pass nitrogen from killed insects to their plant hosts, receiving different carbon nutrients from the plants in return. Fungi harvested after growth on inexpensive materials like chicken droppings are used in agriculture both as fertilizer and as insecticide. Cyclosporine was first discovered in insect-pathogenic fungi. Raymond St. Leger and other scientists working to introduce genetically modified microbes into the environment deeply consider the societal effects of their work, including collaboration with local communities, governmental regulatory bodies, and trusted leaders and tailor their efforts to the regional area. Featured Quotes (in order of appearance): “We really can apply ecological understanding of microbiomes and microbial ecosystems to any environment.” “I think basic research is absolutely essential but I always want to think about what that could lead to in the future.” “Reproducibility is key and extraordinarily difficult in all fields of science due to lack of appropriate funding and a zeitgeist in science that discourages scientists from reproducing one another’s studies.” “We are forever striving to validate the predictions we derive from our descriptive work. We create SO MANY predictions!” “No small dreams, no small goals - go big or go home! At the end of the day, we all want to feel like we’re doing something that makes an impact.” “I love to collaborate. I love to work with other people, brilliant people in the microbiome field” “I’m often accused of not being focused enough. What does Jack Gilbert do? Well, I do a little bit of everything - as long as there’s a microbe involved! I like it like that; it keeps me energized.” Links for this episode Jack Gilbert website at University of Chicago Jack Gilbert TedxNaperville Talk Earth Microbiome Project home page Dirt is Good - new book by Gilbert and Rob Knight History of Microbiology Tidbit: Joshua Lederberg piece in The Scientist on ‘microbiome’ nomenclature in 2001. Send your stories about our guests and your comments (email or recorded audio) to jwolf@asmusa.org.

¡Hola hola, vasos y vasas! Bienvenidos a un nuevo episodio, internacionalmente conspiranonico, de ASM Podcast: tu podcast del molar. Un especial ASM, porque siempre es especial. Pero sobretodo por dos motivos: Hay una terrible conspiración que Pitiflí nos desvelará, donde se entrecruzan asesinatos de ex-banqueros, suicidios simulados, redes internacionales de hackers y vasos de café. Tenemos […]

¡Hola hola, Juanes de la Cosa y Chinito Nakatones! Bienvenidos a un nuevo episodio, Angelísimamente Garóico, de ASM Podcast: tu podcast del molar. El meltdown (colapso) de Charlie Sheen Estados Unidos fue apoteósico, seguido por millones, y emocionante hasta el final. Explotó un día cualquiera, con el hombre golpeando al director de 2 and 1/2 […]

¡Hola hola, Conspiradores y Hackers de la cuenta de Instagram de Britney Spears! Bienvenidos a un nuevo episodio, experimentísticamente conspiranoico, de ASM Podcast: tu podcast del molar. Recordemos lo que nos pasó en el episodio anterior: Samoano volvió en a nuestro espacio-tiempo usando el lazo temporal del AutoLoop, volviéndolo todo del revés, por lo que ahora […]

¡Hola hola, saltinbanquis, trapecistas y demás personajes cirquenses! Bienvenidos a un nuevo episodio, pequeñísimamente cirquense, de ASM Podcast: tu podcast del molar. Recordemos lo que nos pasó la temporada anterior: entramos en un vórtice temporal mega-chungo, y lo que para vostros fue un año, nosotros estubimos danzando con las estrellas, en terrenos post apocalípticos de […]

  ¡Hola hola, apocalípticos y apocalípticas! Bienvenidos a un nuevo episodio, apocalípticamente nuevo, de ASM Podcast: tu podcast del molar. Os parecerá que llevamos un año exacto sin podcastear, pero para nosotros, ha sido solo una semana de portales espacio-temporales, batallas galácticas, loops temporales de guerras apocalípticas y finalmente, vuelta al status quo, con un […]

¡Hola hola, cuartetos y cuartetas! Bienvenidos a un nuevo episodio, musicalmente solfamístico, de ASM Podcast: tu podcast del molar. Hemos vuelto! Como Alf, en forma de chapas. Bueno, os dejamos con un especial canciones sandungueras para toda la familia: Noticias noticiosas del mundo mundial La sección de Ziri. Y hasta el próximo podcast, ménglers!

¡Hola hola, Balaseros! Bienvenidos a un nuevo episodio, balaserísticamente balasero, de ASM Podcast: tu podcast del molar. Bueno, os dejamos con: Noticias noticiosas del mundo mundial La sección de Ziri. Y hasta la semana que viene, ménglers!

Hola hola, Clashintheclevers y Clashinteclevars, Bienvenidos a un nuevo episodio, cleverísticamente clashero, de ASM Podcast: tu podcast del molar. Bueno, os dejamos con: Noticias noticiosas del mundo mundial Cine: la gran película CLASH IN THE CLAVERS, que ha pasado desapercibida en los cines, pero que según la crítica es una joya que no os podéis […]

Welcome back to ASM Podcast ep 29 recorded in New ASM Studios. What a result on the weekend! We present to you a review of the Man City result in another moan free episode! We answer a question from a listener from Sweden, before we get Shirt Fronted with a review of the 2007-2008 Home shirt - Yes the 125th Anniversary shirt... what are your thoughts? Listen to John's review.... We SHOOT! back in time for a look at the british football landscape through the eyes of SHOOT! magazine - March 1982. We then discuss our recommendations of the weekend. If you have a question please tweet or email us or post of Facebook at the below addresses : Twitter @spurssackagain Email : anothersackedmanager@gmail.com Facebook and Instagram : another sacked manager our blog is anothersackedmanager.wordpress.com Please like and review us on iTunes ! Thank you for your continued support of the podcast!!! Onwards to Monaco and Swansea! #COYS #StoppinHO