Finding Genius Podcast

Curious about one of the newest discoveries in the nature of viruses? This discussion explores an exciting find in virus behavior and their ability to communicate: quorum sensing by bacteriophages. Listen and learn What a team in Israel discovered in 2017 about viral communication that set the groundwork for Charles Bernard's research, How the importance of virus and host balance dictates virus survival and therefore initiates this communication regarding density, and What therapeutic applications might develop from viruses using quorum sensing to control bacteria life cycles. Charles Bernard is a PhD student at Sorbonne Université in Paris, working on microbiome communication. He says that quorum sensing means the "minimal number of bacteria or viruses to be present for a collective behavior to be efficient and therefore triggered." But what is viral communication? An important discovery was made in Israel in 2017 when a lab found that a temperate bacteriophage communicates by taking over the cellular machinery of their host bacteria. It signals to other viral particles in a way that determines the host-to-bacteriophage density. In other words, the virus must decide whether to replicate quickly via a lytic cycle or slow down and keep its host alive through a lysogenic cycle, which protects the host. That decision is determined by the ratio of bacteria to bacteriophage: the more bacteria, the better the lytic tradeoff works. The less bacteria, the more host the virus needs to preserve to be able to survive. The genome of the bacteriophage contains genes that produce a signal and a receptor. They use this back-and-forth from within the bacteria to discover the ratio. In other words, they're assessing their odds to determine which replication cycle they should enter. Charles has continued looking at other bacteriophage communications and has been the first to find a bacteriophage with two different communication signals. These findings can translate to therapies by using bacteriophages to control bacteria. For example, if phages can signal in such a way to prevent bacteria from producing spores, scientists could control certain bacterial infection rates. As Charles says, "who gets to decide when it is time to sporulate? We used to think it was the bacteria, but, in fact, maybe it is the phages manipulating its host's biology . . . like a puppet master. " For more, see his lab's website: Team AIRE. Available on Apple Podcasts: apple.co/2Os0myK

HIV's effect on the gut immune cells appears significant. This implies that gut-associated lymphoid tissue (GALT) stands as a possible viral replication reservoir. Virologist Guido Van Marle is researching how and why this happens and how gut infection affects systemic infection. Listen in as he and Richard explore every step of HIV infection. They discuss What the difference between the acute and dormant stage is and why it's termed dormant rather than latent, Why some infected individuals are long-term non progressors and others develop AIDS, and What happens when the virus attacks the gut-associated lymphoid tissue and why this is significant. Guido Van Marle is an associate professor in the Department of Microbiology, Immunology, and Infectious Diseases at the University of Calgary. He focuses on viruses, specifically molecular virology techniques of West Nile Virus and the HIV-1 life cycle. He offers listeners numerous molecular mechanism examples of HIV. He takes special care to designate the different stages of viral infection, explaining how in the early stage, called the acute or primary infection phase, the virus replicates and destroys some of the immune system cells. When it moves into the dormant stage, this activity dies down and the immune system is able to rebound. Significantly, the gut immune cells don't rebound the way other systems do. In fact, his research has found that there is high load of infection going on in these gastrointestinal tract cells in that early acute phase post-HIV transmission, which means the area experiences a lot of cell death and inflammation: this allows pathogens to enter the tract and exit into the blood stream. He explains the molecular mechanisms of biology that lead to leaky gut in this process. Furthermore, when doctors deliver antiviral therapy, and the patient's immune cells increase in number, they don't increase as much in the gut. He has focused on this area of infection for his research with the hopes of understanding disease progression as a whole. Available on Apple Podcasts: apple.co/2Os0myK

Tuberculosis is the world's longest-running pandemic and kills about two million world citizens a year. While often it is the immune response to bacterial infection that's so dangerous, tuberculosis adds a complexity that is especially challenging. Anna Coussens zeros in on several of these complexities in her research. Listen in and learn How the immune response differs dramatically among those infected and how Dr. Coussens is trying to understand why, What is the disease progression and ways the immune response harms the infected individual, and How she is working on "host-directed therapy" as a way to combat the complexities of the disease. Anna Coussens is a Laboratory Head in the Division of Infectious Diseases and Immune Defense with the Walter and Eliza Hall Institute of Medical Research. Her work in infectious diseases microbiology focuses specifically on tuberculosis as an immunologist. Because TB is a dominant problem in lower socioeconomic countries, it is often forgotten about in other areas. This has pushed treatment down on the list of common infectious diseases, but Dr. Coussens is working to change this. She helps listeners understand why Mycobacterium tuberculosis is still the cause of so much illness, explaining the interplay of immunity and infection. It can trick T-cells into not recognizing its presence in infected cells through an extra-cellular vesicle sleight of hand. Furthermore, it has a very slow growth pattern, which makes it both hard to treat and hard to study in lab conditions. Many infected persons can exhibit a strong response and inflammation for years before doctors can detect bacteria in their sputum. Dr. Coussens is trying to understand why different cells can react in such varied ways to the bacteria. Her research aims to find a way to treat the individual and the immune dysfunction of that individual through "host-directed therapy." She hopes to help resolve inflammation that might lead to better outcomes for treatment. People who have had TB are actually at a high risk for getting it again, which perpetuates the disease in high-burden areas. Listen as one researcher describes her hard work to bring better treatment to these communities. For more about her work, follow her on Twitter as @AnnaCoussens and see her web page at WEHI. Available on Apple Podcasts: apple.co/2Os0myK

Could a saliva swab detect cancer presence? Researchers are closer than ever to using such noninvasive biomarker tests as diagnostic tools. Why? Well, it's all about balance, even at the smallest level. Researcher Mahmoud Ghannoum joins Richard to discuss the interactions of the human microbiome. Listen and learn What he's found through studies on cancer and digestive health regarding microbiome species abundance and richness, Why biofilms result from a particular microbiome combination and how his research has found ways to inhibit these films for Crohn's disease patients, and How these findings can be used to generate probiotics and bio therapeutics to address health and disease and a healthy microbiome for cancer therapy. Mahmoud Ghannoum is a professor in the Department of Pathology and Dermatology with the School of Medicine at Case Western Reserve University. He also started a company called Biohm Health, which uses microbiology to develop therapeutics for human microbiome health based on gut microbiome research. Microbiome communities live all over us and inside of us, he says, and he researches how they impact our health. He explains that the microbiome is made up of bacterial and fungal communities. The balance between pathogenic and healthy species and the interactions between each community has dynamic health implications, which is why scientist are connecting healthy microbiomes and cancer prevention. When these communities are out of balance, scientist call this dysbiosis. His extensive studies on tongue cancer and head and neck squamous cell carcinoma showed a connection between cancer and the microbiota. The species diversity and richness of bacteria and fungi both decreased in tumor groups. In the case of head and neck squamous cell carcinoma, he was also able to look at metabolites and found high levels of 2-hydroxyglutarate, which means this chemical can serve as a biomarker of disease, enabling noninvasive diagnosis. In 2016, he also published a well-known study showing how pathogenic bacteria and fungi in microbiomes interact and secrete polysaccharides that form biofilms in the guts of Crohn's disease patients. He's developing a therapy to remove these biofilms by inhibiting the hyphae growth of a candida species. He continues to research effective ways to bring health through microbiome balance. For more information, see biohmhealth.com. Available on Apple Podcasts: apple.co/2Os0myK

Managing diabetes as a type 1 through diet and exercise is a constant balancing act, but Eoin Costello feels he is healthier for the efforts he takes. Listen in as he discusses how he's taken this challenging diagnosis head on and helps others understand and manage their own diabetes. He discusses How his routine helps him manage an effective type 1 diabetes insulin regimen, What methods he uses to make his life simpler and easier under insulin action mechanisms, and What lessons he's learned from inspiring guests on his own podcast and how to learn more about him. It was Christmas time, after all, so maybe all the celebrating was causing his symptoms, and the lack of sleep and increased celebratory drinking had led to his fatigue and excessive thirst. But a doctor's call woke him up from that illusion and at age 19, Eion Costelloe learned he had incurable type 1 diabetes. "I was old enough to understand how serious to take this, but young enough to not be set in my ways," he says, showing his general positive outlook that has helped him manage his type 1 diabetes treatment with vigor and care. He already had a healthy lifestyle, heavily involved in sport, but he had to relearn how he went about his activities with this new challenge. After posting what he learned to an Instagram page for a few years, he found he needed to enlarge the format: there was so much to engage with, that he started his own podcast called The Insuleion Podcast: Redefining Diabetes. On this podcast he shares own insights but also brings on guests from around the world with diabetes and lessons to offer. He says that because it's a well-known yet not well-understood disease, the podcast works well to dispel myths but also inspire. He helps listeners with diabetes redefine for themselves what it means to live as a type 1, enlarging their outlook on what they can accomplish. He shares some of the lessons he's learned from some memorable guests and ends this conversation on a positive note on what being a diabetic means to him at this point in life. For more about him, see his web page, insuleoin.com, and find him on Instagram. His podcast is available through most podcast-streaming sites. Available on Apple Podcasts: apple.co/2Os0myK

First, it's just picking up the prescriptions, then it's helping out a little bit around the house, then it's accompanying them to doctor's appointments, and then, suddenly, the words "Oh, so you're the caregiver" come out of the doctor's mouth. Often, the first time someone hears that, it comes as a surprise, followed by a slow realization that it's true. But what does it mean to be a caregiver, and how to prepare for such a role? Tune in to learn: What types of disagreements often arise between family caregivers and guardians, and how to work through them What the difference is between a guardian and a conservator, and a power of attorney versus a living will How to best prepare for the unexpected when it comes to aging loved ones Pamela Wilson is a podcast host, national caregiving expert, author, radio host, and keynote speaker with over 20 years of experience as a court-appointed guardian, power of attorney, and care manager. She has made it her mission to help caregivers through one of the first hurdles they often face: becoming aware of the fact that they're even a caregiver. In addition, she provides ongoing support and advice to caregivers worldwide, and works with companies and groups that want to increase caregiver education and awareness. Wilson describes the duties and responsibilities of caregivers, examples of problems caregivers face and how best to deal with them, self-care for caregivers, the importance of taking preventative measures (which can sometimes be as simple as having some conversations—albeit some hard ones), and more. Press play for all the details, and learn more by visiting her website at https://pameladwilson.com/. Available on Apple Podcasts: apple.co/2Os0myK

Finding a cure for type 1 diabetes includes two essential goals: growing insulin-producing beta cells and introducing them into patients successfully. Those two achievements appear fast-approaching yet also seem elusive. This podcast takes a closer look at these goals, interviewing one researcher studying how beta cells grow and mature. Listen and learn Where current research stands regarding endocrine system physiology, pancreatic beta cells, and diabetes, What scientists understand about pancreatic beta cell development and pancreas function and what is still a mystery, and How current stem-cell derived pancreatic cells are made and how well they function. Diana Elena Stanescu is an assistant professor of pediatrics with the Department of Pediatrics at the Perlman School of Medicine with the University of Pennsylvania. She's a physician scientist, treating patients and researching how beta cells develop, grow, and mature. "As a pediatrician," she says, "everything is about growing, developing, maturing: I keep that perspective across my work." She adds that scientists think an initial cure for type 1 diabetes will center on cell replacement therapy: they're finding ways to make embryonic cells become beta cells that make insulin. By looking at how beta cells develop and mature, she hopes to advise stem cell biologists on making better beta cells. While scientists have been able to make these cells, they are still too inefficient. Her work aims to change that. Developmental biologists like her are therefore informing these stem cell biologists how these cells need to mimic what happens in normal development to a closer degree. They also need to produce an envelope in which to deliver these cells, protecting them from the body's immune system. "We are able to do this in the lab but the problem is taking it from the lab and scaling up to a lot of people," she says. Furthermore, the cells don't make enough insulin to meet the body's demands. She's directing her research towards making higher quality cells, so that the few cells that they are able to include in this envelope are of the best possible quality and efficiency. This means researching how cells determine their glucose threshold before insulin secretion and other issues like hyperinsulin condition, when babies actually make too much insulin. This work will hopefully lead scientists closer to a cure. For more about her work, she welcomes getting in touch via email. See her information page at the University of Pennsylvania for more information. Available on Apple Podcasts: apple.co/2Os0myK

One of the most exciting recent discoveries in microbiology involves an immunological mechanism of a single-celled organism. CRISPR-Cas technology is a technique bacteria use for fighting infection with phages. This podcast dives into the wild world of CRISPR and bacteriophage interplay. Listen and learn How the timeline of CRISPR discovery progressed into tool developments like CRISPR-Cas9, What are the mechanical details of CRISPR, such as how bacteria steal the phage DNA, and How CRISPR phage therapy might progress and what are other bacterial immunology discoveries. Joseph Bondy-Denomy is an associate professor of Microbiology and Immunology at UCSF. His lab focuses on understanding how bacteria deal with their predators like bacteriophages, which are bacteria-infecting viruses. While they don't infect humans, they cover us and inhabit our bodies, looking for prey. CRISPR is one way bacteria protect themselves from phages, and scientists learned how to utilize the CRISPR for their own purposes, enabling foundational techniques for gene editing in the last decade. CRISPR-Cas9 and bacteriophage interaction in particular has made the news because of the usability of the Cas9 protein. Dr. Bondy-Denomy offers listeners effective analogies for understanding how this process works, comparing this to taking a mugshot of a criminal, giving that bacteria information to retain and work from when the same type of phage tries to invade and infect again. He explains exactly how the bacteria do so, storing the DNA snip in a region that lends CRISPR its name, turns it into RNA, and then guides the CRISPR proteins, like Cas9, to the same phage type if it returns, preventing infection. He explains how understanding this mechanism led to two techniques: putting these systems into mammalian cells and showing how they could cut DNA and change a sequence intentionally and turning the mechanism into a programmable binding system. He discusses his own research as well, including continuing to understand how phages avoid CRISPR-Cas immunity and exploring new bacterial immune systems that have been discovered in the last few years. For more about his work, follow him on Twitter as @joeBondyDenomy and see his lab's website: bondydenomylab.ucsf.edu. Available on Apple Podcasts: apple.co/2Os0myK

While many health programs might seek spousal support, rarely is the spouse's health considered on the same level as the patient. Jannie Nielsen seeks to center these surrounding relationships in how doctors address diet, prevention, and treatment of type 2 diabetes. Listen and learn How might school, social circles, and family members affect one's propensity to develop type 2 diabetes, Why type 2 diabetes manifests itself differently in other countries like Uganda and under different socio-economic patterns, and What are mental risks associated with being a partner of a type 2 diabetes and how this might be addressed with her research. Jannie Nielsen is an assistant professor with the Emory Global Diabetes Research Center. Her research focuses on a new angle: she wants to study how people who are socially or biologically related resemble and affect each other regarding diabetes development and health consequences. In other words, she'd like to quantify in more solid terms how relationships, whether spousal or social, determine behavioral risk factors of diabetes. She mentions a study in England that showed the higher BMI of a spouse, the higher chance that person has diabetes. This certainly has a logic to it, and she therefore asks, "Why don't we then include the spouses when we try to make people healthier?" Her research may help to do just that. She also discusses fascinating differences across cultures and societies reflected in our health, from a cross-sectional study in Uganda to a look at sample populations on islands off of New Zealand. She says that type 2 diabetes and related pancreas function differ across the world. For example, one man in Uganda they worked with who had type 2 diabetes was 55 and never had weight issues. Yet he has severe complications from type 2 diabetes derived from one of the common causes like malfunctioning pancreatic beta cells. For him, she says the challenges to improve his health centered on accessing a more diverse diet, which, without resources, is especially challenging. She's now working on gaining funding for a "complex interventions" study that touches on many variables. For more about this issue, she suggests checking out the Emory Global Diabetes Research Center. Available on Apple Podcasts: apple.co/2Os0myK

The fundamental goal of Juan Alvarez's research? "In a nutshell," he says, "I'm trying to cure diabetes." This podcast discusses the exciting potential of his goal by exploring the specific elements of pancreas function and metabolic misfires that lead to diabetes. Listen and learn How he's working on a substitution for pancreatic beta cells by developing islets in a laboratory, How he's untangling two common causes of type 2 diabetes, namely pancreatic beta cells losing maturity and insulin receptors losing efficiency, and How one promising approach addresses the importance of eating and fasting rhythms on pancreatic beta cell function. Recently awarded an NIH Diabetes Grant, Juan R. Alvarez is an HHMI LSRF Research Fellow with Melton Laboratory at Harvard University. His research investigates causes of diabetes such as the connection between nonfunctioning pancreatic beta cells and diabetes and the impaired uptake of insulin in adipose and muscle tissue. These describe two common causes of type 2 diabetes. In the first case, his group hypothesizes that the pancreas's beta cells are over worked—an overwhelming demand for insulin exhausts the cells and many begin to lose their mature function or phenotype. They believe these cells protect themselves and prevent cell death by returning to this progenitor state. The other common cause of type 2 diabetes is often termed "insulin resistance." It's the job of insulin to encourage muscle and adipose tissues to take up glucose from the blood and use it as fuel. These tissues have insulin receptors to do just that, but in some cases, these receptors become less efficient due to genetics or other metabolic issues or a combination of the two. Dr. Alvarez discusses some promising ways to address these causes, including a focus on the effects eating and fasting rhythms may have on the insulin-producing cells and how a jarring of that rhythm could lead to the beta cells losing their mature state. If they understand this, they might find a protein to reactivate or a molecule to inhibit to bring the beta cells back to their mature phenotype. He and Richard discuss other health connections between diabetes and disease such as cancer and chronic pancreatitis and diabetes. Listen in for how one top researcher is working on a cure for diabetes. For links to Dr. Alvarez's published research, see his page at Harvard: hscrb.harvard.edu/people/juan-alvarez. Available on Apple Podcasts: apple.co/2Os0myK