Finding Genius Podcast

Cancer cells disrupt the body's circadian clock. Researcher Brian Altman works to understand why and how this happens and what therapeutic findings may result. He tells listeners How our 24-hour cycle works and how cancer cells create a type of circadian rhythm disorder, Why cancer cells gain an advantage over other cells under this circadian rhythm disorder, and Why this information could prove useful in fighting cancer with circadian rhythm cancer treatments. Brian Altman is an assistant professor in the Department of Biomedical Genetics at the University of Rochester Medical Center. He's always been interested in the metabolism of cancer and did a post-doc that involved the circadian clock and rhythms. He describes his lab's basic interest as centered on this disruption of normal circadian rhythms by cancer, which gives the tumor cells an advantage over normal cells by allowing them to outcompete the normal cells. This, they hope, is something that can be taken advantage of and manipulated. He makes the connection for listeners between our circadian clock and metabolism and explains that cancer wants to engage in maximal metabolism all the time; therefore, this trend may break the circadian clock. Studies on mice allowed them to ask which genes are mutated in cancer that might impact the clock and they've focused on a cancer gene called MYC. This gene cranks up the biosynthesis of some cancers. He explains that the two main focuses of the lab's work includes identifying which tumors disrupt the circadian clock and how they can use this to inform therapeutic choices. Finally, he adds that they're getting close to showing that slowing the circadian clock can slow the growth of tumor cells. They are investigating the best way to restart the circadian clock in patients who've been disrupted by cancer to slow this cell growth. See his lab's website to find out more: urmc.rochester.edu/labs/altman.aspx. Available on Apple Podcasts: apple.co/2Os0myK

Professor Aditi Uday Gurkar asks why the aging process produces such disparate results under the same chronology for different people. Her research investigates How DNA damage reprograms a cell's metabolism and is it possible to intervene, How post-mitotic cells respond to DNA damage, and What might a unique molecular fingerprint look like for biological age based on markers, metabolites, and the metabolome. Aditi Uday Gurkar is a principal investigator and an assistant professor of medicine in the Division of Geriatric Medicine at the University of Pittsburgh. Growing up with her grandparents gave her an early view of the aging process, but the difference between each grandparent's health and strength struck her most of all. This question of why people age so differently drives her research. She explains the causes of DNA damage and mechanisms of DNA repairing, and adds that her lab's focus is on how cells respond to the damage. They believe they've found those responses are integral to different levels of health as one ages. It's estimated that one cell will undergo 70,000 lesions or damage on any particular day. She explains to listeners that there are many causes of DNA damage, such as sun exposure and resulting UV radiation. The DNA repairing signals kick in after the polymerase finds a lesion too big for its pocket as it reads the DNA during copying and drops off. She explains the different types of repairs in detail and that an over-activation of repairs can lead to a cell responding as if it is in constant stress, which drives aging. The goal of her research is to understand how to intervene and modulate how the cell responds, especially in reference to its metabolism. She describes how their work with model organisms has shown promise with such modulations and also tells listeners about other studies, future goals, and next steps. For more, follow her on twitter with @healthspan_AUG and see her lab's website: agresearchlab.com. Available on Apple Podcasts: apple.co/2Os0myK

Researcher Richard J. Martin works predominantly on filarial parasites and how to develop drugs with the best parasite cleanse ability that can evade resistance. He explains How various filarial parasites move through their lifecycle, enter humans through biting insects, and affect various parts of the body; How the worms themselves have a nervous system that helps them seek different parts of the body and release chemicals to trick the human immune system; and Why social and political factors are a part of this battle against parasites and what anti parasitic medication for humans may offer at least a medical solution. Richard J. Martin is the Clarence Hartley Covault Distinguished Professor and the Dr. E.A. Benbrook Endowed Chair in Pathology and Parasitology at Iowa State University. He specializes in filarial parasitology and tells listeners about their impact on human health as well as describes their physiology and ecology. For example, he describes the life stages and habits of the worms that cause river blindness and elephantiasis and how these diseases result from the worm number and activity. He explains challenges to eradicating parasites completely by discussing the heartworm parasite existing in the U.S. despite effective sanitation. Therefore, in struggling countries with bad sanitation, effective anti parasitic medication for humans is a key part of the battle. He also ties this battle to social and political forces that make this anti parasitic effort especially challenging. For example, better governance and a different motivation for medication funding could make differences in a country's ability to clean and sanitize these areas as well as motivate drug companies to relieve the suffering of those with these parasites. In the effort to find the best parasite cleanse that is not prone to resistance, the ideal looks like a drug that can be take once a year to treat and prevent all the filarial parasites. Dr. Martin describes one drug that is moving to phase 3 trials, and says that if it gets through, it will be a big breakthrough. To find out more, google him and find his research on research gate or send him an email. His university website is genetics.iastate.edu/people/richard-martin. Available on Apple Podcasts: apple.co/2Os0myK

Gavin Douglas and colleagues published a paper assessing microbiome research and assertions that the human microbiome explains missing heritability in nature. He discusses this issue and explains What are classic ways of understanding genetic variation in humans and how recently microbiome research has entered this understanding, What the holobiont model is and how it involves claims regarding the microbiome and missing heritability in nature, and How their paper views the microbiome as more of potential element in genetic variation in humans and necessitates more consideration regarding how to integrate it outside of the strict, holobiont model. Gavin Douglas is a PhD Candidate in the Langille Lab in the Deptartment of Microbiology and Immunology at Dalhousie University. His background is in human genetics and he has just published an intriguing paper called "Re-evaluating the relationship between missing heritability and the microbiome" in the journal Microbiome. He helps listeners understand the basics regarding the issue by explaining heritability as the proportion of variation in a phenotype in a given population explained by genetic variance. He offers more background to this standard and then explains the "case of the missing heritability," which basically indicates the variation that isn't explained. Several hypotheses have emerged to explain this missing heritability, several of which are tied to the human microbiome. He describes how, for example, a holobiont model of a human organism puts forward a hologenome—a combined genome that includes the microbiome and might capture the missing heritability. The article discusses this theory and points out ways it doesn't quite fit. For example, the holobiont doesn't present a combined evolutionary unit that transmits over generations. But he does think the microbiome plays a role in this mystery. He explains how and why and different ways scientists use these ideas. For more, follow him on twitter as @gavin_m_douglas and read the open-access paper here: Re-evaluating the relationship between missing heritability and the microbiome. Available on Apple Podcasts: apple.co/2Os0myK

Computational biologist and evolutionary genomics researcher Eugene Koonin touches on several timely topics about biology, evolution, and what computational biology can teach us. In this podcast, he discusses How the molecular clock works as a null hypothesis and enables deviation studies and a better understanding of functional and ecological changes, How comparative genomics provides specialized ways to understand similarities and differences and explains this in terms of coronaviruses, and What are the mechanics of evolution, theories of the beginnings of life, and the coevolution of viruses. Eugene V. Koonin is a Senior Investigator at the National Center for Biotechnology Information (NCBI) and an NIH Distinguished Investigator and works in evolutionary systems biology. This includes genomic comparative analysis of everything from the human genome to coronaviruses. He shares his vast knowledge with listeners and explains how the molecular clock functions in a computational role. He gives concrete ways this can be understood, such as comparing the same gene in an animal and a human genome. He explains the basics of comparative genomics, a key advancement of our era of biological evolution study, and how it allows for an alignment for scientists to maximize similarity comparisons. They can then compare nucleotide sequences directly with similar life forms and make conclusions about their relationships and functional predictions. He explains how this works using coronaviruses as an example: anything shared between highly virulent strains but is not present in milder strains gives researchers vital information. He also discusses various elements of evolution like punctuated evolution and the math of speciation. He also describes theories of the beginnings of life and Darwin's Last Universal Common Ancestor, or LUCA, as well as how the first genomes might have evolved from RNA and ribosomes that catalyzed various reactions including nucleotide polymerization. Finally, he addresses advancements in his field on the near horizon. For more, search for him in Google Scholar and see his NCBI web page: ncbi.nlm.nih.gov/research/groups/koonin/. Available on Apple Podcasts: apple.co/2Os0myK

Tying the importance of economics to technological innovation is key to advancing developing countries. Eric Verhoogen's research asks why firms in industrial countries aren't adopting technologies already developed by richer countries. He tells listeners about some microeconomics concepts his research explores. For example, he explains How a variety of incentives within a company can inhibit adopting a new technology, How understanding and eradicating organizational barriers to concepts like profit sharing could lift such barriers, and Why connecting microeconomics concepts with effective government intervention is essential in approaching pay-for-performance export incentives. Eric Verhoogen is a professor in the Department of Economics and School of International and Public Affairs at Columbia University. He researches the importance of economics in adopting new technologies by examining organizational barriers to these technologies. He explains this research by telling listeners about a specific example involving the introduction of a less wasteful technology into soccer ball production in several Pakistani firms. He describes his particular research experiment that resulted in pinpointing the barrier to implementing this technology on workers who would lose money in their per-piece system. He discusses why this was the case and what was different about one firm that chose to take on this technology and why that was significant. His example relays other barriers to taking on new technology such as owners unwilling to undergo too much organizational reworking as well as the mysteries behind the lack of much "knowledge spill over." Such research opens up keys to ways government could effectively intervene in terms of tariff reduction and trade organizations. He also discusses his other research projects such as incentivizing surgical goods innovation through a contest and a project in Tunisia on pay-for-performance export production and subsidies. To find out more, see his Columbia website, columbia.edu/~ev2124/, and find him on Twitter as @EricVerhoogen. Available on Apple Podcasts: apple.co/2Os0myK

Ian Birrell is a contributing editor of The Mail on Sunday, has a weekly column in the i newspaper, and has written for a number of publications, including The Times, The Washington Post, the Daily Mail, and the Guardian. Over the course of his career, he has reported for more than 60 countries worldwide. In this episode, he shares what he knows about the origins of COVID-19 and the COVID-19 situation in general. Press play to learn: Who China's 'Bat Woman' is and the significance of her role in the information and theories surrounding COVID-19 What characteristics of the virus are unusual What evidence suggests that COVID-19 did not originate from a wet market in China as we've been told Like most of us, Birrell began hearing about COVID-19 around February when stories began breaking in the media about a potential Chinese cover-up regarding the virus. Considering it a "potential" pandemic at the time, Birrell focused his investigative research on these allegations, including one which placed the World Health Organization (WHO) in collaboration with China in cover-up efforts. He wrote a couple of pieces covering evidence which suggests that the infectious virus broke out earlier than claimed, and that the wet market theory of origin might not be true. Birrell explains what's wrong with the wet market theory of origin, citing the original Lancet paper on the wet market which showed that the very first cases identified were not linked to the wet market, a report in the South China Morning Post showing cases going back to mid-November which were not linked to the market, and several early investigative journalists who published articles which have since been censored and removed from most social media websites. In particular, Birrell discusses evidence which suggests that Chinese officials knew by mid-December that human-to-human transmission was possible, and that the entire genetic code of the virus had been sequenced by January 2nd. That genetic sequencing data—data that would have allowed for earlier research on an effective treatment or a vaccine—was not shared until more than a week later, when it was posted on a public access site by an Australian scientist on behalf of a Shanghai professor, who had his lab shut down just two days later. Birrell also discusses the potential of a laboratory leak of the virus, unusual characteristics of the virus, how different nations have responded to the virus, and the need to be wary of vested interests in journalism and science pushing particular narratives about what's going on. Learn more at http://www.ianbirrell.com/about-me/ and find Birrell on Twitter at @ianbirrell. Available on Apple Podcasts: apple.co/2Os0myK

Returning guest Jo Bhadi discusses using new platforms and technologies to predict cancer probability as well as what he's learned about how cancer evolves. He also discusses how Quantgene seeks to serve its customers. He addresses How Quantgene uses the human genome sequence, artificial intelligence, liquid biopsies, and other technology platforms to identify cancer patterns; How they've put together a monthly subscription turnkey service for early cancer detection; and How cancer itself develops and how they approach detection with this layering of different types of information to achieve a specificity of detection above 90%. Jo Bhakdi started Quantgene in 2015 at a UC Berkeley Lab with a goal of early disease detection. The company uses quantitative science for a new level of precision. They started in cancer detection spaces using cell-free DNA sequencing with what is known about the human genome sequence. They saw a tremendous opportunity opening up based on new technology platforms, sequencing, and AI recognition algorithms. In a nutshell, they pursued how to look at cell-free DNA shed by cancer in the bloodstream and recognition patterns to identify the 15 most deadly cancers. They sell their services directly to patients but include physicians and genetic counselors in the process. He explains their business model in further detail but also covers the complications of detecting and understanding cancer progression, from the heterogeneity of tumors to advantages of cell-free DNA sequencing compared to tumor biopsies. He explains the systemic insight into cancer a liquid biopsy offers. He describes other limitations of tumor biopsies and how the question of heterogeneity of a tumor is surprisingly complex. In fact, he adds that the whole concept of quantifying tumor heterogeneity is a very new concept. He describes many characteristics of cancer and its evolution in more detail and then addresses how Quantgene layers many degrees of information, including medical and genetic history, to produce a highly precise probabilistic model. For more about the company, see quantgene.com. To find out about the direct-to-consumer service, see chooseserenity.com. Available on Apple Podcasts: apple.co/2Os0myK

Researcher Jean-Frederic Colombel has studied Inflammatory Bowel Disease treatment (IBD) for about forty years. He explains for listeners What complications occur with Crohn's disease and ulcerative colitis, which are included in the IBD designation; Why IBD can be brought into remission but is not considered cured; and How researchers are studying this autoimmune disease to understand causes and prevention. Jean-frederic Colombel is a professor of medicine and gastroenterology with the Feinstein IBD Clinical Center at the Icahn School of Medicine at Mount Sinai. He came to Mount Sinai about 10 years ago and had been researching in Lille, France. He tells listeners how treatment of this autoimmune disease has progressed over 40 years and what scientists are still trying to understand. He explains that even though doctors are able to bring patients into deep remission with current inflammatory bowel disease treatment where they have no symptoms and show a perfect colonoscopy, there is not a real cure. As soon as they stop taking the medications, the disease makes headway. Since coming to Mount Sinai, he's worked on better predication and prevention measures. He tells listeners that Crohn's disease and ulcerative colitis overlap and differ. For example, medications that work for one also often work for the other. Differences include how much of the digestive tract and layers of the bowel are being affected. Crohn's disease, for example, can result in a fistula—basically a "communication" or opening and track across the perennial area. They can result in painful abscesses and difficult day-to-day symptoms. He then addresses known causes and describes how much is unknown. IBD is a young person's disease, often showing up around age 25, and early diagnosis is key to preventing complications. He describes studies to better understand the disease, such as a large scale serum sample collection of the U.S. Army to look at biomarkers, as well as treatment efforts beyond drugs such as fecal transplants to microbiome alterations. For more see his page at Mount Sinai: mountsinai.org/profiles/jean-frederic-colombel. Available on Apple Podcasts: apple.co/2Os0myK

As an associate professor in the Department of Economics at the University of Virginia, Anton Korinek studies macroeconomics and international financial stability. He shares details of his work and his input on the COVID-19 situation. Press play to discover: What "externality" means in economics, how it affects each of us every day, and why it's important How the COVID-19 situation has impacted the economy and in what ways in may continue to do so What types of externalities have arisen as a result of COVID-19 The study of economics rests on the premise that the market economy is a very powerful force in society—one that has enabled much progress, but has also been known to lead society astray from the greater good. The force referred to here is called an externality. Korinek explains that externalities arise when people who engage in economic activity do so in a way that affects others without their consent. Consider, for example, a company that dumps waste in a river which runs through your property. Or anyone who produces greenhouse gasses which contribute to global warming. These are externalities, or forces which produce a negative impact on individuals and society at large. Most recently, Korinek has been asking what kind of externalities have arisen from the COVID-19 situation. Mask mandates, social gathering restrictions, economic limitations…these are just a few topics that have become a serious issue of debate in recent months. Many people believe that these mandates infringe upon our civil liberties, but even more are disturbed by a seeming lack of evidence to support the idea that these restrictions are indeed helping the situation. As an economist, Korinek weighs in on these matters. He talks about the ways in which his opinions and viewpoints have changed over the course and development of the COVID-19 situation, the economic cost and effect of social distancing mandates, and what he thinks is likely to happen in the near and long-term future. Tune in, and check out www.korinek.com for more. Available on Apple Podcasts: apple.co/2Os0myK