Podcasts about mice

No Robbie this week - but we've doubled up on the Cody! Joining Cody on this week's roundup is the other Cody - also known as Alaska here at Blood Origins - who produces the Blood Origins podcast. Cody and Alaska talk about the Maine ‘right to food' lawsuit, a proposal to strip hunters' property rights in New Jersey, the state of discourse in the US, the Recovering America's Wildlife Act, and more!  See more from Blood Origins: https://bit.ly/BloodOrigins_Subscribe Music: Migration by Ian Post (Winter Solstice), licensed through artlist.io Learn more about your ad choices. Visit megaphone.fm/adchoices

Paul Shaner leads us through a story of tumors, boils and mice.

Mon nouveau podcast: Real Life French Apple Podcast: https://podcasts.apple.com/fr/podcast/real-life-french/id1628949690?l=en Spotify: https://open.spotify.com/show/400GRC4Cg6epiVJj84PIu5?si=0efca496740d41da ------------------------------------- Texte: Une activité cérébrale perturbée pendant le sommeil des souris, en particulier durant la phase de mouvements rapides des yeux, peut empêcher les animaux de se souvenir de choses apprises dans la journée. Traduction: Disrupting brain activity in sleeping mice, specifically during the rapid eye movement phase, can stop the animals remembering things they learned that day. Learn more about your ad choices. Visit megaphone.fm/adchoices

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Videos: 1. The great recycling LIE (what really happens to plastic) (10:44) 2. Is It Game Over? New NASA Report (5:30) 2. You won't believe what Justin Trudeau's government just did | Redacted with Clayton Morris (13:26) 3. Neil Oliver – Who pulls the strings – Pandemic Treaty, Wealth & Power? (2:00) 4. He's EXPOSING the truth in Syria and they don't like it | Redacted conversation w/ Kevork Almassian (first 10:00) 5. Russian Ruble now best performing currency in the world this year… another example of how US sanctions have failed. 6. Vanessa Beeley and Eva Bartlett are smeared by the Guardian for reporting the truth (3:07) 7. Kim Iversen: Inside The SECRET Bilderberg Meetings Between Spies, War Hawks And World Leaders (9:28) 8. New Rule: The Misinformation Age | Real Time with Bill Maher (HBO) 9. https://theduran.locals.com/post/2311112/title  10. https://www.youtube.com/watch?v=3maIN4-ZJl8    Strawberry Compound Shown to Protect Against Alzheimer's, Memory Loss Salk Institute for Biological Studies, June 16, 2022  The thought of losing your mind is a frightening one, but one in three Americans die with Alzheimer's or some other form of dementia. Regardless how frightening the possibility is, the chances of it happening to you aren't exactly slim, which means prevention should be at the forefront of your mind. A recent study from the Salk Institute for Biological Studies indicates prevention could be as simple as a natural foods diet—rich in fruits (such as strawberries) and vegetables containing something called fisetin. Fisetin is a flavonol found in strawberries, mangoes, cucumbers, and other vegetables and fruits. Researchers with the Salk Institute found this simple compound can actually reduce the risk of Alzheimer's in mice, and could be effective in humans as well. Maher and her team have documented that fisetin has both anti-inflammatory and antioxidant properties in the brain. It is also able to turn on a cellular pathway related to memory function. The team looked to a type of mouse with mutated genes making them vulnerable to Alzheimer's. At three months old, the researchers began feeding the mice a diet enriched with fisetin. Mice who hadn't received the fisetin began struggling in the mazes at nine months of age, but the fisetin mice performed as well as normal (non-predisposed) mice at both nine and twelve months of age. Avocados may hold the answer to beating leukemia University of Waterloo (Canada), June 16, 2022 Rich, creamy, nutritious and now cancer fighting. New research reveals that molecules derived from avocados could be effective in treating a form of cancer. Professor Paul Spagnuolo from the University of Waterloo has discovered a lipid in avocados that combats acute myeloid leukemia (AML) by targeting the root of the disease – leukemia stem cells. Worldwide, there are few drug treatments available to patients that target leukemia stem cells. “The stem cell is really the cell that drives the disease,” said Professor Spagnuolo, in Waterloo's School of Pharmacy. “The stem cell is largely responsible for the disease developing and it's the reason why so many patients with leukemia relapse. We've performed many rounds of testing to determine how this new drug works at a molecular level and confirmed that it targets stem cells selectively, leaving healthy cells unharmed.” Inability to stand on one leg for 10 seconds in mid to later life linked to near doubling in risk of death Exercise Medicine Clinic-CLINIMEX (Brazil) and University of Eastern Finland, June 21, 2022 The inability to stand on one leg for 10 seconds in mid- to later life is linked to a near doubling in the risk of death from any cause within the next 10 years, finds research published online in the British Journal of Sports Medicine This simple and safe balance test could be included in routine health checks for older adults, say the researchers. The researchers wanted to find out whether a balance test might be a reliable indicator of a person's risk of death from any cause within the next decade, and, as such, might therefore merit inclusion in routine health checks in later life. Participants were asked to stand on one leg for 10 seconds without any additional support.  To improve standardization of the test, participants were asked to place the front of the free foot on the back of the opposite lower leg, while keeping their arms by their sides and their gaze fixed straight ahead. Up to three attempts on either foot were permitted. In all, around 1 in 5 (20.5%; 348) participants failed to pass the test. The inability to do so rose in tandem with age, more or less doubling at subsequent 5 year intervals from the age of 51-55 onwards.  The proportions of those unable to stand on one leg for 10 seconds were: nearly 5% among 51-55 year-olds; 8% among 56-60 year-olds; just under 18% among 61-65 year-olds; and just under 37% among 66-70 year-olds.  More than half (around 54%) of those aged 71-75 were unable to complete the test. In other words, people in this age group were more than 11 times as likely to fail the test as those just 20 years younger. During an average monitoring period of 7 years, 123 (7%) people died: cancer (32%); cardiovascular disease (30%); respiratory disease (9%); and COVID-19 complications (7%). The proportion of deaths among those who failed the test was significantly higher: 17.5% vs. 4.5%, reflecting an absolute difference of just under 13%. Anxious Children have Bigger “Fear Centers” in the Brain Stanford University School of Medicine, June 16, 2022 The amygdala is a key “fear center” in the brain. Alterations in the development of the amygdala during childhood may have an important influence on the development of anxiety problems, reports a new study in the current issue of Biological Psychiatry.

 Researchers at the Stanford University School of Medicine recruited 76 children, 7 to 9 years of age, a period when anxiety-related traits and symptoms can first be reliably identified.  The researchers found that children with high levels of anxiety had enlarged amygdala volume and increased connectivity with other brain regions responsible for attention, emotion perception, and regulation, compared to children with low levels of anxiety. They also developed an equation that reliably predicted the children's anxiety level from the MRI measurements of amygdala volume and amygdala functional connectivity.

The most affected region was the basolateral portion of the amygdala, a subregion of the amygdala implicated in fear learning and the processing of emotion-related information.

 Our study represents an important step in characterizing altered brain systems and developing predictive biomarkers in the identification for young children at risk for anxiety disorders,” Qin said.  New research: Olive oil compound destroys cancer cells in 30 minutes Rutgers University & Hunter College, June 12, 2022  Oleocanthal, a polyphenolic, therapeutic compound found in olive oil is the subject of a new anti-cancer study performed by nutritional science and cancer biology researchers with The School of Environmental and Biological Sciences at Rutgers and Hunter's College in New York City. Programmed cell death, known as apoptosis takes approximately 16-24 hours. Dynamic new research just published in the Journal of Molecular and Cellular Oncology blew scientists away – when exposed to oleocanthal, a polyphenol compound found in olive oil, cancerous cells died within 30 minutes to an hour. While researchers previously understood that compounds in olive oil were capable of killing cancer cells, until now, such short apoptosis had not been observed. Even more fascinating was when the team looked closely to surmise why apoptosis was occurring under such swift circumstances – they discovered that cancer cells were being killed by their own enzymes. And, not only one isolated type of cancerous cell, but all of the cancerous cells they were examining. Unlike chemotherapeutic pharmaceuticals that devastate healthy cellular activity, the therapeutic polyphenolic compound found in olive oil kills cancer while maintaining vitality among healthy cells. As Paul Breslin, one of the study's authors at Rutgers noted, while cancerous cells died, healthy cells were not harmed, but rather the oleocanthal “put them to sleep.” The lifecycle of healthy cells was only temporarily affected in this way, without any negative observations and in approximately 24 hours, the healthy cells resumed their life cycle.  Sports, not screens: The key to happier, healthier children University of South Australia, June 21, 2022 Whether it's sports practice, music lessons or a casual catch up with friends, when children are involved in after-school activities, they're more likely to feel happier and healthier than their counterparts who are glued to a screen. In a new study conducted by the University of South Australia, researchers found that children's well-being is heightened when they participate in extra-curricular activities, yet lowered when they spent time on social media or playing video games. Published in BMC Pediatrics, the study analyzed data from 61,759 school students in years 4 to 9, assessing the average number of days per week children participated in after-school activities (3–6pm), and measure these against well-being factors—happiness, sadness, worry, engagement, perseverance, optimism, emotion regulation, and life satisfaction. It found that most students watched TV about four days of the school week and spent time on social media about three days of the week. Our study highlights how some out-of-school activities can boost children's well-being, while others—particularly screens—can chip away at their mental and physical health. “Screens are a massive distraction for children of all ages. And whether children are gaming, watching TV or on social media, there's something about all screens that's damaging to their well-being. Students in lower socio-economic backgrounds who frequently played sports were 15% more likely to be optimistic, 14% more likely to be happy and satisfied with their life, and 10% more likely to be able to regulate their emotions. Conversely, children who played video games and used social media almost always had lower levels of well-being: up to 9% less likely to be happy, up to 8% to be less optimism and 11% to be more likely to give up on things.

As a few young men secretly plan for war, they don't realize one thing: the mice might be listening. Dovie Thomason shares a story about mice who have the people's best interests at heart.

HauntScene LIVE!  Author Jackie Sonnenberg Special Guests:  Author Jackie Sonnenberg comes into the studio to talk about "Mice" - a new book that is a twisted take on the story of Cinderella!Social Mediawww.JackieSonnenberg.comFacebook.com/AuthorJackieSonnenberg Instagram.com - sonnenbooksTwitter - @sonnenbooksEmail – sonnenbooks@gmail.comIf you listen on Apple Podcasts, please be sure to leave us a REVIEW. Visit HauntScene.com for our updated Florida Haunted Attraction Directory!FOLLOW us on our social media channels:LIKE us on Facebook – Facebook.com/hauntsceneFOLLOW us on Twitter – Twitter.com/hauntsceneFOLLOW us on Instagram – Instagram.com/hauntsceneSUBSCRIBE to our YouTube: YouTube.com/hauntsceneSupport the show

There ain't a man alive that Steve wouldn't fight for $100K, however, mice.  Gahhhdog!!! See omnystudio.com/listener for privacy information.

Rückblick auf die wichtigsten News der Woche für Events, Messen, Incentives, Meetings und Kongresse - ausgewählt und kommentiert von der Redaktion des BlachReport.

In this episode the family discuss the worst cinema performances, we hear a heart warming Grand Final story you might've missed and Liam Gallagher does his best French accent while offering Eric Cantona a sleeping bag.  To read about everything that's talked about in this episode of The Matty Johns Podcast, and for everything Matty.....go to dailytelegraph.com.au and get yourself a subscription, or download the Daily Telegraph app at your app store.   See omnystudio.com/listener for privacy information.

You've probably heard of Carbon Dating, but how are Astronomy, Biology, and Nuclear Physics involved? What are the problems with having babies in space, and how many animals have had babies in space? (surprisingly more than you'd think!) And what is the history of nail polish, and more importantly, our relationship with painting nails? Videos we talk about: - Mice in Space Support us on Patreon! Join our Discord! We also learn about: counting the rings in a carbon atom, Dendrochronology, Space & Life & Radioactivity, unstable tennis balls, a surprise callback to last episode, shoutout to baltimore! oh shit we can carbon date anything!! Ella is good at guessing, a rewrite of history??? OES, the real carbon dating was friendship, definitely points, what do you name a space baby? the ISS is not a safe form of contraception, sea urchin space sex, freeze dried mouse sperm resembling instant coffee, space sushi, space babies look cuter, jellyfish that don't know the right way up, but snails do! how humans might evolve in space, Disney's Moon Mouse Colony, what the moon teaches about Earth, Polish vs Varnish, our favorite color, fashion always goes in cycles, mummified pharaohs with nail polish, Van Gogh wasn't color blind, he just had cheap paints, Mary Cobb was a girl boss if you will, car paint gave us nail polish, wear nail polish if you want to! Sources: --- History of Radiocarbon Dating Radiocarbon Revolution Janet Ambers on Chronological Methods Dendrochronology Fritz Schweingruber on Dendrochronology Cosmic Rays and Carbon Dating Libby's Nobel Address Libby Carbon Dates Everything Carbon Dating going 75,00 years Back Overly Dramatic Carbon Dating Error Article OES (Ostritrch Egg Shell) Carbon Dating gets Updated IntCal20 Calibration Curve Emilie Jager on Geochronology --- Fertilization in Microgravity Sea Urchin Space Sperm Freeze Dried Mouse Sperm Sperm Count in Space Rats Mouse Space Baby Development Jellyfish in Space Snails in Space Dizzy Space Rats Space and Bone Density Space Adaptations Russian Space Cockroach Mice Adapting to Microgravity --- The History of Nail Polish Cleopatra and Nailpolish Nail Polish History How Stuff Works Nail Polish Hagley History of Nailpolish History of Cosmetics Nail Polish Trends

Got Faded Japan ep 645 In this action packed episode…. Johnny's still lost in limbo so Tom and Jeremy take care of business and get this podcast about Japan, booze and the weekly wild news on track like drunken sailors on shore-leave.  FADE ON!     -------------------------------------------------------------------------------- Supporting GOT FADED JAPAN ON PATREON directly supports keeping this show going and fueled with booze, seriously could you imagine the show sober?? Neither can we! SUPPORT GFJ at: https://www.patreon.com/gotfadedjapan   -------------------------------------------------------------------------------- CHECK OUT OUR SPONSORS AND SUPPORT THE SHOW!!!! 1. THE SPILT INK: Experience art, buy art and get some original art commissioned at: SITE: https://www.thespiltink.com NFT: https://rarible.com/thespiltink ETSY: https://www.etsy.com/shop/TheSpiltInk?ref=hdr_shop_menu --------------------------------------------------------------------------------  2. Soul Food House https://soulfoodhouse.comAddress:2-chōme−8−10 | Azabujūban | Tokyo | 106-0045 Phone:03-5765-2148 Email:info@soulfoodhouse.com Location Features:You can reach Soul Food House from either the Oedo Line (get off at Azabujuban Station and it's a 7-minute walk) or the Namboku Line (get off at Azabujuban Station and it's a 6-minute walk). --------------------------------------------------------------------------------  3. Ghost Town Pomade FADE IN STYLE with Ghost Town Pomade.Get yours today by contacting: ghosttownpomade@gmail.com  -------------------------------------------------------------------------------- 4. MITSUYA LIQUOR in ASAGAYA: 1　Chome- 13 -17 Asagayaminami, Suginami Tokyo 166-0004　 Tel & Fax: 0303314-6151Email: saketoyou0328@gmail.com --------------------------------------------------------------------------------   5. Harry's Sandwich Company 1 min walk from Takeshita Street in HarajukuCall 050-5329-7203 Address: 〒150-0001 Tokyo, Shibuya City, Jingumae, 1 Chome−16−7 MSビル 3F https://www.facebook.com/harryssandwichco/ -------------------------------------------------------------------------------- 6. Share Residence MUSOCO “It's a share house that has all that you need and a lot more!” - Located 30 minutes form Shibuya and Yokohama - Affordable rent - Gym - BAR! - Massive kitchen - Cozy lounge space - Office work units - A spacious deck for chilling - DJ booth and club space - Barber space - AND MORE! Get more info and move in at: https://sharedesign.co.jp/en/property.php?id=42&property=musaco&fbclid=IwAR3oYvB-a3_nzKcBG0gSdPQzxvFaWVWsi1d1xKLtYBnq8IS2uLqe6z9L6kY -------------------------------------------------------------------------------- GET YOURSELF SOME GOT FADED JAPAN MERCH TODAY!!! We have T-Shirts, COFFEE Mugs, Stickers, even the GFJ official pants! BUY NOW AND SUPPORT THE SHOW: http://www.redbubble.com/people/thespiltink/works/16870492-got-faded-japan-podcast  -------------------------------------------------------------------------------- The Got Faded Japan Podcast gives listeners a glimpse of the most interesting side of Japan's news, culture, peoples, parties, and all around mischief and mayhem. Hosted by Johnny and Jeremy who adds opinions and otherwise drunken bullshit to the mix. We LOVE JAPAN AND SO DO YOU! Send us an email on Facebook or hell man, just tell a friend & post a link to keep this pod rolllin' Fader! Kanpai mofos!

Mr. Hollywood, Mr. Cat,  and Mr. Diegoth talk Truth Cult, Gel, The Catburglars, Man or Astroman, Tzompantli, Horsegirl, Wilco, Sam Stansfield, The Verlaines, The Mice, Dark Thoughts, Generación Suicida, and This Is My Fist. Joey guest stars. 

A former Consulting Actuary to Fortune 100 companies -- including Sony Music, Chanel and Exxon -- David Wood left his cushy Park Avenue job 20 years ago to build the world's largest coaching business. He became #1 on Google for "life coaching," serving an audience of 150,000 coaches and coaching thousands of hours across 12 countries.Alongside his clients' successes, David is no stranger to overcoming challenges himself, having overcome a full collapse of his paraglider and a fractured spine, witnessing the death of his sister at age 7, severe anxiety and depression, and a national Gong Show!He is the author of "Get Paid for Who You Are," and most recently "Mouse in the Room - Because the Elephant Isn't Alone."  He was nominated to the exclusive Transformational Leadership Council alongside such thought leaders as Don Miguel Ruiz, John Gray, and Marianne Williamson.In this episode, David talks about the importance of naming your mice, the hurdle of instant gratification and being unapologetically authentic. What does it mean to have 30% more courage?Hear about the art of dealing with rejection, when not to follow your courage, and get David's advice to his younger self, all on today's episode of How'd It Happen.To learn more, follow David at:Website:          https://focus.ceoPodcast:            https://focus.ceo/tough-conversations-with-david-wood-podcast/Podcast:            https://focus.ceo/extraordinary-focus-podcast Twitter:            @_focusceoInstagram:       @_focusceoFacebook:       @extraordinaryfocusLinkedIn:         https://www.linkedin.com/in/focus-ceoBook:                 https://mouseintheroom.comTo Connect with Mike:Website: https://mikemalatesta.com/LinkedIn: https://www.linkedin.com/in/mikemalatesta/Please LIKE

Welcome to a special episode of The Today's Leader Podcast. This week we feature David Wood, a leading high-performance coach, with his latest book release Mouse in the Room. Because the Elephant Isn't Alone. This conversation showcases the brilliant content in the book and how to take the learnings to grow yourself and deal with the little things that are holding you back.The Mouse in the Room is now available, Tune in to discover how naming your mice will enhance your life.--------------------------------------------------------Discover Mouse in the Room:Website – https://mouseintheroom.com/Website - https://focus.ceo/—————————————————————————-If you are looking to build better leadership skills, check out The Today's Leader website at todaysleader.com.auWe are driving a leadership revolution and BUILDING TOMORROW'S BEST LEADERS, TODAY!Today's Leader is a collective, The mindset to make a difference and the ability to create an impact. Our Emerging Leaders Masterclass can be found at https://www.tomorrowsbestleaders.com/course/emerging-leaders-roundtable-masterclass#/homeThink & Grow Business Hosts our Today's Leader Masterminds. TAGB where we focus on personal, professional, and business growth. Book your free 30-minute discovery call at https://thinkandgrowbusiness.com.au/book-your-free-discovery-call/You are standing Stronger, Braver, and Wiser. Don't forget the golden rule – Don t be an A-HoleCheck Out our Top 10 Leadership Podcasts: https://todaysleader.com.au/the-best-leadership-podcasts-for-2021/#purpose #leadership #communication #conversations #clarity #todaysleader #tomorrowsbestleaders #mentoring #mondaymentoring #development #developmentplan #highpotentiall #techready #careerskills #management #people #process #crisisleadership #simplebusiness #productivity #legacy #carolsanford #businessparadym#personalgrowth #leadershipgrowth #business #recruitment

TWiV discusses the situation with monkeypox, risk factors for SARS-CoV-2 infections of cats and dogs, and a lineage-tracing mouse model for studying papillomavirus infections. Hosts: Vincent Racaniello, Rich Condit, and Brianne Barker Subscribe (free): Apple Podcasts, Google Podcasts, RSS, email Become a patron of TWiV! Links for this episode Monkeypox update (CDC) SARS-CoV-2 infection of cats and dogs (Emerg Inf Dis) Mouse papillomavirus identification (Vet Patrol) Mouse model for papillomavirus infection (eLife) Vincent interviews Harald zur Hausen (virology blog) Letters read on TWiV 907 Timestamps by Jolene. Thanks! Weekly Picks Brianne – Microbes Rule! at Liberty Science Center Rich – Artemis I update:  Mission diagram, mission in photos, launch dates Vincent – Eco-sustainable 3D printed house – Tecla Intro music is by Ronald Jenkees Send your virology questions and comments to twiv@microbe.tv

Honestly! Most people think that winter is a “dead time” in the garden. But if you haven't had a go at growing peas, you'd never know how easy that is. First of all, gardeners often grow a “green crop” in winter that gets dug into the soil in spring to add Nitrogen for the next growing season; We often use peas and other legumes for that task and the key is to dig them in before they set seed. Of course, those “green crops” are never sown for eating! But if you want edible peas, for instance, you could plant the seeds right now in the garden amongst the wintery conditions and frosts, and they'd germinate as well… were it not for the hungry birds, who are keen to devour some sown pea seeds in those lean winter months as there are few nutritious sources of food available at that time of the year. Oh and not just birds! Rats and Mice are in a similar boat… craving food. I prefer to sow them in a hidden spot (glass house or tunnel house) in seed-pots and let them grow until they are 5, 6, or 7 cm tall, with true leaves (not just the cotyledons). At that stage most of the valuable nutrients will have been used from the pea seeds and the transplanted young plants will be relatively safe from the birds and rodents. Seed raising mix in sowing cells works well for me; depending on the temperatures, you'd be looking at 2 weeks germination and an extra week or so to get some height on the little plants. When ready for transplanting, create a nice garden bed with good, weed-free soil, some grains of slow-release fertilisers and carefully put them into their spot… A bit of a “climbing rack” might keep them off the wet ground and results in harvesting cleaner pods. Then it's just a matter of letting them grow and set their own “seeds” in seed pods we call “peas”. To be quite honest, few things taste fresher than new peas. While our peas and beans are so cooperative in terms of germinating in winter, think about their relatives, the Broad beans. They too will come up in the coldest months of the year, some can germinate at 4 degrees. Ideally plant the seeds from March (in the very coldest conditions) to May and Mid-June (elsewhere). These plants do not like too warm conditions. Broad beans are quite heavy plants and prone to collapsing when they grow, so a bit of support would be appreciated. The Sugar snap peas need a little bit of warmth to get going, so wait until late Early to Late Spring. But you know…. It's something to look forward to! 

Thanks for joining the discussion, leaving that 5 Star Rating, and Subscribing! Leave a Question or a Comment. Email BrightBlackwood@gmail.com or go to https://www.brightblackwood.com/ Blog https://brightblackwoodtarot.wordpress.com/ The Purpose of The Bright Blackwood Tarot Podcast is to Motivate, Empower & Encourage. As always take what resonates with you and leave what does not. Handy Tools For Fortune Tellers Lenormand Fortune Teller's Journal: https://smile.amazon.com/Lenormand-Fortune-Tellers-Journal-Diary/dp/B096CXLRZG/ref=sr_1_6?dchild=1&keywords=lenormand+fortune+teller+journal&qid=1625505196&sr=8-6 For more discussion and articles related to this and other motivational topics visit: https://www.brightblackwood.com/blog Check out a few of these topics: Can I manifest more money? https://www.brightblackwood.com/post/nothing-but-questions-can-i-manifest-more-money Fear of Success? https://www.brightblackwood.com/post/nothing-but-questions-fear-of-success Affirmations: Your Inner Resume' https://www.brightblackwood.com/post/affirmations-your-inner-resume So What's Stopping You? https://www.brightblackwood.com/post/short-note-so-what-s-stopping-you Get Happy - Life Is Good https://www.brightblackwood.com/post/get-happy-life-is-good The Friendship Test https://www.brightblackwood.com/post/the-friendship-test Defensive vs Intention Thinking https://www.brightblackwood.com/post/defensive-vs-intention-thinking Getting Unstuck https://www.brightblackwood.com/post/getting-unstuck --- This episode is sponsored by · Anchor: The easiest way to make a podcast. https://anchor.fm/app Support this podcast: https://anchor.fm/bright-blackwood-tarot/support

Monologue Dr. Joel Wallach begins the show discussing Alzheimer's, osteoporosis and MS. Stating that they all have many symptoms in common. Contending they are all due to nutritional deficiencies. Asserting that everyone should be supplementing with all 90 essential nutrients. Pearls of Wisdom Doug Winfrey and Dr. Wallach discuss a study of the health benefits of ginger and chili peppers. The study found that combining 6-gingerol found in ginger and capsaicin found in chili peppers reduced the amount of tumors in mice with lung cancer. Mice with lung cancer that were given just one or the other of the compounds didn't see that same result. Callers Lisa is pre-diabetic with hypothyroidism and is overweight. Lee is obese a type 2 diabetic with spinal stenosis, high blood pressure and kidney failure. Sheryl has high blood pressure, kidney disease and heart failure. Diana's aunt is suffering anxiety and panic attacks. Call Dr. Wallach's live radio program weekdays from noon until 1pm pacific time at 831-685-1080 or toll free at 888-379-2552.

It doesn't take long after getting into beekeeping and then repeatedly, as long as you have beekeeping equipment laying around or stacked neatly, until you have to deal with small furry pests. Mice, rats and other critters love the shelter, warmth, relative safety and often food, found in beekeeping equipment. In today's episode, Jim Tew talks with Jeff Ott, from Beekeeping Today Podcast, about Small Furry Pests. There are ways to deal with mice and rats. What works in a bee yard? The guys talk about the use of poisons and traps and non-lethal approaches minimizing the damage these little critters can quickly do. The “why's” of wanting to manage or avoid small furry pests are almost instinctually known. They chew through wood (and plastics) as if it is not even a barrier. They destroy frames and foundation (and car wiring harnesses), they urinate and defecate where they live. They can make a real mess of stored equipment. They love to get into hives late in the fall and winter when the bees are clustered.  Have you ever picked up a hive box to have mice drop out and scurry off? What if one seeks the relative safety of the nearest dark opening… such as your pant leg? Jim has. Listen to find out your options should you face this quickly evolving situation! Like all other pests you will deal with as a beekeeper, you will come to your own management approach that suits your personal philosophy on life (and death) when it comes to small furry pests. Like everything else, it is good to learn from the mistakes - and adventures - of others and chose your own way forward. Listen in as Jim and Jeff discuss Small Furry Pests. If you like the episode, share it with a fellow beekeepers and/or let us know by leaving a comment in the show notes. We'd love to hear from you! ___________________ Thanks to Betterbee for sponsoring today's episode. Betterbee's mission is to support every beekeeper with excellent customer service, continued education and quality equipment. From their colorful and informative catalog to their support of beekeeper educational activities, including this podcast series, Betterbee truly is Beekeepers Serving Beekeepers. See for yourself at www.betterbee.com ______________________ Honey Bee Obscura is brought to you by Growing Planet Media, LLC, the home of Beekeeping Today Podcast. Music: Heart & Soul by Gyom, Walking in Paris by Studio Le Bus, original guitar music by Jeffrey Ott Copyright © 2022 by Growing Planet Media, LLC

Dom Clonen is the Founder and CEO of TechBridge Market, a tech-enabled recruitment services company Headquartered in Singapore. Their mission to reinvent traditional recruitment services. Instead of charging large commissions for a role, they have developed a highly optimised talent acquisition process that guarantees predictable hiring outcomes at a fraction of the usual cost. Dom is from the UK and graduated from the University of Oxford with a Bachelors in Modern History. He spent the better part of 14 years as a Managing Partner for MICE companies, developing and commercialising niche technology conferences and exhibitions in the US, Europe, and Asia Pacific. After moving to Singapore in 2006 he co-founded a global peer-to-peer community for leading enterprise technologists before becoming the sole Founder of TechBridge Market. Show notes at: https://www.jeremyau.com/blog/dom-clonen

In this episode of the BTP Podcast, Pouya speaks with Tugrul Guner, a Physicist by training and Machine Learning Engineer by trade. Enjoy!   Tugrul's Social:  Twitter: https://twitter.com/Tugrul_Guner LinkedIn: https://www.linkedin.com/in/tugrulguner/   Pouya's Social: Instagram: https://www.instagram.com/pouyalj/ Twitter: https://twitter.com/pouyalj LinkedIn: https://www.linkedin.com/in/pouyalajevardi/   Episode Transcript... ----more----   SUMMARY KEYWORDS quantum optics, arrogance, imaging, materials, physics, degree, confidence, observe, kinda, people, agree, thinking, science, human, quantum mechanics, postdoc position, field, evolved, point, question SPEAKERS Pouya LJ, Tugrul   Pouya LJ  00:00 Well hello, ladies and gentlemen, welcome back to yet another episode of the b2b podcast. We've been away for a while I have for sure. But I am back with a very great friend of mine, tool gunner, and I am happy to introduce him to you what a legendary man he is. He has okay. Oh, you know what? I'm not gonna give you the introduction. I'll let him introduce himself the way he he sees fit. Hey, Joe, how are you doing?   Tugrul  00:43 I'm good, by the way, are legendary?   Pouya LJ  00:48 No, no, I know you well enough to give you that, you know, give you that adjective. So that's all well deserved? For sure. All right, turtle. So why don't you give us a very brief but comprehensive background about yourself, the way you see yourself from your academic background personally. Yeah, go ahead.   Tugrul  01:10 Yeah, sure. Sure. I will start with when everything changed in my life. I was like, I was not cared about anything before, like last year of my high school. So I was like, playing video games going out like playing soccer. And the classes were like, I wasn't. I had zero interest at all. But I wonder I was reading a lot. I was like, I was kind of reading lots of different books, different types of books, mostly like fantasy books, like Dragon land series, forgotten mediums. It all started with a lot of things by the way. Yeah, anyway, but that was also another story. My father, like, gave that present to me like a lot of drinks book. But the second book, he just grabbed a random book from there probably, like, just grab the second book. And then I Oh, what's this looks let me read the first one. Then I started with the Lord of the Rings. Okay. But back then I was reading this Dan Brown's book called demons and angels, or whatever. Demons.   Pouya LJ  02:22 Read the book, but I've watched the movie. Okay.   Tugrul  02:24 Yeah, I also watched the movie, but I don't know. Like, it was a good book. I'm not sure. But the thing that just like was interesting to me when they were talking about like, antimatter. So I just, like stuck at that point, like, Oh, my God, what is this? Like, I never heard of this before antimatter. Like, I wasn't even interested in physics. Okay. No, no, no, no, but antimatter was like, something changed. What? I never heard of this before. And I realized that I mean, we have lots of things we don't know. That was the, like, a break point in my life. Okay. We're, we're just pretending that we are we know stuff that based on our observations, these are like a micro sis macro systems that we are observing daily, like mostly, like, wearing like an eternal outdoors, we all know, so we just ever have that. Like, I mean, if you drop something, it just falls down. Like it's a gravity, I mean, this kind of stuff. But I that was something different. You can observe it you need to be in that field to know what is antimatter. So that was a some kind of like, a break point in my life. Okay, then, I started to read a couple of things about it, then I noticed that oh my god, this is something else. There's another world inside of this like, like quantum mechanics, even though I had no idea what quantum mechanics is, but I was like reading uncertainty principles, something is not clear. But something sounds are like, interesting, like, Oh my God, what's happening here, like the universe is not really like, observed something more and more. I mean, then, last year, in my high school, I develop interest in the physics as you expect, like, then I was like, for the my bachelor degree, I have to study physics. And I have to I have to become a theoretical physics physicist. I mean, because I really wanted to understand everything. That didn't happen, of course, but I'm gonna mention that I'm going to talk about it. So So I in in my country, for bachelor's degree, you have to take an exam and after the exam, you need to write the university and discipline like this university physics. This university for example, electrical engineering   Pouya LJ  05:00 to give his background so when you're originally from Turkey, so you do your Bachelor's there. Yes. Okay. Go ahead.   Tugrul  05:10 Yeah, yeah, my masters and PhD there too, but Right, so, so you have limits, of course. So you can just write 20 University and 20 different subnets. So I wrote physics for all of them. Because I was like, obsessed. So, yeah, I just got into physics. But it was kind of disappointing. Like, okay, I was kind of, I mostly like, thinking about this ideas, thinking about how universe should work. And this kind of like a philosophical way of Lego discussions, I've kind of mostly like that way of it. But mathematics. When it starts to become complicated, you start to lose control of your thoughts. Also, sometimes, like, if it gets too complicated, you start to focus mostly on the mathematics to solve that problem. You're getting away from your first idea, and you can find yourself with into different concepts, different mathematical tools. Of course, it can guide you different discoveries, of course, but you need to, you need to have that skill to have fun with this mathematics. I didn't have that one. So still, I was like, kinda stubborn. So I wanted to do my master's degree also in physics, which did the quantum mechanics from from the fundamentals, which was focusing on the foundations of it like, main things like fundamental things. So we published a paper about quantum tunneling. Because there was a problem about estimating time in quantum mechanics. And tunneling is a phenomenon that happens in time, even though there were people that researchers like arguing about maybe instantaneous, maybe it's not time dependent, but we found the time for that, which we published. It was a nice journey for me, but then I changed my topic, like, very like a, like a 100 watt, like 180 degrees, like, just back with like, a different direction. Which I started doing my like a PhD in material science and engineering, talking about the relevant components.   Pouya LJ  07:35 The way you say. It was 180 degrees deviation. One would think this is a you went to art since fallen artists. No, I'm kidding. Within the realm of physics, you didn't want it okay. Yeah,   Tugrul  07:51 I mean, like, change my direction, like, I mean, it all you can also call it 90 degrees to I mean, I was just like I did, I was like, spanning somewhere else. Yeah, I started to work on some applications. I was kinda materials, material scientist, I was working on polymers, polymer composites, emissive materials, like I was mostly working on alternative materials for the white LEDs, because in LEDs, especially white LEDs, you were using phosphorus, which they contain, like rare earth elements. So I was trying to develop new materials or trying to increase the efficiency of the this phosphor materials inside the tube. It was nice, it was a efficient pH like I published like kinda 20 papers, because it's an application is not a theoretical physicist. So it was kinda like it's highly liked, like you can publish papers, as long as you develop something and you showed us an increase those improvement, it works. Or you even you can come up with a new material, which we were there was like a sample. One kind of material was very popular back then we even published a couple of papers awarded called halide perovskites. Yeah, so I was kinda like optimistic about my postdoc. Because like, 20 papers, so I was like, okay, I can find a good postdoc position around the world, but it didn't go that way. I applied like 600 700 positions with a detailed applications. I didn't get a response from most of it. Probably some I didn't even send the second secondary email to them, but probably they went and noticed, like one of them just, he's a Turkish professor. Also, he's a professor in Montreal,   Pouya LJ  09:59 Montreal. Canada, yes,   Tugrul  10:00 that's Montreal in Canada. So that's he sent me like the position and offered me the postdoc position, which was an amazing subject. It's called water fast electron transmission electron microscopy, which transmission electron microscope by itself is a characterization tool that can image materials at nano scale, which is like 10 to the minus nine is like, how much like 1000 Lower magnitudes higher magnitudes than the human hair, right in 1000, it was micron, so, probably around 1000. Similar things from the human hair. Even more, I don't know, like, probably some that kind of scale. So we were basically imaging nanomaterials at the Nano scale, like we were characterizing them trying to understand the shape some of the properties, but this is regular transmission electron microscopy, ultra fast transmission electron microscopy is where you are integrating your microscopy with laser. Now, you don't only have this imaging, you also have this laser, which you can also send it to your material and observe what's happening when your metal or nanoparticles are interacting with the laser. Which brings, we call it the time dependency for your observations, which is from imaging, a now you start to record movies, and you can visualize what they're doing and understand the interaction of places in time. So, by the way, my professors professor in Caltech, his name was like Zewail, he, like, got the Nobel Prize for this invention, mostly, you got the Nobel Prize for them to chemistry, but this was the part of the invention. So yeah, that that, in today in the world, there are only four or five facilities that can do this. ultra fast transmission electron microscopy is an expensive tool. After that, like I studied two and a half years in Montreal, Canada for as a postdoc, and my second postdoc, I came to Ottawa in Canada again. This time, it is a completely different lab, it is a quantum optics lab, because I also like I am enjoying it. I know I love quantum mechanics. So I came also like to learn quantum optics. And I was planning to apply some of my AI skills. Of course, I don't have any professional skills because I didn't study AI. I didn't study machine learning in any of my degrees. But I, since I love AI and coding, I always like, during my free time as a hobby. I also I tried to improve myself a lot. So then I started to combine quantum optics with deep learning because in quantum optics, you have noisy like results and etc. So you can combine them with the deep learning etc, we   Pouya LJ  13:27 can we take a step back, so can you tell tell me like what is actually quantum optics? Like, can you delve into it? What does that mean? Okay, optics is? Oh, yes, in the quantum, but how do they go together?   Tugrul  13:38 Yeah, of course, I cannot explain that like an expert of it because I work from the burning. But   Pouya LJ  13:43 even if you did, I wouldn't understand.   Tugrul  13:47 In Visual optic isn't just that it's the light. So you don't have to you don't need to have a like coherency, which means that like some kind of like, coherent motion or coherent interaction of your light. Like as a, like a physicist standpoint is like, How can I select it's not random, the photons in the light, if they're not acting random, they are acting in a coherent way. So they have some kind of correlation between them. So regular light is you don't have this year. They're just like, moving. They're just moving like in spacetime. But when you're talking about quantum optics, you need to use some kind of generator of this coherent light because light itself is not generating it with regular light sources. For example, we were using different crystals. You're sending your laser to these crystals. And these crystals are so special that they create coherent light, which they are correlated in the momentum. degrees of freedom. And I mean, they go into two different paths read up, I mean, when you hit them with the laser, out of the crystal, you have two life paths. One goes one direction, or the goals pregnant, the perpendicular direction. The main property of this two beam is their entangled, momentum entangled. So   Pouya LJ  15:25 this one, so the past crystal,   Tugrul  15:28 yeah, after they passed, the crystal crystal generates, of course, what was the efficiency of this generation like 8% 10%, maybe, I mean, it's a lot less not that high,   Pouya LJ  15:41 so you get better you preserve. So the light that comes up at the end of it is less than 50% of what you actually put into it.   Tugrul  15:49 Of course, yes, of course. So you have less light now, but you see that they are momentum in the momentum, degree of freedom, they are correlated, I mean, entangled. One is plus one is exactly the same moment with the negative value. What we can do is that, so if you observe the two beams, so imagine that you have two cameras, one is observing the, one of the beams or the other one is observing the other view. So you have triggers for these cameras. So one photon, when one photon hits one camera, it checks exactly the same time, the other one grabs any photon signal. So if the two photon hits the camera at the same time, you're saying that, okay, two entangled photons, alright. Other than that, you're not capturing anything. These cameras are own only when two photons are era, photons arrive these two different cameras at the same time. Because they, of course, you're designing your optical path in such a way that they like they travel the same distances. Yeah. Okay, because its speed of light is constant. So they have to travel the same distance. So they're like interesting applications of this, if you put an object in one of these beams, if you try to collect the other beam, it gives you the image of the object without touching it. What I mean is that, for example, you have two beams. And in one of the path of one of the beams, if you put an object, you know that right, so some of light is going to pass some of them not because they're gonna be absorbed or reflected by the object. Yeah, so other beam says they're correlated and entangled. So when you get the camera when these photons get the camera, so they are going to be triggered only with the other photons that are passed and reach to the camera. So you're going to have a kind of image of the object with other beam, which has nothing on this path. I mean, this kind of the this is called Ghost imaging. Maybe I just was so bad.   Pouya LJ  18:12 No, no, I think I think so. Yeah. Yeah. Not good boy. Yeah.   Tugrul  18:16 Let's go. Yeah, it's I mean, it was like I was kind of trying to develop a deep learning algorithm to make the resulting images better increase the resolution of it, because you can guess that there's a noisy array. So they're very noisy. Yeah, no, that was a nice thing. Also, I was enjoying working with the group and professional. But so like, last year? Yes, this year right. Now, this year, this is not last year. So I just got an offer. This is really hard to keep track of time. Yeah, exactly. Thanks to COVID. I received an offer from a company, which is not related to my research background, I started to work as a machine learning operations engineer, which are used my skills that I developed during my free time, which I recall, was considering them as my hobbies. Yeah. Yeah, that's a kind of Sir. I mean, I am kinda like, also, like, not because only that was just happened in that way. Not because of that, but also kinda like jumping from subject to subject. Because, I mean, there are lots of things to learn. And I know I'm not gonna be able to learn everything that I want to learn, but still, I'm trying to do my best to learn there's   Pouya LJ  19:47 a there's a huge degree of attention people give to, you know, specializing in something which is like, of course important. I'm not debating the significance of that but I think I Sometimes it gets missed how, how good it is to actually do these jumps between in between topics in that, it gives you a broader sense of understanding because sometimes some knowledge that you gain in one field, although it's not necessarily you're not a specialized, you're not an expert in that field per se. But then it can that knowledge can be analogous in a different field. So it gives you some sort of perspective, I feel. At least that's my personal I had a similar experience, I have a similar experience. And I even for my academic background, I had a similar experience. I didn't know really what I wanted. So I really liked physics. I really like computer science programming, software engineering. I don't know I liked philosophy. I liked psychology I liked, you know, I even liked cinema, like I still do. Photography, cinematography. So it took me a long while to land on where I landed, ultimately. But so yeah, I did jump around quite a bit, too. And I think it is important not to discount it. I'll do a specialization is very important. Again, I'm not doubting that. But I think sometimes when we focus Oh, yeah, you have to specialize. It's what do they say? There's a good thing. Yeah, I don't remember the same but something something and then master of none. Anywhere. Yeah. So it means like, you're you're, you know, so many things, but then you're not a master in any of them. And they see that in it in a in a in a negative direction. Not that either. But there's in a negative way with a negative connotation, meaning it's a bad thing. And I understand they're saying, okay, mastery is important. Of course it is. But one of the things you can master is how to learn different things. And I think that is also important. Anyways, sorry to cut you off, but I just wanted to Yeah, but   Tugrul  21:59 you're right. I think I learned how to learn during all of this time. Yeah,   Pouya LJ  22:03 that's right. That's right. And, and how to think how to think because, again, when you, when you become a master in one very narrow, specific field, then you're very comfortable learning things in that field, but not necessarily in other fields. And you'll get used to and accustomed to thinking a certain way, but not another. If you will, your neural pathways are very much aligned with a certain thing. And I guess in in AI, you're saying you're kind of like memorizing that, that the training set, right. You're overfitting in a way. So that's, that's, that's that's the danger with with over mastering in a very narrow field. I think it's, it's my, from from a personal perspective, of course, it's not going to harm anybody, per se, but it can harm you mentally, not physically.   Tugrul  22:57 But also the other side of it is like, okay, but other than that, like he was, you also, can there's also risk that you can be like, underfitting, I mean, like, he is like, you can have some generalization issue. So, I mean, you can stay like it's not overfitting sense, but I'm kinda you can stay like a generalized way. How can I describe like, you don't have for example, for myself, I have some confidence issues too. So I never I in my life, I never think I am 100% sure of anything. Maybe that's the issue. If you are if I got an expert on some kind of special if I have some kind of specialty if I study or work on something that 20 years, maybe I can build that confidence that level, but   Pouya LJ  23:53 it's tricky. Yeah. Yeah, no, I know. i It's very tricky. I think I agree with you. I don't I don't think I know. I can be 100% Like, I will never give the number 100 I'm 100% sure I'm even if I'm really 100% Sure. I'm 99.999% Sure. Yeah, and okay, but maybe that's part of it. But it's a tricky line though. There's a very fine line between between confidence and arrogance, I think and and that's another issue that arises like you know, when you're too much of an expert in something you're one of the very few in the world who knows something about something then then the ego plays a role and then sometimes it seems it may seem like confidence, but it is actually arrogance. And we see that like I mean the academia that there's plenty of it of course in industry there's plenty of it. There's everywhere like there's plenty of it right? So yeah, I know I confidence aside, you need to like Grow your confidence and all that of course you know you personally but like the rhetorical you any individual needs to go to come Because, of course, but then there's also another aspect of it that I think, you know, I like the fact that I am I remain not 100% Sure on things because I always give myself room to self correct to admit that I was wrong too. Because like, for example, otherwise you become like this politicians like didn't do clearly they're not even sure like, they're not even like if you talk to them in person in a backroom, with nobody listening, no microphones, no nothing with their buddies, for example, they're gonna be like, Yeah, and I don't know, maybe. But then but then they come out and, you know, say with such confidence, because that's how they have to play the game of politics. Right. But then again, you but then that makes them not able to self sorry, course correct. You know, acknowledge mistakes. So I think the fact that you're, you, myself included, like we are, you know, not? How do we say is not? I'm not saying they're not sure, but we leave room for error, or mistake. Because it's how I look at it. It's, even if I am very much comfortable in the field, let's put the word expert or master aside, even if I'm very comfortable in the field, and I have sufficient knowledge i i feel uncomfortable saying that I am 100% sure that something is true or not, or I think that's me leaving myself room that, you know, maybe when I may even caveat that did saying that the current knowledge. And with my current understanding, yes, I'm 100% Sure. But okay, there might be something that I don't know about that, but certainly something that I don't know about and a lot of different ways, maybe in that particular field too. And maybe there's error in the way I think about the world because if history is any indication. Most people most of the time have made mistake, I don't know any famous or infamous individual in the history that you can name that did everything perfectly. Yes. Just outright impossible. And if they if the written record, say that, which I have never heard of any individual, but let's say even if the hidden rows are written record, say that you don't know if they're hidden lives. And anyway, so that's what I think. I don't know. My point is that I think that's not necessarily a bad thing. Although it can have some downfalls in sometimes you seem, may may not even be because I know you'd like your to your humble individual. And sometimes you you know, you're not comfortable. being super confident in your but then, like, I know you like I know that the grasp of your knowledge is high enough that you if you were an arrogant prick, you would be like, Yeah, I'm 100% Sure, get get lost. Right. So, but then you're not that's that's the whole   Tugrul  28:01 thing. No, I mean, I don't understand how you can be like that. How you can be 100% Sure for something doesn't make sense. I mean, today we don't we have so many questions, even Newton dynamics, you can question them, even people came up with like a modification or to Newton dynamics, you can't be 100% Sure, even your observations are like, sinful to fit. With the models you have no, I mean, you can miss something your brain evolved some millions of years as a result of like, trillions of different paths, like a survival tricks, like some extinction, etc, etc. But you're still evolving, your brain is still evolving Darla, so you don't know how much room left for your brain that can evolve, which can be huge, which I think can be huge, because we are probably far from being like reaching the optimal optimum point. I don't even know if there is an optimum point. I don't think so even though we have here like we have full of weaknesses, flaws. And we are not even sure that our brain is really a good tool, even like a perfect tool. Even understanding nature. Maybe this is our problem. Maybe we are not going to be able to solve the universe because our brain is not capable enough of understanding it.   Pouya LJ  29:23 Yeah, no. No, I don't I honestly don't know how you can do that. I think it's not that being too short is a byproduct of arrogance. That's my guess. Like, because the more humble people I've seen, the less sure they seem people who tend to be more humbled who tend to not be arrogant or egotistical. They seem that, you know, they don't seem like that they lack confidence. They're fairly confident, but they're very comfortable admitting that I don't know everything. And I can't possibly know everything. And I may be wrong from time to time. I may I may be wrong a lot of the times, I think that is, again, this is my observation. I don't have empirical evidence to back this hypothesis. But this is my personal observation, the more you know, grounded people I've seen the more humble people I've seen, the less they have that ability to be like, No, this is done. This is settled. And, and let's, let's take a point recently, something from a very recent history, and that was like during COVID, the COVID science, there was plenty of arrogance from very established either scientists or officials in the authorities of science, quote, unquote, that they were like, saying things that you know, this is established science, you should believe it. This is no, this is true. The lab leak is no, I'm not saying that. The you know, COVID leaks from the lab, but they were not even they were they were treating you as a either stupid or racist if you even questioned it. And I was like, How can you be so sure it leaks from not leaked from the lab, and it came from nature, when you don't even know the source of sort of like the origin of species of this thing? How can you be so arrogant about it? And then I gave myself the answer. I was really thinking that and I gave myself the answer. I was like, yeah, that's arrogant. That's why like, there should be no room for arrogance, the human arrogance and, or any kind of arrogance as matter of fact, but we only know one kind. And that's the human arrogance. There should be no room for arrogance in science, but unfortunately, there is. So I think that's that. I think I'd rather being too sure. Is a symptom of arrogance is or is a byproduct of arrogance, I don't know. But they go together. I think that's what that's where he I see it.   Tugrul  31:56 I think this guy, this is kinda like a defense mechanism like this kind of people. I think, probably I'm not sure, of course. They think that they think that maybe, if they're if people start to think that there is a room of questioning their knowledge, they think, in this case, they think they're weak. So that's why they are pretending that they know 100 person, should they become like arrogant? No, you cannot question my knowledge. Yeah. Because they don't want to be seen weak, or maybe they have a higher position in somewhere. If they, maybe they think that if they seem weak, they can lose their status, they lose their position, whatever. I think that's the opposite.   Pouya LJ  32:45 Yeah, so okay, I completely agree. But I also disagree that is completely opposite. I think it's kind of the opposite, depending on how you depending on the area, I think, so for, for, for somebody who's claiming that they are the authority, like a king, or an emperor, or a queen, or whatever, right. So that person needs to maintain that authority. So they need to be listened to and accepted. Right. Okay. So that's that. But that's why I'm saying this should be. So that's, of course, the end. And they lose the grasp if they don't, or they feel that way. Again, it's not necessarily true, I agree with you, if, if a Emperor King was humble, and was like, you know, I'll do my best or even a political leader, I do my best to the best of my abilities to lead, but I'm a human, I'll make mistakes, if they admitted that they probably win a lot of votes. But that's aside, when you're talking about science and technology, you know, specifically science because it's in my mind need to present it should represent something very pure, and remove the elements of human human nature, but rather be a method to evaluate to think essentially. That's why we call it the scientific method, right? It has to leave the interpersonal inter, to like within the human character, human species, ugliness out of it. Of course, it's not going to happen because it's just humans. So I think that's exactly that's the specific area that I agree with you it actually is not. If if you're wrong, and you admitted it, that's the sign of strength. And, and I think people do, maybe not consciously understand that themselves, or or think about it that way. But they really appreciate when you admit a mistake, because then they can rely on your words. Be like, you know what, this guy is not full of shit. This guy admits when he's wrong. If somebody constantly when they when they caught in a lie, or when they caught in a mistake, they still insist, then how can I trust them? So I think I agree with you They just feel that they lose. It's a defense mechanism, they feel like they're losing the grasp on of authority, which is not really true. They're they're losing it when they enforce it too harshly. There was a quote, I don't remember where I heard it or who I heard it from. But basically, it was saying power is like sand in your fist, the more you try to hold on to it, the easier it will spill out of your fist. And if you doubt that just go on a beach someday, not you, anybody who's listening and go grab a because I thought that I thought about I tried to go grab a handful of fist so sad. and strengthen the tighten your wrist fist, rather, and squeeze, the sand will spill out at some point you will not but then the more you squeezed, the more it spills out of your your fist. So that's what they're doing. They feel like they have to, like hold on to this sand tight and make sure it doesn't spill out of their fist, but then doing that they're actually squeezing it out of their, their fists, because by tightening their fist, actually, they're occupying the room that the sand should ergo the sand will spill out because their fingers will not get you know, break the nylon screws that tight. Anyways, so So I agree with you. But the issue is that the thinking is wrong, I think.   Tugrul  36:30 Yeah, but I think yeah, I think the root of this behavior is probably we can investigate, like we can discuss in evolutionary evolutionary way. Probably because of the past like, not too long, like like, if you go to check the history even go like ancestors. Being sure is probably this is above, like a, like a living or death issue, life or death issue. Basically, he has to be shared for a couple of things, really. Because otherwise you can die me somebody can write Okay, so maybe it is rooted somewhere there this kind of behavior? Because you instinctively you want to think that you will surely you have to show us your data, you have to strong you have to seem strong.   Pouya LJ  37:20 Because if you're not so sure you remain indecisive. And that's   Tugrul  37:25 it worse than being so sure in the past, like any evolutionary point of view, probably so, but so sorry, sorry, interrupting you. But sorry, what I was thinking is that, like, when I was saying the opposite is better, like not being sure, I was just thinking in the future. So we already evolved, we already have some complex understanding we already not in the part of nature anymore, we don't we're not scared of like, hunted by like a tiger on the way but so we are even like, not natural about like artificially selected. Because we have our system, everybody surviving. So feature, because we don't have these issues in more which is good, which means that we have a long way to go ahead of us that can focus only on humans feature like including science, technology, etc. So we are also like, complex enough to think about our thoughts. We are in a machine that can question itself. And so we are at this level, and so we can start acting like in a mental like in it, we have to start thinking that we have lots of rules that we can improve ourselves and we can learn a lot with no need to be so sure for everything we are not going to die.   Pouya LJ  38:48 Yeah, yeah. So this is where I classify actually I have this because I've thought about this and I wasn't thinking about it right now but I've thought about this in the past, I actually have I call it I mean I don't have a literal definition out there, but I have internal definition I call it these are two different things though. One is how short I am in theory versus how sure I am theory sorry, practically. So how sure I am in theory okay in theory nobody's chasing me. I have all the time in the world to doubt myself. In practice, in real life, when you're facing life or death or or matters of extreme importance, that can be very costly, either monetary or, or, you know, matter of life and literally metal of life and death then then then it becomes important. So then when it's in practice, then I think you should basically act on the best information you have. Like the highest confidence degree you have about anything, you just act on it. That's it. You're done. You don't need to think, think twice or three times. My point is that you can I agree with you, it's probably something evolved in us. But you can still even in that environment in a chaotic West West world, or or even, you know, rules of the jungle kind of thing, you can still have this element of I'm not so sure about everything and still survive. So long as you're like, I'm not 100% Sure, but I'm 90%. Sure. And that 90% is above everything else I'm sure about. So I'm going to act on that knowledge. That's fine. that'll that'll get you out of it and actually, actually probably get you out of it the best. Because you're not acting on a random information, you're acting on the information that you have the highest confidence. You're most shorter, but basically, but you don't have to say I'm 100% sure about that. You just have to be like, I'm sure enough, but I'm going to act on it. And then the question comes, okay, now I'm sure about something 90% on your shirt about something, some what number of a percent, and we have to do one or the other. And then we get into a fight about who's more sure. So it becomes messy. I understand. That's what I'm trying to say. But But anyway, so that's a theoretical, doubting of yourself. And then the practical being sure of yourself. It's Yes, I agree, sometimes being indecisive because when you don't choose, that's a choice. Sometimes people don't choose because they're terrified of their choice. And then that's the choice itself. They don't choose because if they feel if they don't choose they are they can make a mistake. But then that's the mistake itself, because by not choosing, you're choosing. Anyway, it's not to get too philosophical. But I agree. I think it's it's evolved to be in us because if we weren't so sure, then we were indecisive and would be would be eaten by bears and tigers and such.   Tugrul  42:02 So more. And also, I think we just recently learned what is what does that mean that being sure, I think it's it just came with it like a science and technology or understanding about how we can share about something this came with the some physical philosophical questions, because other than that, we can question about being sure because you don't know what, what is it? I mean, being chill. What does that mean? before?   Pouya LJ  42:30 I think there is a meaning before science in the like, Okay, if we take it to before, 2000 years before,   Tugrul  42:37 like, first of all, let's go down to a Greek oak, but the   Pouya LJ  42:41 Greeks will do the same thing. They would disprove each other. Right? They would but but that's but they were doing science. So I grant that. But let's go even further back, let's go 10,000 years ago, I think there was a degree of being sure and unsure. And I think that was linked to discovery because let's say a caveman that went out of the cave, and they were debating is like, No, I'm sure there's something beyond this hill, I gotta go see it. And the other guy was like, How can you be so sure? I don't know. Like, there is nothing beyond that he'll under you're gonna die and we're gonna starve in the cave because you're the hunter. So   Tugrul  43:11 sorry, I don't agree. I think that okay. Mice kind of my story is like, a guy who is like a strongest one on this, like a society that they had just decides instinctively, everybody follows. There was no debate probably.   Pouya LJ  43:27 Right. But but then he can personally be shown that he his confidence was false. For example, He's sure that there's a, you know, there's nothing beyond the hill. But then to prove himself, he goes, and then he realizes, oh, there's something down the hill. So I was wrong.   Tugrul  43:43 Yeah, I agree. I agree. Probably, like a personal, like, initial level of being sure. Very minor. They didn't question the list.   Pouya LJ  43:51 No, I don't I think you may be right. I think it's it started from the ancient Greeks when they started philosophizing and thinking semi scientifically, yes, I think I think   Tugrul  44:02 because you have different information to be understanding, okay, for the same concept, we have two ideas. Okay, which one is correct? Then you can think about, okay, how we can be so sure about which one is more correct. And compare? Yeah, maybe you need the comparison for ideas, at least. Yeah. Yeah. I don't know. Like,   Pouya LJ  44:20 I mean, I think, I think for that, as far as we know, at least, as far as I personally know, I think for that you have to, we can only go as far as the ancient Greeks probably. I mean, I think you may be right if we can, or maybe we just don't know about it, because it wasn't well documented. Who knows? Yeah, again, I'm not sure.   Tugrul  44:40 You never know. I mean, you know, you have to go there and observe it.   Pouya LJ  44:43 Even then, you know,   Tugrul  44:46 because we are we're creating stories based on our findings from like for sales, etc, etc. Like his drawings on the cave. They're all good models, but their stories still, like backed by evidences but that everything can be can still satisfy a like all these findings, but in a different way. So you never know you have to go there and observe it with a time machine, which is not possible. But there was that's what all I got all we got.   Pouya LJ  45:17 Yeah, and, you know, these are very interesting questions, and I think we should explore them more. And I'm very happy that we're going to do this. Okay. So for the audience who are wondering, we will be doing more of these kinds of episodes. Now, this was introductory for us to, you know, discuss with turtle get to know Him and who he is where he came from academically. Because not that not in the sense that academic academia is very important, but because first of all, you spend a lot of your life there. And second of all, because I think that kind of tells you what your interests are, where you're coming from where your perspective is at so. So this was the, you know, introductory episode, but we'll continue this discussions, probably from maybe a little bit more narrowed and talk about specific things into future episodes. But for now, before we come to a close, is there something you want to talk about, whether about yourself or about what we talked about or about anything, really, before we close for this episode?   Tugrul  46:22 No, no, I enjoyed this a lot. So I'm just looking forward to other episodes like we can discuss, but I wasn't expecting to talk about cavemen.   Pouya LJ  46:34 That's the beauty of it. I think. I do like some structure in the in the podcasts, but I don't. And I know everybody has a different, you know, style. And I like those who are super structured and those who are completely unstructured. But for myself, I like to be surprised in my conversations in a way that as you said, I didn't expect so. So anyhow. Yeah, there's a degree of chaos and too much control me ruin it. A little bit, just just as ordered enough that it makes sense. Okay, so with that. Thank you all for listening. And thank you all for joining us with the promise of many more of   Tugrul  47:18 these kinds. Of course, of course, I'm looking forward. Thank you.   Pouya LJ  47:22 Fantastic. And thank you all for tuning in. Tune in for more episodes in the weeks and months to come.

Tim and Ted tackle one of the most pressing, and complex, issues in the world of technology. But first: news you can use about some misleading pictures going around and Ted details his increasing cinematic fame. Support Tep Talk on Patreon: patreon.com/TechTalkPod

Got Faded Japan ep 644 In this action packed episode…. Johnny is stranded in the US, so Tom and Jeremy take the ropes and fire up some old school fading like true playaz do. Oh yes, beers were killed, stories were told and the weekly bizarre and wacky news was reviewed just like it was in the 70's by sauced to perfection weatherman. FADE ON!     -------------------------------------------------------------------------------- Supporting GOT FADED JAPAN ON PATREON directly supports keeping this show going and fueled with booze, seriously could you imagine the show sober?? Neither can we! SUPPORT GFJ at: https://www.patreon.com/gotfadedjapan   -------------------------------------------------------------------------------- CHECK OUT OUR SPONSORS AND SUPPORT THE SHOW!!!! 1. THE SPILT INK: Experience art, buy art and get some original art commissioned at: SITE: https://www.thespiltink.com NFT: https://rarible.com/thespiltink ETSY: https://www.etsy.com/shop/TheSpiltInk?ref=hdr_shop_menu --------------------------------------------------------------------------------  2. Soul Food House https://soulfoodhouse.comAddress:2-chōme−8−10 | Azabujūban | Tokyo | 106-0045 Phone:03-5765-2148 Email:info@soulfoodhouse.com Location Features:You can reach Soul Food House from either the Oedo Line (get off at Azabujuban Station and it's a 7-minute walk) or the Namboku Line (get off at Azabujuban Station and it's a 6-minute walk). --------------------------------------------------------------------------------  3. Ghost Town Pomade FADE IN STYLE with Ghost Town Pomade.Get yours today by contacting: ghosttownpomade@gmail.com  -------------------------------------------------------------------------------- 4. MITSUYA LIQUOR in ASAGAYA: 1　Chome- 13 -17 Asagayaminami, Suginami Tokyo 166-0004　 Tel & Fax: 0303314-6151Email: saketoyou0328@gmail.com --------------------------------------------------------------------------------   5. Harry's Sandwich Company 1 min walk from Takeshita Street in HarajukuCall 050-5329-7203 Address: 〒150-0001 Tokyo, Shibuya City, Jingumae, 1 Chome−16−7 MSビル 3F https://www.facebook.com/harryssandwichco/ -------------------------------------------------------------------------------- 6. Share Residence MUSOCO “It's a share house that has all that you need and a lot more!” - Located 30 minutes form Shibuya and Yokohama - Affordable rent - Gym - BAR! - Massive kitchen - Cozy lounge space - Office work units - A spacious deck for chilling - DJ booth and club space - Barber space - AND MORE! Get more info and move in at: https://sharedesign.co.jp/en/property.php?id=42&property=musaco&fbclid=IwAR3oYvB-a3_nzKcBG0gSdPQzxvFaWVWsi1d1xKLtYBnq8IS2uLqe6z9L6kY -------------------------------------------------------------------------------- GET YOURSELF SOME GOT FADED JAPAN MERCH TODAY!!! We have T-Shirts, COFFEE Mugs, Stickers, even the GFJ official pants! BUY NOW AND SUPPORT THE SHOW: http://www.redbubble.com/people/thespiltink/works/16870492-got-faded-japan-podcast  -------------------------------------------------------------------------------- The Got Faded Japan Podcast gives listeners a glimpse of the most interesting side of Japan's news, culture, peoples, parties, and all around mischief and mayhem. Hosted by Johnny and Jeremy who adds opinions and otherwise drunken bullshit to the mix. We LOVE JAPAN AND SO DO YOU! Send us an email on Facebook or hell man, just tell a friend & post a link to keep this pod rolllin' Fader! Kanpai mofos!    

When a lizard gets in a dicey situation it can eject its tail like a sinking ship trying to lose weight, but why and how does this happen? Today we're talking all about detachable limbs and the mighty power of stem cells! Learn more about your ad choices. Visit podcastchoices.com/adchoices

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Our main host is out this week due to other engagements so Angela and the rest of the team take the train ride on the show from awesome news regarding more accessible features from the big step companies, to lots of humor, it's a show you definitely want to have on repeat. Sorry meant to say Dee we got big news from the awesome tech companies regarding more accessibility. Dictation fail

Did you know there were soooo many different fevers a person can get?  I sure didn't.  Join us to learn about a few more fevers.Support the show

Intro Banter - This is the (mostly) unscripted intro to the show! We catch up, play games, talk about games that perhaps did not make the main show, and just gab, Welcome!  Stars of Akarios (Alex) Sneak  Ark Nova Under the Hood:  We roll up our sleeves and talk about games from the perspective of their mechanics! The mechanisms that are present and cover what some of the buzzwords may mean.    Summer Games Epic Campaigns!   Hallmarks of campaign games Progression Narrative driven (player/game) Single unconnected scenarios (Player created narrative, Sentinels of the Multiverse) versus from determined by the book Things to consider Cost of Entry, Expansions? Arkham Horror LCG, Descent 2nd Ed, Mice and Mystics, Group size Consistency of meeting Table size How to “save” the game Campaign versus Legacy Risk Legacy  Charterstone Jurassic World: The Legacy of Isla Nublar   Best Campaign games for 1 player, 2 - 3 player, 4 - 5 player    Alex: Solo : 7th Continent, LOTR the Card Game, Legacy of Dragonholt 2 - 3 Player: Shadows of Brimstone, Pandemic Legacy, Pathfinder Adventure Card Game, Gloomhaven  4 - 5 Player: The Crew, The Initiative, Imperial Assault, The King's Dilemma     Larry: Solo:  7th Continent, Hostage Negotiator Career, Zombiecide Invader,  (Honorable Mention Space Infantry) 2 - 3 Player:  Sword and Sorcery, Mage Knight/Star Trek Frontiers, Mechs Vs. Minions 4 - 5 Player:  Sentinels of the Multiverse, Thunderstone Quest, Gears of War Links:  Podstudio1  BGG  Space Infantry 2.1 Rules  Mice & Mystics Downwood Tales   Music:  As always from the amazing community of gifted musicians, arrangers, and composers over at ocremix.org go visit and support them for the full project and so much more amazing music!   Outro :  De Nuit / by mv feat. Jeff Ball Original Track - The Phantom Forest Album - Final Fantasy VI: Balance and Ruin Project Page - Final Fantasy VI: Balance and Ruin | OC ReMix Content Group - Final Fantasy VI Original Copyright - Square Enix Original Composers - Nobuo Uematsu

Author legend Anthony Horowitz joins us this week to chat about his hilarious new book in the Diamond Brothers series, Where Seagulls Dare. And we hear Roald Dahl classics coming to life through some of Britain's most loved comedians.. this week we hear some of James Acaster's impromptu singing for his reading of James and the Giant Peach, its all in this weeks Book Worms Podcast! Get in touch to let us know what you are reading at funkidslive.com! See omnystudio.com/listener for privacy information.

This week we've got a special one for y'all! Ayleph runs us through a very fun game of Mausritter! Mousey shenanigans ensue. Mice up your life!Mausritterhttps://losing-games.itch.io/mausritterLauren's Mom's GoFundMe:https://www.gofundme.com/f/emergency-funding-for-yvonne-and-the-gangDice Funk:https://austinyorski.podbean.com/Lauren's Mother's GoFundMe:https://www.gofundme.com/f/emergency-funding-for-yvonne-and-the-gangOpening Arguments:https://open.spotify.com/show/2fpbVK2Ry4P9qgcjOdmyvNLauren's Onlyfans:onlyfans.com/rawrgliciousLauren's Paypal:paypal.me/rawrgliciousLet's Talk About Snacks:https://open.spotify.com/show/1fVjUPlm967tApMypgyWkLBethany's Comic:https://eonscomic.kitmyth.net/

A story about clever Judith and brave Jimmy Mouse. A grand portrait of a cat is hanging on the wall of the cafe. The mice who lived their are convinced it comes alive at night. What is the truth of the mystery? Sponsored by Athletic Greens.

CLIP: Klein has a mouse problem and you will not believe how much they're wanting to charge to get rid of it

We wrap up the week with a patron episode featuring our good friend Eric Lohrenz. He focuses on the year 2002, picking out two albums and two songs for discussion: ...And You Will Know Us By the Trail of Dead -  Source Tags & Codes Interpol - Turn on the Bright Lights Longwave -  "Everywhere You Turn"  Bats & Mice -   "Worst Comes to Worst"  Subscribe to Rockin' the Suburbs on Apple Podcasts/iTunes or other podcast platforms, including audioBoom, Spotify, Google Podcasts, Amazon, iHeart, Stitcher and TuneIn. Or listen at SuburbsPod.com. Please rate/review the show on Apple Podcasts and share it with your friends. Visit our website at SuburbsPod.com Email Jim & Patrick at rock@suburbspod.com Follow us on the Twitter, Facebook or Instagram @suburbspod If you're glad or sad or high, call the Suburban Party Line — 612-440-1984. Theme music: "Ascension," originally by Quartjar, covered by Frank Muffin. Visit quartjar.bandcamp.com and frankmuffin.bandcamp.com

CLIP: Klein thought is was just plastic. Turns out, like always, he's wrong

a brief history of some of my favorite cats, and their favorite drug of choice. Spoiler alert: like many of the stories in this series, it is sad. --- This episode is sponsored by · Anchor: The easiest way to make a podcast. https://anchor.fm/app Support this podcast: https://anchor.fm/twochocolatecakes/support

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Check a look at this cool ass friendship, as it develops live in front of you between myself and fellow independent pro wrestler and podcaster Red Dawg Cliff Miller.   https://linktr.ee/The_reddawg85

This month on Episode 36 of Discover CircRes, host Cynthia St. Hilaire highlights original research articles featured in the April 29 and May 13 issues of Circulation Research. This episode also features a conversation with Dr Patricia Nguyen and Jessica D'Addabbo from Stanford University about their study, Human Coronary Plaque T-cells are Clonal and Cross-React to Virus and Self.   Article highlights:   Zanoli, et al. COVID-19 and Vascular Aging   Wang, et al. JP2NT Gene Therapy in a Mouse Heart Failure Mode   Harraz, et al. Piezo1 Is a Mechanosensor in CNS Capillaries   Zhao, et al. BAT sEVs in Exercise Cardioprotection   Cindy St. Hilaire:        Hi, and welcome to Discover CircRes, the podcast of the American Heart Association's journal, Circulation Research. I'm your host, Dr Cyndy St. Hilaire, from the Vascular Medicine Institute at the University of Pittsburgh. And today, I'll be highlighting the articles from our April 29th and May 13th issues of Circulation Research. I also will speak with Dr Patricia Nguyen and Jessica D'Addabbo from Stanford University about their study, Human Coronary Plaque T-cells are Clonal and Cross-React to Virus and Self.   Cindy St. Hilaire:        The first article I want to share is titled Vascular Dysfunction of COVID 19 Is Partially Reverted in the Long-Term. The first author is Agostino Gaudio and the corresponding author is Luca Zanoli. And they're from the University of Catania. Cardiovascular complications, such as endothelial dysfunction, arterial stiffness, thrombosis and heart disease are common in COVID 19. But how quickly such issues resolve, once the acute phase of the illness has passed, remains unclear. To find out, this group examined aortic and brachial pulse wave velocity, and other measures of arterial stiffness in 90 people who, several months earlier, had been hospitalized with COVID 19. These measurements were compared with data from 180 controls, matched for age, sex, ethnicity and body mass index, whose arterial stiffness had been assessed prior to the pandemic. 41 of the COVID patients were also examined 27 weeks later to assess any changes in arterial stiffness over time. Together, the data showed arterial stiffness was higher in COVID patients than in controls. And though it improved over time, it tended to remain higher than normal for almost a year after COVID.   Cindy St. Hilaire:        This finding could suggest residual structural damage to the arterial walls or possibly, persistent low-grade inflammation in COVID patients. Either way, since arterial stiffness is a predictor of cardiovascular health, its potential longterm effects in COVID patients deserves further longitudinal studies.   Cindy St. Hilaire:        The second article I want to share is titled Gene Therapy with the N-Terminus of Junctophilin-2 Improves Heart Failure in Mice. The first author is Jinxi Wang and the corresponding author is Long-Sheng Song from the University of Iowa. Junctophilin-2 is a protein with a split personality. Normally, it forms part of the heart's excitation contraction coupling machinery. But when the heart is stressed, JP2 literally splits in two, and sends its N-terminal domain, JP2NT, to the nucleus, where it suppresses transcription of genes involved in fibrosis, hypertrophy, inflammation and other heart failure related processes. However, if this stress is severe or sustained, the protective action of JP2NT is insufficient to halt the progressive failure. This group asked. "What if this N-terminal domain could be ramped up using gene therapy to aid a failing mouse heart?"   Cindy St. Hilaire:        To answer this question, they injected adenoviral vectors encoding JP2NT into mice either before or soon after transaortic constriction, or TAC, tack, which is a method of experimentally inducing heart failure. They found, in both cases, that the injected animals fared better than the controls. Animals injected before TAC showed less severe cardiac remodeling than control mice, while those treated soon after TAC exhibited slower loss of heart function with reduced ventricle dilation and fibrosis. These data suggest that supplementing JP2NT, via gene therapy or other means, could be a promising strategy for treating heart failure. And this data provides a basis for future translational studies.   Cindy St. Hilaire:        The third article I want to share is titled Piezo1 Is a Mechanosensor Channel in Central Nervous System Capillaries. The first and corresponding author is Osama Harraz from the University of Vermont. Neurovascular coupling is the process whereby transient activation of neurons leads to an upsurge in local blood flow to accommodate the increased metabolic needs of the cell. It's known that agents released from active neurons trigger changes in local capillaries that prompt vasodilation, but how these hemodynamic changes are sensed and controlled is not entirely clear. This group suspected that the mechanosensory protein Piezo1, a calcium channel that regulates dilation and constriction of other blood vessels, may be involved. But whether Piezo1 is even found in the microcirculation of the CNS was unknown. This group shows that Piezo1 is present in cortical capillaries of the brain and the retina of the mouse, and that it responds to changes in blood pressure and flow.   Cindy St. Hilaire:        Ex vivo preparations of mouse retina showed that experimentally induced changes in hemodynamics caused calcium transients and related currents within capillary endothelial cells, and that these were dependent on the presence of Piezo1. While it is not entirely clear how Piezo1 influences cerebral blood flow, its pressure induced activation of CNS capillary endothelial cells suggest a critical role in neurovascular coupling.   Cindy St. Hilaire:        The last article I want to share is titled Small Extracellular Vesicles from Brown Adipose Tissue Mediate Exercise Cardioprotection. The first authors are Hang Zhao and Xiyao Chen. And the corresponding authors are Fuyang Zhang and Ling Tao from the Fourth Military Medical University. Regular aerobic exercise is good for the heart and it increases the body's proportion of brown adipose tissue relative to white adipose tissue. This link has led to the idea that brown fat, possibly via its endocrinal activity, might somehow contribute to exercise related cardioprotection. Zhao and colleagues now show that, indeed, brown fat produces extracellular vesicles that are key to preserving heart health. While mice subjected to four weeks of aerobic exercise were better protected against subsequent heart injury than their sedentary counterparts, blocking the production of EVs prior to exercise significantly impaired this protection. Furthermore, injection of brown fat derived EVs into the hearts of mice lessened the impact of subsequent cardiac injury.   Cindy St. Hilaire:        The team went on to identify micro RNAs within the vesicles responsible for this protection, showing that the micro RNAs suppressed an apoptosis pathway in cardiomyocytes. In identifying mechanisms and molecules involved in exercise related cardio protection, the work will inform the development of exercise mimicking treatments for people at risk of heart disease or who are intolerant to exercise.   Cindy St. Hilaire:        Lastly, I want to bring up that the April 29th issue of Circulation Research also contains a short Review Series on pulmonary hypertension, with articles on: The Latest in Animal Models of Pulmonary Hypertension and Right Ventricular Failure, by Olivier Boucherat; Harnessing Big Data to Advance Treatment and Understanding of Pulmonary Hypertension, by Christopher Rhodes and colleagues; New Mutations and Pathogenesis of Pulmonary Hypertension: Progress and Puzzles in Disease Pathogenesis, by Christophe Guignabert and colleagues; Group 3 Pulmonary Hypertension From Bench to Bedside, by Corey Ventetuolo and colleagues; and Novel Approaches to Imaging the Pulmonary Vasculature and Right Heart, by Sudarshan Rajagopal and colleagues; and Understanding the Pathobiology of Pulmonary Hypertension Due to Left Heart Disease, by Jessica Huston and colleagues.   Cindy St. Hilaire:        Today, Dr Patricia Nguyen and Jessica D'Addabbo, from Sanford University, are with me to discuss their study, Human Coronary Plaque T-cells are Clonal and Cross-React to Virus and Self. And this article is in our May 13th issue of Circulation Research. So, Trisha and Jessica, thank you so much for joining me today.   Jessica D'Addabbo:    Thank you for having us.   Patricia Nguyen:         Yes. Thank you for inviting us to your podcast. We're very excited to be here.   Cindy St. Hilaire:        Yeah. And I know there's lots of authors involved in this study, so unfortunately we can't have everyone join us, but I appreciate you all taking the time.   Patricia Nguyen:         This is like a humongous effort by many people in the group, including Roshni Roy Chowdhury, and Xianxi Huang, as well as Charles Chan and Mark Davis. So, we thank you.   Cindy St. Hilaire:        So atherosclerosis, it stems from lipid deposition in the vascular wall. And that lipid deposition causes a whole bunch of things to happen that lead to a chronic inflammatory state. And there's many cells that can be inflammatory. And this study, your study, is really focusing on the role of T-cells in the atherosclerotic plaque. So, before we get into the nitty gritty details of your study, can you share with us, what is it that a T-cell does normally and what is it doing in a plaque? Or rather, let me rephrase that as, what did we know a T-cell was doing in a plaque before your study?   Patricia Nguyen:         So, T-cells, as you know, are members of the adaptive immune system. They are the master regulators of the entire immune system, secreting cytokines and other proteins to attract immune cells to a diseased portion of the body, for example. T-cells have been characterized in plaque previously, mainly with immunohisto chemistry. And their characterization has also been recently performed using single cell technologies. Those studies have been restricted to mainly mirroring studies, studies in mice in their aortic walls, in addition to human carotid arteries. So, it is well known that T cells are found in plaque and a lot of attention has been given to the macrophage subset as the innate immune D. But let's not forget the T-cell because they're actually composed about... 50% in the plaque are T-cells.   Patricia Nguyen:         And we were particularly interested in the T-cell population because we have a strong collaboration with Dr Mark Davis, who's actually the pioneer of T-cell biology and was the first to describe the T-cell receptor alpha beta receptor in his lab in the 1970s. So, he has developed many techniques to interrogate T-cell biology. And our collaboration with him has allowed us and enabled us to perform many of these single cell technologies. In addition, his colleague, Dr Chen, also was pivotal in helping us with the interrogation and understanding of the T-cells in plaque.   Cindy St. Hilaire:        And I think one of the really neat strengths of your study is that you used human coronary artery plaques. So, could you walk us through? What was that like? I collect a lot of human tissue in my lab. I get a lot of aortic valves from the clinic. And it's a lot of logistics. And a lot of times, we're just fixing them, but you are not just fixing them. So, can you walk us through? What was that experimental process from the patient to the Petri dish? And also, could you tell us a little bit about your patient population that you sampled from?   Jessica D'Addabbo:    So, these were coronary arteries that we got from patients receiving a heart transplant. So, they were getting a heart transplant for various reasons, and we would receive their old heart, and someone would help us dissect out the coronary arteries from these. And then, we would process each of these coronary arteries separately. And this happened at whatever hour the hearts came out of the patient.   Jessica D'Addabbo:    So sometime, I was coming in at 3:00 AM with Dr Nguyen and we would be working on these hearts then, because we wanted the samples to be as fresh as possible. So, we would get the arteries. We would digest out the tissue. And then, we would have certain staining profiles that we wanted to look at so that we could put the cells on fax to be able to sort the cells, and then do all the downstream sequencing from there.   Cindy St. Hilaire:        So, in terms of, I don't know, the time when you get that phone call that a heart's coming in to actually getting those single cells that you can either send a fax or send a sequencing, how long did that take, on a good day? Let's talk only about good days.   Jessica D'Addabbo:    Yeah. A lot of factors went into that, sometimes depending on availability of things. But usually, we were ready with all of the materials in advance. So, I'd say it could be anywhere from six to 12 hours, it would take, to get everything sorted. Then, everything after that would happen. But that was just that critical period of making sure we got the cells fresh.   Patricia Nguyen:         So we have to credit the CT surgeons at Stanford for setting up the program or the structure, infrastructure, that enables us to obtain this precious tissue. That is Jack Boyd and Joseph Woo of CT surgery. So, they have enabled human research on hearts by making these tissues available. Because as you know, a transplant... They can say the transplant's happening at 12:00 AM, but it actually doesn't happen until 4:00 AM. And I think it's very difficult for a lab to make that happen all the time. And I think having their support in this paper was critical. And this has allowed us, enabled us, to interrogate kind of the spectrum of disease, especially focusing on T-cells, which are... They make a portion of the plaque, but the plaque itself has not like a million cells that are immune. A lot of them are not immune. So, enabling us to get the tissue in a timely fashion where they're not out of the body for more than 30 minutes enables us to interrogate these small populations of cells.   Cindy St. Hilaire:        That's actually the perfect segue to my next question, which is, how many cells in a plaque were you able to investigate with the single cell analysis? And what was the percentage again of the T-cells in those plaques or in... I guess you looked at different phases of plaque. So, what was that spectrum for the percentage of T-cells?   Patricia Nguyen:         So, for 10X, for example, you need a minimum of 10,000 captured cells. You could do less, but the utility of the 10X is maximized with 10,000. So, many times before the ability to multiplex these tissues, we were doing like capturing 5,000 for example. And the number of cells follows kind of the disease progression, in the sense that as a disease is more severe, you have more immune cells, in general. And it kind of decreases as it becomes more fibrotic and scarred, like calcified. So, it was a bit challenging to get very early just lipid-only cells. And a lot of those, we captured like 3000 or something like that. And efficiency is like 80% perhaps. So, you kind of capture…   Cindy St. Hilaire:        And also, how many excised hearts are going to have early athero? So, it's...   Patricia Nguyen:         Well, there are... nonischemics will have...   Cindy St. Hilaire:        Oh, okay. Okay.   Patricia Nguyen:         So, the range was nonischemic to ischemic.   Cindy St. Hilaire:        Oh great.   Patricia Nguyen:         So, about a portion... I would say one third of the total heart transplants were ischemic. And a lot of them were non ischemic. But as you know, the nonischemic can mix with ischemia. And so, they could have mild to moderate disease in the other arteries, for example, but not severe like 70%/90% obstruction.   Cindy St. Hilaire:        Wow. That's so great. That's amazing. Amazing sample size you have. So T-cell, it's kind of an umbrella term, right? There's many different types of T-cells. And when you start to get in the nitty gritty, they really do have distinct functions. So, what types of T-cells did you see and did you focus on in this study?   Jessica D'Addabbo:    So, the two main types of T-cells are CD4 positive T-cells and CD8 positive T-cells. And we looked at both of these T-cells from patients. We usually sorted multiple plates from each. And then, with 10X, we captured both. But our major finding was actually that the CD8 positive t-cell population was more clonally expanded than the CD4 population, which led us to believe that these cells were more important in the coronary artery disease progression and in the study that we were doing because for a cell to be clonally expanded, it means it was previously exposed to an antigen. And so, if we're finding these T-cells that are clonally expanded in our plaques, then we're hypothesizing that they were likely exposed to some sort of antigen, and then expanded, and then settled into the plaque.   Cindy St. Hilaire:        And when you're saying expansion, are you talking about them being exposed to the antigen in the plaque and expanding there? Or do you think they're being triggered in the periphery and then honing in as a more clonal population?   Patricia Nguyen:         So, that's a great question. And unfortunately, I don't have the answer to that. So basically-   Jessica D'Addabbo:    Next paper, next paper.   Patricia Nguyen:         Exactly. So, we... Interesting to expand on Jessica's answer. Predominantly what was found, as you said, was memory T-cells, so memory T-cells expressing specific markers, so memory versus naive. And these were effector T-cells. And memory meaning they were previously expanded by antigen engagement, and just happened to be in the plaque for whatever reason. We do not know why T-cells specifically are attracted to the plaque, but they are obviously there. And they're in a memory state, if you will. And some of them did display activation markers, which suggested that they clonally expanded to an antigen. What that antigen is, is the topic of another paper. But certainly, it is important to understand that these patients that we recruit, because they were transplant patients, they're not actively infected, right? That is a exclusionary criteria for transplants, right?   Patricia Nguyen:         So, that means these T-cells were there for unclear reasons. Why they're there is unclear. Whether they are your resident T-cells also is unclear, because the definition of resident T-cell still remains controversial. And you actually have to do lineage tracking studies to find out, "Okay, where... Did they come from the bone marrow? Did they come from the periphery? How did they get there?" Versus, "Okay. They were already there and they just expanded, for whatever reason, inside the plaque."   Cindy St. Hilaire:        So, your title... It was a great title, with this provocative statement, "T-cells are clonal and cross react to virus and self." So, tell us a little bit more about this react to virus and self bit. What did your data show?   Jessica D'Addabbo:    So, because of the way we sequenced the T-cell receptor, we were able to have paired alpha and beta chains. And because we knew the HLA type of the patients, we were able to put the sequences that we got out after we sequenced these through an algorithm called GLIPH, which allows us to look at the CDR3 region of the T cell receptor, which is the epitope binding region. And there are certain peptide. They're about anywhere from three to four amino acids long. These are mapped to certain binding specificities to known peptides. And so, basically, we were able to look at which epitopes were most common in our plaques. And we found that after comparing these to other epitopes, that these were actually more binding to virus. Patricia Nguyen:         So let me add to what Jessica stated, and kind of emphasize the value of the data set, if you will. So, this is, I believe, the first study that provides the complete TCR repertoire of coronary plaque, and actually any plaque that I know of, which is special because we know that there is specificity of TCR binding. It's more complicated than the antibody that binds directly from B cells to the antigen, because the T-cells bind processed antigen. So, the antigens are processed by antigen presenting cells like Dendritic cells and macrophages. And they have a specific HLA MHC class that they need to present to. And they need both arms, the antigen epitope and the MHC, to activate the T-cell. So unfortunately, it's not very direct to find the antigen that is actually activating the T-cell because we're only given a piece of it. Right?            Patricia Nguyen:         But we have provided a comprehensive map of all the TCRs that we find in the plaque. And these TCRs have a sequence, an immuno acid sequence. And luckily, in the literature, there is a database of all TCR specificities. Okay. So, armed with our TCR repertoire, we can then match our TCR repertoire with an existing database of known TCR specificities. Surprisingly, the matching TCRs are specific to virus, like flu, EBV and CMB. And also, because this was done in the era of COVID, we thought it would be important to look at the coronavirus database. We did find that there were matches to the coronavirus database. Even though our finding is not specific to SARS, it does lend to some potential mechanistic link there as well.   So, because this is all computational, it is important to validate. So, the importance of validation requires us to put the TCR alpha beta chain into a Jurkat cell, which is a T-cell line that does not have alpha beta chains on it, and then expose it to what we think is the cognate antigen epitote, with the corresponding HLA MHC APC. Because you don't have all those pieces, it will not work. Yes. So importantly, we did find that what we predicted to have the specificity of a flu peptide had specificity to a flu peptide.   Patricia Nguyen:         So then, the important question was, "Okay, these patients aren't infected, right? Why are these things here? Is there a potential cross reactivity with self peptides?"   Patricia Nguyen:         So luckily, our collaborator, Dr Charles Chan, was able to connect us with another computational algorithm that he was familiar with, whereby we were able to take the peptide sequences from the flu and match them with peptide sequencing from proteins that are self and ubiquitous. And we demonstrated, again, these T-cells were activated in vitro. That is why we concluded that there's a potential cross reactivity between self and virus that can potentially lead to thrombosis associated with viral infections. Of course, this all needs to be proved in vivo.   Cindy St. Hilaire:        Sure, sure.   Patricia Nguyen:         It's that first step for other things.   Cindy St. Hilaire:        The other big immune cell that we know is in atherosclerotic plaques and that's macrophages. And they can help to present antigens and things like that. And they also help to chew up the necrotic bits. And so, do you think that this T-cell component is an earlier, maybe disease driving, process or an adaptive process that goes awry as a secondary event? Patricia Nguyen:         So, I'm a fan of the T-cell. So... I'm with team T cell. I would like to think that it is playing an active role in pathology in this case and not a reactive role, in the sense of just being there. I think that the T-cell is actively communicating with other cells within the plaque, and promoting pro fibrotic and pro inflammatory reactions, depending on the T-cell. So, a subset of this paper was looking at kind of the interactions between the T-cell and other cells within the plaque, like macrophages and smooth muscle cells. And as we know, T-cells are activated and they produce cytokines. Those cytokines then communicate to other cells. And we found that, computationally, when you look at the transcriptome, there is a pro-inflammatory signature of the T-cell that resides in the more complex stage. And then, there's an anti-inflammatory signature that kind of resides in the transition between lipid and fibro atheroma, if you will.   Cindy St. Hilaire:        So, do you know, or is it known, how dynamic these populations are? Obviously, the hearts that you got, the samples you got, didn't have active infections. But do you know perhaps even how long ago they happened, or even how soon after there might be an infection or an antigen presented that you could get this expansion? And could that be a real driver of rupture or thrombosis?   Patricia Nguyen:         So, in theory, you would suppose that T-cells expanding and dividing and producing more and more cytokines would then lead to more macrophages coming, more of their production of proteinases that destroy the plaque. Right? So yes, in theory, yes. I think it's very difficult to kind of map the progression of T cell clonality in the current model that we have, because we're just collecting tissues. However, in the future, as organoids become more in science and kind of a primary tissue, where we can... For example, Mark Davis is making organoids with spleen, and also introducing skin to that.   Patricia Nguyen:         And certainly, we could think of an organoid involving the vasculature with immune cells introduced. And so, I think, in the next phase, project 2.0, we can investigate what... like over time, if you could model atherosclerosis and the immune system contribution, T-cells as well as macrophages and other immune cells, you can then kind of map how it happens in humans. Because obviously, mice are different. We know that mice... Actually, the models of transgenic mice do not rupture. It's very hard to make them rupture. Right?   Cindy St. Hilaire:        Well, if you stop feeding them high fat diet, the plaque goes away.   Patricia Nguyen:         For sure, for sure. So I think.. I mean, Mark Davis is a huge proponent of human based research, like research on human tissue. And as a physician scientist, obviously I'm more inclined to do human based research. And Jessica's going to be a physician someday soon. And I'm sure she's more inclined to do human based research. And certainly, the mouse model and in vitro models are great because you can manipulate them. But ultimately, we are trying to cure human diseases.   Cindy St. Hilaire:        Mice are not little humans. That's what we say in my lab. I similarly do a lot of human based stuff and it's amazing how great mice are for certain things, but still how much is not there when we need to really fully recapitulate a disease model.   So, my last question is kind of regarding this autoimmune angle of your findings. And that is, women tend to have more autoimmune diseases than men, but due to the fact that you are getting heart transplants, you've got a whole lot more men in your study than women. I think it was like 31 men to four women. But, I mean, what can you do? It's the nature of heart transplants. But I'm wondering, did you happen to notice...Maybe the sample size perhaps is too small, but were there any differences in the populations of these cells between women and men? And do you think there could be any differences regarding this more prevalence of autoimmune like reactions in women?   Patricia Nguyen:         So, that's an interesting question, but you hit it on the nose when you said "Your sample is defined mainly by men." And in addition, the samples that were women tend to have less disease. And they tend to be nonischemic in etiology. So, I think that kind of restricts our analysis. And perhaps, I guess, future studies could model using female tissues, for example, instead of only male. But the limitation of all human studies is sample availability. And perhaps, human organoid research can be less limited by that. And certainly, mouse research has become more evenly distributed of male and female mice.   Cindy St. Hilaire:        Yeah. Suffice it to say, human research is hard, but you managed to do an amazing and really important study. It was really elegant and well done. Congratulations on what is an epic amount of time. 12-hour experiments are no joke, and really beautiful data. So, thank you so much for joining me today, Dr Nguyen and Miss almost Dr D'Addabbo. Congrats and I'm really looking forward to seeing your future work.   Jessica D'Addabbo:    Thank you so much.   Patricia Nguyen:         Thanks so much.   Jessica D'Addabbo:    Thank you for having us. This is wonderful.   Cindy St. Hilaire:        That's it for the highlights from the April 29th and May 13th issues of Circulation Research. Thank you so much for listening. Please check out the Circ Res Facebook page and follow us on Twitter and Instagram with the handle @Circres and #Discover CircRes. Thank you to our guests: Dr Patricia Nguyen, and soon to be Doctor, Jessica D'Addabbo, from Stanford University.   This podcast was produced by Ishara Ratnayaka, edited by Melissa Stoner, and supported by the editorial team of Circulation Research. Copy text for the highlighted articles was provided by Ruth Williams. I'm your host, Dr Cindy St. Haler. And this is Discover CircRes, you're on the go source for the most exciting discoveries in basic cardiovascular research. This program is copyright of the American Heart Association 2022. The opinions expressed by the speakers of this podcast are their own and not necessarily those of the editors or of the American Heart Association. For more information, visit aha journals.org.  

On this week's SciFiles, your hosts Chelsie and Daniel interview Charlotte Best. Charlotte works in a lab that studies the influence of the gut microbiome (all the bacteria in our gut) on the brain and behavior. She is in charge of analyzing its effects on individual neurons and she also found that MRI impacts certain neurons in a negative way, which hasn't been documented before.If you're interested in talking about your MSU research on the radio or nominating a student, please email Chelsie and Danny at scifiles89fm@gmail.com. Check The Sci-Files out on Twitter, Facebook, Instagram, LinkedIn, and YouTube!

This week Amanda and Victoria unpack Of Mice and Men, the exploitation of the American worker, and the utter exhaustion of existence. --- Support this podcast: https://anchor.fm/unfortunately-required/support

Scientists at Stanford infused cerebrospinal fluid from young mice into older mice, and found that they could reverse memory loss. ThePrint's Sandhya Ramesh explains the science behind the new findings and why such treatments are still far away for humans. ----more---- https://theprint.in/health/wondering-why-your-child-suddenly-rebelled-at-13-stanford-study-on-teenage-brain-has-answer/943594/   

GUEST HOST: MIKE TOSAW, ST. CHARLES WEALTH MANAGEMENT CO-HOST: ANDREW GIOVINAZZI, THE OPTION PIT IN THIS EPISODE UNCLE MIKE AND THE ROCK LOBSTER BREAK DOWN: THE LATEST IN THE OPTIONS MARKETS VIX AND VOLATILITY IN THE MARKETS MOST ACTIVE EQUITY OPTIONS INCLUDING DIS, COIN, TWTR, TSLA, AMC, AAPL UNUSUAL OPTIONS ACTIVITY IN CIM, MFA, AON, AMC HOW TO USE YOUR BUTTERFLIES APPROPRIATELY WHAT'S ON OUR RADAR FOR THE REST OF THE WEEK AND WEEKEND AND MUCH MORE

Diets high in fiber associated with less antibiotic resistance in gut bacteria United States Department of Agriculture, May 10, 2022 Healthy adults who eat a diverse diet with at least 8-10 grams of soluble fiber a day have fewer antibiotic-resistant microbes in their guts, according to a study published by Agricultural Research Service scientists and their colleagues in mBio. Microbes that have resistance to various commonly used antibiotics such as tetracycline and aminoglycoside are a significant source of risk for people worldwide, with the widely held expectation that the problem of antimicrobial resistance (AMR)—the term that refers to bacteria, viruses, and fungi that are resistant to antibiotics—is likely to worsen throughout the coming decades.  In this study, the researchers were looking for specific associations of the levels of antibiotic resistance genes in the microbes of the human gut with both fiber and animal protein in adult diets. The researchers found regularly eating a diet with higher levels of fiber and lower levels of protein, especially from beef and pork, was significantly correlated with lower levels of antimicrobial resistance genes (ARG) among their gut microbes. Those with the lowest levels of ARG in their gut microbiomes also had a greater abundance of strict anaerobic microbes, which are bacteria that do not thrive when oxygen is present and are a hallmark of a healthy gut with low inflammation. Bacterial species in the family Clostridiaceae were the most numerous anaerobes found. The strongest evidence was for the association of higher amounts of soluble fiber in the diet with lower levels of ARGs. Soluble fiber, as its name suggests, dissolves in water and is the main type of fiber found in grains like barley and oats; legumes like beans, lentils and peas, seeds (like chia seeds) and nuts; and some fruits and vegetables like carrots, berries, artichokes, broccoli and winter squash. Probiotics stop menopause-like bone loss in mice Emory and Georgia State universities, May 6, 2022 Probiotic supplements protected female mice from the loss of bone density that occurs after having their ovaries removed, researchers at Emory University School of Medicine and Georgia State University have shown  The findings suggest that probiotic bacteria may have potential as an inexpensive treatment for post-menopausal osteoporosis. However, clinical evidence that probiotics can have a lasting effect on the mix of bacteria in the body is limited. Emory and Georgia State researchers found that in mice, the loss of estrogen increases gut permeability, which allows bacterial products to activate immune cells in the intestine. In turn, immune cells release signals that break down bone. Probiotics both tighten up the permeability of the gut and dampen inflammatory signals that drive the immune cells, the team found. Researchers led by Pacifici treated female mice twice a week with Lactobacillus rhamnosus GG (LGG), a type of bacteria found in some yogurts, or with a commercially available mix of eight strains of bacteria known as VSL#3. Good nutrition positively affects social development, research shows University of Pennsylvania, May 6, 2022  Proper nutrition during childhood can positively affect a child's social behaviors and development. It's a unique take on a field that often focuses on how poor diet negatively influences early childhood development. For this study, the scientists analyzed a sample of 1,795 3-year-old children from Mauritius, an island off the eastern coast of Africa with a population of about 1.3 million people. They focused on four aspects of physical health related to nutrition and four indicators of social development. Physical health factors included anemia expressed by low hemoglobin levels, reflecting iron deficiency; angular stomatitis revealed by cracked lips and a lack of vitamin B2 and niacin; and insufficient protein intake indicated by thin or sparse hair and hair discoloration.  The researchers considered a child with just one of the quartet as “suffering from nutritional deficits.” However, children with more malnutrition indicators showed more impaired social behavior. Social interactions studied included friendliness, extent of verbalization, active social play and exploratory behavior.  Examining the relationship between these components after the fact, they teased out a neurocognitive link between nutrition and comprehensive social behavior. It's a connection undiscovered to this point. “The bigger message is give children good nutrition early on,” Liu said. “Not only will it enhance cognitive function but, importantly, promote good social behavior,” which is essential to brain development and intelligence. “In the same study,” Raine said, “we've shown that children with positive social behavior, eight years later, they have higher IQs.” Diabetes almost doubles risk of death from COVID University of Aberdeen, May 10, 2022 People with diabetes were almost twice as likely to die with COVID and almost three times as likely to be critically or severely ill compared to those without diabetes. However, the study conducted by researchers from the University of Aberdeen, which reviewed data from hundreds of thousands of people from all over the world, also found that good management of the condition can mitigate against the risks.  Specifically, the collaboration with King's College, London, found that while diabetes presents a significant risk of severe illness and death with COVID, good control of blood sugar in these patients can significantly reduce this risk.  The researchers reviewed findings from 158 studies that included more that 270,000 participants from all over the world to determine how COVID affects people living with diabetes.  Eating nuts linked to lower risk of colon cancer Seoul National University College of Medicine (Korea), May 6, 2022 Eating nuts has been linked to a number of health benefits, such as a reduced risk of obesity, diabetes and heart disease. Now, new findings from South Korea suggest that a nut-rich diet may also reduce a person's risk of colon cancer.  The researchers found a reduction in this risk for both men and women. Eating a serving of nuts three or more times a week appeared to have a big effect on risk. In the study, a serving of nuts was considered to be 15 grams (0.5 ounces). That's a smaller amount than what's considered a serving in the United States (A serving in the U.S. is 28 g, or 1 oz.) Although the researchers included many types of nuts in their analysis, peanuts were the most widely consumed nuts among people in the study. This may be due to the availability of peanuts in South Korea, the researchers said. The researchers found that men who reported eating three or more servings of nuts a week had a 69 percent lower risk of colon cancer than those who reported eating no nuts. Women who ate three or more servings had an 81 percent lower risk than those who ate no nuts, according to the study. Nicotinamide riboside repairs features of Alzheimer's disease NIH's National Institute on Aging, May 6, 2022 Researchers have found that an NAD+ precursor helped mice with features of Alzheimer's disease perform better on learning and memory tests… The brain's usual DNA repair activity is impaired in Alzheimer's disease, leading to inflammation and dysfunction. A compound that the brain needs to regulate DNA repair and other key signalling pathways is known as nicotinamide adenine dinucleotide (NAD+). Because NAD+ declines with age, scientists have wondered whether boosting the level of NAD+ could help ageing brain cells (neurons) to function better. One way to increase the cellular level is by giving an NAD+ precursor compound, such as nicotinamide riboside (NR). NR is a form of vitamin B3. The team found that the NR-treated mice had less DNA damage, lower levels of neuron damage and death, increased production of new neurons, and lower brain inflammation than control mice. Mice who received NR had reduced tau in their brains, too, but amyloid-beta levels were unchanged. The NR-treated mice performed better than control mice on many learning and memory tests, such as a water maze. In addition, NR-treated mice had better muscle strength and endurance than controls. The research team also tested human cells from people with and without Alzheimer's disease. As in the mouse studies, NR decreased DNA damage in the cells from people with Alzheimer's. Videos: 1. Sensational Charge Against Global Pharma Lobby, Government Hints At Vax Lobby Role In W.H.O Report (4:55) 2. ‘Zelensky is a puppet'; Col. Douglas Macgregor upsets Fox host. (2:18) 3. The Clinton & Gates Foundation were brokers for Big Pharma (4:43)

Recorded  May 9, 2022If there is one thing I got from this episode is that adulthood involves navigating a lot of anxiety producing situations and that it would have been nice to have invited a therapist on the episode to describe healthy ways to address the issues we unearthed. Ok that was two things but they are important take-aways from this show.  With May being Mental Health month, it's a good time to acknowledge any fears that are negatively impacting our daily lives and dedicate some time working toward overcoming them. That said, we still had a laugh-out-loud good time revealing our more light-hearted but very real fears. Join us!Please support our podcast:Please rate/review, subscribe and share!!Shop: Etsy storeCashapp Tip Jar: $GirrrlPodcastDonate: PatreonHave a question or topic you want us to talk about? We want to hear from you!!Twitter: @girrrlpodcastInstagram: @girrrlpodcastFacebook: @girrrlpodcastEmail us: Talk2Us@girrrlpodcast.com

Congrats to everyone who did #Sprint4Syngap.  Thanks to Stoke for joining! https://twitter.com/StokeTx/status/1523651977594703872 WEBINAR: This Thursday May 12, 2022 join us for the Webinar with #Syngap Grandparent and USC Law Professor, Richard Peterson.  Register at https://syngap.fund/IDEA  STUDY: Have you signed up for the Eye Tracking study yet? https://syngap.fund/eyetrack  TWITTER: Here is the thread on Praxis: https://twitter.com/cureSYNGAP1/status/1521852433713950721  GETA: Conference, sign up to hear Ingrid & Steve: https://www.eventbrite.com.au/e/geta-2022-sydney-tickets-302049868287  MICE: Help us Make 2!  https://syngap.fund/2mice RESEARCH: Ben talking about his SYNGAP1 work: https://www.youtube.com/watch?v=U6Z4UDYgGi4  EVENTS: - June 11 in Philly - Support our team https://syngap.fund/srfmdbr22  - June 25 in DFW - Join us for a family meeting and hear from Dr. Perry - October 8 in NJ - Caren Leib Gala https://www.syngapresearchfund.org/get-involved/fundraising/caren-leib-gala - October 8 in SC - Scramble for SYNGAP https://www.syngapresearchfund.org/get-involved/fundraising/scramble-for-syngap  - November 12 in GA - Sparks of Hope Gala https://www.syngapresearchfund.org/get-involved/fundraising/syngap-soiree  - December 1 in TN - Syngap Science Meeting - Stay tuned   EVERYONE SHOULD SIGN UP FOR CIITIZEN ASAP: https://www.ciitizen.com/syngap1/  This is a podcast: subscribe to and rate this 10 minute #podcast #SYNGAP10 here https://www.syngapresearchfund.org/syngap10-podcast  Apple podcasts: https://podcasts.apple.com/us/podcast/syngap10-weekly-10-minute-updates-on-syngap1-video/id1560389818    Episode 59 of #Syngap10 - May 9, 2022 #F78A1 #Syngap #epilepsy #autism #intellectualdisability #id #anxiety #raredisease #epilepsyawareness #autismawareness #rarediseaseresearch #SynGAPResearchFund #CareAboutRare #PatientAdvocacy #GCchat #Neurology 

Comedian Atsuko Okatsuka and Emma get overrun by mice, meet a fancy cat and finally untangle the mystery of the Rat King. With guests Dr. Bobby Corrigan, Cameron Jay, and Lynzie Rogers.