Podcasts about T2

World Golf Hall of Fame member Nancy Lopez begins her story growing up and learning the game under the watchful eye of her father in Roswell, New Mexico. She had astounding success as a junior player winning her state's amateur title as a 12, 13 and 14-year-old. Nancy played on the boy's team in high school after successfully challenging an arcane rule that stood in her way. She won the U.S. Girls Junior, the Women's Western Junior 3 times and, competed in the Women's U.S. Open twice (with a T2 as Low Am in 1975) all before starting college. She was an All-American at Tulsa, the Women's collegiate champion, a Curtis Cup Team member (meeting the Queen) and won the Women's Western Amateur before deciding to turn professional after two years of college. Nancy finishes this episode reflecting on a couple of her near-misses in the Women's U.S. Open including her tough loss to Alison Nicholas in 1997. Nancy Lopez begins her life story, "FORE the Good of the Game."

Charlie and T2 discuss a story about a little girl attacked by a raccoon. Charlie tells T2 a story about his brother who was bitten by a rabid fox. Charlie talks about a sheep dog that was attacked by a pack of 12 coyote. The sheep dog took out 8 of them before they ran off.  Another case of refusal to provide services to same sex marriages.

Charlie discusses the twitter files dropped by Elon Musk. Charlie discusses the advanced weaponry sent to Ukraine from the US. Charlie and T2 discuss a recipe of eggnog that calls for Hellman's mayonnaise.  

Charlie and T2 discuss a story about a little girl attacked by a raccoon. Charlie tells T2 a story about his brother who was bitten by a rabid fox.

Charlie and T2 discuss Super cars that are now cheap due to inflation. 

Charlie and T2 discuss Super cars that are now cheap due to inflation. Gavin Newsome has mad a new promise to his subjects in California. Charlie talks about Hunters laptop scandal and a story of a woman who shut off another's ventilator at the hospital.

“Lies for Power” “Federal Business” “Canceling Mr. Rogers” “Christmas Tradition with T2”

【S6E4-VOL131】花絮2：现在的T2环境怎么了？

Drew McKissick joins the show to talk to Charlie about Current events. Charlie talks about weird superstitions with T2. Charlie talks about Elon Musk's fight against twitter bots. He discusses random deaths around the country.

Charlie discusses the possibility of Nicki Haley running for president. Charlie and T2 talk about a study that show Toyotas at the top of the list for high mileage cars. Charlie discusses the left's obsession with eating bugs.

Charlie and T2 talk the end of Thanksgiving and the start of Christmas. Charlie talks about upcoming company layoffs. 

「SIRUI、フルサイズアナモルフィックレンズやアクセサリーなど8製品発売」　SIRUIは、「35mm T2.9 1.6×フルサイズアナモルフィックレンズ」、「100mm T2.9 1.6×フルサイズアナモルフィックレンズ」、「1.25x アナモルフィック アダプター」、マルチファンクション一脚、三脚、LEDビデオライト、Bi-Color Soft LEDパネル、LEDチューブライトを2023年1月上旬に発売する。ラインアップと希望小売価格は以下の通り。

Charlie and T2 talk the end of Thanksgiving and the start of Christmas. Charlie talks about upcoming company layoffs. Charlie talks about the impact of Unions and the keystone pipeline.

Tara and Lea discuss the feud between Elon Musk and the radical left. Tara and T2 talk about near car accidents they have experienced.

Charlie talks about the left's reaction to Elon Musk's recent moves with his Twitter Company. Charlie reports a story of a man who pulled a gun in the middle of a Monopoly game over the recent Holiday. Charlie and T2 discuss board games they like to play. Charlie discusses Klaus Schwab, the World Economic Forum and the agenda of the Elite.

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.11.29.518330v1?rss=1 Authors: Casella, C., Vecchiato, K., Cromb, D., Guo, Y., Winkler, A. M., Hughes, E., Dillon, L., Green, E., Colford, K., Egloff, A., Siddiqui, A., Price, A., Cordero Grande, L., Wood, T. C., Malik, S., Teixeira, R. P. A. G., Carmichael, D. W., O'Muircheartaigh, J. Abstract: Our current understanding of focal epilepsy is evolving as increasing evidence suggests that tissue abnormalities may extend beyond the focus. In adults, widespread structural changes remote from the epileptic focus have been demonstrated with MRI, predominantly using morphological markers. However, the underlying pathophysiology of these changes is unclear, and it is not known whether these result from ongoing disease processes or treatment-related side-effects, or whether they emerge earlier. Few studies have focused on children, who typically have shorter disease duration. Fewer still have utilised quantitative MRI, which may provide a more sensitive and interpretable measure of tissue microstructural changes. In this study, we aimed to determine if there were common spatial modes of changes in cortical architecture in children with drug-resistant focal epilepsy, and secondarily if changes were related to disease severity. To assess cortical microstructure, quantitative T1 and T2 relaxometry (qT1 and qT2) was measured in 89 children - 43 with drug-resistant focal epilepsy [age-range=4-18 years] and 46 healthy controls [age-range=2-18 years]. We assessed depth-dependent qT1 and qT2 values across the cortex, as well as their gradient of change across cortical depths. As a post-hoc analysis, we determined whether global changes seen in group analyses were driven by focal pathologies in individual patients. Finally, we trained a classifier using qT1 and qT2 gradient maps from patients with radiologically-defined abnormalities (MRI-positive) and healthy controls, and tested if this could classify patients without reported radiological abnormalities (MRI-negative). We detected depth-dependent qT1 and qT2 increases in widespread cortical areas, likely representing loss of structure such as altered cortical stratification, gliosis, myelin and iron alterations, oedema-associated increases in free-water, or a combination of these. Changes did not correlate with disease severity measures, suggesting they may appear during cerebral development and represent antecedent neurobiological alterations. Using a classifier trained with MRI-positive patients and controls, sensitivity was 62% at 100% specificity on held-out MRI-negative patients and controls. Our findings suggest the presence of a potential imaging endophenotype of focal epilepsy, detectable irrespective of radiologically-identified abnormalities, and possibly evident at a pre-symptomatic disease stage. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Charlie discusses the weird similarities between Balenciaga and minor attracted people, how ad photography works. Charlie talks about the mainstream media, how they use sex to sell products. Charlie and T2 talk about people who die using everyday Tech.

Charlie and T2 discuss their favorite old TV show themes

Charlie and T2 discuss their Thanksgiving Day and Holiday decorations. Covid is back in China. China has begun lockdowns again in reaction to the latest Covid outbreak. Charlie talks about the elite agenda to replace the American Dollar with digital currency.

Charlie talks about a story about liberals justifying transgenderism because most gender individuals were abused as children. Charlie and T2 discuss their favorite old TV show themes. Charlie explains to Tim what he missed on the Macy's Day Parade.

Last week Bill and I were getting geared up for El Tour de Tucson and Ironman Arizona. Today we are going to give a first-hand report on the pro races at Ironman Arizona and do a recap of El Tour de Tucson.   Show Sponsor: UCAN Generation UCAN has a full line of nutrition products to fuel your sport. UCAN uses SuperStarch instead of simple sugars and stimulants to fuel athletes.  UCAN keeps blood sugar steady compared to the energy spikes and crashes of sugar-based products. UCAN also has hydration products focused on giving you the sodium you need when hydrating, including several clean and light flavors. Steady energy equals sustained performance and a faster finish line!   Use UCAN in your training and racing to fuel the healthy way, finish stronger and recover more quickly!  Use the code 303UCAN for 20% off at ucan.co/discount/303UCAN/ or ucan.co   In Today's Show Feature Discussion IM Race Mistakes and How to Avoid Them Endurance News Ironman Arizona Race Report El Tour de Tucson Recap What's new in the 303 How to Prepare Your Bike to Travel   Feature Discussion: IM Race Mistakes & How to Avoid Them Swim DNF: At IMAZ Sunday, approximately 150 athletes DNFd during the swim. The most common cause seemed to be hypothermia or simply being too uncomfortable in cold water to push through. The water temperature was a cool 60.8 degrees (mandatory wetsuit) and I admit that's approaching my limit for comfort.   Tips to Avoid Swim DNF: Be a good swimmer. If you are swimming the Ironman distance you should be swimming at least 10K per week and preferably 15-20K. Your longest swim should be around 5K (longer than the 4.2K of IM). Cold water exposure in the two weeks leading up to the race. This can be ice baths at home or properly supported cold open water with or without wetsuit as appropriate to be exposed to very cold water. Have a good fitting long-sleeve wetsuit with a 5mm or thermal jersey Neoprene cap that fits snugly but doesn't constrict airway (optional double cap) Booties allowed at 65 degrees or colder Vaseline for your face   Bike: The two issues I observed this weekend were mounting and mechanical. Since this was Ironman and most people have their shoes on coming out of the changing tent, not to mention the soft grass surface of the transition area, most do not have the flying mount problem where you can't get your feet in the already clipped in shoes. Most of the near collisions were due to athletes still feeling wobbles from the swim.   One guy had his chain get caught I his rear derailer and he nearly made it worse by trying to ride on it.   Another had a flat the moment he rode out of T1. He had replaced his perfectly fine tubes with brand new ones the day before the race and apparently pinch flatted them. Billy and I helped him fix his flat. Shame.   Tips to Avoid a Bike Mount Disaster: Practice mounts and dismounts Practice change tubes Shake out the bike setup at bike check in If when an issue arises, take a deep breath and slow down   Run: Chaffing - avoidable by using anti chaffing products, testing what you will be wearing on race day during race rehearsals and changing into clean and dry run gear in T2. Dehydration - having practiced your nutrition several times before showing up on race day   News Sponsor Buddy Insurance: Buddy Insurance gives you peace of mind to enjoy your training and racing to the fullest. Buddy's mission is simple, to help people fearlessly enjoy an active and outdoor lifestyle.    Get on-demand accident insurance just in case the unexpected happens. Buddy ensures you have cash for bills fast.  Go to buddyinsurance.com and create an account.  There's no commitment or charge to create one.  Once you have an account created, it's a snap to open your phone and in a couple clicks have coverage for the day.  Check it out!   Endurance News: El Tour de Tucson and Its Dual Personality in the Desert By Bill Plock   November 22, 2022, Tucson: El Tour de Tucson circled the fragile ecosystems surrounding Tucson where Saguaro cacti come to life, thirsty rivers cut the desert, and dreamers come to dream. For thousands of years, people have thrived in this at-first-glance difficult environment. Its dry and hot reputation, while well deserved in summer hibernates in November and offers the perfect weather to ride or race.  It's this dual purpose that gives this tour a dual personality and makes it unique.   Top racers from around the country (the world really) converge in the desert to compete. Riders can qualify for Platinum status to give them a more favorable starting position and a better shot at winning Tissot watches—no monetary prizes.  Riders choose 32, 63, or 102 miles. Said ride director TJ Juskiewicz, about 500 race and the other 7,000 enjoy a well-supported tour.   The logistics of closing roads and controlling intersections for 7,500 riders to ride or race so many miles during most of the day in a big city is incredible. The winner in the 102-mile race was able to average almost 27 mph thanks to top-notch police support. I took about twice as long and received the same support.   I chose to chat as I do, meet some folks and not bonk on undertrained legs and lungs! I made it in part thanks to my podcast partner and close friend, Rich Soares who pulled me more than I pulled him, by a lot! This tour showcased so many personal missions. Whether it was the couple recently married on their honeymoon ride. Or 7-year-old Ariana who rode all 102 miles in about seven and half hours and set a record as the youngest known person to ride a century. Or, Timothy from the Pueblo Road Warrior team (supported by We Ride 4) rocked the 102 miles in his tennis shoes and smiled the whole way.   The vibe oozes a recipe of seriousness, fun, and gratefulness. The contrast of colorful cyclists streaming through the desert, pecan farms, airplane graveyards, and adobe buildings on sleepy streets made the time pass fast. Aid stations all featured friendly bike valets to hold your bike. Kids from the Optimist club or the Boy Scouts or many other local groups smiled big and made us feel very welcomed. Said Rich Soares, “The volunteers were great ambassadors of Tucson and the friendly bike valets were a nice touch and surprise”   That feeling of gratefulness is not an accident. Said Juskiewicz, “We gave away 550 free bikes to kids and our 50+ non-profit partners raised over $5,000,000 for their charities through the  El Tour partnership.”   Coloradans were all over the place. Executive Director of Team Evergreen, Jen Barbour won her age group, and Pete Piccolo, Executive Director of Bicycle Colorado was 22nd overall in a very competitive field that included Primal Ambassador and Tour de France star Jens Voigt who finished 53rd. Other ex-pro's like George Hincapie, Bob Roll, and Christian VandeVelde joined in the fun and said Juskiewicz, “having the rock star pros there was something that took this year over the top.”   Maybe this tour reflects the native Saguaro cactus more than we know. It takes 75 years for Saguaros to grow “arms” to help for better reproduction and continue to flourish and spread more seeds. They stand tall in the desert and have supported human life for thousands of years.  Less than one in a million seeds germinate for this defining plant only found in this area.   As this tour ages and grows, it attracts more and more cyclists and helps more and more people. Its arms are dreams and a safe harbor for so many charities raising money to spread more seeds and help humanity. As a late-season destination, a challenging well-run ride, a trip to Tucson makes for a nice warm-up to enjoy Thanksgiving week and reflect on what's important.   IRONMAN Arizona 2022 - Pro Race, Age Group Kona Slots, Observations There were reasons to be excited about this pro race. On the women's side you had Sarah True, Skye Moench, Lauren Brandon, Melanie McQuade and others. On the men's side you had 70.3 World Champs 2nd place Ben Kanute taking his first swipe at the full distance. Familiar names like Sam Long, Matt Hansen, Joe Skipper and Bart Aernouts.   Pro Women: Lauren Brandon, Sarah True and Skye Moench were 1, 2 and 3 out of the water. Skye would take Sarah's spot at mile 28. By mile 66 Laruen Brandon dropped back to 3rd with Skye leading the way and Sarah just biding her time. Skye entered T2 about 3 minutes before Sara True and Lauren Branden arrived 2 minutes later. About a mile into the run, Sarah True took the front and held that position the rest of the run. By mile 8, Melanie McQuaid moved up to 3rd, but she would fall back to 6th by then finish. At mile 14 they came through and I was giving the pro women splits. Sarah True held on to 1st, Skye Moench held on to 2nd and Daniel Lewis would finish 3rd.   Pro Men: Andrew Hosfall-Turner was first out of the water with Ben Kanute on his heels. By mile 30, Ben Kanute was in control with Joe Skipper in 3rd, Matt Hanson in 5th and Sam Long in 7th. Billy Edwards and I saw them come through and called out splits. At T2 it was Kristian Hogenhaug in first, followed by Joe Skipper in 2nd, Ben Kanute in 3rd, Sam Long in 4th and Matt Hanson in 5th. My mile 5, Matt has passed Sam and swapped positions. By mile 12 Joe Skipper and Hogenhaug swap positions. Hogenhaug blows at mile 23 and it's now the podium of Joe Skipper Matt Hansen and Ben Kanute in that order.   What's New in the 303: Leaving On A Jet Plane: How To Travel With Your Bike Article and photos by: A.V. Schmit   With the major airlines removing the draconian fees associated with flying with a bike, you may be tempted to bring your bike with you on your next vacation. Passengers on American, United and Delta will pay the same amount for a bike as they would for any other piece of checked luggage under 50 pounds — about $30. That's a far cry from the $150 each way to fly with a bike, only a years ago.   International flights typically offer two checked bags per passenger with no additional cost, so the idea of traveling for an international IRONMAN or IM 70.3 is a lot more approachable. And… If you plan on racing, having the bike you trained with is an essential part of being successful.   “Woot, woot, I can travel with my bike,” they thought, until they realized, “Oh wait, I don't know how to pack my bike for travel.”   Fear not, I can show you some pretty simple techniques to keep your “baby” safe on a plane.   If you are my age, I'm sure you remember the 1970's American Tourister luggage commercial with the Gorilla. And if you don't recall, here it is on YouTube:   The point is… baggage handlers typically tend to be a lot less careful than you might want them to be with your bike. So you need to take steps to prepare your bike for travel the best that you can.   For airline travel, there are really two basic categories of luggage to carry a bike — Padded soft case or hard plastic case. Both have their advantages and disadvantages. With a padded soft case, you typically have to disassemble less of the bike, especially on a triathlon bike. But a soft case does not offer as much protection as a rigid case.   With a rigid bike case, your bike has more protection, but more of it needs to be disassembled to fit. A rigid hard case does offer more protection than a padded soft case. In the event of a catastrophic situation, like a very heavy piece of luggage falling from a height or the bike case falling off the luggage carrier, either event will likely damage the bike contained within either type of case.   Sci-Con TSA 3.0 Triathlon Travel Bag " Trico Iron Case Left, Sci-Con Aerocomfort TSA 3.0 Triathlon Travel Bag. Right, Trico Iron Case.   OK, onto packing a bike for travel. In this example I'm packing a Cervelo P5 three in a Sci-Con Aerocomfort 3.0 padded triathlon bag.   Step 1 – Remove the pedals, and wipe the grease off the spindles with a paper towel or shop rag. Don't worry, we are going to pack a bit of bike grease for re-assembly when we get to our destination. I tend not to want to travel with a full tube of grease, rather I like to squirt a small blob into a heavy-duty zip lock bag. It's lighter, and you are less likely to run afoul of any hazardous chemical limits.   Step 2 — Remove bottle cages and other accessories. Wrap them in bubble wrap for protection and storage later in the process. And, while you're at it, remove any CO2  cartridges, as compressed gas of any kind is not allowed on a plane. Be sure to get replacements at your travel destination.   Bottle cages, pedals and rear derailleur ready for removal and padding.   Step 3 — If you don't have access to a bike stand, then it makes the most sense to remove the wheels from the bike and use the alloy cradle of the bag to support the bike for the rest of the procedure. A P5, as well as many tri-bike frames, has horizontal drop outs, so you will need to slide the rear end of the bike into the Frame Defender Armature and then use the quick release at the front to secure the forks.   If your bike uses thru axles, you will need them to secure the bike frame to the armature.   Step 4 — At this point, I like to wrap the frame in closed cell foam to protect the finish from accidental chips or dings. With the popularity of online shopping, you probably have some thin closed cell foam hanging around the house. If not, you might stop by your local bike store to see if they have any leftover foam packing material from in-bound bike shipments. You can also use “bubble wrap,” but I've found it to be less effective than closed-cell foam.   Step 5 — Since the advent of 11-speed drive trains, virtually all road / triathlon groupsets have a “master link” in their chains. A master link is a special link that uses a mechanical connection to connect the chain. With a simple pair of specialized pliers, it's easy to remove the chain and package it in bubble wrap.   While many boxes and bags make chain removal optional. It's my thinking the more you can do to protect the frame from damage, the better. A chain moving around inside a bag or box can really do a number on your bike's paint. Just take it off.   Step 6 — Remove the rear derailleur. On a Shimano Di2 or SRAM AXS, this is a very straightforward procedure. For Di2 you simply unplug the E-Tube wire and use a hex wrench to remove the derailleur. On a SRAM system, simple use a hex wrench and remove the rear derailleur. It is advisable to remove the battery in the case of SRAM AXS as well, prior to placing it in a zip-lock bag and bubble wrapping it.   For Di2, just make sure the shifters and the battery are disconnected to prevent accidental “shifting” during travel from draining your battery.   For a traditional mechanical derailleur, remove the mounting bolt with the appropriate hex wrench, wrap the derailleur in bubble wrap and tuck it in-between the chain stays and secure it. Be careful not to kink the cable housing.   Step 7 — Remove the quick release skewers from the wheels and place them in the pockets on the left and right side of the bag.   If your bike uses disc brakes, it's recommended that you remove them prior to packing the bike. I know, it's a pain, but so is a slightly bent disc that is rubbing as the wheel rotates. Most disc wheels are either 6-bolt or center-lock.   If your wheels are 6-bolt, you will likely need a T25 Torx wrench to remove and reinstall them at your destination. And if it is 6-bolt, you may want to bring a few extra bolts just in case 1 or 2 of the T25 heads get stripped during the process.   If your wheels use center-locks, be sure to pack the tools you will need to get them back on.   Step 8 — After you have removed the pedals, chain, rear derailleur, water bottle cages and accessories. Wrap them carefully in bubble wrap and place them in the storage bag that will be placed under the down tup of the frame and secure the bag. This is also a great place to stow the tools you will need to put the bike back together when you arrive at your destination.   Step 9 — Add additional padding to delicate parts of the bike, including the shifters mounted on the aero extensions.  Insert the wheels into the pockets on the left and right of the bag. Be sure to remove your skewers and wrap them in bubble wrap before you stow them in the bag.   Secure the Velcro and other straps and prepare to close the bag. Before you do, it is a good idea to take some pictures of your packing job so there is no question about how the bike was packed in the event there is an incident during travel.   Step 10 — BONUS — If you use an iPhone, then I would highly recommend you place an Apple AirTag somewhere in the bag. This gives you extra piece of mind that your bike has made it on the plane safely. An AirTag is a blue tooth device that can use the location data of any iPhone it encounters to pinpoint the position of your bike.   Your bike arrives in tact, you've taken the time to put it back together and now it's time to rack it and race the next day.   Video of the week: Skip This Week   Closing: Thanks again for listening in this week.  Please be sure to follow us @303endurance and of course go to iTunes and give us a rating and a comment.  We'd really appreciate it! Stay tuned, train informed, and enjoy the endurance journey!

Welcome back to another fantastic episode of the just Spitballin Podcast! We have a fun episode! Paul recap his trip to New York to visit the spitballers we have there! Second topic and the third topic is One Piece related. So be SPOILERS AHEAD! Timestamps: T1: 1:05, T2:39:07 T3: 1:00:00 If you like what you hear be sure to Follow our social media: Facebook: Just lol Spitballin Ent. Twitch:JSE4GAMING. Twitter: @JSpitballin Instagram: justspitballin_ent YouTube: Just Spitballin --- This episode is sponsored by · Anchor: The easiest way to make a podcast. https://anchor.fm/app

Charlie tells T2 the price of a turkey dinner at K Mart in the 1970's. He discusses crypto and random shootings around the country. God not the Government gives our rights to us. Charlie explains this to his listeners. The Biden administration shares talking points with their followers for this year's holidays. Charlie discusses ad agencies who advertised questionable content.

Gheobhaidh na mílte dalta ar fud na tíre torthaí an Teastas Sóisearaigh inniu. Seo an chéad uair an múnla nua T1 agus T2 bheith dá mheas i gcás na Gaeilge.

Charlie and T2 talk about thanksgiving and anxiously anticipate one of the greatest holidays of the year. 

Charlie and T2 talk about thanksgiving and anxiously anticipate one of the greatest holidays of the year. Charlie talks about things in our country's history that we should be thankful for. Charlie talks about the run off in Georgia how Raphael Warnock has conducted business in the past.

Charlie and T2 discuss foods they would give up for thanks giving. Charlie discusses the mentality of mass shooters; if they are what the left deem them to be.

Charlie and T2 talk Black Friday stories. We encourage all to be mindful and respectful to others who may be shopping on Friday. Charlie and T2 discuss a story about Jack Daniels suing a dog's chew toy company.

The secret to personal development lies in your ability to become self aware. T2 are notorious for their Human Iceberg model. In this video Martin Johnson and Spencer Locker talk through the three layers of self awareness. --- Send in a voice message: https://anchor.fm/martin-johnson3/message

Charlie and T2 discuss the radical left how they have no one and nothing to be thankful for. TRUMP IS BACK on Twitter. Charlie discusses the hypocrisy of the radical left how they are losing their minds over Trumps return to Twitter.

Simply Bitcoin Podcast Host Nico Muran joins the show to Charlie about how crypto currency and Bitcoin works. Caller Paul from Inman joins the show to ask Charlie if real homesteaders can run the government. Charlie and T2 discuss the types of razors they use to shave with.

Our special guest will be 36 year veteran from TROY FD Battalion Chief Tom Miter. His sons Justin and Jeremy Miter, are also members of the Troy Fire Department. Prior to being hired as a Firefighter during his high school days Tom was a wheel washer at Station 2 for many years. In 1986 He began working as a firefighter going to E5, M2, M3, and then back to E5. He was promoted to LIEUT 1994 working in T1 and T2. He was promoted to CAPT. June 1998. He left on deployment in the Air national Guard twice in 2002 and 2004 to Iraq. After returning he was promoted to BATT. CHIEF JULY 2015. he just retired in 2022. Tom was a past executive board member of the Troy Uniformed Firefighters Association Local 86. He has been to many memorable jobs over the years, been a teacher of leadership and mentoring skills, and has maybe pissed of a chief or two...maybe my kind of guy ;) ...You don't want to miss this one. You can also Listen to our podcast ...we are on all the players #Troy #GOAT #lovethisjob #givebackmorethanyoutake www.youtube.com/gettinsaltyexperience---Connect with Us---OUR MERCH WEBSITE : https://gettinsaltyapparel.com/INSTAGRAM: https://www.instagram.com/saltydoginc/FACEBOOK: https://www.facebook.com/gettinsaltyapparelTWITTER: https://twitter.com/saltydogapparelSPOTIFY: https://open.spotify.com/show/4QSZ6kGOIXa3YuqHv8m0FuSPREAKER: https://www.spreaker.com/show/gettin-salty-experience-podcastAPPLE PODCAST : https://podcasts.apple.com/us/podcast/gettin-salty-experience-podcast/id1497426893

Go online to PeerView.com/MKN860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. Eosinophilic esophagitis (EoE) is an increasingly prevalent, chronic, T2 inflammatory disease triggered by food and/or environmental allergens. Due to underlying tissue inflammation, patients suffer diminished quality of life due to symptoms such as weight loss, difficulty swallowing, and heartburn. Patients can experience these symptoms for a long time before receiving a proper diagnosis. Once diagnosed, treatment options have historically been limited. Fortunately, therapies that treat other type 2 disorders are in development or are approved to treat EoE. At a recent live event, experts used patient cases to discuss the diagnosis, underlying causes, and the newest treatments for EoE, including biologic therapies. Watch this on-demand version now! Upon completion of this activity, participants should be better able to: Distinguish signs and symptoms of eosinophilic esophagitis (EoE) among children and adults to enable an earlier diagnosis and minimize complications due to uncontrolled disease; Recognize underlying mechanisms of EoE, including the role of key cytokines such as interleukins -4, -13, and -5 as drivers of type 2 inflammation and how this relates to emerging treatment; and Apply the latest expert recommendations and clinical evidence to the treatment of patients with EoE, particularly as novel and emerging agents become available.

On Episode 22 of the Stroke Alert Podcast, host Dr. Negar Asdaghi highlights two articles from the November 2022 issue of Stroke: “Estimating Perfusion Deficits in Acute Stroke Patients Without Perfusion Imaging” and “Five-Year Results of Coronary Artery Bypass Grafting With or Without Carotid Endarterectomy in Patients With Asymptomatic Carotid Artery Stenosis.” She also interviews Dr. George Ntaios about his article “Incidence of Stroke in Randomized Trials of COVID-19 Therapeutics.” Dr. Negar Asdaghi:         Let's start with some questions. 1) What is the actual incidence of stroke after COVID-19? 2) In the setting of acute ischemic stroke, can the volume of ischemic penumbra be estimated with just a regular MRI study of the brain without any vascular or perfusion imaging? 3) And finally, can a patient with significant carotid stenosis go through coronary artery bypass graft surgery? We're back here to answer these questions and bring us up to date with the latest in the world of cerebrovascular disorders. You're listening to the Stroke Alert Podcast, and this is the best in Stroke. Stay with us. Welcome back to another issue of the Stroke Alert Podcast. My name is Negar Asdaghi. I'm an Associate Professor of Neurology at the University of Miami Miller School of Medicine and your host for the monthly Stroke Alert Podcast. The November issue of Stroke is packed with a range of really exciting and exceedingly timely articles. As part of our Original Contributions in this issue of the journal, we have a post hoc analysis of the Treat Stroke to Target, or the TST, randomized trial by Dr. Pierre Amarenco and colleagues. We've talked about this trial in our past podcast, and the main study results that were published in New England Journal of Medicine in January of 2020. TST randomized patients with a recent stroke or TIA to either a low target of LDL cholesterol of less than 70 milligram per deciliter or a target LDL of 90 to 110. The main study showed that the low LDL target group had a significantly lower risk of subsequent cardiovascular events without increasing the risk of hemorrhagic stroke. So, from this, we know that achieving a low target LDL is possible and is actually better than the LDL target of 90 to 110 post-stroke. But in the new paper, in this issue of the journal, in a post hoc analysis of the trial, the TST investigators showed that it's not just achieving that magic low target LDL of less than 70 that's important in a reduction of cerebrovascular disorders, but it's also how we achieve it that determines the future of vascular outcomes. So, in this analysis that compared patients on monostatin therapy to those treated with dual cholesterol-lowering agents, that would be a combination of statin and ezetimibe, and showed that in the low LDL target group, only those patients treated with dual therapy had a significant reduction of subsequent vascular events as compared to those in the higher LDL category. But the same was not true for patients on statin monotherapy, even though they had all achieved a low target LDL. Think about this for a moment. Both groups, whether on statin monotherapy or on dual anti-cholesterol treatments, achieved the same low target of LDL, but only those on dual therapy had a lower risk of subsequent vascular events as compared to those that were in the higher LDL target group. Very thought-provoking study. In a separate paper by Dr. Shin and colleagues out of Korea, we learned that survivors of tuberculosis, or TB, are at a significantly higher risk of ischemic stroke than their age- and risk factors–matched non-TB counterparts. The authors used data from the Korean National Health Insurance Services and studied over 200,000 cases diagnosed with TB between 2010 and 2017 and compared them to a pool of over one million non-TB cases for matching. And they found that the risk of ischemic stroke was 1.2 times greater among TB survivors compared to matched non-TB cases after adjusting for the usual confounders, health behavioral factors, and other comorbidities. Now, why would TB increase the risk of stroke? The authors talk about the pro-inflammatory state of this condition, thrombocytosis, that is a known complication of chronic TB amongst other putative and less clear mechanisms. But what is clear is that findings from a large-scale population-based cohort such as the current study support an independent association between TB and ischemic stroke. As always, I encourage you to review these papers in addition to listening to our podcast today. My guest on the podcast today, Dr. George Ntaios, joins me all the way from Greece to talk to us about the much discussed topic of the risk of stroke in the setting of COVID-19. Dr. Ntaios is the President of the Hellenic Stroke Organization and an experienced internist who has been fighting this pandemic in the front lines since the beginning. In an interview, he talks about his recently published paper, his experience, and the lessons learned on balancing scientific rigor against the urgency of COVID-19. But first, with these two articles. In the setting of a target vessel occlusion in patients presenting with an acute ischemic stroke, distinguishing the ischemic core from the ischemic penumbra is of outmost importance. The success of all of our reperfusion therapies heavily lies on our ability to differentiate between the tissue that is already dead, which would be the ischemic core, from the tissue that is not dead yet but is going to die unless revascularization is achieved. That is the ischemic penumbra. Over the past two to three decades, there's been lots of debate over how these entities of dead tissue versus going-to-die tissue are best defined, especially when we're making these distinctions under the pressure of time. We don't even agree on the best imaging modality to define them. Should we rely on CT-based imaging? Do we stop at CT, CT angiogram? Should we do single-phase CTA or multiphase CTA? When do we perform CT perfusion, and what perfusion parameters best define core and penumbra, or should we rely on MRI-based modalities altogether? These questions have all been asked and extensively studied, which is why, as a field, I think, we have at least some agreements today on the basics of core and penumbra definitions. And I also think that overall we are becoming better at doing less imaging to be able to predict tissue outcomes in real time. And there's definitely a growing interest in trying to estimate tissue fate based on a single-imaging modality. So, I think you're going to find an Original Contribution in this issue of the journal, titled "Estimating Perfusion Deficits in Acute Stroke Patients Without Perfusion Imaging," really interesting. In this paper, Dr. Richard Leigh from the National Institute of Neurological Disorders and Stroke, National Institutes of Health, in Bethesda and colleagues evaluated patients with acute ischemic stroke enrolled between 2013 to 2014 in the NINDS Natural History of Stroke study. A little bit about the study: It enrolled stroke patients presenting to three hospitals in Washington, DC, and Maryland with serial MRI scans during the acute and subacute time period after ischemic stroke. For this particular paper, they included patients who received MRI and perfusion-weighted imaging and included only those who were thrombolized. That was their way of ensuring that all patients in their study were in the hyperacute stage of stroke. They then looked at their MR imaging, specifically the fluid-attenuated inversion recovery, or FLAIR, images, for a presence of something called hyperintense vessels in the ischemic territory. Now, this is an audio-only podcast, so unless you're Googling FLAIR hyperintense vessels on MRI, to follow along, I have to take a bit of time explaining this entity. What do we mean by FLAIR hyperintense vessels? We are not just talking about the T2 hyperintense signal that's sometimes noticeable at the site of proximal occlusion. For example, in the setting of an M1 occlusion, we may be able to detect a T2 hyperintense signal at the site of M1 on FLAIR. That's not the point of this paper. The point is to look throughout the area supplied by that said target occlusion, in this case all of the MCA, and see whether there is hyperintense signal in all arteries in that potentially ischemic tissue and how the area delineated by these FLAIR hyperintense vessels could potentially correspond to the area of perfusion deficit on conventional perfusion imaging. It turns out that these hyperintense vessels actually map a pretty large area. So, this is the point of this study. The investigators developed a FLAIR hyperintense vessel scoring system and called it NIH, obviously, because this was a National Institutes of Health study, FHV, which stands for FLAIR hyperintense vessel, scoring system. And the score is based on presence of these hyperintense vessels in three vascular territories: ACA, MCA, or PCA. Now, seeing that MCA is a larger territory, they had to further divide it into four sub-regions: frontal, insular, temporal, and parietal. So, in total, we have six regions now. Each of them would get a score of zero if there were no hyperintense vessels in them, and a score of two if there were three or more FLAIR hyperintense vessels in a single slice, or if there were three or more slices that contained FLAIR hyperintense vessels. And, of course, a score of one would be anything in between. So, we have six regions in total, each maximum getting two points, to give us a composite score of maximum 12 for this scoring system. So, they wanted to see whether there's a correlation between the FLAIR hyperintense vessel score and the volume of perfusion deficits that is detected by conventional perfusion imaging, which is their main study result. But before we go there, it does seem like a lot of work to learn all these regions and count all these hyperintense vessels in these six regions and come up with an actual score. So, they had to do an interrater reliability to see how easy it is to score and how reliable are these scores. So, they had two independent reviewers for their study. On average, the scores of these two independent reviewers differed by one point for a κ of 0.31, which is quite a low interrater reliability. But when they looked at a more liberal way of assessing interrater reliability, where partial credit was given, when the raters were at least close in their scoring, the κ improved to 0.65 for a moderate degree of agreement. So, what that means is that it's not easy to learn the score, and potentially I can give a score and another colleague can give a different score. So, we have to keep that in mind. But I want to emphasize that in the field of stroke neurology, we are kind of used to these poor interrater reliability agreements in general. For example, the interrater reliability of the ASPECTS score, a score that is commonly used in our day-to-day practice, and especially in the acute phase, we communicate the extent of early ischemic changes by using the ASPECTS score, has a pretty poor interrater reliability, especially in the first few hours after the ischemic stroke. So, we can make due with a κ of 0.65. Now on to the results of this study. They had a total of 101 patients. Their median age was 73. The median FHV, which is that FLAIR hyperintense vessel score, in their entire cohort was four. And close to 80% of patients enrolled in their study had some perfusion abnormalities on their concurrent perfusion-weighted imaging. Now, briefly, they defined perfusion deficits as areas with delay in the relative time to peak map, or TTP maps, after applying a six-second threshold to these TTP maps. Of note, half of those patients with a perfusion deficit had a significant perfusion deficit, which meant that they had 15 cc or more of perfusion deficit. OK, now on to the main study results. Number one, the score obtained by NIH FLAIR hyperintense score highly correlated with the volume of perfusion deficit. In fact, every one point increase on the NIH-FHV score was approximately equal to 12 cc of perfusion deficit. That's a really useful way of thinking about this score. Each score translated in 12 cc of perfusion deficit. Number two, when they looked at the predictive ability of this score in predicting the presence of significant perfusion deficit, that is 15 cc or more of perfusion delay, the area under the curve was 0.9, which is quite high. This is quite reassuring that the FHV score was sensitive and specific in predicting the presence of significant perfusion deficit. Next finding, how does this score do in predicting a significant mismatch? They calculated mismatch ratio by dividing the perfusion volume to that of ischemic core as measured by diffusion volume as it's done conventionally, and then did the same for the score with the exception that instead of using the perfusion volume, they actually used this score and divided it by diffusion volume. And it turns out that FLAIR hyperintense mismatch ratio had a strong predictive capability in predicting the mismatch ratio of 1.8. So, in summary, if this score is validated in larger studies, it can potentially be used as a quick and dirty way of calculating the amount of perfusion deficit in the setting of target vessel occlusion. And, of course, it can also be used as a predictive way of presence of significant perfusion deficit, which is perfusion deficit of over 15 cc. This is all without the need to do actual perfusion imaging. Now, all we've got to do is to get comfortable with this scoring system and, of course, be able to multiply it by 12 to give us a quick guesstimate of the perfusion volume. And one final word on this is that I think the future of stroke imaging is not in doing more images, but to be able to extract more information from less imaging in the acute setting. Stroke physicians were frequently consulted to see patients that are scheduled to undergo coronary artery bypass graft surgery, or CABG. The stroke consult would be for the optimal perioperative management of an often incidentally found carotid disease. Now, why do I say we were frequently consulted? Because at least anecdotally in my own practice, I feel that over the past decade, the number of these consults has substantially reduced. Why is that? Well, let's dive into this topic and review some of the literature. First off, around 40% of patients who have active coronary artery disease and are scheduled to undergo CABG have concurrent carotid disease, and about 10% of CABG patients have evidence of hemodynamically significant carotid disease. And seeing that the risk factors for coronary artery disease are similar to those causing carotid disease, these high percentages are not surprising at all. But the question to ask is, can we put a patient with significant carotid disease through cardiac surgery? What is the perioperative risk of stroke in this situation? And importantly, should the carotid disease be surgically treated during carotid surgery? This is referred to as synchronous carotid endarterectomy, or CEA plus CABG. Or the carotid disease should be treated either surgically or endovascularly before CABG? We refer to this as staged carotid surgery or post-CABG. This is known as reverse staged carotid surgery. All of these questions are asked from the stroke physicians in that consult, and, like many of you, I have struggled to find the evidence to answer some of them. So, let's briefly review some of the current literature on this topic. The CABACS trial, the acronym stands for the Coronary Artery Bypass Graft Surgery in Patients With Asymptomatic Carotid Stenosis, was a randomized controlled trial that included patients undergoing CABG who are found, exactly like that consult, to have an asymptomatic carotid disease of equal or greater than 70% stenosis. The carotid disease for this trial had to be amenable to carotid endarterectomy, or CEA, and the patients were randomized to either receive synchronous CEA plus CABG or just go through with the CABG alone. The trial started in 2010 and planned to enroll over a thousand patients, but was stopped, unfortunately, prematurely in 2014 due to slow recruitment and withdrawal of funding after only 129 patients were enrolled from 17 centers in Germany and Czech Republic. The original study was published in this journal in 2017. So, what did it find? In their intention-to-treat analysis, the primary outcome of any stroke or death at 30 days was 18% in patients receiving synchronous CEA plus CABG as compared to only 9% in patients receiving isolated CABG. Ouch, a double risk of stroke in those who had concurrent surgical treatment of their carotid disease in addition to CABG. Now, this was an underpowered study, and the results should be understood in that context, but it really didn't appear that synchronous CEA plus CABG would decrease the rate of stroke in the first 30 days. Now, how about the long-term outcomes of these patients? We know that asymptomatic carotid disease carries a cumulative annual risk of stroke, and it's important to see if the risk of subsequent stroke was lower downstream if the carotid was already fixed early on. So, in the current issue of the journal, the CABACS trial investigators, led by Dr. Stephan Knipp from the Department of Thoracic and Cardiovascular Surgery in Essen, Germany, and colleagues are back with the five-year results of this trial. How did synchronous CABG plus CEA do as compared to CABG alone? Well, by five years, the rate of stroke or death was 40% in the combined group and 35% in the CABG-only group. This was not a statistically significant difference. Now, when they broke down the primary outcomes, the rate of death from any cause was similar in the two groups. By five years, the mortality rate was 25% in the combined group and 23% in the CABG-only group. And the same was true for the rate of nonfatal strokes. And also the cumulative rate of nonfatal strokes from year one to year five was similar between the two groups, which meant that the higher stroke risk early on in the CABG plus CEA group was not counterbalanced by decreased rate of stroke later on during the long-term follow-up. And finally, they looked at the rate of disability-producing stroke. First of all, after the first year, no new disabling strokes were observed in either group. That's great news. However, in the early period, unfortunately, close to half of strokes that had happened after the combined CEA and CABG were disability-producing, and about a third of strokes that happened after CABG alone were also disability-producing. So, in summary, even though this study is quite underpowered, it appears that performing synchronous CEA plus CABG increases the preoperative morbidity and mortality in patients with asymptomatic carotid disease without providing any long-term benefits to these patients. Coronaviruses are important human and animal pathogens. By now, I think it's safe to say that most of the population of the world has heard of at least one of the members of the coronavirus's family, which was first identified in late 2019 as the cause of a cluster of cases of pneumonia in Wuhan, China. In the early months of 2020, COVID-19, the disease caused by this novel coronavirus, would rapidly spread to involve much of the world. And on March 11 of the same year, the World Health Organization declared COVID-19 a pandemic. Today, over two and a half years have passed since that day, and an avalanche of scientific papers have since been published about COVID-19, not just in medicine, but in each and every imaginable field of life. Neurology's, of course, no exception. The clinical presentation of COVID-19 largely depends on the severity of the disease and may range from a simple asymptomatic infection to a severe, lethal, multi-organ disease. In the world of neurology, a myriad of neurological symptoms, from loss of sense of taste and smell to headache, all the way to encephalopathy and seizures, have been reported in association with this disease. Early in the pandemic, some studies suggested that COVID-19 is indeed a risk factor for stroke. Like many severe infections, COVID-19 can potentially cause a prothrombotic state and can be associated with thromboembolic events. But most of these earlier studies were smaller observational studies that were completed in an inpatient setting, including those with severe COVID. In fact, to date, we still don't have an accurate and reliable estimate of stroke incidence among patients with COVID-19. On the other hand, stroke is the second leading cause of death globally and the fifth cause of death in the US. In the United States, every 40 seconds, someone has a stroke, and every four minutes, someone dies of a stroke. So, I think the question that everyone should be asking is, has COVID-19 changed this statistic? In this issue of the journal, in the study titled "Incidence of Stroke in Randomized Trials of COVID-19 Therapeutics: A Systematic Review and Meta-Analysis," Dr. Ntaios and colleagues aim to get us a step closer to answering this very important question. Dr. Ntaios is an Associate Professor of Medicine at the University of Thessaly in central Greece, and he's the current President of the Hellenic Stroke Organization. It is my great honor to have Dr. Ntaios today in our podcast to discuss this paper and all things stroke-related COVID-19. Good afternoon, George, and welcome to our podcast. Dr. George Ntaios:          Thank you for the invitation, Negar, and for highlighting our work. It's a pleasure to be here with you today. Dr. Negar Asdaghi:         Thank you for being here, and congrats on the paper. George, can you start us off by discussing the pathophysiological mechanisms through which COVID can potentially cause a stroke? Dr. George Ntaios:          Well, one of the most attractive things about stroke, which makes it fascinating for all of us, is its complexity. So many different pathologies can cause stroke, and, quite frequently, identifying the actual cause of stroke can be really challenging. And in a similar way, the pathophysiological association between COVID and stroke seems to be, again, complex. Different pathways have been proposed. Internal, we talk about two broad mechanisms. One is the vascular inflammation and thrombosis, and the other is cardioembolism. And there are several pathways which are involved in vascular inflammation and thrombosis: activation of the complement, activation of the inflammasome, activation of thrombin, increased production of [inaudible 00:24:47] constriction, state of stress, platelet aggregation, vascular thrombosis. So, collectively, this thromboinflammation could lead to damage of the neurovascular unit and consequently to stroke. And in a similar way, there are several cardiac pathologies which can cause stroke in a COVID patient, like acute left ventricular dysfunction, which can be caused, again, by several mechanisms, like coronary ischemia, stress-induced takotsubo cardiomyopathy, myocarditis inflammation, or also as a result of direct effect of the coronavirus at the myocardial cell. And, of course, we should not forget about atrial fibrillation, which seems to be more frequent in COVID patients. So, we see that the proposed mechanisms behind the association between COVID and stroke, that is, vascular thromboinflammation on one hand, or cardioembolism on the other hand, are complex, but whether these derangements they have a clinically relevant effect or they are just biochemical derangements without any clinical effect is a debate. For example, the incidence of myocarditis in COVID is about 0.2%. That is, in every 500 COVID patients, you have one patient with myocarditis. But myocarditis has a very wide clinical spectrum ranging from subclinical elevation of myocardial enzymes to full and life-threatening disease. So, obviously, the incidence of severe myocarditis is even lower than 0.2%. And the same is true also for the incidence of myocarditis after COVID vaccination. The CDC estimates that one case of myocarditis occurs every 200,000 vaccinations, with the number being slightly higher in young men after the second dose. And this is extremely rare, and the huge majority of these myocarditis cases, they're mild. So, this is about ischemic stroke. Now, with regard to hemorrhagic stroke and its association with COVID, again, it seems to be, again, very rare. The best estimate that we have comes from the Get With The Guidelines – Stroke Registry and is about 0.2% and involves mainly patients who are already on anticoagulants. So, they had already a risk factor for ICH. So, again, whether all these pathophysiologic derangements in COVID patients, they have a clinical meaningful association with stroke risk or not, I think it's a matter of debate. Dr. Negar Asdaghi:         Wow, George, it was a simple question, but it seems like the answer was not that straightforward. Let me just recap some of the things you mentioned. So, first of all, the answer is not straightforward and depends on whether we're talking about ischemic stroke or hemorrhagic stroke. There seems to be a lot of connecting points, at least, so to speak, between COVID and either forms of stroke. But you touched on two major sort of broad mechanisms. One is the idea of vascular thromboinflammation that goes along the lines of many sort of hyperacute, hyperinflammatory processes that can occur, especially in the setting of severe COVID. You touched on activation of thrombin, complement activation, platelet aggregation, sort of an activation of that microvascular or vascular unit in a sense. And then a second mechanism you touched on is the impact of COVID on the myocardium on sort of many different pathways. Again, you talked about acute left ventricular dysfunction, stress-induced myocarditis, and the impact of COVID on perhaps increasing the rate of atrial fibrillation. Again, these are all very complex associations, and some could be already present in a patient who is perhaps of an older age, and COVID is just a modifier of that risk factor that was already present in that particular person. And you also touched on how COVID can potentially increase the risk of hemorrhagic stroke, but the study seems to suggest that those patients already had risk factors for the same. And perhaps, again, COVID is a modifier of that risk factor. All right, so with that information, a number of studies early on, especially, in the pandemic and later, some meta-analyses, have aimed to estimate the incident rate of stroke post-COVID. Can you please briefly tell us what were their findings, and how is your current paper and current meta-analysis different in terms of methodology from those earlier studies? Dr. George Ntaios:          Yes. Well, it all started from this letter to the editor at the New England Journal of Medicine. It was published very early in the pandemic during the outbreak in New York. And in this letter, the authors had reported that within a period of two weeks, they had five young patients with COVID and large artery stroke, which they commented that it was much higher than their typical, actually their average, of 0.7 cases during a two-weeks period within the last year. And remember that back then, we knew literally nothing about COVID. So, this letter was really a huge, loud alert that something is going on here and that perhaps our hospitals would be flooded with COVID patients with stroke. So, subsequently, several reports were published aiming to estimate the incidence of stroke in COVID. Rather contradictory with the incidence, estimates are ranging from as low as 0.5% to even 5%. However, these estimates could well be inaccurate. They were observational studies. Most of them were limited to the inpatient setting. Most of them were single-center studies. Most of them, if not all, were retrospective studies. So, there was really a high risk of registration and assessment bias, as well as reporting bias. And also remember that back then during the outbreak, people were really reluctant to visit the hospital, even if they had a serious condition like stroke, an urgent condition, which means that the real incidences could be even higher. So, it was our feeling that these estimates were perhaps inaccurate. And there are also some meta-analyses of these studies which estimate that the incidence of stroke in COVID is about 1.5%. But, of course, any meta-analysis is as good as the studies it includes. So, we tried to find a way to have a more accurate estimate than these estimates. And we followed a different methodology. We studied randomized trials of COVID therapeutics, and we looked for strokes reported as adverse events or as outcome events. And the good thing about randomized trials is the rigorous assessment and reporting of outcomes in adverse events. So, we think, we believe, that this methodology provides a more reliable and a more robust estimate of stroke incidence in COVID patients. Dr. Negar Asdaghi:         OK. George, it's very important what you just mentioned, so I wanted to recap for our listeners some of the things you mentioned. It all started with a letter to the editor of New England Journal of Medicine on a report of five young patients that had large vessel occlusion in the setting of COVID. And then, basically, the floodgates opened in terms of all these observational studies that basically reported the same. And subsequent to that, meta-analyses that were completed containing those observational studies predominantly gave us an incident rate of 0.5 to 5%. That's much, much higher than basically the non-COVID–associated incidence rate of stroke in the population-based studies, and basically suggested that COVID-19 is indeed a major risk factor for all types of stroke. So, that's where it all started. And, as you alluded to, these numbers had to be reverified in bigger settings, more controlled setting. And you already answered my next question, which is the difference between those studies and prior meta-analyses to the current meta-analysis is that you basically took the simple question and started looking at it in a controlled setting of randomized trials. And you already answered this question of the methodology, but I want to recap. You took basically patients included in randomized trials of therapeutics for COVID-19, various therapies for COVID-19, and you did a meta-analysis to see what were the incident rate of stroke as an outcome in these trials. So, with that, could you please tell us a little more about the population that you had in this meta-analysis in terms of their age, the types of therapies that these randomized trials had looked at, and the duration of the follow-up, please? Dr. George Ntaios:          The follow-up included 77 randomized trials, which corresponds to more than 38,000 COVID patients. The mean age of these patients was about 55 years of age, and they were followed for an average of 23 days after study enrollment. With regard to the set strategy, I think it was not strict at all. I would rather say it was very liberal. We allowed trials of any drug in COVID patients of any age, of any severity, coming from any setting: outpatient, inpatient, either general ward or intensive care unit. And from any country. I don't think that we could achieve a wider inclusion than this strategy did. And the huge majority of patients, more than 95%, they were hospitalized patients. So, by definition, they had severe COVID disease. And the drugs studied in these trials included everything that was actually tried in COVID, including tocilizumab, IL-6R inhibitors, steroids, remdesivir, chloroquine, azithromycin, ritonavir, interferon, ivermectin, and many other drugs. So, I think we tried to include as many trials as possible. Dr. Negar Asdaghi:         OK. So, let me see if I got it. You basically included 77 randomized trials. It is a younger population of patients in these trials, median aged 55. You had a total of over 38,000 patients. It's a great sample size for this meta-analysis. And importantly, the duration of follow-up is median of 23 days. And it's just about any treatments we've heard that have been tried for COVID, from dexamethasone to remdesivir and ivermectin. And a rigorous methodology. So, I think we're ready to hear the primary results of this meta-analysis. How many strokes happened in these patients? Dr. George Ntaios:          In the overall population, that is both in the hospital and in the outpatient setting, there were totally 65 strokes in these 38,000 COVID patients, which corresponds to one stroke every 600 COVID patients or else an incident of only 0.16%, 0.16%. This is very low, much lower than the previous estimates. And, of note, all strokes occurred in hospitalized patients. There were no strokes at all in the ambulatory COVID patients. So, just to repeat the result, we just found that only one patient will have a stroke every 600 COVID patients who are either hospitalized or are ambulatory. Dr. Negar Asdaghi:         OK. So, I need to have these numbers, I think, committed to memory, especially when we speak to family members and patients in the hospital. Ninety-five percent of the patient population of this meta-analysis were inpatient COVID. So, by definition, they must be sicker in terms of the severity of their COVID disease. Out of 38,000 patients, you had 65 events of stroke. So, these are very, very important numbers, a lot basically lower than the incidence rate reported from prior studies. So, I wanted to ask you about the sensitivity analysis that was done in the meta-analysis. Dr. George Ntaios:          Yes. When we designed the analysis, we were expecting that we would find numbers was similar to those reported before. So, we thought that perhaps a sensitivity analysis would be able to increase the confidence and the robustness of the results. That's why we did this sensitivity analysis. However, it proved that the number of strokes, the number of outcome events was much lower than what expected. So, the power for those sensitivity analysis to show a meaningful conclusion was low. So, actually, that's why we don't comment at all on those sensitivity analysis because there were so few strokes to support such an analysis. Dr. Negar Asdaghi:         OK. So, basically, you had a priori design the meta-analysis based on the assumption that the incidence rate of stroke would be a lot higher, but then later on, when the incidence rates was lower, then the sensitivity analysis didn't really give any meaningful data to us. So, I mean, I think we already talked about this, but I want to ask you, why do you think that the incidence rates were so much lower in your analysis than the prior meta-analysis? Dr. George Ntaios:          I believe that our estimate is quite accurate. I think that the reports of stroke incidence published during the pandemic possibly overestimated the association. I think that the early concern that we all had in the beginning, that we would be flooded with strokes during the pandemic, was not confirmed. I think that we can support with decent confidence that stroke is a rare or perhaps very rare complication of COVID. Dr. Negar Asdaghi:         Right. That's great news. That really is great news, and we take every bit of good news in these trying times. George, something that was not touched on in the paper, but I want to ask you and basically get your opinion on this matter, is a much talked about concept in the COVID literature of how COVID could potentially modify certain risk factors. There are much talk about how people with pre-existing diabetes or obesity can potentially develop more severe COVID and, hence, have more complications of COVID, including stroke. What is your clinical experience on this matter, and do you think there are certain predictors of development of COVID-associated stroke? Dr. George Ntaios:          That's a very good point. For the last two years, I was involved in the hospitalization management of COVID patients. So, what we see is what is also described in the literature, that there are certain patient characteristics that predispose them to severe COVID. For example, obesity, for example, older age, pregnancy. Perhaps our analysis was not designed to respond to this question. The data available on the studies that were included, they could not support such an analysis. So, I cannot provide information from our study. But the fact that all strokes in our study, they occurred in hospitalized patients and none of them occurred in ambulatory patients, confirms what is known, that those strokes occurred in patients who, by definition, they have severe COVID disease. So, they confirm this putative association that perhaps severe COVID is associated with stroke rather than just mild COVID. Dr. Negar Asdaghi:         All right. Thank you. And I just want to end with this simple question that I get asked often, and I want to see how you respond to patients or their loved ones when you're asked this question: "Doctor, did COVID give me a stroke?" How should we answer that question? Dr. George Ntaios:          Yes. As we discussed, I think that stroke is a rather rare or perhaps very rare complication of stroke and certainly less frequent than we initially thought. And in those stroke patients who had already other pathologies which can cause stroke, I would be rather reluctant to attribute it to COVID. I would be perhaps more willing to do so in younger patients, but again, only after exhaustively looking for another cause, like PFO, dissection, etc. I mean, the concern is that if we as the treating stroke physicians assume that the stroke is caused by COVID, then we might discourage patients from doing the necessary diagnostic workup to find the actual cause of stroke. And if it happens, then perhaps an underlying pathology may be missed, which means that the patient will remain vulnerable to stroke recurrence. So, in general, I'm rather very reluctant to say that the stroke is caused by COVID unless a really thorough diagnostic workup shows nothing else at all. Dr. Negar Asdaghi:         All right. Very important message now to all practicing clinicians is don't stop at COVID. Don't just say simply, "Oh, this is COVID. COVID gave you a stroke." Keep looking for potential causes of stroke. Still do put that patient in the category of potentially ESUS or cryptogenic stroke if no other causes are found. And keep in mind that stroke is rare or, as George said, a very rare complication of COVID. Dr. George Ntaios, this is an exceedingly timely topic and a very important contribution to the field. Congratulations again on your paper, and thanks for taking the time to chatting with us today. Dr. George Ntaios:          Thank you for the wonderful discussion, Negar, and for the focus of our work. Dr. Negar Asdaghi:         Thank you. And this concludes our podcast for the November 2022 issue of Stroke. As always, please be sure to check out the table of contents for the full list of publications, as we can only cover a fraction of the incredible science published in this journal each month. And don't forget to check our fantastic Literature Synopsis. In this month's issue, we read a short summary of the ACST-2 trial published in Lancet on the results of a randomized comparison of stenting versus endarterectomy in asymptomatic carotid disease patients with over 60% of carotid stenosis. We also have the results of the CASSISS randomized trial, which was published in JAMA earlier this year, and it studied the effect of stenting plus maximal medical therapy versus maximum medical therapy alone on the risk of subsequent stroke and death in patients with symptomatic intracranial stenosis, either in the anterior or in the posterior circulation. CASSISS did not show that stenting was superior to maximum medical therapy, and sadly, these patients remain at a substantial risk of recurrent stroke despite being on best medical therapy. But I wouldn't be too despondent about the future of interventional therapy for intracranial atherosclerotic disease. After all, we've come a long way since Dr. Charles Thomas Stent, an English dentist, started experimenting with products to advance the field of denture making around 1865. The work that Dr. Stent had started would be continued by his two sons, both dentists, to eventually make its way to products to create surgical tools. But it would be another 100 years before the first percutaneous coronary procedure was completed in 1964. And in honor of Dr. Stent's pioneering work, the device used to keep the coronaries open was named, you guessed it, stents. Today's stroke care cannot be imagined without the use of various stents, and there's no doubt the future is promising for ways in which we will be able to safely treat intracranial atherosclerotic disease amongst all other vascular disorders. And what better way to keep our enthusiasm than staying alert with Stroke Alert. This program is copyright of the American Heart Association, 2022. The opinions expressed by speakers in this podcast are their own and not necessarily those of the editors or of the American Heart Association. For more, visit AHAjournals.org.

Charlie and T2 discuss the moon whether we should go back to it or not. 

Charlie discusses the upcoming cases against the democrat party. Charlie and T2 discuss the moon whether we should go back to it or not. Charlie discusses the alleged crimes of the Biden family how the republicans want an investigation in to all of their scandals.

Go online to PeerView.com/MKN860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. Eosinophilic esophagitis (EoE) is an increasingly prevalent, chronic, T2 inflammatory disease triggered by food and/or environmental allergens. Due to underlying tissue inflammation, patients suffer diminished quality of life due to symptoms such as weight loss, difficulty swallowing, and heartburn. Patients can experience these symptoms for a long time before receiving a proper diagnosis. Once diagnosed, treatment options have historically been limited. Fortunately, therapies that treat other type 2 disorders are in development or are approved to treat EoE. At a recent live event, experts used patient cases to discuss the diagnosis, underlying causes, and the newest treatments for EoE, including biologic therapies. Watch this on-demand version now! Upon completion of this activity, participants should be better able to: Distinguish signs and symptoms of eosinophilic esophagitis (EoE) among children and adults to enable an earlier diagnosis and minimize complications due to uncontrolled disease; Recognize underlying mechanisms of EoE, including the role of key cytokines such as interleukins -4, -13, and -5 as drivers of type 2 inflammation and how this relates to emerging treatment; and Apply the latest expert recommendations and clinical evidence to the treatment of patients with EoE, particularly as novel and emerging agents become available.

Go online to PeerView.com/MKN860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. Eosinophilic esophagitis (EoE) is an increasingly prevalent, chronic, T2 inflammatory disease triggered by food and/or environmental allergens. Due to underlying tissue inflammation, patients suffer diminished quality of life due to symptoms such as weight loss, difficulty swallowing, and heartburn. Patients can experience these symptoms for a long time before receiving a proper diagnosis. Once diagnosed, treatment options have historically been limited. Fortunately, therapies that treat other type 2 disorders are in development or are approved to treat EoE. At a recent live event, experts used patient cases to discuss the diagnosis, underlying causes, and the newest treatments for EoE, including biologic therapies. Watch this on-demand version now! Upon completion of this activity, participants should be better able to: Distinguish signs and symptoms of eosinophilic esophagitis (EoE) among children and adults to enable an earlier diagnosis and minimize complications due to uncontrolled disease; Recognize underlying mechanisms of EoE, including the role of key cytokines such as interleukins -4, -13, and -5 as drivers of type 2 inflammation and how this relates to emerging treatment; and Apply the latest expert recommendations and clinical evidence to the treatment of patients with EoE, particularly as novel and emerging agents become available.

Go online to PeerView.com/MKN860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. Eosinophilic esophagitis (EoE) is an increasingly prevalent, chronic, T2 inflammatory disease triggered by food and/or environmental allergens. Due to underlying tissue inflammation, patients suffer diminished quality of life due to symptoms such as weight loss, difficulty swallowing, and heartburn. Patients can experience these symptoms for a long time before receiving a proper diagnosis. Once diagnosed, treatment options have historically been limited. Fortunately, therapies that treat other type 2 disorders are in development or are approved to treat EoE. At a recent live event, experts used patient cases to discuss the diagnosis, underlying causes, and the newest treatments for EoE, including biologic therapies. Watch this on-demand version now! Upon completion of this activity, participants should be better able to: Distinguish signs and symptoms of eosinophilic esophagitis (EoE) among children and adults to enable an earlier diagnosis and minimize complications due to uncontrolled disease; Recognize underlying mechanisms of EoE, including the role of key cytokines such as interleukins -4, -13, and -5 as drivers of type 2 inflammation and how this relates to emerging treatment; and Apply the latest expert recommendations and clinical evidence to the treatment of patients with EoE, particularly as novel and emerging agents become available.

EPISODE 99 - Fred Rutman - Living Life After Dying Twenty Times.  Fred's new book is coming out March 9th 2024Fred Rutman, aka “Repeatedly Dead Fred” was a marketer/consultant and then went into academia as a college professor. He taught MBA, Marketing and Finance for a number of years. After acquiring his MBA, his weight really ballooned, up to 340 pounds. He did all the CICO methods, tried a bariatric doctor (no surgery) and exercised his butt off. He eventually got down to about 280, where he plateaued. Then, the summer of 2009 came crashing down on him and forced him into permanent medical leave.His heart was stopping and was clinically dead dozens of times. Each time his heart stopped, he collapsed and hit his head, sustaining multiple concussions. In 2018, he learned about intermittent fasting and life hasn't been the same for Fred since. He attributes the large majority of his recovery to the healing powers of IF. He reversed T2 diabetes and some of its related issues, and is no longer asthmatic. His sleep apnea even went away. There is still some perpetual anxiety, PTSD and Post-Concussion Syndrome but it gets better every day. Visit https://www.linkedin.com/in/fredrutman/ to learn more or to connect with Fred.Fred Shared these great book suggestions in this episodeBird by Bird: Some Instructions on Writing and Life - Anne Lamott___https://livingthenextchapter.com/podcast produced by: https://truemediasolutions.ca/Have a podcast and need a great website? Try Podpage!Dave's Audio Book Recommendation for November 2022Surrender: 40 Songs, One Story - Bono Bono—artist, activist, and the lead singer of Irish rock band U2—has written a memoir: honest and irreverent, intimate and profound, Surrender is the story of the remarkable life he's lived, the challenges he's faced, and the friends and family who have shaped and sustained him. Narrated by the author, Surrender is an intimate, immersive listening experience, telling stories from Bono's early days in Dublin, to joining a band and playing sold out stadiums around the world with U2, plus his more than 20 years of activism. Throughout a remarkable life, music has always been a constant for Bono and in the audiobook, his distinctive voice is interwoven with a very personal soundtrack adding atmosphere and texture to each and every scene. From moments of classic U2 hits to snippets by The Clash, Patti Smith, Verdi, Johnny Cash and Mozart, Surrender also exclusively features clips of newly recorded re imagined versions of U2 songs including ‘Sunday Bloody Sunday', ‘With Or Without You', ‘One', ‘Beautiful Day' and more, glimpsed for the first time on Surrender: 40 Songs, One Story.

Charlie discusses a new official branch in Greenville designed to force companies to be more inclusive. Charlie and T2 talk Thanksgiving foods. They discuss what foods they would get rid of. Charlie reveals his Dressing recipe and T2 talks about Macaroni and Cheese. Charlie talks to T2 about random facts about laundry detergents.

Charlie and T2 discuss Yellowstone and Woke TV shows. Charlie talks about Mitch McConnell's favorability rating. He discusses other election results and questions there validity. Charlie discusses an official who lives an interesting lifestyle. Charlie links the official to the democrat Party. The women on The View claim the republicans want to raise the voting age to 28 years old. 

My guest this week is Dr. Amie Hornaman also deemed, “The Thyroid-Fixer”. In this episode, Dr. Amie and I discuss functional medicine workup and protocols for thyroid imbalances. First, we talk about the conglomeration of symptoms those with thyroid imbalances may be experiencing, how the autoimmune switch gets turned on & possible underlying causes of thyroid issues, what role gluten plays in thyroid health, as well as the various thyroid hormones, especially T2.  Dr. Amie shares how to get into “optimization land”; starting with the one question all physicians need to be asking and often don't, what thyroid labs you need to ask your physician for, why we need Iodine and how to supplement (pool swimmers, listen up!), and tips for weight loss, fasting, cold therapy, and more.   Learn more about Dr. Aime and her thyroid support products at here and use code NAT10 for 10% off.     ------     Follow Dr. Amie: Website Facebook Instagram YouTube     ------     Episode Sponsors Oxford HealthSpan brings us Primeadine, which upregulates autophagy and mitophagy, helps the immune system to rejuvenate plus it protects DNA and supports deep sleep, hair skin and nails!  It's a staple in my supplement stack! If you haven't tried it yet, go to Primeadine's website to learn more and use promo code BIONAT15 to save 15%.   Mitopure from Timeline Nutrition is a scientific breakthrough for our cells. Ten years of research has led to the discovery of Urolithin A; a mitochondrial powerhouse that assists in mitophagy, protecting cells from cellular decline. Mitopure is clinically proven to enhance muscle health and performance. It comes in a powder, capsules or a berry powder (it tastes good!). There is a 3-month trial so you can try them all! To learn more, visit www.timelinenutrition.com and use code NAT10 for 10% discount!     ------     Episode Takeways [06:50] Let's talk about thyroid & what symptoms to look out for?… [09:50] Why are so many people having thyroid issues?.. [12:30] Is gluten bad for the thyroid?.. [17:30] What are the basic thyroid tests people need?.. [30:50] The importance of being in a functional lab value range… [32:00] What should we be looking for as far as ideal lab ranges?.. [35:28] How to help your thyroid with food, thyroid replacement and supplements… [52:30] Fasting and thyroid… [57:10] Dr. Amie's unique thyroid support supplement line…     ------     Follow Nat Facebook Facebook Group  Instagram Work with Nat: Book Your 20 Minute Optimization Consult

Lindsey Graham says republicans are favored to win the next election cycle. Charlie tells T2 about his first attempt at baking bread. Mitch McConnell is negotiating with his peers about ditching the MAGA Republicans.

La novena sinfonía de Robo-Beethoven / Grave fallo en los Pixel / Auriculares que se desinfectan solos / Gran avance en predicción de huracanes / 18 años de Firefox 1.0 Patrocinador: BluaU de Sanitas es el nuevo complemento digital del seguro médico de Sanitas que incorpora la más alta tecnología para ayudarte en el cuidado de tu salud y la de tu familia. — BluaU lanza Cuida Tu Mente, un nuevo servicio que se centra en la prevención como en el tratamiento de posibles problemas psicológicos en nuestra familia. — Descubre más en BluaU.es La novena sinfonía de Robo-Beethoven / Grave fallo en los Pixel / Auriculares que se desinfectan solos / Gran avance en predicción de huracanes / 18 años de Firefox 1.0

We're back and talking about one of the greatest sequels ever made, James Cameron's Terminator 2: Judgment Day aka T2. Not only do we discuss this Arnold Schwarzenegger classic, from its production to its story and action, but we also have some laughs with tangents throughout, and make sure we at least spent a few minutes lampooning the sequels that came after it. So travel back in time with us to 1991 and let's talk T2! Subscribe to the podcast free on your preferred app and please tell a friend who loves movies about the show, just tell em to look up "Just Like the Movies" on any podcast app! Thank you for listening and as always remember to be kind, rewind, relax, and enjoy the show.

 In this ISACA Podcast episode, ESET's Chief Security Evangelist, Tony Anscombe, joins ISACA's Principal, Emerging Technology Professional Practices, Collin Beder to discuss ESET's recently released T2 2022 Threat Report. As a global leader in cybersecurity, ESET's T2 2022 Threat Report summarizes the most notable trends that have shaped the threat landscape for the past four months. This report dives into CloudMensis, the previously unknown macOS malware discovered by ESET researchers. To read the full ESET report: https://www.welivesecurity.com/wpcontent/uploads/2022/10/eset_threat_report_t22022.pdf. For more information, check out ESET's award-winning blog: WeLiveSecurity. Make sure to follow ESET Research on Twitter for the latest news from ESET Research. To listen to more ISACA Podcasts, please visit www.isaca.org/podcasts.

Terminator 2: Judgement Day is one of the greatest science fiction movies ever made. Michael Benton and Alejandro Espinoza are HUGE FANS. This two part miniseries is them dissecting two major themes from the film: the threat of artificial intelligence and today's subject... NUCLEAR ANNIHILATION.They will discuss the famous nuclear blast nightmare sequence from T2, the development of the Big Ol' Bomb, and what the future may look like. They will also be discussing the mechanics and realism of the film's depiction of a nuclear blast with Dr. Jeffrey Lewis, professor at Middlebury Institute and an expert in nuclear weapons, as well as working for a world with as few nuclear weapons as possible.Support the show

Last week brought exciting racing at the IRONMAN 70.3 World Championship in St. George UT with commanding wins by Taylor Knibb and Kristian Blummenfelt. Taylor, Kristian and other big names from last weekend are off to Bermuda for the World Triathlon Championship Series. Show Sponsor: UCAN Generation UCAN has a full line of nutrition products to fuel your sport. UCAN uses SuperStarch instead of simple sugars and stimulants to fuel athletes. UCAN keeps blood sugar steady compared to the energy spikes and crashes of sugar-based products. UCAN also has hydration products focused on giving you the sodium you need when hydrating, including several clean and light flavors. Steady energy equals sustained performance and a faster finish line! Use UCAN in your training and racing to fuel the healthy way, finish stronger and recover more quickly! Use the code 303UCAN for 20% off at ucan.co/discount/303UCAN/ or ucan.co In Today's Show • Feature ○ World Triathlon Series Championship in Bermuda • Endurance News ○ Ironman 70.3 World Championship • What's new in the 303 ○ 2023 Season Race Dates Announced ○ TriDot Pre Season Project ○ Bicycle Colorado - Support bike advocacy and win prizes • Video of the Week ○ Worlds Best Drone Video Extreme Mountain Bike Feature: Bermuda World Triathlon Series 2022 World Triathlon Championship Series Bermuda 2022 World Triathlon Championship Series Bermuda marks a return to this beautiful island for a third edition of WTCS Bermuda and the first since 2019. Much has happened on and off the blue carpet since we were last here, not least Bermuda's very own Flora Duffy making history by becoming the first triathlete to win both the Olympic and World titles in the same year, becoming Bermuda's first ever Olympic gold medallist and more recently the first to defend a Commonwealth Games triathlon title. This weekend, we return to the island for the penultimate Championship Series racing of 2022, and elite men's and women's events that have the potential to make a huge impact on the battles to become this year's World Triathlon Champions. The triathlon world's eyes will be fixed on this beautiful corner of the Atlantic and can expect another dose of high-octane entertainment from the world's best athletes. The island will also host a wealth of Age-Group and kids triathlon races, and it is always gratifying to see our sport continuing to grow among so many people at all levels of the sport. It is precisely these weekends that will inspire future generations to take up the magic of swim bike run and that can be the spark behind the fire of the next Flora Duffy. Bermuda has a strong and important history of triathlon and also with the WTCS, having hosted many professional events since 1987, including three WTCS (formerly ITU World Cups) in the 90's where Flora Duffy, Olympic gold medalist and multiple World Champion, watched as a young aspiring triathlete. Age Group - Saturday, November 5th 8am Elite Men - Sunday, November 6th 11am Elite Women - Sunday, November 6th 2pm Temperature in November varies between an average high of 74 degrees to a low of 67 degrees Fahrenheit. The water temperature also comes down to 73 degrees, however, water visibility remains at 100-120 feet. View on Triathlon Live - TriathlonLIVE Start List: Elite Women • 2022 World Triathlon Championship Series Bermuda • World Triathlon Start Num First Name Last Name YOB Country 1 Flora Duffy 1987 BER 2 Beth Potter 1991 GBR 3 Taylor Spivey 1991 USA 4 Laura Lindemann 1996 GER 5 Sophie Coldwell 1995 GBR 6 Anabel Knoll 1996 GER 7 Taylor Knibb 1998 USA 8 Kirsten Kasper 1991 USA 9 Maya Kingma 1995 NED 10 Miriam Casillas García 1992 ESP 11 Summer Rappaport 1991 USA Start List: Elite Men • 2022 World Triathlon Championship Series Bermuda • World Triathlon Start Num First Name Last Name YOB Country 18 Kevin McDowell 1992 USA 26 Matthew Mcelroy 1992 USA 29 Ren Sato 1995 JPN 30 Seth Rider 1997 USA 38 Chase Mcqueen 1998 USA 48 Brent Demarest 1995 USA 49 Gregor Payet 1995 LUX 50 Miguel Tiago Silva 1998 POR 51 Kristian Blummenfelt 1994 NOR 52 Martin Demuth 1995 AUT 53 Kyotaro Yoshikawa 2000 JPN 54 Gustav Iden 1996 NOR 56 Tyler Smith 1998 BER News Sponsor Buddy Insurance: Buddy Insurance gives you peace of mind to enjoy your training and racing to the fullest. Buddy's mission is simple, to help people fearlessly enjoy an active and outdoor lifestyle. Get on-demand accident insurance just in case the unexpected happens. Buddy ensures you have cash for bills fast. Go to buddyinsurance.com and create an account. There's no commitment or charge to create one. Once you have an account created, it's a snap to open your phone and in a couple clicks have coverage for the day. Check it out! Endurance News: Taylor Knibb Powers to Victory at 2022 Ironman 70.3 World Championships It was the Taylor Knibb show at the 2022 Ironman 70.3 World Championship in St. George as the 24 year-old American put on a master class of racing to take her first-ever 70.3 World title. A master class in racing was held in St. George, Utah this morning during the women's pro race at the Ironman 70.3 World Championship. The instructor: 24 year-old Taylor Knibb, who delivered a confident and commanding swim, bike, and run to take the win in 4:03:20. The Swim Lucy Charles-Barclay and Lotte Wilms finish the women's pro swim leg during the 2022 IRONMAN 70.3 World Championship. After much speculation about whether or not the swim would be shortened after a cold front moved through southern Utah on race week, race morning arrived with 63 degree F water temperatures and the full 1.2-mile swim. Naturally, many assumed this would work to the advantage of defending champion Lucy Charles-Barclay, who is known for building a considerable lead in any swim leg she races. But instead of surging to the front as usual, she found she had company: Lotte Wilms of the Netherlands and American Taylor Knibb were on her feet. At the halfway point, Wilms surged to attempt a pass, and Charles-Barclay matched her speed; Knibb held on in the draft, eventually reeling the two back in. The trio powered through to the swim exit, with Charles-Barclay's 23:50 swim split just barely edging out Wilms' 23:51 at the first timing mat; Knibb followed in 23:54. The Bike With air temperatures hovering around 38 degrees F at the start of the bike leg, it was clear the race would belong to the one who could best manage the cold. Clad in gloves and thermal cycling attire, Knibb wasted no time taking charge on the bike leg, moving to the front within the first mile. With an average speed of 28.2 MPH in the first 20 miles, Knibb's lead only grew: one minute at mile 10, 2:30 at mile 20. But Knibb wasn't the only one moving quickly. Duffy also pushed hard in the initial miles of the bike, shooting out of the rolling hills of Sand Hollow with laser-like focus to move into second place by mile 10. Behind her, India Lee (GBR) and Findlay were the only athletes to match Knibb's blistering pace, and they were each rewarded with a Duffy pass and a turn at second place before mile 30. At mile 40, Charles made her move, pushing back into second place with Findlay and Duffy close behind as they entered Snow Canyon. Lawrence, spent from the cold and the early charge, was unable to respond and fell behind. Within the walls of Snow Canyon, Knibb's lead only grew. With almost five minutes on the chase pack, the young American sailed up the notoriously steep climbs; behind her, Findlay, then Duffy, then Charles-Barclay (again) attempted to drop the hammer, but no one was willing to give up the fight. As the three crested Snow Canyon and powered to T2, they were greeted by Knibb, who was already well into the run course. The message was unspoken, but clear: Knibb's impossibly fast 2:14:41 bike split had given her a lead of six minutes and 44 seconds. The Run From the first steps out of T2, it was clear that Knibb saw the run as a mere formality to the win. With a consistent 5:58 min/mile pace, Knibb's lead grew – and grew, and grew. By mile 4, she had more than 7:30 over her closest competition. Though the victory was all but decided, there was still an intense race going on to see who would get boxed out of the podium. Duffy, Findlay, and Charles-Barclay ran as a pack, each daring the others to make a move. At the halfway point, Charles-Barclay began to fall back, and Duffy's form began to show signs of fatigue. Findlay, sensing it was time to make a move, began to slowly pull ahead. Over the course of the next three miles, she was able to put in more than 40 seconds on Duffy and Charles. But an out-and-back section of the course revealed that those two weren't the only competitors Findlay had to worry about – a hard-charging Pallant-Browne was clocking 5:56 min/mile splits in hopes of running her way from ninth place off the bike and onto the final podium. She made easy work of it, overtaking Duffy and Charles in the final mile of the race. In the end, Knibb's 1:21:48 run and 4:03:20 finishing time was more than enough to stamp her name on the history books as the youngest woman to win the title of Ironman 70.3 World Champion. Findlay followed in 4:08:57, and Pallant-Browne rounded out the podium with a run split of 1:17:45 and an overall finishing time of 4:10:45. A Rollercoaster 70.3 World Championship, Kristian Blummenfelt Holds on for the Win A relentlessly close swim, a controversial penalty, and a run battle for the ages - the pro men's race at the 2022 Ironman 70.3 World Championship was a high-stakes, high-drama affair that had viewers on the edge of their seats from the very start to the very finish. A relentlessly close swim, a controversial penalty, and a run battle for the ages – the pro men's race at the 2022 Ironman 70.3 World Championship was a high-stakes, high-drama affair that had viewers on the edge of their seats from the very start to the very finish. The moment of catharsis came in the form of a Kristian Blummenfelt victory in a staggering 3:37:12 on one of the toughest courses on the 70.3 circuit. Men's Race: The Swim With water temperatures at 62 degrees F and air temperatures at 40 degrees F, the theme of the day was the same as the women's race prior: managing the cold conditions of late fall in southern Utah. Aussie Aaron Royle set the pace, with Americans Ben Kanute and Marc Dubrick hot on his heels. Royle emerged from the water first in 22:20, followed by Marc Dubric and Ben Kanute. But what came next was a rare sight in middle-distance racing: In the span of only 20 seconds, a pack of 19 athletes rushed out of the water as if one unit. It was no surprise, then, that T1 was a bit of a circus, with athletes jockeying for position. The pack, which included Denmark's Miki Taagholt and Magnus Ditlev, Norwegians Kristian Blummenfelt and Gustav Iden, Americans Eric Lagerstrom and Jason West, Germans Mikia Noodt and Frederic Funk, and Canadian Brent McMahon, rushed out of transition as quickly as they entered. Two minutes down from the lead, another chase pack formed, this one containing Canadian Jackson Laundry and American Sam Long. In 34th and 40th place, respectively, it was clear that if they wanted a fighting chance at the podium, they were going to have to put in some big work on the bike to catch their competition. The Bike Blummenfelt had no intention of sitting in the pack and watching the race unfold in front of him. He pushed hard from the very start, setting out at a burning pace of 28 mile per hour in the rolling hills out of Sand Hollow. Sam Long, who had ridden his way from 40th to 8th place in the first 20 miles, was the one who took the hit. After getting caught in a tight spot during a pass involving Laundry, Long found himself with a controversial call-out from the referee and a five-minute stand-down in the penalty box. With a gap of 2:25 and an enormous chase pack of 18 athletes close together whizzing past the yellow penalty tent, Long was visibly upset. The pack emerged from Snow Canyon and descended with reckless abandon, barreling toward T2 at 39 miles per hour. Ditlev tucked in tight and tried to get any advantage he could, entering T2 with a bike split of 1:49:59, nine seconds ahead of Blummenfelt and Funk. But that advantage was erased in transition as Blummenfelt moved from bike to run in a seamless 29 seconds while Ditlev floundered for nearly twice that amount of time. In the end, it was Blu who started the run first. Would this mistake cost Ditlev the race? The Run Though Blummenfelt set out at a 5:47 minute-per-mile pace, his lead didn't last long. At mile 2, he had company in the form of Kanute, who was throwing down 5:16 splits. As he passed Blummenfelt, Kanute turned the screws even more, dropping the pace to a staggering 4:55 minutes per mile. But this didn't shake Blummenfelt, who stayed right on his heels and