Podcasts about Mog

Wykład lek. Maciej Walędziaka w ramach w ramach XII Dnia Odkrywców Kampusu Ochota Uniwersytetu Warszawskiego [21 marca 2026 r.]Otyłość nie jest wyłącznie skutkiem braku silnej woli ani prostym problemem nadmiaru spożywanych kalorii. To przewlekła, złożona choroba, na której rozwój wpływają czynniki biologiczne, hormonalne, genetyczne, psychologiczne, społeczne i środowiskowe.Lek. Maciej Walędziak wyjaśnia, jak współczesna medycyna podchodzi do leczenia otyłości. Pokazuje, dlaczego samo zalecenie „proszę mniej jeść i więcej się ruszać” często okazuje się niewystarczające oraz dlaczego skuteczna terapia powinna być dostosowana do sytuacji konkretnego pacjenta.Punktem wyjścia jest właściwe rozpoznanie choroby i ocena jej wpływu na zdrowie. Znaczenie mają nie tylko masa ciała i wskaźnik BMI, lecz także rozmieszczenie tkanki tłuszczowej, obwód talii, występowanie chorób współistniejących oraz dotychczasowe próby redukcji masy ciała.Otyłość zwiększa ryzyko wielu poważnych problemów zdrowotnych, między innymi cukrzycy typu 2, nadciśnienia tętniczego, chorób układu krążenia, bezdechu sennego, przeciążenia stawów, stłuszczenia wątroby i niektórych nowotworów. Może również wpływać na sprawność, samopoczucie psychiczne, relacje społeczne i jakość życia.Podstawą terapii pozostaje trwała zmiana sposobu odżywiania i codziennych nawyków. Nie chodzi jednak o krótkotrwałą, restrykcyjną dietę, lecz o stopniowe wprowadzanie rozwiązań, które pacjent jest w stanie utrzymać przez długi czas. Ważną rolę odgrywają również aktywność fizyczna, sen, ograniczenie stresu i praca nad mechanizmami sprzyjającymi nadmiernemu jedzeniu.Leczenie otyłości może wymagać współpracy wielu specjalistów: lekarza, dietetyka, psychologa, fizjoterapeuty, a w niektórych przypadkach także chirurga. W zależności od stopnia zaawansowania choroby i stanu zdrowia pacjenta stosuje się leczenie zachowawcze, farmakologiczne lub operacyjne.Farmakoterapia może wspierać redukcję masy ciała poprzez wpływ na apetyt, uczucie sytości i procesy metaboliczne. Nie zastępuje jednak zmiany stylu życia i powinna być prowadzona pod kontrolą lekarza. Dobór leczenia zależy od wskazań, przeciwwskazań, chorób współistniejących i reakcji pacjenta na terapię.Jedną z metod leczenia zaawansowanej otyłości jest chirurgia bariatryczna. Zabiegi bariatryczne nie polegają wyłącznie na mechanicznym zmniejszeniu żołądka. Wpływają także na wydzielanie hormonów regulujących głód, sytość i metabolizm. Mogą prowadzić do znacznego zmniejszenia masy ciała oraz poprawy lub ustąpienia części chorób związanych z otyłością.Operacja nie jest jednak rozwiązaniem automatycznym ani drogą na skróty. Wymaga odpowiedniej kwalifikacji, przygotowania, zmiany sposobu odżywiania, regularnych kontroli i długotrwałej współpracy pacjenta z zespołem medycznym.Wykład zwraca również uwagę na problem stygmatyzacji osób chorujących na otyłość. Obwinianie pacjenta, zawstydzanie go lub sprowadzanie choroby do braku dyscypliny może utrudniać rozpoczęcie leczenia i pogarszać jego skuteczność. Otyłość powinna być traktowana jak inne choroby przewlekłe – z empatią, szacunkiem i wykorzystaniem dostępnych metod terapeutycznych.Czy otyłość można skutecznie leczyć? Jak wybrać odpowiednią metodę? Kiedy wystarczy zmiana nawyków, a kiedy potrzebne są leki lub zabieg chirurgiczny? Wykład pokazuje, że terapia jest możliwa, ale powinna być kompleksowa, indywidualna i nastawiona na długofalową poprawę zdrowia, a nie wyłącznie na liczbę kilogramów.Wykład lek. Macieja Walędziaka odbył się w ramach Dnia Odkrywców Kampusu Ochota Uniwersytetu Warszawskiego.#MaciejWalędziak #Otyłość #LeczenieOtyłości #ChorobaOtyłościowa #Bariatria #ChirurgiaBariatryczna #Odchudzanie #ZdroweOdżywianie #Zdrowie #Dietetyka #AktywnośćFizyczna #Farmakoterapia #Cukrzyca #Insulinooporność #ZdrowieMetaboliczne #Medycyna #KampusOchota #UniwersytetWarszawski #DzieńOdkrywców #Wszechnica

Cześć. Tutaj Leszek. Niedoszły alkoholik.  Żyjemy w kraju ogromnym problemem. W Polsce każdego dnia do południa schodzi 500 000 małpek. Pół miliona małych butelek mocnego alko na śniadanie. To jest do południa. Bo do północy schodzi ich 3 miliony. Codziennie każdego dnia. 3 miliony tylko tych małych butelek. W Polsce Żabka nie otworzy się jeśli w danej lokalizacji nie ma szans na koncesję. No dobra są takie trzy. To mnie przeraża. Tak samo jak otyłość wynikająca nie tylko że złej diety, tylko z ilości wypijanego alkoholu każdego tygodnia, miesiąca, roku. Ile to jest kcal? Tak samo przykro mi jest obserwować jak wiele osób uprawia sport po to by pić i pije coraz więcej, bo uprawia sport. Zrobiłem o tym nawet cały film. O tej pułapce: Mogę dzisiaj wypić butelkę wina, bo dużo jeździłem. A jutro będę dużo jeździć, bo jutro też chcę się napić. Mówisz sobie, że Ci smakuje. A tak naprawdę chodzi o coś zupełnie innego. O to, że alkohol jako jedyny daje Ci to uczucie zdjęcia łańcucha z klatki piersiowej. Rozluźnia Cię, poprawia nastrój. Resetuje stres i problemy skryte cholernie głęboko. Być może nawet te z trudnego dzieciństwa.  Dlatego uważam siebie za niedoszłego alkoholika. Niedoszłego tylko dlatego, bo kiedyś udało mi się wychwycić ten schemat, ale co najśmieszniejsze nie u siebie.  Wychwyciłem patrząc z boku. Wychwyciłem będąc w grupie kolarzy, gdzie każdy był na kacu. Każdy narzekał na upał, zmęczenie, ból, zły nastrój, ale nie dlatego, bo trasa była wyjątkowo skomplikowana, a temperatura wyjątkowo wysoka.  Kiedyś zapytałem siebie po co tutaj jestem. Dla roweru czy dla wieczorów przy browarach po każdym powrocie do bazy. Rano ruszając juz myślami byłem przy wieczornym stoliku  Jestem niedoszłym alkoholikiem też dlatego, bo spełniam wszystkie warunki osoby o wysokim ryzyku uzależnienia od alkoholu: Mam zdiagnozowane zaburzenia lękowe, jestem osobą o niskim poczuciu własnej wartości. Do tego alkohol w moim przypadku łagodzi przewlekły stres i napięcie. Niweluje stres. Po alkoholu jestem zabawny i pocieszny. Rozwiązuje praktycznie wszystkie moje codzienne troski. Nawet jedno piwo sprawia, że unoszę się te kilka milimetrów nad ziemią. Lubię to uczucie. Jest praktycznie takie samo jak po wjechaniu Bieńkówki na czas.  Jak każdy Polak żyję w otoczeniu gdzie jest powszechna kultura picia alkoholu podczas każdego spotkania. Każda uroczystość to alkohol. Chrzciny, urodziny, komunia, stypa. Kiedyś wjeżdzała wóda, teraz bardziej prestiżowe barwione alko, wina i piwo. Osoba niepijąca na imprezie to dzikus.   To nie jest nasza wina. To pewna tradycja i kultura. Zauważcie nawet, że nawet w serialu Rodzina Zastępcza na którym się wychowywaliśmy w każdym odcinku był alkohol. Po czasie to dla mnie też masakra. Chociaż może przesadzam? W kolarskiej kulturze też kiedyś było tak, że każda wspólna trasa to meta z piwkiem. Bo piwo jest mokre i zimne i dobrze wchodzi po wysiłku. Na szczęście zauważam, że wiele dobrego pod tym względem zrobiły napoje funkcjonalne i piwa zero.  Tylko nie wiem ile osób aktywnych sportowo potem samemu pije w domu. Ile osób narzeka na nadwagę wiedząc, że to nie wina złego jedzenia, tylko tego, że nie potrafią rzucić alkoholu. Sporo z nas nawet nie wie ile kcal ma butelka wina i deska serów. Co weekend. Każdy weekend. Dobra, dzisiaj poszaleję, od poniedziałku znowu dieta. W poniedziałek stajesz na wadze i znów wyrzuty sumienia. Masz wyrzuty, to więcej musisz jeździć, żeby zbudować deficyt na weekend. Nie chciałbym zostać źle zrozumianym. Nie mam nic do alkoholu. Nie mam nic do sprzedawania go na każdym rogu. Tak samo nie mam nic jak ktoś obok mnie zamawia piwo do kolacji. Bo ma taką ochotę. Tak samo jak lampka wina do obiadu czy prosecco na śniadanie jak u południowców. Mi chodzi tylko o regularność oraz schematy. O warunkowanie. O to, że zawsze grill to alkohol, zawsze dzień wolny od pracy to alkohol. Albo każdy wieczór to też alkohol.  Nie dlatego, bo piwo super uzupełnia kcal, bo wino super smakuje. Picie dla smaku to inne picie, niż picie pod pretekstem dobrego smaku czy dobrej okazji. Gdzie głęboko w sercu wiesz, że po wypiciu przyjdzie ten moment rozluźnienia. Przez całą trasę na rowerze myślisz o tym, że rozluźnisz się przy piwie. Albo przez cały wujowy tydzień w pracy myślisz, że w weekend przyjdzie okazja do napicia się. Tak. Ja kiedyś też czekałem. Szedłem ze skrzynką do sklepu specjalistycznego na wymianę butelek.  Dlaczego dzisiaj piję raz do roku a nie co drugi wieczór? Ja nie przestałem pić z dnia na dzień, chociaż miałem takie momenty, kiedy przez rok nawet nie powąchałem alko. Byłem wtedy na redukcji po zakupie drugiej szosy. Chciałem jak najszybciej zjechać że 103 na 79. Wiedziałem że alkohol jest największym niszczycielem wszelkich postępów. Ponieważ uruchamia u mnie jeszcze dodatkową gastro fazę. Nie tylko dlatego, bo do piwa idealnie pasuje pizza. U mnie wyłączały się wówczas wyrzuty sumienia, które wracały z podwójną siłą następnego poranka. Stąd ta zerojedynkowa decyzja z dnia na dzień.  Tak samo przestałem czytać o nowych piwach kraftowych i oddałem kaucyjną plastikową skrzynkę do sklepu bez wymiany na nową.  Nawet nie zdajesz sobie sprawy jak ta decyzja mi pomogła. OK, przez pierwsze 2 tygodnie było ciężko, psychicznie. Bo wiesz, że w domu nie czeka zimne piwo. Tak samo jak nie czeka czekolada i paczka chrupek. Jednak po 3 tygodniach ból zamienił się w lekkie pieczenie, a po 6 tylko szczypanie. Co prawda musiałem omijać alejki z piwami, ale jakoś dawałem radę. Po dwóch miesiącach widziałem zdecydowaną różnicę w wyglądzie i samopoczuciu. Miałem mniej dni z epizodami nerwicy lękowej czy depresji. Dziwnie lekko na sercu i na wadze. Okazało się też, że leki, które przyjmuję mogą lepiej działać gdy nie łączę ich z alko. Pamiętam też jak smakowało pierwsze po roku piwo. Jedno. Wypiłem jedno, a nie trzy. Bo była super okazja. Naprawdę wyjątkowa.  Gdy ustabilizowałem wagę to włączył mi się tryb oszczędzania kalorii. Zaczęło mi być szkoda pracy, którą włożyłem w to wszystko. Mówiąc o kaloriach mam na myśli nie tylko te z alkoholu, ale przede wszystkim te wynikające z późniejszej gastrofazy. Nauczyłem się też odmawiać, mówiąc wprost, że mojego bilansu energetycznego nie stać dziś na więcej.  Dlatego przez ostatnie 10 lat upiłem się tylko raz. Raz miałem kaca i to tylko po to, aby upewnić się w przekonaniu, że nie chcę więcej do tego wracać.  Zacząłem używać alkohol tak jak rzodkiewkę. Kiedy jadłem ostatnio rzodkiewkę? Nie pamiętam. Kiedy zjem kolejną? Nie mam pojęcia. Czy przeszkadza mi ktoś kto obok mnie je rzodkiewkę? Nie. Tak samo w sklepie może być cały dział z rzodkiewkami. Przejdę obojętnie.  Dzisiaj mamy lipiec w kalendarzu. Ostatnie dwa piwa wypiłem w grudniu. Taka statystyka powiela się u mnie już chyba drugi rok. Jakie odczuwam korzyści z niemal całkowitej abstynencji?  Zawsze jestem kierowcą.  Ale też mniej wydaję na taksówki A tak na serio, największe korzyści czuję na wyjazdach. Mam zarąbistą regenerację. O wiele lepszą. A w trakcie samej jazdy mniej narzekam. Lepiej śpię. Fizycznie czuję się naprawdę super. Na codzień i na rowerze. Doszedłem do wniosku, że na obozach piwo przyjmuje ujemny współczynnik regeneracji. Dokłada ciału dodatkowy wysiłek, psuje jakość snu, metabolizm, resyntezę glikogenu, obciąża wątrobę i przede wszystkim łeb. Nastepnego dnia już nie czuję się jak nadmuchana beczka.  Umiem odmawiać do perfekcji. Wszystko zrzucam na sport, zawody, cele. Przygotowuję się do czegoś tam, w związku z czym nie piję alkoholu. Jutro mam test FTP, za dwa tygodnie wyścig. Wszyscy to łykają i już bez pytania otwierają mi zerówkę albo colę. Nie boję się już braku akceptacji w grupie jak powiem, że nie piję. Mam też oczywiście mniejsze wahania wagi. 76/77 kg niezmiennie. Oszczędzam mnóstwo kcal, które mogę zagospodarować sobie inaczej. Zamiast alko mogę sobie kupić draże korsarze, chrupki orzechowe albo żelki. Raz w tygodniu walnąć kebsa.  Policz też ile kasy zostawiałeś w knajpach na alkohol. A ile w skali roku wychodzi na ten kupowany w sklepie. Można się śmiać, ale jeśli to jest tysiak rocznie, to można go przewalić na inne głupoty. Na ceramiczne łożyska suportu.  Jak można spróbować to ogarnąć samodzielnie? Pierwsze pytanie jest w pełni szczere. Do samego siebie. Pijesz bo Ci smakuje, czy pijesz dla uczucia gilgotania. Jak dla smaku to luz. Jesli dla odreagowania i często o tym myślisz, to znaczy, że gdzieś, kiedyś może być problem. Tym bardziej jeśli tak jak ja słowo PROBLEM masz wypisane na twarzy. To stwarza ryzyko w przyszłości. Wtedy możesz spróbować po prostu stopniowo zmniejszać ilość alko w Twoim życiu. Bo z dnia na dzień może być ciężko.  Gorzej jeśli zdarza Ci się pić do ocinki, do zerwania filmu. To jest ogromna czerwona flaga. Tak samo jak ukrywanie się z piciem czy robienie zapasów, by nigdy w domu nie zabrakło. Druga kwestia to motywacja. Jeśli masz do zrzucenia kilka kilogramów to wiedz, że tyje się nie tylko od jedzenia. W cholerę ludzi jest otyłych przez alkohol. Raz, że każde piwo to pół paczki chipsów, numer dwa to gastro.  Trzy to wpływ na formę. Zwłaszcza na wyjazdach. Po 4 dniu jazdy z imprezami co wieczór wysiadasz. Zamiast cieszyć się sportem walczysz tak naprawdę z kacem, który siada na nogi i głowę. Tak samo cofają alkoweekendy, albo alcoweekendowe wyprawy rowerowe. Stówka w kołach, ale czteropak piwka skasował aktywność. Pamiętaj też, że Twoi sportowi idole też mocno ograniczają procenty, bo to nie licuje z progresem formy. Cztery to jest naturalne pragnienie. Po rowerze lecisz do żabki po piwo, bo jesteś odwodniony. Wychlej litr wody przed wejściem do sklepu. bmwChce Ci się ogólnie pić, a nie pić piwo.  Kup sobie coś gazowanego, kostki lodu, albo najlepiej saturator i koncentraty napojów. Masz fanty, mirindy, lemoniady po kokardy i to bez kaucji.  Numer pięć to zmiana kulturowa w Polsce jak i społeczności kolarskiej. Coraz więcej osób po prostu nie pije. Dlaczego? Bo ktoś inny też nie pije. Jest to bardziej akceptowane, mniej antyspołeczne niż jeszcze 10 lat temu. Dziś na impreze czuję dumę, że jestem trzeźwy i wracam autem do domu. Tak samo dumnym można być w nowy rok, który zaczynam zarąbistym treningiem na trenażerze a nie z głową w misce.

Miguel Ángel González Suárez te presenta el Informativo de Primera Hora en 'El Remate', el programa matinal de La Diez Capital Radio que arranca tu día con: Las noticias más relevantes de Canarias, España y el mundo, analizadas con rigor y claridad. Una excelsa España se impone a Francia y logra el pase a su segunda final mundialista dieciséis años después. Hoy hace dos años: Oyarzabal marca el gol que le da a España su cuarta Eurocopa ganando a Inglaterra. Y hoy hace un año: El PP propone declarar persona non grata a Pedro Sánchez en Lanzarote, donde veranea. Hoy se cumplen 1.608 días de guerra entre Rusia y Ucrania. 4 años y 140 días. Hoy es miércoles 15 de julio de 2026. Día Mundial de las Habilidades de la Juventud. En el año 2014 la Asamblea General de la ONU proclamó el 15 de julio como el Día Mundial de las Habilidades de la Juventud, para divulgar la importancia de impulsar a los jóvenes a través de la adquisición de habilidades y destrezas, que les permitan acceder al mercado laboral global. 1738: Se funda la Real Academia de Medicina en Madrid. 1834: Finaliza de forma oficial el Tribunal de la Santa Inquisición gracias a un decreto de la reina Isabel II. 1916: en Seattle (Washington) (Estados Unidos), William Edmund Boeing funda la compañía aeronáutica que lleva su nombre: Boeing. 1924.- Se publica "20 poemas de amor y una canción desesperada" del chileno Pablo Neruda. 1977.- Unión de Centro Democrático (UCD) gana las primeras elecciones legislativas democráticas en España desde la II República. El 15 de julio de 1997 muere el diseñador de moda italiano Gianni Versace en los escalones fuera de su mansión de Miami tras ser disparado en la cabeza por Andrew Cunanan. 2006.- Lanzan el servicio de la red social Twitter, creada el 21 de marzo por Jack Dorsey, al que se unen Biz Stone y Evan Williams. 2008.- Vicente del Bosque es nombrado seleccionador español de fútbol. 2014.- El conservador luxemburgués Jean-Claude Juncker es elegido presidente de la Comisión Europea. Patrocinio del santo de cada día por gentileza de la Casa de las Imágenes, en la calle Obispo Perez Cáceres, 17 en Candelaria. Santos Rosalía, Julia, Justa, Buenaventura y Felipe. Del Tratado de Utrecht hasta una verja con los días contados: ¿cuál es la historia de Gibraltar? La Audiencia de Badajoz condena a David Sánchez, hermano del presidente, a 9 años de inhabilitación para empleo público. El Gobierno confía en la "inocencia" de David Sánchez y ve la sentencia como un intento para "derribar" al Ejecutivo. El juez Peinado reclama a Begoña Gómez que demuestre que fue a la graduación de su hija a Reino Unido. Confirmado por Revolut: traerá sus cajeros automáticos a Canarias antes de que termine el año. El banco digital supera los 120 cajeros en España un año después de su lanzamiento y prevé extender su red a las Islas. Mogán recurre al Supremo la anulación de la tasa turística y la mantiene en vigor hasta que haya una sentencia firme. El Ayuntamiento defiende la legalidad del gravamen de 0,15 euros por persona y día, asegura que no tiene un fin recaudatorio y estudia incrementar su cuantía si el Tribunal Supremo falla a su favor. El Gobierno de Canarias rechaza la tasa turística y defiende la recaudación a través del IGIC. El portavoz del Ejecutivo regional, Alfonso Cabello, ha precisado que de esta manera el cobro puede ser distribuido en el conjunto del territorio de manera que no se genere la idea de que “los municipios que son más turísticos tienen más ingresos”, cuando otras zonas con menos pernoctaciones también reciben un impacto por los visitantes. El 11,2% de los menores presenta un riesgo suicida elevado. El primer diagnóstico integral de Unicef y la Consejería de Educación del gobierno autonómico asocia el uso intensivo de las pantallas con un incremento del malestar emocional entre los estudiantes, cuya edad media de acceso al primer móvil se sitúa en los 10,69 años. Los aeropuertos de Canarias han registrado en los seis primeros meses de 2026 un total de 26.847.826 pasajeros, un 0,7% menos que en el mismo periodo del año pasado. De los 26.729.685 viajeros comerciales, 10.647.275 lo hicieron en vuelos nacionales, un 0,2% menos que en los primeros seis meses de 2025, y 16.082.410 lo hicieron en vuelos internacionales, un 0,8% menos. Paso decisivo para hacer realidad la central hidroeléctrica de Tenerife: tendrá un gran impacto en la generación de energía y la economía de la isla. El Consejo de Ministros otorga la titularidad de la infraestructura a Red Eléctrica de España para blindar el almacenamiento público de energía en los barrancos de Güímar que fueron utilizados como plantas de extracción de áridos. Salvamento Marítimo rescata a 37 migrantes de una neumática a la deriva al este de Lanzarote. Una llamada desde la precaria embarcación alertó de una avería en el motor y el helicóptero Helimer 205 la localizó este martes. Un 15 de julio de 1924.- Se publican "20 poemas de amor y una canción desesperada" del chileno Pablo Neruda. Luis Eduardo Aute publica en 1986 un doble LP que parafrasea y da la vuelta a ese título para convertirlo en “20 Canciones de Amor y un Poema Desesperado”

Miguel Ángel González Suárez te presenta el Informativo de Primera Hora en 'El Remate', el programa matinal de La Diez Capital Radio que arranca tu día con: Las noticias más relevantes de Canarias, España y el mundo, analizadas con rigor y claridad. Puerto de la Cruz revive este martes su cita más multitudinaria con la Virgen del Carmen. Los actos festivos incluyen concursos de pesca, tómbola, cucaña y festival folclórico, además de la eucaristía y la procesión marítima. Hoy martes 14 de julio a las 20:00 horas semifinales del mundial entre Francia y España. AT&T Stadium (Estadio Dallas), Arlington, Texas, Estados Unidos. Las apuestas están: Francia: 39-40% de probabilidad implícita. España: 29-30%. Hoy hace un año: Una misión comercial canaria viaja a Japón para promocionar vinos y el sector audiovisual. Se pretenden ampliar las vías comerciales y de comunicación con uno de los países de mayor crecimiento económico de los últimos años. Hoy se cumplen 1.607 días de guerra entre Rusia y Ucrania. 4 años y 139 días. Hoy es martes 14 de julio de 2026. Día Internacional del Auxiliar de Enfermería. El 14 de julio se celebra el Día Internacional del Auxiliar de Enfermería, para destacar la labor y compromiso de estos profesionales esenciales de la salud, durante la hospitalización y recuperación de pacientes. Además de para reconocer su trabajo, la creación de esta efeméride pretende reivindicar los derechos laborales y necesidades de estos trabajadores fundamentales de la salud. El auxiliar de enfermería asiste a médicos y enfermeras, en los cuidados auxiliares de pacientes y residentes de centros asistenciales de salud, hospitalarios y geriátricos, interviniendo en su proceso de ingreso, hospitalización y recuperación. 1789.- El pueblo de París toma la prisión-fortaleza de la Bastilla. Comienza la Revolución Francesa. 1853.- Apertura de la Exposición Universal de Nueva York. 1881.- Asesinado el legendario pistolero norteamericano Billy "El Niño". 1900.- Se inauguran en París los II Juegos Olímpicos de la Era Moderna. 1931.- Apertura de las primeras Cortes de la II República española, con carácter constituyente. Julián Besteiro, elegido presidente. 1990.- Elegido el nuevo Politburó y Secretariado del Partido Comunista de la URSS, con Mijail Gorbachov como secretario general. 1997.- Millones de personas se manifiestan en toda España, en la mayor movilización popular de la historia del país, contra la violencia de ETA, tras el asesinato del concejal del PP Miguel Angel Blanco. 1998.- Se comercializa en Gran Bretaña una prueba de saliva que permite verificar la paternidad. 2005.- La ONU lanza oficialmente la iniciativa "Alianza de Civilizaciones", propuesta por el presidente español José Luis Rodríguez Zapatero. El 14 de julio de 2007, comienza probarse el Gran Telescopio Canarias, el más grande del mundo. Tras siete años de construcción y un costo de 130 millones de euros, el Gran Telescopio de Canarias en La Palma es capaz de captar algunas de las imágenes más distantes del universo, siendo el telescopio óptico de apertura simple más grande del mundo. 2016.- 84 muertos por una atentado islamista en Niza durante la celebración de la Fiesta Nacional francesa, cuando un camión arrolló al público que festejaba el evento en el paseo marítimo. Patrocinio del santo de cada día por gentileza de la Casa de las Imágenes, en la calle Obispo Perez Cáceres, 17 en Candelaria. santos Camilo de Lelis, Francisco Solano y Humberto. Trump restablece el cerco naval a Irán y aplicará un peaje del 20% por proteger buques en Ormuz. Un incendio en un bar de Bangkok deja al menos 27 muertos y 35 heridos. Identificados seis de los 13 fallecidos del incendio de Almería: un español y cinco extranjeros. Sánchez y Moreno agradecen la labor de las instituciones en el fuego de Los Gallardos: "La emergencia climática mata" El Gobierno exige a Feijóo desautorizar a Rajoy, al que acusa de haber metido a España en "un lío diplomático" con Francia. El TSJC decide que la tasa turística de Mogán es nula de pleno derecho. Aunque la sentencia no lo cita expresamente, la consecuencia lógica es que el Ayuntamiento tenga que devolver todo lo recaudado hasta ahora por esta vía. El Gobierno de Canarias se reunirá este martes en Tenerife con la Federación Canaria de Municipios (FECAM) para abordar las líneas del marco presupuestario del Fondo de Desarrollo de Canarias (FDCAN) para el decenio 2027-2037 y fijar las nuevas prioridades de las inversiones, tal y como pidieron las corporaciones locales en mayo. Dichas prioridades son, como ya se anunció en su momento, la construcción de vivienda pública y crear nuevas infraestructuras sociosanitarias en el archipiélago. Ecologistas en Acción insta a suprimir las excursiones turísticas a motor en La Graciosa. En sus alegaciones a la modificación de la Ordenanza Reguladora del Tráfico en la isla, solicita que el transporte de visitantes sea sustituido por un programa de visitas guiadas a pie o en bicicleta en coherencia con la “especial fragilidad ambiental” del entorno. Feijóo presentará de manera oficial la candidatura de Poli Suárez a la Alcaldía de Las Palmas de Gran Canaria el próximo jueves. Suárez es actualmente consejero de Educación, Formación Profesional, Actividad Física y Deportes del Gobierno canario, además de secretario general del PP de Canarias. Arrancan las negociaciones del Cabildo de Gran Canaria con las constructoras para la reforma del estadio: «Estudiaremos rebajar algunas de sus pretensiones» El Ejecutivo insular abrirá un procedimiento negociado tras quedar desierta la licitación y revisará con el equipo redactor el alcance del proyecto, cuyo coste real podría alcanzar los 220 millones de euros. Un día como hoy en 1979: en la Plaza de la Concordia de París (Francia) el músico Jean Michel Jarre desarrolla un concierto audiovisual reuniendo a más de un millón de personas al aire libre con motivo del éxito de sus álbumes Oxygène y Equinoxe, iniciando la era de los megaconciertos.

The "Community Meets Clinic" podcast series introduces clinicians and healthcare personnel specializing in rare neuroimmune disorders. In this episode, Krissy Dilger of SRNA spoke with Dr. Ayşe Altıntaş, Professor of Neurology at Koç University School of Medicine in Istanbul, Turkey, which has been designated as a Center of Excellence in Rare Neuroimmune Disorders. Dr. Altıntaş described the unmet needs in rare neuroimmune disorders and noted her role on an international panel developing updated NMOSD diagnostic criteria [00:03:40]. She outlined current research on mechanisms of optic neuritis, pregnancy complications and aquaporin-4 antibodies, and developing accessible biomarkers beyond CSF with a future goal of remote monitoring [00:06:01]. Dr. Altıntaş also explained Koç University's multidisciplinary demyelinating disease center model, emphasizing coordinated consultations, advanced MRI capabilities, shared decision-making, and the value of specialized centers, while expressing hope due to rapid advances in biomarkers and targeted therapies [00:11:43]. You can view the medical profile of Dr. Ayşe Altıntaş here:https://www.kuh.ku.edu.tr/doctors/ayse-altintasAyşe Altıntaş, MD is a professor of neurology at Koç University School of Medicine in Istanbul, Türkiye. She graduated from Ege University Faculty of Medicine in 1986 and completed her neurology residency there in 1992. She received early training in neuroimmunology as a fellow at Mayo Clinic under Prof. Moses Rodriguez and later continued her research at Mayo Clinic with Prof. Claudia Lucchinetti and Prof. Brian Weinshenker, focusing on the animal model, immunopathology, and imaging correlates of multiple sclerosis.Prof. Altıntaş served at Istanbul University Cerrahpaşa School of Medicine for 23 years before joining Koç University in 2018, where she established a neuroimmunology laboratory and continues to lead clinical and translational research. Her work focuses on multiple sclerosis, neuromyelitis optica spectrum disorders (NMOSD) and MOG antibody-associated diseases (MOGAD), with an emphasis on biomarkers and disease mechanisms. She is actively involved in international organizations, including BioMS-eu, The MOG Project, Siegel Rare Neuroimmune Association (SRNA), MEDEN, the MSBase Scientific Leadership Group, and the Guthy-Jackson Charitable Foundation International Scientific Consortium.00:00 Welcome and Guest Intro01:39 Why Neurology03:40 Choosing Rare Disorders06:01 Current Research Projects11:43 Clinic Team and Workflow15:48 Advanced Imaging and Coordination17:20 Self Care and Balance20:20 Advice for New Patients22:17 Hope for the Future24:34 Closing

Dr. GG deFiebre of SRNA spoke with Dr. Michael Levy and Dr. Benjamin Greenberg about CAR-T therapy for aquaporin-4-positive NMOSD. They described why targeting B cells may reduce aquaporin-4 antibodies over time and could enable long-term remission or reduced need for ongoing drugs [01:37]. The physicians outlined an autologous Phase 1 study at Mass General and UT Southwestern [07:02]. They discussed eligibility rationale and how lessons from this NMOSD-focused trial could inform future neuroimmune disorder research [09:10]. You can find more information about the trial here:https://clinicaltrials.gov/study/NCT07573332?cond=NMOSD&intr=CAR-T&viewType=Card&rank=1Benjamin M. Greenberg, MD, MHS is a Professor and the Cain Denius Scholar in Mobility Disorders in the Department of Neurology [https://utswmed.org/why-utsw/departments/neurology/] at UT Southwestern Medical Center in Dallas, Texas. He currently serves as the Vice Chair of Translational Research and Strategic Initiatives for the Department of Neurology. He is also the interim Director of the Multiple Sclerosis Center [https://utswmed.org/locations/aston/multiple-sclerosis-and-neuroimmunology-clinic/] and the Director of the Neurosciences Clinical Research Center. In addition, he serves as Director of the Transverse Myelitis and Neuromyelitis Optica Program and the Pediatric Demyelinating Disease Program [https://www.childrens.com/specialties-services/specialty-centers-and-programs/neurology/demyelinating-disease-program] at Children's Medical Center.Dr. Greenberg earned his medical degree at Baylor College of Medicine before completing an internal medicine internship at Chicago's Rush Presbyterian-St. Luke's Medical Center. He performed his neurology residency at the Johns Hopkins School of Medicine. He also holds an M.H.S. in molecular microbiology and immunology from the Bloomberg School of Public Health, as well as a bachelor's degree in the history of medicine – both from Johns Hopkins. Prior to his recruitment to UT Southwestern in 2009, Dr. Greenberg was on the faculty of the Johns Hopkins Division of Neuroimmunology, serving as the Director of the Encephalitis Center and Co-Director of the nation's first dedicated Transverse Myelitis Center.Dr. Greenberg splits his clinical time between adult and pediatric patients at William P. Clements Jr. and Zale Lipshy University Hospitals, Parkland, and Children's Medical Center. His research focuses on better diagnosing, prognosticating, and treating demyelinating diseases and nervous system infections. He also coordinates clinical trials to evaluate new treatments to prevent neurologic damage and restore function to affected patients. Michael Levy, MD, PhD is a recognized neurologist with over 15 years of clinical and research expertise in rare neuroimmunological disorders. He established the Neuroimmunology Clinic and Research Laboratory at Massachusetts General Hospital and is the Research Director in the Division of Neuroimmunology and Neuroinfectious Disease. Previously, Dr. Levy was on the faculty at Johns Hopkins University and was the founding Director of their Neuromyelitis Optica Clinic. Clinically, Dr. Levy cares for patients with MOG antibody disease (MOGAD), neuromyelitis optica spectrum disorder (NMOSD), and idiopathic transverse myelitis (TM). Dr. Levy is also the principal investigator (PI) on numerous patient studies and drug trials for new and improved treatments for these disorders. In 2022, Dr. Levy became the lead principal investigator for the two worldwide clinical trials in MOG antibody disease. In the lab, Dr. Levy's research focuses on the development of animal models of NMO and MOG with the goal of tolerization as a sustainable long-term treatment. Dr. Levy has more than 200 peer-reviewed research articles, reviews and editorials, and 3 patents covering NMO tolerization therapy, TM diagnostics, and stem cell regeneration approaches.

Welcome to the NeurologyLive® Mind Moments® podcast. Tune in to hear leaders in neurology sound off on topics that impact your clinical practice.In this Mind Moments episode, Grace Gombolay, MD, associate professor of pediatrics at Emory University School of Medicine and director of the Pediatric Neuroimmunology and Multiple Sclerosis Program at Children's Healthcare of Atlanta, joins Varun Kannan, MD, assistant professor of pediatrics in the Department of Neurology at Emory University School of Medicine and Children's Healthcare of Atlanta, for a discussion on acute disseminated encephalomyelitis (ADEM), a rare inflammatory demyelinating syndrome that remains an important diagnostic consideration in pediatric neuroimmunology. The conversation provides a practical overview of how clinicians should recognize ADEM, distinguish it from conditions such as multiple sclerosis, MOG antibody-associated disease (MOGAD), and neuromyelitis optica spectrum disorder (NMOSD), and approach treatment in the absence of FDA-approved therapies. Gombolay and Kannan review the clinical and radiographic hallmarks of ADEM, the role of MRI and antibody testing in the diagnostic workup, and current treatment strategies involving corticosteroids, IVIG, and plasma exchange. They also discuss long-term outcomes, the evolving relationship between ADEM and MOGAD, emerging biomarkers such as neurofilament light chain and cytokine profiling, and common misconceptions that can complicate diagnosis and management in clinical practice. Looking for more Multiple sclerosis & demyelinating disorders discussion? Check out the NeurologyLive® Multiple sclerosis & demyelinating disorders clinical focus page.Episode Breakdown: 1:15 – Recognizing the clinical and imaging features of ADEM 3:30 – Distinguishing ADEM from MS, MOGAD, and NMOSD 7:20 – Current treatment approaches and management strategies 10:10 – Neurology News Network  12:40 – Long-term outcomes and monitoring after recovery 15:55 – Emerging biomarkers and improving diagnostic precision 19:10 – Preventing future attacks and reducing relapse risk 21:10 – Remaining research gaps and unanswered questions in ADEM The stories featured in this week's Neurology News Minute, which will give you quick updates on the following developments in neurology, are further detailed here: FDA Allows AMT-130 Huntington Disease Data to Support Planned BLA Submission Under Accelerated Approval Pathway Teva Submits NDA for Ecopipam, Potential First New Tourette Syndrome Treatment in Over a Decade FDA and EMA Accepts Regulatory Applications for Cemdisiran in Generalized Myasthenia Gravis Thanks for listening to the NeurologyLive® Mind Moments® podcast. To support the show, be sure to rate, review, and subscribe wherever you listen to podcasts. For more neurology news and expert-driven content, visit neurologylive.com.

Ta książka trafi prosto w serduszka dzieci, które mają ukochane zabawki, bo będą rozumiały, że dbanie o nie to wielka sprawa.Powinny ją jednak też przeczytać maluchy, które często proszą o nowe rzeczy, chcą więcej i więcej, choć mają naprawdę sporo.”Kubuś i ukochany miś” uśmiechają się do nas z okładki najnowszej części książek tworzonych przez Jakuba Tylmana i Ewę Podleś. Znasz tego chłopca? Kubuś jest przedszkolakiem, a o jego przygodach opowiadałam już na blogu Aktywne Czytanie kilka razy, bo to moja patronacka seria. Lubię ją za pokazywanie dzieciom codziennych sytuacji, ale z takim głębszym przesłaniem, niż tylko codzienność. Tym razem sprawa dotyczy zepsutego misia. Urwana łapka to wypadek, który zdarzył się podczas zabawy z kolegą. Jest smutek, są przeprosiny, ale one przecież łapki misia nie przykleją z powrotem.Tu do akcji wkracza mama, która zaprasza chłopców do naprawienia maskotki. Raz dwa i miś wygląda jeszcze lepiej niż przedtem, jest gotowy do dalszych zabaw. Czy to koniec przygody?Mogłoby się wydawać, że to książka o małym konflikcie (zepsuta zabawka) i rozwiązaniu problemu. Też, ale to nie koniec historii, bo tym przeżyciem chłopcy dzielą się z dziećmi w przedszkolu.Nauczycielka natomiast wykorzystuje temat do rozmowy o dawaniu drugiego życia przedmiotom. Tyle zabawek można naprawić, zamiast wyrzucać i domagać się nowych! Na tym opiera kolejne zajęcia z dziećmi, każdy przynosi coś z domu i zaczyna się wielki reperowanie.To takie ważne, żebyśmy pokazywali dzieciom, jak wiele radości może przynieść naprawienie zepsutej zabawki, czasem więcej niż dostanie nowej. Przecież maluchy często przywiązują się do ukochanych pluszaków, autek czy kolekcji kamieni. Warto pielęgnować to przywiązanie i na nim budować świadomość ekologiczną. Pomyśl o zabawkach swojego malucha, czy któraś potrzebuje naprawy? Do dzieła! #kubuśiukochanymiś #zabawki #ekologicznezabawki #książkidladzieciaktywneczytanie 

Det är midsommar och vad kan passa bättre än några småläskiga sägner om just midsommar, eller i sista sägnens fall med lite midsommarfeeling. Varför inte varva ner lite mellan midsommardansen och blomsterplockandet med några sägnerSägner i detta avsnitt Småfolket dansar, sägnen uppges komma från Mogärde i JämtlandJättarnas brudkrona, sägnen uppges komma från området runt betarsjön i Ångermanlandbåda är hittade här https://sagenresan.sagobygden.se/Hårgalåten, sägnen uppges komma från Hårga i Hälsinglandhttps://sv.wikipedia.org/wiki/H%C3%A5rgadansenljudet av steg kommer från Iamgiorgio på https://freesound.org/people/Iamgiorgio/sounds/371785/ hårgalåten är skapad med hjälp av midifil från http://www.folkwiki.se/Musik/1038

ZAPIS NA LISTĘ ZAINTERESOWANYCH WEBINAREM: Jak przestać słuchać Zaburzonego Głosu? - od "wiem co zmienić, ale nie potrafię" do prawdziwej zmiany" - https://bit.ly/webinar-zainteresowaniRestrykcje, ograniczenia, intensywne treningi - a to wszystko po to, by później i tak usłyszeć w swojej głowie głos, który mówi “Zawaliłaś”, “Mogłaś zrobić to lepiej”, “Należy Ci się kara”. Nie ważne, jak bardzo próbujesz spełnić oczekiwania Zaburzeń Odżywiania i tak, w pewnym momencie jesteś zalewana falą wyrzutów sumienia. Znajome?00:00 Wstęp01:39 Dlaczego czujesz poczucie winy, gdy jesz?05:17 5 kroków, by nie nie mieć wyrzutów sumienia po jedzeniu30:07 Twój Komfortowy Kącik - “za sikanie jakoś się nie obwiniasz”33:40 ZakończenieHej! Nazywam się Weronika Cieślak. Jestem Psychodietetyczką i przyszłą Psycholożką. Pracuję z osobami z zaburzeniami odżywiania. Edukuję w Internecie o zdrowej relacji z jedzeniem i sobą, podając "wiedzę na talerzu"

El programa comienza analizando el grave cariz que toma la trama Ferraz, con la figura de "Leire 10", quien se reúne en la Fiscalía General del Estado con cargos relevantes, lo que genera críticas a la Moncloa por su aparente inacción. Un tema central es la visita del Papa León XIV a Arguineguín, Gran Canaria, para encontrarse con migrantes y las organizaciones que los acogen. Se destaca la crisis migratoria en las islas, la labor de acogida del pueblo canario y las críticas de la alcaldesa de Mogán a la gestión del gobierno central. En la actualidad nacional, se informa sobre un incendio con dos fallecidos y 24 heridos en un bloque de viviendas en Magaluf, Mallorca, y otro incendio forestal que ha calcinado 3500 hectáreas en Villanueva de los Castillejos, Huelva, ya estabilizado. En política regional, se constituye el nuevo parlamento andaluz y Alfonso Fernández Mañueco jura su cargo en Castilla y León con el apoyo de VOX. Finalmente, varios expertos deportivos comparten sus ...

Federico entrevista a Onalia Bueno, alcaldesa de Mogán, por la visita del Papa a Canarias.

Krissy Dilger of SRNA welcomed University of Washington neuroimmunologist Dr. Shuvro Roy for an open Q&A on transverse myelitis (TM). Dr. Roy explained how TM can be both a presentation and a diagnosis, with “idiopathic TM” used when extensive testing finds no underlying cause and noted that recurrence should prompt reevaluation for conditions like NMOSD, MOGAD, or neurosarcoidosis and consideration of preventive immunotherapy [00:06:16]. He addressed audience questions about lifestyle and rehabilitation topics including diet, metabolic health, exercise, sleep issues, and safe considerations around CBD or THC-containing gummies, and reviewed approaches to chronic pain, spasticity, physical therapy timelines, and spinal cord stimulation (including ArcX) [00:13:20]. Dr. Roy also discussed the current status of peptides and stem cells, highlighted emerging cell-based therapies like CAR-T, and answered a case question about a high MOG antibody titer and its diagnostic implications [00:24:53].Shuvro Roy, MD is an Assistant Professor of Neurology at the University of Washington, specializing in neuroimmunology, with a specific focus on multiple sclerosis (MS) and related neuroimmunologic disorders. He is Co-Director of the UW SRNA Center of Excellence for Rare Neuroimmune disorders. He is also a core teaching faculty member for the UW Medicine Multiple Sclerosis Center's fellowship program, contributing to clinical education and research initiatives like the ECHO MS program in collaboration with the National MS Society. Dr. Roy is actively engaged in projects aimed at improving access to care, addressing healthcare disparities, and enhancing patient safety for individuals living with MS and related conditions. He has co-authored recent research articles in medical journals on a variety of topics, including studies on stiff person syndrome, encephalomyelitis, MOG-antibody disorder, and multiple sclerosis treatment protocols. Dr. Roy is dedicated to helping his patients thrive amid challenging, lifelong neurological conditions.00:00:00 Welcome and Introductions00:01:24 What Is Transverse Myelitis00:03:30 Common Causes and Mechanisms00:06:16 Diagnosis Versus Presentation00:10:39 Monophasic or Recurrent00:13:20 Diet Do's and Don'ts00:17:25 Aging and Long-Term Health00:24:53 Peptides and Stem Cells00:33:07 Fatigue Sleep and CBD or THC-containing gummies00:37:58 Chronic Pain Options00:43:55 Physical Therapy Recovery00:47:56 Spinal Cord Stimulation ArcX00:51:46 Stopping Pregabalin Safely00:52:59 Trials and Rehab at Any Age00:56:00 MOG Titer and Diagnosis01:00:02 Closing

Mogłoby się wydawać, że w tej sprawie na linii premier-prezydent rozpęta się piekło. Po deklaracji Karola Nawrockiego na temat chęci odebrania Wołodymyrowi Zełenskiemu Orderu Orła Białego, ministrowie rządu Donalda Tuska rzucili się do krytykowania głowy państwa. Nawrocki ostro zareagował po tym, gdy prezydent Ukrainy nadał jednej z jednostek Sił Zbrojnych swego kraju imię "Bohaterów UPA". Ukraińska Powstańcza Armia dokonała w czasie II wojny ludobójstwa Polaków na Wołyniu i w Małopolsce Wschodniej. Jej członkowie zamordowali wówczas od kilkudziesięciu do ponad 100 tys. ludzi, w tym kobiety i dzieci. Order Orła Białego przyznał ukraińskiemu przywódcy prezydent Andrzej Duda wiosną 2023 r. Sam Duda kilka dni milczał po deklaracji obecnego prezydenta Polski. W korespondencji z Onetem w mijającym tygodniu jednak i on Zełenskiego bronić nie chciał: "Wołodymyr Zełenski otrzymał Order Orła Białego w innym czasie i gdy warunki były inne. Teraz one się zmieniły i zachowanie Wołodymyra Zełenskiego także. I to wyraźnie" — napisał nam Andrzej Duda. I dalej: "Dziś wobec zaistniałych ostatnio faktów decyzja należy do pana prezydenta Nawrockiego. Oczywiście prezydent wysłucha opinii kapituły i z pewnością podejmując decyzję, weźmie pod uwagę wszelkie okoliczności i fakty. A te są różne — nie wszystkie pamiętane, nie wszystkie szerzej znane i nie wszystkie dostrzegane w obecnej atmosferze". Niespodziewanie do grona otwartych krytyków Kijowa w tej sprawie dołączył Donald Tusk. Jasno stwierdził, że trzyma stronę Karola Nawrockiego, choć być może sam zareagowałby inaczej niż prezydent. Całą odpowiedzialność za kryzys zrzucił na Kijów i zasugerował Ukraińcom, by to ci znaleźli rozwiązanie tej sytuacji. O tym, że Ukraina zorientowała się, iż napięcia w relacjach z Polską mogą być kosztowne, świadczy fakt, że Wołodymyr Zełenski wysłał do Warszawy swojego zaufanego człowieka Kyryło Budanowa, który kieruje jego kancelarią. Ten spotkał się w piątek i sobotę w stolicy Polski z koordynatorem służb specjalnych Tomaszem Siemoniakiem, wiceszefem MSZ Marcinem Bosackim, wicepremierem i szefem MON Władysławem Kosiniakiem-Kamyszem, a także prezydenckim ministrem Marcinem Przydaczem. Kosiniak-Kamysz nagrał specjalne oświadczenie skierowane do Ukraińców, w którym tłumaczy, dlaczego dla Polski ruch Wołodymyra Zełenskiego ws. uhonorowania UPA jest nie do przyjęcia. Wystąpienie zostało opublikowane w czwartkowy wieczór w serwisie informacyjnym największego kanału telewizyjnego na Ukrainie. Kamil Dziubka i Dominika Długosz dyskutują również m.in. o sytuacji małopolskiej Koalicji Obywatelskiej, której struktury właśnie rozwiązał premier Donald Tusk, awanturze wokół projektu ustawy o wsparciu artystów, a także pewnym pijanym pośle PiS, którego będzie rozliczał inny polityk tej partii z alkoholowym ekscesem na koncie. 

Final Fantasy VI - Episode 8 This Week: Go back to Mobilzgo to Triangle Island, get eaten by the Zone Eater, explore the Zone Eater's tum-tum and find a new friend. This new friend is special. He mimics whatever the person before him did. He can also do the special attacks of a ton of other characters, but you have to go to set him up correctly. To do that, go to Status and Set Commands. Choose whatever you want, Tools, Blitz, Steal, Throw, the world is your oyster! Fly to the pentagon shaped mountain (this is the phoenix cave, go check it out.) Investigate Narshe, bring Locke. Pick up Mog and Mog's friend while you are there. Bonus things to do:Return to Sabin's Cabin and get his ultimate Blitz (this takes five minutes and makes Sabin good.)Return to Doma Castle and make Cyan Great Again (as long as he has haste.) Climb the Cultist's TowerCleanse the Cursed Shield (this isn't as difficult as it seems. Just go to the sad island Celes was on and give the person with the Cursed Shield a ribbon and then let monsters die 250 times.) Explore the Ancient Castle (take a ride on Figaro Castle and when it gets stuck, hop out and go through the entrance you used in the prison cells of the castle.)Go fight a dagron at the Opera House. Kill Deathgaze. Next Week: Raid Kefka's Tower and finish the game What's a video game book club? Exactly what you think! Some clubs read books, we play video games. Join us! Discord: https://discord.gg/hfnusHE Email: squelchcast@gmail.com Listen: www.squelchcast.com Support: www.patreon.com/Squelch or www.twitch.tv/dan0play 

We took the mobile studio down to Lewisville, Texas, to sit down with local legends Carlos and Lisa Uranga at the brand-new Full Gas Cycling Fit Studio. Before we dive into the black magic of bike fitting, Brad and Kevin debrief the absolute mudfest at Unbound 2024. We break down Keegan Swenson's F1-style pit stops, the utter dominance of the Specialized Crux, and the momentum building behind Scott's winning 32-inch prototype in the XL field.Then, we get down to the nuts and bolts of how a proper bike fit can give you free watts, fix that nagging lower back pain, and keep you smiling on those ultra-endurance pushes. Carlos and Lisa break down why buying a bike before getting fit is a massive gamble—especially in the era of expensive, integrated cockpits. Whether you are building up a brand-new MOG, tweaking a trusty Fargo, or stubbornly mashing a single-speed, this episode is packed with fit philosophy that will change how you look at your rig.In this episode, we cover:The Unbound 2024 Fallout: Mud, marginal gains, and why a good team dynamic is just as important as tire clearance.The 32-Inch Wheel Revolution: Will it become the new standard for ultra-endurance and bikepacking?The Pre-Purchase Fit: Why you should get mapped on a fit bike before dropping $10k on a rig with an integrated cockpit.Short Crank Science: The mechanical advantage of dropping down to 160mm or 165mm cranks to open up your hip angle and improve aerodynamics.Solving the "Hot Foot": Why standard wide shoes (we're looking at you, Shimano) might be failing you, and how surface area, socks, and custom insoles make or break a 100-mile ride.Direct-to-Consumer Risks: The pros and cons of buying Chinese carbon frames like X-Lab or Quick Pro without a proper geometry consultation.Links & Resources:Full Gas Cycling Fit Studio: fullgasfitstudio.comFind Carlos & Lisa Urrenga's studio off 121 in Lewisville, TX for your next pre-purchase mapping or fit follow-up.0:00 New Location Intro00:22 Meet Full Gas Fit Studio01:31 Unbound Tech Talk 32s05:27 Fit Implications of 32s08:54 Unbound Weather Recap11:11 Wheel Swap Drama14:12 Crux Bike vs Talent16:14 Fit Basics Stack Reach21:57 Buy Fit Before Bike27:28 Integrated Cockpit Headaches34:18 Hot Feet Troubleshooting39:49 Fitting Riders on Flats40:58 Flats Versus Clips41:47 Leg Length Shims42:40 Short Crank Setup44:27 Q Factor Explained45:10 Pedal Options Today47:04 Fit Across Bike Types50:02 Goals Drive Fit51:35 Common Pain Triggers52:50 How Often Refit55:53 Injuries And Compensation57:41 Tools And Assessments59:47 Free Watts For All01:01:14 Modern MTB Geometry01:02:44 Droppers And Setback01:05:24 Hip Angle Blood Flow01:08:08 Watching Pros Critically01:09:52 Three Contact Points01:11:55 Ultra Endurance Fits01:14:16 Pre Fit Before Buying01:17:34 Partnering With Shops01:20:14 Fit Included On 10K Bikes01:20:38 Custom Spec Bikes01:21:05 Booking a Fit01:21:57 Four Hour Fit Day01:23:30 When MOG Won't Fit01:24:38 Testing Cockpits Fast01:26:00 Fit Bike vs Your Bike01:27:19 Pricing and Transfers01:28:24 Why Fits Matter01:30:48 Follow Ups and Fees01:33:54 Crank Length Debate01:37:07 Short Cranks Stories01:44:45 Trends and Geometry01:46:08 DTC Brands and LBS01:50:03 Wrong Bike Problem01:51:32 Wrap Up and Contact

Twenty-five years of being dismissed, misdiagnosed, and told it was all in her head. By the time Elena Herning finally got answers, she had lost her home, her belongings, her ability to drive, and very nearly her life. In this episode of Integrative Cancer Solutions, Dr. K sits down with Elena Herning, patient advocate and TruDOSE™ ambassador, to trace her harrowing journey through undiagnosed Lyme disease, co-infections, toxic mold exposure, mast cell activation syndrome, POTS, MOG antibody disease, and COVID - and the single therapy that finally turned it all around. Elena breaks down what dose-specific IV platelet-rich plasma (TruDOSE™) actually does inside the body, why it crosses the blood-brain barrier, how it unwinds inflammatory loops that conventional medicine never addresses, and what it felt like to go from writing goodbye letters to her children to logging mile six on a treadmill. If you or someone you love is caught in the chronic illness spiral with no answers and no end in sight, this episode is for you. Key Takeaways: 0:00 Introduction  1:52 Undiagnosed for 25 years and what that looked like day to day  3:29 How a hysterectomy became the breaking point that revealed Lyme  9:04 Why Lyme is rarely the only problem  27:00 After energy healers, ozone, and a near liver transplant 29:38 What TruDOSE™ IV PRP is and how it differs from standard PRP  32:11 First treatment results and how fast things shifted  37:17 How dose-specific platelets cross the blood-brain barrier  Schedule a Free 15-Min Cancer/Lyme Consultation at The Karlfeldt Center: 208-338-8902 Resources: TruDOSE™ — https://trudose.com Medical Disclaimer: This content is for educational purposes only and is not intended to diagnose, treat, cure, or replace professional medical advice. Always consult your physician or qualified healthcare provider regarding any medical condition or treatment decisions. ____________________________________WORK WITH DR. KARLFELDT:The Karlfeldt Center offers the most cutting-edge and comprehensive Lyme therapies available. To schedule a Free 15-Minute Discovery Call with a Lyme Literate Naturopathic Doctor, contact us at:

Skąd wziąć w partii dziewczyny, kiedy się nie jest Januszem Korwin-Mikke? Szukamy pomysłów. Mogą być głupie, byle skuteczne. Kontestacja - słuchać, wbijać, kontestować!

Skąd wziąć w partii dziewczyny, kiedy się nie jest Januszem Korwin-Mikke? Szukamy pomysłów. Mogą być głupie, byle skuteczne. Kontestacja - słuchać, wbijać, kontestować!

En este episodio de NeuroLink de ScienceLink, el Dr. Raúl Medina Rioja, especialista en neurología cognitiva y trastornos del movimiento, dialoga con la Dra. Lizeth Zertuche, neuróloga especialista en enfermedades desmielinizantes adscrita al Centro Médico Naval y al Hospital Ángeles Pedregal. En el marco del Día Mundial de la Esclerosis Múltiple, los especialistas profundizan en la fisiopatología de esta enfermedad inmunomediada y analizan su gran impacto epidemiológico, al ser la principal causa de discapacidad neurológica no traumática en adultos jóvenes.Durante la charla, repasan la reciente simplificación de los criterios diagnósticos de McDonald y enfatizan la importancia de realizar un diagnóstico diferencial exhaustivo para descartar otras entidades desmielinizantes, como la neuromielitis óptica y la enfermedad por anticuerpos anti-MOG.En cuanto al tratamiento, destacan un importante cambio de paradigma: la tendencia actual favorece el inicio temprano de terapias modificadoras de alta eficacia para frenar la discapacidad irreversible.Preguntas realizadas durante el episodio:¿Cuál es la definición clínica de la esclerosis múltiple?¿Qué cambios recientes se han integrado a los criterios de McDonald y de qué manera simplifican el diagnóstico?¿Cómo se identifica una lesión yuxtacortical en una resonancia magnética?¿Cuáles son los principales diagnósticos diferenciales que deben considerarse ante la sospecha clínica o radiológica de una enfermedad desmielinizante?¿Qué nuevos biomarcadores se están utilizando para evaluar y dar seguimiento al daño inflamatorio y degenerativo?¿Cuáles son los mayores retos en el manejo de la progresión de la enfermedad?Fecha de grabación: 14 de mayo de 2026.Referencia:Este contenido se basa en la interpretación crítica de la evidencia científica disponible, así como en la experiencia clínica del o los ponentes como profesionales de la salud en instituciones de referencia.Para profundizar en los conceptos discutidos, se recomienda al profesional de la salud consultar literatura científica vigente, guías clínicas internacionales y la normatividad aplicable en su país.

Masz wziąć kasę od klienta z góry za sprawę? Absurd!Przecież twój klient buduje nową fabrykę glazury. Albo twoja klientka właśnie sobie stawia albo kupuję nową daczę we Francji…A poza tym, jego (jej) nowa bryka, to już właściwie jest u dealera, więc ty - jako dobry wujek albo dobra ciocia swojego klienta - nie będziesz przecież brać kasy z góry prowadzenie jego sprawy. Ty masz przecież MISJĘ! Skoro on właśnie stawia fabrykę, to już z tego powodu jest bez sensu upominanie się o jakiekolwiek hajsy. Po co ci kasa za sprawę z góry? Ty przecież masz, klient nie ma. Ty tam ten milion robisz miesięcznie albo rocznie bez wysiłku, więc możesz sobie pozwolić na to żeby sfinansować sprawę klienta… i pozwolić mu budować fabrykę glazury, czy daczę... Tak naprawdę, oprócz tego, że prowadzisz kancelarię, jesteś też instytucją kredytową. Co więcej najlepszą instytucją kredytową ever! Udzielasz kredytów bez BIKu, bez poręczycieli, bez weksli i bez sprawdzania stanu majątkowego klienta. Po prostu jesteś najlepszą ofertą na rynku. Gratulacje! Szacun! Mogę zobaczyć twój roczny PIT? Witam w 36. odcinku podcastu Togz bez wroga, który dzisiaj jest dość brutalny. Opowiada o mecenasach i mecenaskach dobrych wujkach, dobrych ciociach. Podcast jest o błędach, które notorycznie popełniacie w relacji z sobą i klientem, przez co kasa się nie zgadza. I macie przez to dość!Nie mówię że ty - ty pewnie nie… ale już ty być może. Popełniacie te błędy notorycznie, i pakujecie się przez to w duże kłopoty - w brak rentowności, brak wydajności, skazujecie się na bycie w kołowrotku i skrajnym przemęczeniu. Kosztem siebie, swojej rodziny, przyjaciół, dzieci…[autopromocja]#togabezwroga #prawnikodnowa #adwokat #radcaprawny #prawnik

Final Fantasy VI - Episode 7This Week: Follow the pigeon. Fight in the Veldt with only three people in your party. Go to the cave on the Veldt, go to the Dragon's Neck Coliseum and bet the Ichigeki. Go to Jidoor and explore the giant mansion. Go to the Cultists Tower. Head to Thamasa and then to Ebot's Rock.  Next Week: Go back to Mobilzgo to Triangle Island, get eaten by the Zone Eater, explore the Zone Eater's tum-tum and find a new friend. This new friend is special. He mimics whatever the person before him did. He can also do the special attacks of a ton of other characters, but you have to go to set him up correctly. To do that, go to Status and Set Commands. Choose whatever you want, Tools, Blitz, Steal, Throw, the world is your oyster! Fly to the pentagon shaped mountain (this is the phoenix cave, go check it out.) Investigate Narshe, bring Locke. Pick up Mog and Mog's friend while you are there. Bonus things to do:Return to Sabin's Cabin and get his ultimate Blitz (this takes five minutes and makes Sabin good.)Return to Doma Castle and make Cyan Great Again (as long as he has haste.) Climb the Cultist's TowerCleanse the Cursed Shield (this isn't as difficult as it seems. Just go to the sad island Celes was on and give the person with the Cursed Shield a ribbon and then let monsters die 250 times.) Explore the Ancient Castle (take a ride on Figaro Castle and when it gets stuck, hop out and go through the entrance you used in the prison cells of the castle.)Go fight a dagron at the Opera House. Kill Deathgaze.  What's a video game book club? Exactly what you think! Some clubs read books, we play video games. Join us! Discord: https://discord.gg/hfnusHE Email: squelchcast@gmail.com Listen: www.squelchcast.com Support: www.patreon.com/Squelch or www.twitch.tv/dan0play 

We build durable cyclists. New performance videos every week on YouTube:

Krissy Dilger of SRNA moderated an open Q&A on acute disseminated encephalomyelitis (ADEM) with pediatric neurologist Dr. Linda Nguyen of the University of Texas Southwestern Medical Center. Dr. Nguyen discussed how widespread MOG antibody testing has shifted many cases previously labeled ADEM to MOG antibody-associated disease, recommended MOG testing at onset, and reviewed relapse risk, mimics, and follow-up imaging [00:05:07]. Questions from the community covered acute treatments, recovery, guidance on pseudo-relapse, rehabilitation, and transition from pediatric to adult care [00:14:41].Dr. Linda Nguyen completed her MD, PhD training at West Virginia University in 2017, and then pediatric neurology residency at the University of California, San Diego in 2022. She then completed a combined pediatric and adult neuroimmunology fellowship at the University of Texas Southwestern in 2024, where she now serves as an Assistant Professor in the Department of Pediatrics. Dr. Nguyen currently sees patients in the Demyelinating Disease Clinic at Children's Medical Center Dallas.00:00 Welcome and Guest Intro01:08 What Is ADEM01:51 Causes and Who Receives This Diagnosis02:55 Early Signs and Onset04:20 Diagnosis and MRI Criteria05:07 MOG Antibodies and ADEM07:21 Testing and Relapse Risk09:06 Recurrent ADEM and Labels12:34 Mimics and Differential Diagnosis14:41 Acute Treatment Options15:38 Recovery Timeline and Rehab17:47 Long Term Effects and Seizures21:23 Family Support and Accommodations24:47 Follow Up Imaging and Relapse Signs27:25 Managing Fatigue and Headaches29:31 Supplements, Vaccines, and Genetics33:40 Pseudo Relapse and Exercise Balance37:41 Research and Predicting Outcomes43:14 Transition to Adult Care45:36 Weakness Sleep Issues and Final Thoughts

„Mogę coś słodkiego?" „Jeszcze jedną czekoladkę." „Ale on dostał, dlaczego ja nie mogę?"

"To bardzo zły kandydat - jest współodpowiedzialny ze wszystkie patologie, jakie narosły w Instytucie Pamięci Narodowej w ostatnich latach. Wybór Mateusza Szpytmy na prezesa IPN oznacza zachowanie przez Prawo i Sprawiedliwość kontroli nad tą instytucją" - powiedział w Popołudniowej rozmowie w RMF FM prof. Paweł Machcewicz, historyk z Instytutu Studiów Politycznych Polskiej Akademii Nauk. Skrytykował pochwały wicemarszałka Sejmu Piotra Zgorzelskiego pod adresem Szpytmy. "Mogę tylko ubolewać, że takie słowa padają ze strony ważnego polityka" - ocenił.

Caper - No ShadeJeff Lagos feat. Ehmsay - Smoke A Lotmu$an€ta - youPassport Rav & Bloo Azul - Paying for My SinsLegit x HostileProd - Raising the Culture Part 3 (Remix)David Rey - Shoulda Been YouBenefit - Cruel EyesRemz Rage – Nice & Slow (Valentine's Day Riddim)LRD feat. Jaya Kosa & Trajbrown - KneeKidd Called Quest feat. Mav - Many MenKbiz - Run It UpVincebyvince & Tophe - Out OutJusto the MC x Jay Rilez - Souls of MischiefSWIR - Fake SmileFreestyle Session - LypheNapoleon Da Legend feat. Crazy DJ Bazarro & Maitre D - Star WarsNacious - SMTA (Send Me The Addy)Real Triggz - Shutdown ModeWestbay - Secret Son Lee & Maine The Medicine - ObscurityEcho x BhramaBull - Higher ConsciousnessSankofa & Burnt Bakarak - Bronson StathamFonzse - da onleh weigh aht iz frooEs x Nec Nymbl - Celebrity WarshipAlias Molombo x Justo the MC - TunnelVisionGreg Cypher feat. Headkrack & Tuesday Talaga - BlindersSoltuv feat. NuphZed - HoneyPrince Dale - Ride OutShowrocka, Fuego Base, Chi Sees - We Don't CareObleak & Yotto Beatz feat. Ruste Juxx & Rockness Monsta - Three In The ChamberKut One feat. RJ Payne, Rockness Monsta - HittersB1 The Architect & Young Reese Dude feat. E.Smitty - Reach For The StarsTribal John, MOG, Werd & Lewis Findlay - Excess

Although rare, recognizing NMOSD is crucial for improving patient outcomes through correct diagnostic and treatment approaches. Reports of atypical forms and increasing knowledge of clinical, imaging, and laboratory-specific features are fundamental for the accurate recognition of this condition. Research on targeted therapies and biomarkers measuring and predicting disease activity will improve NMOSD management. In this episode, Gordon Smith, MD, FAAN, speaks with Sara Mariotto, MD, PhD, coauthor of the article "Neuromyelitis Optica Spectrum Disorder" in the Continuum® April 2026 Multiple Sclerosis and Related Disorders issue. Dr. Smith is a Continuum® Audio interviewer and a professor and chair of neurology at Kenneth and Dianne Wright Distinguished Chair in Clinical and Translational Research at Virginia Commonwealth University in Richmond, Virginia. Dr. Mariotto is a neurologist in the Neurology Unit in the Department of Neurosciences, Biomedicine, and Movement Sciences at the University of Verona in Verona, Italy. Additional Resources Read the article: Neuromyelitis Optica Spectrum Disorder Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @GordonSmithMD Full episode transcript available here Dr Smith: Neurology is an increasingly therapeutic specialty, and across many of our subspecialty areas, lots of new drugs are being approved. Are you interested in learning more about a historically disabling disorder for which we now have a spectrum of new therapies that, if used appropriately and promptly in the right clinical situation, promise to dramatically improve patient outcomes? If so, keep listening. My name's Dr Gordon Smith. Today I'll be talking with Dr Sara Mariotto about her article on neuromyelitis optica spectrum disorder or NMOSD, which she wrote with Dr Romain Marignier. This article appears in the April 2026 Continuum issue on multiple sclerosis.  Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast.  Dr Smith: This is Dr Gordon Smith. Today, I'm interviewing Dr Sara Mariotto about her article on neuromyelitis optica spectrum disorder or NMOSD, which she wrote with Dr Romain Marignier. This article appears in the April 2026 Continuum issue on multiple sclerosis. Sara, welcome to the podcast, and maybe you can start by introducing yourself to our audience.  Dr Mariotto: Yes. Thanks, Gordon. I'm Sara Mariotto. I'm a neurologist, and I work at the Neurology Unit, University of Verona, where I do both clinical diagnosis and research into neuroimmunology---so, in particular, autoimmune encephalitis, NMOSD, and MOGAD.  Dr Smith: Well, this is a super exciting area. Whenever I hear about NMOSD, I think of one specific patient I had, and I always think of her when I come across something like your article, which is really fantastic. So, before we dive into the details, I wonder if maybe you can just explain to our listeners who aren't up to speed on what NMOSD is, what the disorder is, and maybe why it's so important that all of our listeners learn how to recognize it quickly and get people started on therapy.  Dr Mariotto: Yes, sure. So, neuromyelitis optica is an inflammatory autoimmune CNS disorder usually associated with aquaporin-4 antibodies, although there are a few cases, around 10%, who can be antibody-negative. And I think it's very much important to have in mind this disease and recognize it because it can be severe, as you pointed out; can present with very severe optic neuritis, myelitis, the brain stem, or area postrema syndrome. So, it can be really severe, affect quite young people around 40 years of age---although it can affect also the pediatric population and elderly people---and, importantly, it can be treated. It's very much important to treat this patient in the acute stage very quickly with steroids or plasma exchange in addition, and then to start a chronic treatment. So, we have treatment for this condition. So, it's very much important to, to recognize it quickly and treat the patient properly.  Dr Smith: So, I wonder if we can talk a little bit about the diagnostic criteria and boundaries of NMOSD, right? So, someone who comes in with bilateral op- severe long segment optic neuritis or long segment myelitis, we think about it. But what are the boundaries? Should we be looking for this, for instance, in someone who comes in with a unilateral optic neuritis or looks like typical multiple sclerosis? Is it important to get aquaporin-4 antibodies in those patients? What do the diagnostic criteria say about this?  Dr Mariotto: So, I wouldn't test aquaporin-4 antibodies in all patients with demyelinating conditions because although aquaporin-4 antibody assay is very specific, as for all assay and all antibody testing---also for MOG antibodies, for example---some false positive results can come out. So, I would suggest to test aquaporin-4 antibodies not in typical MS cases but in those who could be suggestive for not being MS, so in all those cases with atypical optic neuritis and myelitis or other syndromes. For those cases, it's important to test aquaporin-4 antibodies, but I wouldn't test them in all typical, classical MS cases. As I said, it's quite specific, the assay, so it's uncommon to have false positive results, but it can be.  Dr Smith: Serum, CSF, both?  Dr Mariotto: So, for aquaporin-4 antibodies, they're usually present in serum. They can be positive also in the CSF. And there are a few reports of isolated CSF positivity. But if we analyze larger samples volume, then it becomes clear that isolated CSF positivity is so, so rare that it's not recommended to test them in the CSF when serum is negative. So, for aquaporin-4 antibodies, the recommended matrix of testing is serum, which is different for MOG, which is not the topic of our article but is important to mention because MOG antibodies should be tested in serum and CSF. But aquaporin-4, I would recommend to test serum.  Dr Smith: What are the boundaries between MOGAD and NMOSD? And you talked about the differential testing of antibodies, which I was going to ask about. But when should we think of NMOSD relative to MOG? Dr Mariotto: Yeah. There are aspects which are the one mentioned in the criteria, highly suggestive for NMOSD. But the clinical spectrum can be similar to that of MOGAD. Usually, although there are some clinical aspect---like, for example cortical encephalitis or ADEM, which is more typical for MOGAD, or others like area postrema syndrome, which are more typical of NMOSD. The spectrum can be similar among the two conditions, so that's why in our clinical experience, usually they ask both aquaporin-4 and MOG antibodies in patients. It's- for experts, it can be easy to differentiate the two conditions, but for nonexperts can not be so easy.  Dr Smith: Can you define area postrema syndrome? I think not all of our listeners see that every day.  Dr Mariotto: Yeah, sure. This is a syndrome which is highly suggestive of NMOSD. That's why I mention it. And it's characterized by nausea, vomiting, hiccups are known as the syndrome. And it is very, very suggestive because of the expression of aquaporin-4 in that area of NMOSD. That's why I strongly recommend for all patients who comes out to have this syndrome to test for aquaporin-4 antibodies. MOGAD is hardly ever positive for that, so I think that whenever you see a patient with that syndrome, you should think about NMOSD.  Dr Smith: I'm just curious, aquaporin-4 is a water channel, which is kind of an interesting concept. Our conversation, I really want to make sure we give clinically important information to folks, but it's so curious to me at least, how does this actually result in a inflammatory demyelinating syndrome? For a simple neuromuscular guy, what's the immunopathogenesis of this?  Dr Mariotto: Yeah, the immunopathogenesis is quite complicated, as in all CNS disorders. And of course, aquaporin-4 antibodies are the main focus, but they are not the only one. As you said, aquaporin-4 antibodies have a target, this water channel, which is at the basis of the disease, and they are produced by the interplay between T cells, B cells, and plasma cells. But then also eosinophils, macrophages, cytokines, and chemokines are involved, enter the CNS, and then another important component is complement, which is highly activated in this disease. At the end, we have astrocyte damage because astrocytes are the main target of the disease, but also axon and myelin are involved. So, it's a quite complex pathogenesis based on the antibodies, but not only on that.  Dr Smith: And this will become important when we start talking about treatment. There seems to be a recurring theme of long segment demyelination, right? Optic neuritis is typically a large percentage of the length of the optic nerve, and obviously the myelitis se- more than three segments. Do you see other long segment areas of CNS demyelination, corpus callosum or things like that? Any ideas why that is, if that's true?  Dr Mariotto: Of note, this is quite interesting because usually when we have NMOSD, we have a longitudinal involvement, especially of the optic nerve and spinal cord, while brain lesions are quite different. Like, we usually do not have the typical Dawsen fingers-like lesions that we have in MS, for example, or the classical periventricular or subcortical extensive lesions that we can see and we have in mind when we think about MS. In some cases with NMOSD, the brain is completely negative, so we do not see anything. And Dawsen lesion's quite suggestive of NMOSD. So, you're right. I mean, this is related partially to the expression of aquaporin-4, and that's why we have this typical involvement also for area postrema, for example, and maybe also our other examples of clinical aspect that we can see in these conditions. But it's basically linked with the expression of aquaporin-4, which is the main target of the disease. And that's why usually the brain doesn't show so much involvement as we can see in MS, for example.  Dr Smith: I was actually really interested in some of the unusual manifestations or phenotypes, and I don't want to get into arcadia, really, but which of these should our listeners be familiar with that would really suggest that they should be thinking about NMOSD beyond the area postrema and other features that we've already talked about that are part of the core criteria?  Dr Mariotto: Yeah. I mean, I think that the encephalic syndromes or also ADEM, which is most typical of MOGAD but can be observed also in NMOSD or PRES, for example, are syndromes that can be considered in patients with NMOSD. There are the typical ones, which are the ones showed in the criteria, but whenever we have a brainstem involvement or, like, these encephalic syndromes or also PRES, we should think about NMOSD also.  Dr Smith: Another area I was interested in are red flags. In your article, you talk about red flags that might suggest an alternative diagnosis, right? And then this presumably is particularly important in seronegative patients, which 10% is not a reasonably high number, I suppose. What are red flags we should be thinking about for some other diagnosis?  Dr Mariotto: Yeah. I would here mention two very important red flags. The first one is a very hyperacute onset. Usually these conditions, these inflammatory conditions have a subacute onset, so whenever you have a very, very acute onset, you should think about something else. This can occur sometimes also in NMOSD, but hardly ever occur. Like, a very acute myelitis, the first thing we should think about is a vascular origin, for example, with a lot of pain and not about NMOSD, although sometimes the differential diagnosis is not so easy. The second thing is a progression independently of relapses, which hardly ever occur in NMOSD. Usually in NMOSD, we have the onset, and then we have a relapsing disease course. That's why we have to treat patients always and not to stop treatment. But we do not have progression in the meanwhile, while we can have, for example, this in MS. Same thing is for MOGAD. So, these are two things that I think is very much important to keep in mind.  Dr Smith: I want to pivot to talk about treatment because that's been super exciting. But rumor has it there are new diagnostic criteria coming for NMOSD in the next year. I bet you know a bit about those. Can you give our listeners any indication about kind of where the puck is going on this? Not so much what the criteria are specifically, but what sort of diagnostic challenges are the new criteria going to help us with once they come out?  Dr Mariotto: Yeah. So basically, we are working on that, so you will read them in the next future. This is the good point of the conversation on the new criteria. And we work a lot on the definition, on the new definition and nomenclature of NMOSD; on the definition of seronegative NMOSD, which is also quite tricky; and then on the assay we should use to test aquaporin-4 antibodies, and also on potentially new syndromes which should be included into the main feature of the disease. But hopefully you will read about this very soon.  Dr Smith: Looking forward to it. And Continuum Audio listeners, you heard it here first, so thank you. Let's pivot to treatment. This has been super exciting, and I wonder if the way to approach this is to start with acute management and then sort of chronic management. Would that make sense?  Dr Mariotto: Sure.  Dr Smith: Let's say I go on service on Friday, and I have a patient who comes in with positive aquaporin-4 and bilateral optic neuritis. What's the acute approach to managing that patient?  Dr Mariotto: So, the first approach is to administer intravenous steroids, but I would not wait to escalate to plasma exchange. There is quite good evidence that we should treat the patient with additional plasma exchange very quickly, and every day of delay of plasma exchange can cause increased disability. So, we should treat patients with steroids first, and then if we are not satisfied by the recovery, soon start with a plasma exchange. There is also some evidence, although less, for IVIG, but it's important to try to treat them very quickly, even if it's Friday, you know, there is the weekend and so on. But I think it's very much important to start with steroids after excluding other infectious causes or so on, and then to start quickly with plasma exchange. The main problem could be that we do not have the results of the antibody yet.  Dr Smith: Right. So, let me ask that question. You know, let's say my patient comes in on Friday, and clinical syndrome that really looks like NMOSD, and we're waiting for the aquaporin-4. There are many places where it's hard to get plasma exchange over weekends. And so, in that setting, are you better off doing the steroids over the weekend then PLEX on Monday, or should we just give IVIG because maybe it's as good as PLEX? What's your advice there? I'm trying to get ready for Friday because I know one's coming in.  Dr Mariotto: That's true, that's true. Usually they come on Friday or Saturday. I think it's acceptable to have three days of steroids and see how the patient improves, and then after three days to start with plasma exchange. Actually, we have a very good improvement if we start between three and five days after onset. So, I think waiting for three days is acceptable just because we can see if the steroids work properly or not, and then we can quickly start to plasma exchange. But I would not wait, like, 10 days, you know, before starting with a plasma exchange, and I would not wait for antibody results.  Dr Smith: Got it. Super helpful. And I'm actually not joking around, I learned recently that I have a reputation among our residents for having lots of optic neuritis when I'm on service, which I think is sort of karmic justice for being a peripheral nerve expert. But let me ask another question. So, let's say we do that, and the patient gets three or five days of pulse methylprednisolone and five courses of PLEX, and they're not doing well. Do you then just move right along into another agent B cell depletion therapy? I mean, what's your next step in escalation in the acute setting?  Dr Mariotto: I would for sure start to, as you said, with steroids, plasma exchange, and in case IVIG, and then quickly move to chronic treatment. And for patients who are not recovering well, I would think of something which has a quick effect so we can really start treating patients very quickly. There are different options. And all over the world, there are different rules for using immunosuppression in NMOSD. Like in Italy, for example, it's different from US or other countries, Germany, for example. There are different approved treatments and different rules of using them before or after rituximab, for example. We all know that there are treatments approved for NMOSD all over the world. But in some countries, like for example in Italy, we should use rituximab first, and then if it doesn't work, escalate to the approved treatment. I know in the US it's different. But anyway, for a patient who does not improve quickly, I would start with something which has a quick effect on the disease.  Dr Smith: And then rituximab versus inebilizumab, you know, CD20, CD19, what's your advice there? Is one preferable to the other, you know, if we have options to do either?  Dr Mariotto: Yeah. So, between rituximab and inebilizumab, we know that the target, well, is different, but is anyway B cells, so CD19 and CD20. With CD19, we can affect both plasma blast, plasma cells, and B cells. That's why the target is broader. And of note, this is an approved drug, while rituximab is, in most countries, used as off-label treatment.  Dr Smith: So inebilizumab would probably be preferable if we're able to do that.  Dr Mariotto: Unfortunately, there are not so many studies comparing rituximab with the approved drug, which is, of course, a pity, but that's the case. While we have clinical trials for all the approved drugs, and although the trials were designed differently, as we mentioned in the Continuum paper, we can argue something of the comparison between the approved drugs. But it is not so clear the comparison between rituximab and the new drugs, which is also something that we should work on.  Dr Smith: And then for chronic suppressive management, what other options are there?  Dr Mariotto: So, in addition to B cells, target can be interleukin-6, as we know with tocilizumab or satralizumab, and then complement with eculizumab. These drugs are both based on the pathogenesis of the disease. That's why we also discuss it in the paper, which shows a clear involvement of complement, and among cytokines of interleukin-6. So, targeting these made clear that could improve the disease quite well, and that's why they designed some clinical trials on these drugs, which are now approved, as we said, for NMOSD.  Dr Smith: Wow, so many options, and a lot of questions, but limited time. Let me just ask a couple of more. I see a lot of myasthenia patients, and there's a lot of variability, as you know, in patients with myasthenia, the extent to which complement is an important mechanism versus other, you know, important mechanisms. To what extent is response to a complement inhibitor kind of uniform across NMOSD? Or there's some patients who just don't respond to a complement inhibitor and others that respond really well. And then just, I'll just give my second question out is, you know, what about combination therapies for patients who have particularly challenging NMOSD?  Dr Mariotto: So usually these patients have a terrific response to complement inhibitors, and this is also shown by the clinical trials where we saw how eculizumab have a very impressive effect on the disease. And also, maybe this is also your experience, a very quick effect. So that's why there are also thoughts on using it in a very acute stage of the disease. That was what I was thinking about before. But then it has a very huge effect on complement, which is a major factor involved in the pathogenesis of NMOSD also in the chronic disease stage, and that's what also we see from clinical trials. Usually, we prefer to switch treatment from one to another and not to combine them. Of course, in very difficult cases, this can be considered, but the recommendation is to switch from one of these approved drugs to the other, or from rituximab to one of the approved drugs, and try to find out the best for our patient before combining them. Dr Smith: The complement inhibitor trials are breathtaking, at least for me. If I'm trying to convince students to go into neurology, I'll say, "Take a look at that paper," because anyone who claims that we're "diagnose and adios" is so wrong. It's so exciting. So, at a high level, this must have fundamentally changed outcomes for patients. I mean, it's still a difficult disease, but what is the kind of prognosis for that patient I described who comes in, gets the therapy you talked about? What does their long-term outcome look like in this modern therapeutic environment? Dr Mariotto: So, NMOSD is almost always a relapsing disease. That's why, as we mentioned, we have to treat patients always. But the prognosis changes a lot since we were also able to use all these drugs for the disease. So, the prognosis changes if we recognize it properly and early, and if we treat NMOSD properly with immunosuppressives. So, whatever we choose it's important to start it quickly, and this is the only way that we have to improve the prognosis of this disease. We have very active cases, but we have also cases who responds quite well to this immunosuppressive treatment, since now we have, as mentioned, these ones which are very impressive and show incredible results. So, the prognosis of the disease change in the last year, thanks also to the improvement of the diagnosis and of the treatment choices for the disease.  Dr Smith: I'm just... I- maybe my last question, you know, just at a personal level, not only for you as an expert who's caring for these patients, but in the patient community, this must have been a pretty exciting period of time, right? I mean, these, these drugs are coming fast and furious, and what a change. What's the kind of zeitgeist in the community, both your professional community and amongst the patient community about where we are? Dr Mariotto: Yeah, you're right. The last years were defined the years of NMOSD and also MOGAD because we had finally approved drugs which is relevant for all the disease that we treat and changed the landscape of the disease for clinicians, but also for patients. And we have more than one, as we said, so we have more options that we can also discuss with patients to try to choose the best one in terms of activity, but also route of administration or time. Some years ago, we just had rituximab, which is not approved in most of the countries, and now we have different approved drugs. And we improved the diagnosis of the disease thanks to the availability of live cell-based assay. And then we are working a lot also on biomarkers like GFAP, for example, which has been shown to be a very attractive biomarker able to mark disease activity and maybe also prognosis on this disease. So, you're right. I mean, in the last years, the landscape of NMOSD changed a lot.  Dr Smith: Sara, thank you so much for talking with me. I could keep going for another half an hour, but I would be in trouble with my editor, so I think we probably need to wrap it up. But thank you so much. This has been very informative.  Dr Mariotto: My pleasure. Dr Smith: Mine too. Thank you. Again, today I've been interviewing Dr Sara Mariotto about her article on NMOSD, which she wrote with Dr Romain Marignier. This article appears in the April 2026 issue of Continuum on multiple sclerosis. Be sure to check out Continuum Audio episodes from this and other issues, and thanks to you, our listeners, for joining us today. Dr Monteith: This is Dr Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at continpub.com/audioCME. Thank you for listening to Continuum Audio.

Join us for part two of the Clavicular cringe saga. We're mogging all over the podcast with our cringe-maxxxing!  References: Channel 5 interview https://www.youtube.com/watch?v=-_6mni6k0Zw Clavicular slapped at club https://www.instagram.com/reels/DWG9y6rocyO/ Clavicular & Whoa Vicky speed date https://www.youtube.com/watch?v=bzpF_B5vCmY Clavicular ditches Whoa Vicky after she acts sketchy https://www.tiktok.com/@clipsfye/video/7626610744070638878 Tip Toe Maxxing from Jack Mac interview https://www.tiktok.com/@jackmacbarstool/video/7621320406657420558 Clavicular's home tweet/x https://x.com/Clavicular0/status/2044362432823411176 Michael Knowles interview https://www.youtube.com/watch?v=e8qj9RNA938 Write us some of your cringe stories at nervouslaughterpodcast@gmail.comThe socials: Instagram | Facebook | Twitter

The "Community Meets Clinic" podcast series introduces clinicians and healthcare personnel specializing in rare neuroimmune disorders. In this episode hosted by Krissy Dilger of SRNA, we met Dr. Grace Gombolay and Dr. Varun Kannan, both from Emory University and Children's Healthcare of Atlanta, designated Centers of Excellence in Rare Neuroimmune Disorders. Dr. Kannan discussed learning alongside families as conditions like MOG antibody disease emerged clinically and his focus on tailoring treatment and supporting clinical trials in a field with few approved therapies [03:37]. Dr. Gombolay outlined her research on biomarker development, a Children's biobank, advanced MRI collaborations, and participation in the Network of Pediatric MS Centers covering disorders such as MOGAD, NMOSD, optic neuritis, ADEM, and TM [06:36]. They described their multidisciplinary clinic team, highlighted home infusions and telemedicine to reduce burden, and shared personal self-care strategies [10:22]. Dr. Gombolay and Dr. Kannan expressed hope for more trials, remyelination, prevention, and earlier diagnosis aided by AI prompts [20:43].You can view Dr. Grace Gombolay's medical profile here:https://www.choa.org/doctors/grace-gombolayYou can view Dr. Varun Kannan's medical profile here:https://www.choa.org/doctors/varun-kannanGrace Gombolay, MD, MSc, FAAN is an Associate Professor at Emory University and Director of the Pediatric Neuroimmunology and Multiple Sclerosis Clinic at Children's Healthcare of Atlanta. Her research interest involves biomarker development in pediatric neuroinflammatory diseases including autoimmune encephalitis, multiple sclerosis, MOGAD, and NMOSD.Varun Kannan, MD graduated from Emory University School of Medicine in 2017. He then completed child neurology residency in 2022, followed by pediatric neuroimmunology and multiple sclerosis fellowship at Baylor College of Medicine and Texas Children's Hospital in 2023. He returned to Emory and Children's Healthcare of Atlanta in 2023, where he has worked closely with Dr. Grace Gombolay in the neuroimmunology program. He is interested in clinical research regarding severe/relapsing forms of rare neuroimmune disorders including autoimmune encephalitis and MOGAD. He is currently involved in multiple upcoming phase 3 clinical trials exploring new disease modifying treatments for pediatric rare neuroimmune disorders. He is also passionate about medical education and is currently one of the Associate Program Directors for the Emory child neurology residency.00:00 Welcome01:56 Dr. Grace Gombolay's Journey03:37 Dr. Varun Kannan's Path05:06 Kannan's Research Focus06:36 Biomarkers and Biobank10:22 Clinic Team and Care13:44 Self Care and Balance16:15 Children's Healthcare of Atlanta20:43 Hopeful Future Ahead24:49 Closing

Familiarity with the clinical, MRI, CSF, and serologic features of MOGAD can help neurologists recognize this condition in clinical practice. Awareness of the utility and pitfalls of the MOG antibody test is critical. The current therapeutic approach is guided by retrospective studies and the application of immunotherapies used in other autoimmune neurologic disorders. In this episode, Gordon Smith, MD, FAAN, speaks with Eoin P. Flanagan, MBBCh, coauthor of the article "Myelin Oligodendrocyte Glycoprotein Antibody–Associated Disease" in the Continuum® April 2026 Multiple Sclerosis and Related Disorders issue. Dr. Smith is a Continuum® Audio interviewer and a professor and chair of neurology at Kenneth and Dianne Wright Distinguished Chair in Clinical and Translational Research at Virginia Commonwealth University in Richmond, Virginia. Dr. Flanagan is a professor of neurology and the division chair of the Division of Multiple Sclerosis and Autoimmune Neurology in the Department of Neurology at Mayo Clinic in Rochester, Minnesota. Additional Resources Read the article: Myelin Oligodendrocyte Glycoprotein Antibody–Associated Disease Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @GordonSmithMD Full episode transcript available here Dr Smith: So, what neurological disorder can cause bilateral optic neuritis, transverse myelitis, ADEM, or can mimic acute flaccid myelitis, intracranial hypertension, viral encephalitis, or cause seizures? Sounds like the great imitator, perhaps. If you want to know and learn more about this syndrome and how you can treat it---and it is very treatable---keep listening. My name is Gordon Smith, and today I have the great opportunity to talk with Dr Eoin Flanagan from the Mayo Clinic on his article on myelin oligodendrocyte glycoprotein antibody associated disease, or MOGAD, which is in the April 2026 issue of Continuum on Multiple Sclerosis and Related Disorders.  Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast. Dr Smith: This is Dr Gordon Smith. Today I'm interviewing Dr Eoin Flanagan about his article on myelin oligodendrocyte glycoprotein associated disease, or MOGAD, which appears in the April 2026 Continuum issue on multiple sclerosis and related disorders. Eoin, welcome to the podcast, and please introduce yourself to our audience.  Dr Flanagan: Yeah, thanks so much. I'm Eoin Flanagan. I'm a neurologist at the Mayo Clinic. I'm originally from Ireland. I work in the neuroimmunology lab at the Mayo Clinic, and work and see patients with MS, MOG, and autoimmune disorders here in Rochester, Minnesota.  Dr Smith: Your article is super interesting, I think, and this has been a really rapidly evolving area over the last, you know, many years. We have many more antibodies, and MOG is something that's been around for a while, but we've certainly learned a lot more about it. This is a topic that I think will be familiar to most of our listeners, but I wonder if maybe you can just begin by laying the foundation. Like, what is MOG? What's its typical presentation?   Dr Flanagan: So, MOG is a protein on the surface of the oligodendrocyte or its CNS myelin, and it was always of interest as a potential antibody target, and initially it was investigated in multiple sclerosis. But subsequently, we recognized that the antibodies to MOG have a specific syndrome, of which about a quarter of patients are pediatric and then the remainder are adults. And they can present with a variety of syndromes, probably most commonly optic neuritis, but also acute disseminated encephalomyelitis, or ADEM. Transverse myelitis can also occur, and then some other unusual brain and brainstem cerebellar syndromes can also occur.   Dr Smith: I was really impressed in the very broad phenotypic spectrum of MOG. We'll talk more about that, of course. But I wonder if maybe you can tell us when we should be ordering MOG antibody? Given this broad variability, does anyone who has a CNS demyelinating disease need a MOG assay, only specific phenotypes? What guidance do you have for our listeners?   Dr Flanagan: Yeah. It's a great question. So, I think you have to be a little bit careful because the MOG antibody test is a little bit sticky. So sometimes we can see some low-positive false positives. So, we don't wanna order it in every single patient with classical MS. So, I suppose we'll start with who not to order it in. I think it's also a very optic nerve- and optic neuritis-central disease, so I think you really need to be considering this in a patient with optic neuritis who does not have lesions in the brain suggestive of multiple sclerosis. And then we think about some of the features: if the lesion, the enhancement along the optic nerve is long, if it's bilateral, if there's a lot of optic disc edema accompanying that, we tend to think about MOG antibodies. And then children with demyelinating disease, MOG is over-represented in that cohort, so it accounts for about a third of those. So, if you have a child with CNS demyelinating disease, particularly if they're under twelve, with ADEM presentations or other presentations, you probably want to be ordering the MOG antibody test. And then a longitudinally extensive transverse myelitis in adults, certain types of cerebral phenotypes that we can get into, you would want to consider ordering MOG antibodies too.   Dr Smith: Now, you point out in the article that it's really important that laboratories use the cell-based assay for MOG as opposed to an ELISA, for instance. Is this something folks need to be very attentive to, or are all of the commercial laboratories now using a cell-based assay?   Dr Flanagan: Yeah. I think all of the commercial labs are using cell-based assays, so we don't really get into much of an issue. There are some differences between serum and CSF, so really, serum is the optimal sample to order. There is also some differences between the live cell-based assay and the fixed cell-based assay, where the live cell-based assay may have some advantages in terms of sensitivity. And then CSF is kind of still under evaluation about its role in the condition. So in general, it's a serum test. And then we have to remember that the antibody tends to be highest at the onset, and then it goes down over time. So, if you delay your testing or you're testing a patient long after the condition, it can go negative, for example. So it tends to be highest both around the relapses and particularly at the onset of the condition.   Dr Smith: You mentioned earlier that the test is sticky, which I take to mean that there is some risk for low-titer false positives. How do you navigate that situation? When should we be suspicious about a false positive?   Dr Flanagan: Yeah. I think there's some very useful features that can help you. You know, the main differential diagnosis is going to be multiple sclerosis, particularly in the US, in regions of the northern US where MS is particularly common. So, you really wanna be making sure that if you get a positive result, low positive, that it's not multiple sclerosis. And some of the best discriminating features are CSF oligoclonal bands. They're about 85% in MS and about 15% in MOG, so an easy number to remember, 85 and 15. And then the lesions in MOG, the brain lesions, tend to disappear over time. So, if you have the advantage of that follow-up MRI a year down the line, about 70% of lesions in MOGAD will resolve, while in MS, as we know, the term means multiple scars, so the MS lesions tend to persist over time. So, they are two quite useful features that can help discriminate.   Dr Smith: And how about specific phenotypes or areas of involvement or imaging abnormalities that suggest MOG? One of the things I found really interesting in your article is there are a host of different syndromes that I think had largely been previously described, many of them, that became clear later that these were really tied to MOG antibodies. Presumably, that's helpful in interpreting the antibody assay in that patients who have, perhaps, a borderline low titer, for instance, but have a very typical phenotype are more likely to have MOG than those who have a more clearly MS-type phenotype.   Dr Flanagan: Yeah, absolutely right. Yes. So, there's certain phenotypes that we don't tend to see with MS. The acute disseminated encephalomyelitis, or ADEM, is one that's particularly common in children. And about half of people that have ADEM will be positive for the MOG antibody. So that's a syndrome you need to look out for, which would be often in children, encephalopathy, and they would have multifocal white matter lesions, sometimes involving the gray matter. A second syndrome that was an interesting discovery from a Japanese group was this unilateral cerebral cortical encephalitis, where patients can have this swelling and T2 hyperintensity, often just on one side of the brain. And it's in the cortex, and some of those patients won't have any white matter lesions. And in that situation, it's important to order the MOG antibody, and that seems to be a specific phenotype of MOGAD. But sometimes people don't think about it because the white matter is not involved. So, if you see these patients, they often present with seizures, sometimes they even have fever accompanied by it. And if you see those patients and see this radiological feature, then you really want to consider ordering the MOG antibody too.   Dr Smith: Yeah, I found that really interesting. And I- actually, my next question is perhaps a good follow-up on that, is, what are the diagnostic pitfalls? You give a lot of examples of situations and I think some cases where it's easy to get tripped up and misdiagnose someone who has MOG with another fairly common neurological problem.   Dr Flanagan: Yeah, I think some of the things that can help you when you're determining if the MOG is a true positive or false positive is the level of the antibodies. The super high titers, if it's a clear positive or very strong positive, the likelihood is that that is much more likely to be MOGAD than those low positives just above the cutoff. So that can be useful to help you discriminate from false positives. Those lesions, again, if all the lesions persist over time, that's going to be more suggestive of multiple sclerosis. Other diagnostic pitfalls, I suppose, if it's a syndrome that's not really associated with MOG, like peripheral neuropathy or other syndromes where we'll see some case reports, but usually I would be very cautious about those kind of presentations. So usually, having the antibody at a high level, and then also if they've had other symptoms suggestive of MOGAD, like if a patient has had recurrent optic neuritis and then they have an unusual brain syndrome, or they start out with an unusual brain syndrome and then have recurrent optic neuritis. You know, there are situations that make it more likely if they're having other typical phenotypes of the MOGAD where we can kind of expand the spectrum, but we have to be careful.   Dr Smith: I was really curious about the dynamic imaging findings. And you point this out both in terms of the resolution of imaging findings, but also in that patients who have an acute MOG syndrome often have very rapid evolution of the imaging abnormalities. I'm just curious, you know, why is that, and what do you make of it? Does it have a mechanistic implication, do you think?   Dr Flanagan: I don't think we know for sure. I think there's probably a lot more happening than we see on MRIs sometimes. What sometimes can happen in about 10% of patients is the initial MRI can be normal. We don't tend to see that with multiple sclerosis or NMOSD. Then what we see is it evolving over time. So, at that time, if you do a CSF, you'll often see inflammation, but we don't see the lesions. Now, that might be because the MRI is not very good at picking up cortical involvement. That can be difficult to see in MRI. Or there could be other factors. It could be a functional effect on the MOG but without frank demyelination yet, for example. Or there could be edema that you- myelin edema that you can't see as a lesion yet on MRI. But we do see that if you repeat the MRI, sometimes it'll change a lot. So, you may go from one or two lesions on the first MRI to twenty lesions on the second MRI a week later. So, it does tend to change a lot. And then over time, those lesions also resolve. So, what I say is if it's a very suspicious situation---like a child comes in with new-onset encephalitis, has inflammatory CSF---you might wanna consider repeating that MRI down the line and seeing if it's changing. And then over time, you know, a repeat MRI a year after the onset when there's brain or spinal cord lesions can be very helpful just to make sure you're on the right track, because lots of those lesions will then disappear, and that's a very clear discriminator from multiple sclerosis.   Dr Smith: Yeah, thanks. I mean, I was wondering the same thing about whether that particular feature might imply, you know, a functional abnormality as opposed to more of a structural abnormality. So probably a lot more to learn as we move forward. There are now consensus diagnostic criteria that were published a couple of years ago. I think you've already touched on kind of the general approach, but do you want to speak to those? I found your summary pretty helpful.   Dr Flanagan: Yeah, I think that those criteria are quite useful. They have three main parts to them. The first part is having a characteristic clinical syndrome. So, we talked about ADEM, we talked about cerebral cortical encephalitis, transverse myelitis that's often longitudinally extensive, and optic neuritis being the main syndromes, but sometimes other brainstem or cerebellar involvement can be seen. And then the second part is having a positive MOG antibody. And then there's some caveats there. So, if you have a high positive, then you don't really need any additional supportive criteria. On the other hand, if you're low positive, to get at those sticky antibodies that make sure it's not a false positive, you need some additional supportive clinical or MRI criteria. Or if you're only positive in CSF, you need that additional criteria. You also need to be negative for the aquaporin-4 antibody, because they can overlap clinically. And some of those supportive criteria are things that we talked about a little bit earlier, longer lesions within the optic nerve, bilateral involvement, involvement of the nerve sheath or optic disc edema. This is a situation, MOG antibody disease, where your fundoscope is useful and looking in the back of the eye and seeing swelling, because we don't tend to see that quite as often. It's less common in multiple sclerosis, but we often see prominent edema in MOGAD. And then in the spinal cord, the lesions tend to be central in the cord. Sometimes they form this H sign where it's restricted to the gray matter, and they tend to be longer, sometimes involving the conus. Patients will often have neurogenic bowel or bladder. And then in the brain, deep gray involvement, those large lesions along the cortex with swelling are some of the typical features. And then the final step is exclusion of another diagnosis. Just like with any test that we do in neurology, our final step is going to be to put that into context. So that's just a normal thing that we will always do when we get a group of test results back that we don't know what it means. We have to put it into context. So, make sure it's not multiple sclerosis, everything else does not look like multiple sclerosis, and then you can be on your way to make a diagnosis.   Dr Smith: Definitely encourage listeners to read your article. I guess I say that with every time I- or with everyone I talk to for Continuum Audio, but the images are really fantastic and the cases are fantastic. So, everything you've described is well-illustrated, including really nice schematic sort of diagrams that help differentiate NMO from MOG and MS. So, if you like MRI scans and good imaging frameworks, then this is the article for you.   Dr Flanagan: I think that's true, and the other thing is that the imaging is quite helpful because it takes a while for that antibody to come back. We're lucky at Mayo Clinic, if you work here, it, it comes back faster for you. But for many places, that time of sending it in, so a lot of times you don't know right away. So, looking at scrutinizing that MRI can be very helpful to guide you on your way and to know what you're dealing with and how to approach both the acute treatment and plans to have potentially a steroid taper after the acute treatment and those kind of things that can help guide you in that regard.   Dr Smith: Yeah. So, let's talk about treatment. You know, what's your approach to treating a patient who has an acute demyelinating syndrome related to MOG?   Dr Flanagan: So similar to other things, MOG is very steroid responsive. So, we use high-dose IV methylprednisolone in adults. That would be one gram IV for five days. And then we also will sometimes use oral steroids, twelve hundred and fifty milligrams. That's a bit of a hassle because it's twenty-five fifty-milligram tablets, it doesn't come in a larger tablet version. But it's very helpful to patients because they can get started on it right away. You don't have to set up an infusion center. So, we have used those oral steroids often in people who don't have access to an infusion center, are not in the hospital. And particularly as it's often optic neuritis, some of those patients are seen in the outpatient setting, so we can get in with treatment quickly. In patients where it's more severe, it doesn't recover quickly with steroids, then we would consider escalating to plasma exchange as our second-line treatment, and there's some retrospective data that suggests that plasma exchange can be useful. That's gonna be particularly for those people who don't have that quick response to steroids, or maybe more severe phenotypes like that brain involvement with ADEM or cerebral cortical encephalitis, where those patients might be in the hospital and quite unwell. I will say, we might get on to this, that sometimes MOG can be very, very severe and even fulminant, where there can be increased intracranial pressure, and these patients can be in the ICU, and it can be life-threatening. And so, it's really important to treat those patients aggressively, and some patients have even required hemicraniectomy or additional treatment. Sometimes IL-6 blocking medications have been used in that situation. So, monitoring and treating increased intracranial pressure in those rare patients, probably 2 or 3% that have the very severe attack, is important.   Dr Smith: I think one of the things I found interesting, and then I'd love to get your feedback on this, is that most patients with MOG seem to have a very readily treatable disorder that's monophasic, right? You treat them with steroids, and they do well. On the other extreme, there are these patients that have a much more malignant presentation, and there are some that sound like they benefit from prophylactic or some chronic therapy. What's your approach, right? In MS, we do serial scans to monitor, and obviously, our patients are on, you know, chronic disease-modifying therapy. How do you decide when you're going to provide some sort of prophylactic therapy? How do you monitor it? How long do you continue it?   Dr Flanagan: That's a great point. We don't know for sure yet, but I think for the most part, our approach has been if the patient has a single episode, they recover well from that episode. So, if that's optic neuritis, they're back to twenty/twenty vision. They have recovered well. We don't tend to use chronic maintenance immunotherapy. Sometimes after the first attack, we'll do a little bit of a slow taper, maybe over four, six weeks. We have done longer than that. And then we won't place them on any long-term treatment, because it's about 50% of patients that may have a monophasic disease, so we don't want to treat all those people who are destined never to have another relapse. On the other hand, if a patient had a very severe episode, they're in the ICU, they're intubated, some of those patients then afterwards we will start them at least temporarily on an attack prevention medication for at least a few years to get them through. Some patients will be very fearful of future relapses in that situation. Or if they don't recover well, if they're blind in one eye after an episode and then their other eye is vulnerable, or they're left with some residual deficits neurologically from a myelitis, then we would often sometimes put those patients after the first attack. But most of the time, we're gonna wait and see if they get that second attack, and then once they have the second attack, that is when we would consider a steroid-sparing medication. But I will say that there's no proven medications. We don't have any clinical trial data available yet. So some of those patients with relapsing disease, we'll either try to enroll them in a clinical trial, or we'll use an off-label treatment to try and manage their disease based on what we've learned from neuromyelitis optica or from multiple sclerosis. A few different options seem to be better, and we can maybe get into that too.   Dr Smith: Yeah, let's go there. So, what options are there? You mentioned in more fulminant disease IL-6 inhibitors, and by that I assume you mean tocilizumab, but what are the options when you want to use prophylactic therapy?   Dr Flanagan: So, that tocilizumab can be beneficial in the very acute situation, in that malignant situation. But also as an attack prevention treatment, the IL-6 blockers seem to- some of the retrospective data seems to look like it works reasonably well, so we work and see if we can get that approved. Another medication that can work well is IVIG or subcutaneous immunoglobulin as a maintenance treatment, so we would sometimes give that, like, at least one gram per kilogram once a month. The benefit of that is it doesn't lower your immune system, so there's some advantages there, particularly in people who may be more prone to infections, older people. So, we'll sometimes use that. But we do get into a lot of challenges with insurance coverage, and it can be difficult to get these approved by insurance because we only have retrospective data out there. So then for some patients, if they're in a region where there's a clinical trial available, we might try to enroll them in a clinical trial. And there are some clinical trials underway now, so hopefully in the future we'll be able to have some FDA-approved medications that can have some Class 1 data that we can follow. Because it's hard when you're just following retrospective data or anecdotal reports, it's a little bit difficult to know exactly how well you're doing with your treatments.   Dr Smith: Well, Eoin, I wonder if we could finish up by just looking into the future, right? I mean, it sounds like a fun patient population to take care of because you've got lots of great therapies and can have a durable impact. But sure would be nice to have more evidence-based therapies and an FDA approval. What trials are going on? What's the future look like?   Dr Flanagan: Yep. So, there's some trials going on in the- a couple of worldwide trials. One is on an FCRN blocker called rozanolixizumab, which is kind of like a plasma exchange-type treatment which removes your antibodies, and it's a weekly subcutaneous treatment where adults are enrolled. And the second one is called satralizumab, which is another IL-6 blocking medication. And again, that one's given once monthly under the skin. And the trial for that also includes children down to age eighteen, so for adolescents, too, that can be an option. There are trials, I believe, in Asia for tocilizumab too, and there's one starting in Australia for rituximab. So, the good news is that we're going to have some really good data down the line for lots of different agents, and we'll be able to figure out which treatments work. And this will be really of great benefit to our patients when we get that Class 1 data to kind of guide us on what we should be using and really build on the success of some of the other conditions like neuromyelitis optica spectrum disorder, where we now have four or five approved, medications that work very well.   Dr Smith: Well, Eoin, thank you. This is a great conversation. I will say that it... the topic that I was a little intimidated about. I'm a simple peripheral nerve guy, as you know. But I think moreso than any other Continuum article I've read recently, I'm, like, loaded for bear. I can't wait to go back on the inpatient service and look for some MOG patients, because your article really left me feeling kind of prepared to think through this in a clinical setting. So, thank you for the conversation, and congratulations on a really wonderful piece for Continuum.   Dr Flanagan: Yeah, thanks so much. Always a great honor to be involved in the Continuum, and thanks to all the readers out there.   Dr Monteith: This is Dr. Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at continpub.com/audioCME. Thank you for listening to Continuum Audio.

In this special “Ask the Expert” collaboration between The MOG Project and SRNA, Julia Lefelar and Dr. GG deFiebre welcomed Dr. Benjamin Greenberg of UT Southwestern, who answered questions from the audience. Dr. Greenberg reviewed major advances in MOG antibody disease research and diagnostic criteria [00:05:06]. He discussed efforts to predict relapse risk using sustained antibody positivity, demographic and clinical models, and immune-cell profiling studies [00:07:55]. Dr. Greenberg detailed controversies around low-positive antibody titers and how cell-based assays and dilution thresholds affect specificity [00:21:38]. He outlined concepts and progress in tolerance-inducing approaches such as Tregs and CAR T therapy, described differences from B-cell–depleting drugs like rituximab [00:26:32] Finally, Dr. Greenberg highlighted the satralizumab meteoroid trial and the ongoing cosMOG study of rozanolixizumab, emphasizing community engagement, registries, surveys, and trial participation to accelerate access and potential curative strategies [00:38:36]. You can learn more about The MOG Project here:https://mogproject.org/Benjamin M. Greenberg, MD, MHS is a Professor and the Cain Denius Scholar in Mobility Disorders in the Department of Neurology [ https://utswmed.org/why-utsw/departments/neurology/ ] at UT Southwestern Medical Center in Dallas, Texas. He currently serves as the Vice Chair of Translational Research and Strategic Initiatives for the Department of Neurology. He is also the interim Director of the Multiple Sclerosis Center [ https://utswmed.org/locations/aston/multiple-sclerosis-and-neuroimmunology-clinic/ ] and the Director of the Neurosciences Clinical Research Center. In addition, he serves as Director of the Transverse Myelitis and Neuromyelitis Optica Program and the Pediatric Demyelinating Disease Program at Children's Medical Center [ https://www.childrens.com/specialties-services/specialty-centers-and-programs/neurology/demyelinating-disease-program ].Dr. Greenberg earned his medical degree at Baylor College of Medicine before completing an internal medicine internship at Chicago's Rush Presbyterian-St. Luke's Medical Center. He performed his neurology residency at the Johns Hopkins School of Medicine. He also holds an M.H.S. in molecular microbiology and immunology from the Bloomberg School of Public Health, as well as a bachelor's degree in the history of medicine – both from Johns Hopkins. Prior to his recruitment to UT Southwestern in 2009, Dr. Greenberg was on the faculty of the Johns Hopkins Division of Neuroimmunology, serving as the Director of the Encephalitis Center and Co-Director of the nation's first dedicated Transverse Myelitis Center.Dr. Greenberg splits his clinical time between adult and pediatric patients at William P. Clements Jr. and Zale Lipshy University Hospitals, Parkland, and Children's Medical Center. His research focuses on better diagnosing, prognosticating, and treating demyelinating diseases and nervous system infections. He also coordinates clinical trials to evaluate new treatments to prevent neurologic damage and restore function to affected patients.00:00 Welcome01:44 Hosts and Guest Intro05:06 Research Buckets Overview07:55 Predicting Relapse Risk11:46 Tregs and Immune Brakes17:40 Attack Severity and Relapse19:24 MOGAD Criteria Updates21:38 Titers Explained Simply26:32 Targeting MOG Antibodies29:11 CAR T and Immune Reset32:39 When Criteria Changes33:52 Tolerance Research Boom34:48 From Animals to Trials37:17 Community Drives Progress38:36 Meteoroid and cosMOG Clinical Trials41:39 How These Drugs Work44:02 FDA Approval and Access45:49 Insurance Switch Concerns48:39 Rituximab Dosing Debate52:41 Why Antibodies Develop54:18 Future Attack Patterns55:47 CAR T Versus Rituximab57:10 Lab Research and Support01:00:51 Hope for a Cure01:02:14 Closing and Resources

In this SRNA "Ask the Expert" episode moderated by Krissy Dilger, Dr. John Chen of the Mayo Clinic answered audience questions about MOG antibody disease (MOGAD). He discussed diagnosis and the importance of titers and live cell-based assays given possible false positives [00:02:42]. Dr. Chen reviewed acute management with early high-dose steroids, prolonged tapers, and escalation to plasma exchange for severe or steroid-refractory attacks, as well as evolving long-term options including IVIG/subcutaneous IG and IL-6 blockade [00:04:14]. Audience questions covered relapse prediction, vision recovery timelines, fatigue, pregnancy, heredity, symptom interpretation, and whether to stop immunotherapy when antibodies become undetectable [00:12:13]. Finally, Dr. Chen described current and upcoming research, including a trial that is currently enrolling participants, and future prospects for optic nerve regeneration while cautioning against unproven stem cell clinics [00:41:37].John J. Chen, MD, PhD attended the University of Virginia for his undergraduate and combined MD/PhD degrees and completed his Ophthalmology residency and Neuro-Ophthalmology fellowship training at the University of Iowa. He then took a position at the Mayo Clinic in 2014 where he specializes in Neuro-Ophthalmology. Currently, he serves as a Consultant and Professor of Ophthalmology and Neurology, and Neuro-Ophthalmology Fellowship Director at the Mayo Clinic. Among Dr. Chen's awards and honors are the AAO Senior Achievement Award, Top Doctors in Minnesota, the Heed Fellowship, Real World Ophthalmology Inspiring Academic Leader Award, Ophthalmology Teacher of the Year Award four times leading to induction to the Educators Hall of Fame, and the Mayo Clinic Distinguished Educator Award – awarded to the top educator at Mayo Clinic in Rochester. He is an Associate Editor for Ophthalmology and the Journal of Neuro-Ophthalmology, has authored more than 250 peer-reviewed publications, and focuses his research on ophthalmic imaging, idiopathic intracranial hypertension, and optic neuritis, particularly NMOSD and MOG antibody–associated disease.00:00 Welcome and Introductions01:08 What Is MOGAD?02:42 Causes and Triggers03:23 How MOGAD Is Diagnosed04:14 Acute Attack Treatments06:35 Steroid Side Effects08:13 Testing During Treatment09:09 Long Term Therapies12:13 Interpreting MOG Positivity16:51 Eye Symptoms and Vision Fluctuations20:12 Antibody Titers and Severity21:19 Relapse Risk After First Attack23:09 Seizures and Encephalitis24:17 Vision Recovery After Optic Neuritis25:13 Acute Treatment Window25:57 Hereditary Risk Questions26:35 Stopping Azathioprine Safely29:56 Managing Post Attack Pain30:16 Steroids IVIG and Plasma Exchange32:08 Infections as Triggers33:01 Retesting MOG Antibodies35:01 Fatigue and Workup36:23 Prognosis and Life Expectancy37:45 Tinnitus and Brain Pressure39:05 Pediatric and Pregnancy Concerns41:37 Trials and Future Regeneration46:05 Research Resources and Wrap Up

In this SRNA “Ask the Expert” episode, Krissy Dilger of SRNA spoke with neuroimmunologist Dr. Shailee Shah about paraneoplastic neurologic syndromes—immune-mediated, “off-target” effects of cancer that can affect the brain, spinal cord, or peripheral nerves. Dr. Shah described updated diagnostic criteria and scoring that combine neurologic phenotypes, cancer risk, and high-risk autoantibodies, and she explained how immune checkpoint inhibitors can trigger immune-related neurologic adverse events that don't always fit classic rules [00:01:48]. She reviewed how these syndromes differ from other autoimmune neurologic disorders and outlined common subacute presentations such as limbic encephalitis, brainstem encephalitis, cerebellar ataxia, seizures, and neuropathies [00:08:09]. Dr. Shah emphasized prompt evaluation with neurologic exam, MRI/EEG/EMG as appropriate, blood and CSF antibody testing, cancer screening, and coordinated oncologic and immunosuppressive treatment to prevent worsening disability [00:17:24].Shailee Shah, MD is a Clinical Assistant Professor in the Neuroimmunology Division with Northwestern Medicine and Northwestern University. She is an autoimmune neurologist with expertise in the management of paraneoplastic and autoimmune neurological diseases. She also treats rare neuroimmunological diseases such as neuromyelitis optica and MOG associated disease. She is co-director of the Northwestern Medicine Paraneoplastic Neurological Disease Clinic.00:00 Welcome and Guest Intro00:58 What Is Paraneoplastic01:48 New Criteria and Antibodies04:59 Diagnostic Challenges and ICI08:09 Paraneoplastic vs Autoimmune10:22 How Common Are They13:03 Early Symptoms to Watch17:24 When to Seek Care19:09 Testing and Workup24:20 Paraneoplastic Myelitis27:55 Delays and Specialty Centers31:38 Cancer Link and Treatment37:16 Changing Therapies38:19 Recovery and Prognosis39:58 Patient Advice and Hope42:52 Closing

Książkę znajdziecie tutaj: https://ksiegarnia.uni.lodz.pl/geometria-p-2727.html #współpracapłatnaGeometria, Grecy, Egipcjanie i piramidy, Wszechświat, czarne dziury, tunele czasoprzestrzenne i pomysły na „zgeometryzowanie” mechaniki kwantowej – oto zestaw zagadnień, którymi raczymy Was w najnowszym, jakże treściwym odcinku. Naszym gościem jest prof. Maciej Dunajski, fizyk matematyczny z Uniwersytetu Cambridge, a rozmowę nagraliśmy w Łodzi, w której się urodził i kształcił. Inspiracją do spotkania jest książka profesora pt. „Geometria” – oryginalnie napisana po angielsku, właśnie ukazała się w polskim przekładzie w Wydawnictwie Uniwersytetu Łódzkiego. Odcinek jest elementem współpracy promocyjnej z Wydawnictwem.Korzenie geometrii sięgają starożytności, a jej abstrakcyjną stronę zaproponowali Grecy. Ówczesną wiedzę zebrał Euklides, który spisał słynne aksjomaty na przełomie IV i III wieku przed naszą erą. Musiało minąć grubo ponad 2000 lat, by matematycy zmierzyli się z myślą, że istnieją też inne, nieeuklidesowe geometrie. Jako pierwszy zrobił to w XIX wieku Carl Friedrich Gauss. – Być może najwybitniejszy matematyk wszechczasów – ocenia prof. Dunajski.Geometria nieeuklidesowa okazała się konieczna, by opisać Wszechświat. – Geometria Wszechświata, tak jak ją rozumiemy teraz, jest przestrzenią zakrzywioną (…). Mogą być rejony zakrzywione dodatnio, mogą być też takie, które mają ujemną krzywiznę – opowiada naukowiec. W odcinku rozmawiamy o „szalonych” efektach zakrzywienia czasoprzestrzeni, jakimi są czarne dziury.W wyobraźni wybieramy się na wycieczkę do ich wnętrza, staramy się ominąć osobliwość, szukamy też przejścia przez wormhole, aby wylądować w innym miejscu czasoprzestrzeni (w przeszłość nie da rady, ale jak mówi prof. Dunajski „nie ma silnych przeciwwskazań podróży w czasie do przodu”). W rozmowie pojawia się też Roger Penrose, jeden z najlepszych współczesnych fizyków na świecie, z którym prof. Dunajski pracuje. Gorąco polecamy! 

Legendary British ad man Rory Sutherland invented a fake business on a podcast, a coffee shop appealing to the busy commuter called “Flat White or F**k Off.”But it's one thing to have a post go big on TikTok or Instagram… but to turn that viral moment into an actual COMPANY is a very different challenge.On TWiST, Jason and Lon chat with Charlie Hurst, Tom Noble, and Will Sudlow, founders of the online brand “Flat White or F**k Off,” about how they took a funny little slogan and turned it into a string of popular social media accounts, a line of merch, a pop-up café, and let's face it, an entire lifestyle.PLUS we've got Mog and Dubs from Subnet 75 — Hippius! Hear how they're using the blockchain for decentralized storage, and providing server space much cheaper than their famous hyperscaler rivals.This Week In Startups is made possible by:Plaud - https://Plaud.ai/twistLinkedIn Jobs - https://LinkedIn.com/twist.Wispr Flow - https://wisprflow.ai/twistNorthwest Registered Agent  - https://www.northwestregisteredagent.com/twistTimestamps:00:00:00 Intro00:01:28 Plaud - If your work depends on conversations — interviews, meetings, calls — you need a Plaud NotePin. You can check it out at https://Plaud.ai/twist and use code TWIST for 10% off!00:03:22 What is "decentralized cloud storage"?00:05:42 How Hippius came together00:09:57 LinkedIn Jobs - Hire right, the first time. Post your first job and get $100 off towards your job post at https://LinkedIn.com/twist.00:11:38 Incentivizing miners00:14:25 How many people are contributing?00:18:42 But where does the value accrue?00:20:18 Wispr Flow - Stop typing. Dictate with Wispr Flow and send clean, final-draft writing in seconds. Visit https://wisprflow.ai/twist to get started for free today.00:29:55 Northwest Registered Agent. Get more when you start your business with Northwest. In 10 clicks and 10 minutes, you can form your company and walk away with a real business identity — Learn more at https://www.northwestregisteredagent.com/twist00:35:53 The best places to eat in Dubai00:38:06 The inspo behind "Flat White or F Off"00:42:16 From social media to IRL business00:53:06 The secrets of experiential marketing00:57:28 Hospitality's "Rule of 3s"00:59:33 Inside the Flat White London pop-up01:13:11 Lon and Jason's Oscar picks01:26:06 Lon went "Inside the Manosphere"Subscribe to the TWiST500 newsletter: https://ticker.thisweekinstartups.comCheck out the TWIST500: https://www.twist500.comSubscribe to This Week in Startups on Apple: https://rb.gy/v19fcpFollow Lon:X: https://x.com/lonsFollow Alex:X: https://x.com/alexLinkedIn: ⁠https://www.linkedin.com/in/alexwilhelmFollow Jason:X: https://twitter.com/JasonLinkedIn: https://www.linkedin.com/in/jasoncalacanisCheck out all our partner offers: https://partners.launch.co/Great TWIST interviews: Will Guidara, Eoghan McCabe, Steve Huffman, Brian Chesky, Bob Moesta, Aaron Levie, Sophia Amoruso, Reid Hoffman, Frank Slootman, Billy McFarlandCheck out Jason's suite of newsletters: https://substack.com/@calacanisFollow TWiST:Twitter: https://twitter.com/TWiStartupsYouTube: https://www.youtube.com/thisweekinInstagram: https://www.instagram.com/thisweekinstartupsTikTok: https://www.tiktok.com/@thisweekinstartupsSubstack: https://twistartups.substack.com

Födslotalen dyker i Europa och varför det fortsätter nedåt är en gåta. Vad händer när den europeiska bebiskollapsen blir politik? Lyssna på alla avsnitt i Sveriges Radios app. I land efter land i Europa dyker siffrorna över antalet nyfödda. Demografer famlar efter förklaringar och medan avsaknaden av säkra svar är ett faktum dras nya politiska konfliktlinjer upp. Hör om hur radikalhögern i Europa vill äga befolkningsfrågan och hur Ungerns Viktor Orbán gått fram med en familjepolitik som andra ytterhögerpartier nu tar efter. Däribland AFD i Tyskland, som genom engångsutbetalningar vill uppmuntra kvinnor att föda fler barn. Inte sällan ställs migration mot inhemskt barnafödande och Spanien går mot strömmen när invandrare ses som en framtidslösning. Även i Sverige har befolkningsfrågan hamnat på den politiska dagordningen. I Västerbottens inland söker Konflikt svar på hur framtiden kan se ut och vad som står på spel för våra samhällen.Medverkande: Pieter Vanhuysse, demograf och ekonom vid Syddansk Universitet. Vanessa Behrendt, familjepolitisk talesperson för AFD i Niedersachsen. Weiard Siebels, SPD-politiker i Niedersachsen. Onalia Bueno, borgmästare i Mogán på Kanarieöarna. Cecilia Festin Stenlund (L), kommunalråd i Malå. Tove Lestander, förälder i Sorsele. Marie Quinonez Gonzalez, kommunchef i Sorsele. Pia Sjöberg (S), kommunalråd i Sorsele. Jakob Forssmed (KD), socialminister. Invånare i Hannover, Tyskland samt i Sorsele, Sverige.Reporter i Spanien: Daniel Ekblad, frilansjournalist.Producent och reporter i Västerbotten: Therese Rosenvingetherese.rosenvinge@sverigesradio.seProgramledare och reporter i Hannover: Filip Kotsambouikidisfilip.kotsambouikidis@sverigesradio.seTekniker: Lisa Abrahamsson

A rush of new competition is flooding into areas like space and nuclear. We take a look at what is real, and what is hype. Tyler Crowe, Matt Frankel, and Lou Whiteman discuss: - What space investments look exciting - Areas of the sector that are overcrowded - Why they are cautious about buying into the nuclear hype - Investing stories they are following right now Companies discussed: MOG.A, SES, OKLO, SMR, HHH, JOBY, ACHR Host: Tyler Crowe Guests: Lou Whiteman, Matt Frankel Engineer: Dan Boyd Disclosure: Advertisements are sponsored content and provided for informational purposes only. The Motley Fool and its affiliates (collectively, “TMF”) do not endorse, recommend, or verify the accuracy or completeness of the statements made within advertisements. TMF is not involved in the offer, sale, or solicitation of any securities advertised herein and makes no representations regarding the suitability, or risks associated with any investment opportunity presented. Investors should conduct their own due diligence and consult with legal, tax, and financial advisors before making any investment decisions. TMF assumes no responsibility for any losses or damages arising from this advertisement. We're committed to transparency: All personal opinions in advertisements from Fools are their own. The product advertised in this episode was loaned to TMF and was returned after a test period or the product advertised in this episode was purchased by TMF. Advertiser has paid for the sponsorship of this episode. Learn more about your ad choices. Visit ⁠⁠⁠⁠⁠⁠⁠⁠megaphone.fm/adchoices⁠⁠ Learn more about your ad choices. Visit megaphone.fm/adchoices

W książce „Kiedy życie mówi sprawdzam” użyłam określenia – „opiekun rezyliencji” (za Borisem Cyrulnikiem). Opiekun rezyliencji to osoba, która pełni w naszym życiu określoną rolę. Ma nieść wsparcie, ma nieść opiekę, gdy my wpadamy w tarapaty, ma okazać życzliwość, dać poczucie bezpieczeństwowspierające w powrocie do równowagi po ów tarapatach. Co ciekawe opiekunem rezyliencji nie muszą być osoby namznane. Mogą nimi być osoby przypadkowe. Naprawdę! I o tym jest ta rozmowa. Gdy Magda opowiedziała mi swojąhistorię, a spotkałyśmy się ostatnio na warsztatach z odporności psychicznej, których brała udział. Gdy opowiedziała swoją historię innym uczestniczkom wprawiającje w prawdziwe zadziwienie – wiedziałam, że bardzo chcę, by jeszcze raz opowiedziała ją … w moim podcaście. Poznajcie Magdę Jędrzejewską – Sadecką, z jednej strony finansistkę, z drugiej instruktorkę pilatesu i właścicielkę studia Tricity Pilates. Ale przede wszystkim kobietę, której życie powiedziało sprawdzam. Nie raz. Nie dwa. Posłuchajcie naszej rozmowy o tym, że opiekunowierezyliencji mogą być nieoczywiści, niespodziewani, a pomoc może przyjść do nas z zaskakujących źródeł. To rozmowa o przyjmowaniu pomocy, bardzo trudnymkawałku naszego życia, bo tak bardzo chcemy udawać, że dajemy radę, samotnie isamodzielnie … Ech. Nie udawajmy! Zapraszamy do odsłuchu

Polski wynalazek mógłby usprawnić działanie stomatologów i innych lekarzy, gabinetów kosmetycznych itp. Mogłoby być lepiej, wygodniej, taniej a do tego bardziej ekologicznie - zniknęłaby produkcja tysięcy ton odpadów medycznych! Ale polskie urzędy od lat stają na drodze. Posłuchajcie historii inżyniera Kazimierza Bachanka. #medycyna #wynalazek #narzędziamedyczne

On the Space Cowboys' RIPEcast this week Mancub rocks the decks live from the Mog stage at Breakfast of Champions Jan. 1, 2026. Had an absolute blast playing the Mog stage. Proud of our Bay Area community and enjoyed all the DJs sets. Thank you for having me again! - Mancub

In Part Two we continue with the chirping and muttering of the Mog, who warmly endorses ICE, and praises Trump's global tarrifs, which ironically, have just been declared illegal and void by the Supreme Court. It is strange to hear Bruce D Hales speaking so authoritatively on the governance of great nations, while his own sorry banana republic collapse around his ears, and to hear him enthusing about punitive tariffs while his scandal-stained UBT is prosecuted for tax evasion. But then, what Hales ever scored a passing grade for integrity?After the team has finished politely and respectfully analyzing the Profound Wisdom of the Mog, we move on to some scathing emails from insiders who have much to say about the current leadership. All this is offered to you, dear listeners, free of charge. We don't even require you sign an NDA. Enjoy!Link for Insiders- https://www.dropbox.com/scl/fi/jyal3erc0n29y2a7rtv80/45000-163.mp4?rlkey=6tu9a3mteishtdd4kcsm49lyj&st=kgalcgod&dl=0Link to GOFUNDME for legal suit against Cheryl and the Get a Life podcast- https://gofund.me/e976c9d77Link to articles on ATO raid-https://archive.ph/Mi2wfhttps://www.theguardian.com/australia-news/article/2024/may/24/accounting-firm-controlled-by-exclusive-brethren-church-to-close-after-extraordinary-ato-raid-ntwnfbhttps://archive.ph/TnP7YTo share your story or be a guest on the show, email info.getalife@proton.meGet a Life Paypal donations -https://www.paypal.me/getalifepodcastGet a Life GoFundMe-https://gofund.me/614bcd06Olive Leaf Network- https://oliveleaf.network/Thinking of Leaving Pamphlet and resources - https://oliveleaf.network/resources/Link to Anchor/Spotify- https://open.spotify.com/show/4GhNv1hZp6tjfLyA4s6PMu?si=Gs5euyWpT4y7lOS8OTe4XAPreston Down Trust Decision-https://www.gov.uk/government/news/commission-publishes-report-on-the-preston-down-trustAberdeen incident- https://drive.google.com/file/d/1riImgAqwaqGwjYq6vRQIr4_jscJA0eQN/view?usp=drive_linkIf we walk in the light letters-https://drive.google.com/file/d/14WlgJladl1r95YGxW0FbZ0prYfjlg7FU/view?usp=sharingAdmin/Legal email address:stouffvillelegal-gal@protonmail.comOffice address:22 Braid BendStouffville ONL4A 1R7#plymouthbrethrenchristianchurch #pbcc #abuse #church #cult #religion #trauma #religioustrauma #sexualabuse #mindcontrol #brainwashing #conversation #exmembers #exposingtruth #expose #exposure #whistleblower #getalifepodcast #getalife #podcast #rules #strict #exclusivebrethren #brucehales #BruceHales #BDH #BruceDHales #UniversalBusinessTeam #UBT #RRT #RapidReliefTeam #Aberdeen #OneSchoolGlobal #OSG #johnhales #shutup #withdrawnfrom #worldly #excommunicate #assemblydeath #christiansect #christiancult #canadiancult #canadiansect #sect #worldwidesect #worldwidecult #cultescape #cultescapestory #bully #bullying #brokenfamily #awareness #cultescape #cultandculturepodcast #cultescapee #cultescapeer #cultescapeeinterview #askingforhelp #unispace

The ATO raid on the Plymouth Brethren Christian Church's HQ took place 2 years ago, and since then, a series of consequences and related events has played out, some in public, and some behind closed doors. Like pieces of a jigsaw puzzle, the real picture is a mystery until all these pieces are assembled and that is what Get A Life does for you in this episode. What emerges is three names. Three extremely prominent PBCC leaders whose behavior screams of guilt, and a desperate attempt to evade accountability. We name and shame them.Then we move on to Bruce Hales in person – recordings of a recent fellowship meeting we have obtained, which we will play for you, and offer our commentary on his strange and contradictory ramblings. The profound mutterings of the MOG will be continued on Part 2 of this gripping episode that we have titled “THIEVES”.Link for Insiders- https://www.dropbox.com/scl/fi/t3y5gbssi5aflo6qvxa24/45000-162.mp4?rlkey=pyj6higznc5c2dgvvwhuegqid&st=etwr0zxp&dl=0Link to GOFUNDME for legal suit against Cheryl and the Get a Life podcast- https://gofund.me/e976c9d77Link to articles on ATO raid-https://www.smh.com.au/national/fleecing-the-flock-exclusive-brethren-businesses-raided-by-tax-office-20240321-p5fe6r.htmlhttps://bnnbreaking.com/world/australia/exclusive-brethren-under-tax-office-scrutiny-raid-reveals-potential-financial-misconductTo share your story or be a guest on the show, email info.getalife@proton.meGet a Life Paypal donations -https://www.paypal.me/getalifepodcastGet a Life GoFundMe-https://gofund.me/614bcd06Olive Leaf Network- https://oliveleaf.network/Thinking of Leaving Pamphlet and resources - https://oliveleaf.network/resources/Link to Anchor/Spotify- https://open.spotify.com/show/4GhNv1hZp6tjfLyA4s6PMu?si=Gs5euyWpT4y7lOS8OTe4XAPreston Down Trust Decision-https://www.gov.uk/government/news/commission-publishes-report-on-the-preston-down-trustAberdeen incident- https://drive.google.com/file/d/1riImgAqwaqGwjYq6vRQIr4_jscJA0eQN/view?usp=drive_linkIf we walk in the light letters-https://drive.google.com/file/d/14WlgJladl1r95YGxW0FbZ0prYfjlg7FU/view?usp=sharingAdmin/Legal email address:stouffvillelegal-gal@protonmail.comOffice address:22 Braid BendStouffville ONL4A 1R7#plymouthbrethrenchristianchurch #pbcc #abuse #church #cult #religion #trauma #religioustrauma #sexualabuse #mindcontrol #brainwashing #conversation #exmembers #exposingtruth #expose #exposure #whistleblower #getalifepodcast #getalife #podcast #rules #strict #exclusivebrethren #brucehales #BruceHales #BDH #BruceDHales #UniversalBusinessTeam #UBT #RRT #RapidReliefTeam #Aberdeen #OneSchoolGlobal #OSG #johnhales #shutup #withdrawnfrom #worldly #excommunicate #assemblydeath #christiansect #christiancult #canadiancult #canadiansect #sect #worldwidesect #worldwidecult #cultescape #cultescapestory #bully #bullying #brokenfamily #awareness #cultescape #cultandculturepodcast #cultescapee #cultescapeer #cultescapeeinterview #askingforhelp #unispace

Pisté par la commandante Mog, le Gallinea fonce vers Toxymu, où Yto espère trouver Tym.plus d'infos

Join me as I review The Dragon Isles by Stephen D. Sullivan live! Share your thoughts on this fourth novel in the Dragonlance Crossroads series, released by Wizards of the Coast on December 1, 2002. You can buy a copy here: https://amzn.to/4k9Vsow  https://youtube.com/live/G7_6TTEypEQ About The Dragon Isles The Dragon Isles: abandoned home of the good dragons, land of amazing adventure and legendary treasure. The trouble is, no one knows how to get there. Now Mikal Vardan and his crew have found the hidden route, but they're not the only ones interested in the isles. A beautiful sea elf scavenger thinks the wealth of a lost civilization might be worth killing for, and a menacing sea dragon is determined to bring a reign of terror to the peaceful archipelago. Review Part one of this novel deals with Lady Karista Meinor and her bodyguard Bok hiring a ship to take them to the Dragon Isles where they want to open a trade route. They are using an old poem that is thought to be a prophecy about how to find the mysterious dragon isles. The novel opens with the ship’s captain, Mikal Verdan rescuing one of his sailors, a kender named Tripleknot Shellcracker from a sea monster. THey narrowly escape and are pulled on deck just in time for the crew to near mutiny. THey have not been informed about the point of this excursion and they have been sailing the northern Courrain ocean for longer than anticipated with no end in sight.  They are told they are headed to the Dragon Isles where everyone will get their share of the spoils, and this pacifies them. Then they see floating wreckage which the kender claims has someone on top. It takes a while to intercept but there is a Dargonesti elf chained and unconscious on the wreckage. They bring her aboard and nurse her. It is revealed that she was believed to be cursed by her former shipmates and left to die, because there is  a sea dragon named Tempest trying to enter the Dragon Isles with her dragonspawn Mog. If they can’t get through the veil which protects the isles, no one will. She has been attacking all ships that dare to get near. It is also revealed that the captain, Mik, is having visions of treasure and the dargonesti named Ula, is willing to help him locate the isles and treasure for a percentage. He agrees, but Karista doesn’t. Then Tempest attacks. She capsizes the ship and kills most of the crew. Mik and Trip use the failing magical items to breathe under water but are captured by other Dargonesti and brought to their underwater town. There they will be sold off into slavery or fight. However, Tempest and Mog followed. Once imprisoned they see that Ula and Karista were there and the only other survivors. Then Tempest attacks. They escape together with the help of one of the elves that captured them named Shimmer. He leads them to the Veil and with the aid of a black gem Mik has, they all pass through. Mog follows and narrowly passes through as well. Though Tempest is left on the other side still. Tempest charges at the barrier using all her might and magic and is repelled again and again. She must be content that her spawn is on the other side, following the mortals, waiting to spring a trap and drop the veil once and for all. On the other side, the party comes ashore and is seen by a massive dragon, then a ship rolls up under order of the Brass taking them captive. Ula demands honor by combat rather than them being taken to their lord, and she fights Misa Kell, defeating her. Her brother is furious but honors the bargain. Ula is to take them to the dargonesti kingdom, but Benthor Kell, Misa's brother, holds to the law of shipping the kender to an island where they all dwell. Karista Meinor decides to stay with Kell to have the Order of the Brass negotiate shipping routes with her. The kender is tied up in a cabin, and Ula, Mik and Shimmer are dropped into a boat and leave to the dargonesti home. Once they arrive they see some of the people from the ruined sea elf town outside the veil, and they make their pleas to the lord of this realm. He allows them freedom and Ula, mik and shimmer decide to look for the next key to their treasure by visiting the sea sage. When they arrive it ends up attacking them and they temporarily defeat it, taking its key. Next they head to the gold dragons libraries. There Ula stays at the ship while shimmer and Mik head up, only to be stopped by a copper dragon guard who knows shimmer and lets them pass.  Back on Kell's boat, Trip escapes and jumps overboard, swimming from the pursuing ship. He hides in a cave and finds  a secret entrance to a pirates hide where he takes a sea dragon cloak that allows him free movement and breathing underwater. He escapes his pursuers and gets passage from the pirate Jerrick the Red, an old acquaintance of Miki's. Very convenient. He takes the kender to the same island as his companions, conveniently, and meets Ula there. Mik and shimmer enter the library and mik climbs to the peak and has a vision of the island chain being formed and populated, then gets the next key piece. They come to shore to see Ula, Trip and Jerrick where they bargain for his ship to take them to the final key location. Kell meets with the order of the Bronze and is told to stop Ula and shimmer, retrieving the treasure themselves as payment for the future shipping agreement with Karista. They pursue Jerrick’s ship and their dragon emissary abducts Ula. Shimmer transforms into a bronze dragon, his true form, and attacks the bronze holding Ula. He recovers her as krell seizes control of Jerricks ship with his own. Shimmer crashed on deck with Ula and both sides nearly come to blows when Jerrick speaks up, on working together to split t he treasure. The interjection actually works and they all get together to find the last piece ofthe key.  They find the location and dive under the water, locating the temple where they find the key, but Mog is waiting and attacks a guard, changing into his appearance. He joins the crew and as Mik assembles the key with thenew piece, a stairway appears and ascends into the sky. They begin to go up and swarms of crabs attack, then Karista steals the key from Mik and reveals she is working for Tempest, this stuns Mog and they both race to the temple fighting the heroes all the way. Tempest breaks through the barrier when the group arrives at the temple and the now fully assembled key is a lightning weapon that is turned against the heroes. Factions are blurred and everyone seems to survive incredible wounds but the fight is truly epic. Karista is defeated and the heroes reclaim the key only to have tempest arrive and fight them, killing many people, including Karista, and the all scatter trying to defeat the sea dragon. Eventually Mik faces off against it and it plumets into a volcano, which then erupts and the key seems to offer Mik treasure at the sacrifice of the Dragon Isles. He refuses and throws the key into the volcano as well. The temple of the sky begins to fade and he leaps in to the ocean, sure to drown. He is saved by Ula and they return to the ship, when Trip arrives with a miraculously still alive Shimmer. They all decide to continue searching for treasure in the Dragon Isles together and the novel ends abruptly. There were so many moments where characters should have died over and over again, but I forgive it for the epic scope of that final battle. The author isn't great, but I did find myself enjoying this novel more than I anticipated, even if the story itself was seemingly rushed. I also think it was more epic than the Dawning of a New Age final novel, which while not saying a lot since it want good, does say that this one novel was superior to a trilogy. If you are a fan of the Dragon Isles, and water based adventures, this is a must read. For fans of Dragonlance, it is fun, but not required reading.

Rozmowa z przyjaciółmi i bliskimi o depresji potrafi być trudna. Nawet jeśli mają szczere chęci, bywa, że ich wiedza i rozumienie depresji są ograniczone. Mogą również mieć pytania, na które nie zawsze będziesz wiedzieć jak zareagować i odpowiedzieć.Przygotowanie do takiej rozmowy sprawi, że poczujesz większą pewność siebie. Usłyszysz pytania, które pojawiają się w rozmowach z bliskimi najczęściej i przykładowe wyjaśnienia. Mam nadzieję, że okażą się przydatne.__________Monika Kotlarek jest psycholożką z kilkunastoletnim doświadczeniem. Od 2012 roku prowadzi znany blog psycholog-pisze.pl, na którym opowiada o… psychologii, oczywiście! Jest też autorką książek takich jak „Choroba afektywna dwubiegunowa, czyli ze skrajności w skrajność”, „Depresja, czyli gdy każdy oddech boli”, „Borderline, czyli jedną nogą nad przepaścią” oraz „Wyczerpanie psychiczne, czyli gdy to już nie jest zwykłe zmęczenie” i „Dorosłość z ADHD, czyli między chaosem a kreatywnością”. Prowadzi również własny gabinet psychologiczny online, w którym pomaga pacjentom odzyskać spokój i zdrowie. Dodatkowo prowadzi profesjonalną diagnostykę psychologiczną w kierunku ADHD u osób dorosłych. Prowadzi Psychosklepik z materiałami do pracy własnej m.in. nad pewnością siebie, stratą czy poczuciem wartości oraz budową bliskości wśród par. W social mediach znana jako Psycholog Pisze (@psycholog_pisze), prowadzi podcast i kanał na Youtubie o nazwie „Psychologia Na Co Dzień”.

2026 rang in with another epic year at BOC. We thought the weather might scare some people away, but dance floors were solid all day long and full of lots of smiling faces. Thanks to everyone with rocked out with me on the MOG stage this year. This set is full of some new and old favorites. Happy New Year! TRACK LISTING Born I Music, PEZNT - Doin' My Thing (DBR Edit) Fuzzy Hair, Tommy Vee, Keller - Super Rsquared - Wanna Be Funky (DBR Edit) Hanna Hansen - Let Me Tell You Something (Hazzaro Vs. Jerome Robins Remix) RSquared - What U Need (DBR Edit) Papa Nugs, Luke Alessi - Back It Up (DBR Edit) FDF (Italy) - Rotation (DBR Warehouse Days of Glory Edit) Hatiras - Hypnotized The Cube Guys - Never Leave You SP1DER, Ivax - My Nation FDF (Italy) - Washer Beastie Boys - Shake Your Rump (Jerome Robins Remix) Raumakustik - Panther (FormatB DBR Edit) The Brothers Macklovitch, Tony Romera, A-Trak, Mike Dunn - Bump (DBR Edit) Richard Grey - This Pressure -Brad Robinson

In this episode, Krissy Dilger of SRNA interviewed Dr. Vivien Xie regarding the significance of brain lesions in pediatric MOG antibody disease (MOGAD). Dr. Xie explained the autoimmune nature of MOGAD and the common occurrence of optic neuritis in young patients [00:01:28]. She described her study comparing children with optic neuritis who had brain lesions to those who did not, revealing that brain lesions often did not result in additional symptoms [00:02:41]. The findings suggested that brain lesions didn't significantly impact long-term outcomes, which may provide reassurance for patients with concerning MRI results [00:06:43]. Finally, they discussed the study's implications for better understanding different phenotypes of MOGAD and improving patient prognosis. Future research directions include more detailed MRI analysis and cognitive outcome assessment [00:12:29]. You can read about this multicenter study here:https://pubmed.ncbi.nlm.nih.gov/41167051/Vivien Xie, MD, is a pediatric neurologist and neuroimmunology fellow at Children's National Hospital and MedStar Georgetown University Hospital. Originally from Baltimore, she earned her undergraduate degree in biology from the University of Maryland, College Park and her medical degree from the University of Maryland School of Medicine. She then completed a child neurology residency at Children's National Hospital, where she discovered a passion for helping young patients and their families navigate rare and often life-long neuroimmunologic disorders. Dr. Xie's research interests include pediatric multiple sclerosis and MOG antibody–associated disease, with publications and presentations spanning national and international conferences. She is a committed academic clinician dedicated to advancing clinical trials and research initiatives to improve diagnosis and care for children with rare neuroimmunologic conditions.00:00 Introduction01:28 Understanding MOG Antibody Disease02:41 Research Motivation and Background05:33 Study Design and Methodology06:43 Key Findings and Implications12:29 Future Research Directions14:10 Conclusion and Acknowledgements

In this "ABCs of MOGAD" episode, "Steroid Dependence," Krissy Dilger of SRNA was joined by Dr. Eoin Flanagan from the Mayo Clinic in Rochester, MN. They began with a summary of how steroids are used to manage MOG antibody disease, particularly during acute attacks [00:01:25]. Dr. Flanagan described the mechanics of steroids in reducing brain inflammation and the importance of early treatment [00:04:14]. They discussed the concept of steroid dependence and the complications that arise when tapering down the steroid dose [00:05:46]. Dr. Flanagan highlighted alternative treatments to manage steroid dependence and emphasized the importance of working closely with healthcare providers to safely reduce steroid use over time [00:09:42].Eoin Flanagan, MB, BCh is a Professor of Neurology and Consultant in the departments of Neurology and Laboratory Medicine and Pathology at the Mayo Clinic (Rochester, MN). He completed his medical school training at University College Dublin in Ireland in 2005. He did a medical residency in Ireland and then completed neurology residency, fellowships in neuroimmunology and a master's in clinical and translational science at Mayo Clinic (Rochester, MN). He works in the Autoimmune Neurology and Multiple Sclerosis Clinics and the Neuroimmunology Laboratory at the Mayo Clinic.His clinical expertise and research are focused on inflammatory myelopathies and their imaging patterns, myelin oligodendrocyte glycoprotein (MOG) antibody associated disorder, neuromyelitis optica spectrum disorders, autoimmune encephalitis, paraneoplastic neurologic disorders, and multiple sclerosis. He is principal investigator on an NIH RO1 grant studying MOG antibody associated disorder.00:00 Introduction01:25 Understanding Steroids in MOG Antibody Disease04:14 Steroid Dosage and Administration05:46 Steroid Dependence in MOGAD Patients09:42 Managing Steroid Dependence14:02 Balancing Inflammation Control and Steroid Risks17:31 Conclusion

Clauses of Christmas cinema and hosts of the Linoleum Knife podcast (@linoleumcast), Alonso Duralde (@alonso.duralde) and Dave White (@dlelandwhite), come back into frame to chat about animated holiday favorites that don't often get top billing: Mog's Christmas, Ziggy's Gift, A Walt Disney Christmas, Mickey's Christmas Carol, Santa and the Three Bears, and Arthur Christmas. What's Making Us Feel Cozy This Christmas? Descanso Gardens' Enchanted Forest of Light Christmas throw pillows (Target and Costco) Have Yourself a Movie Little Christmas Max and Helen's Animated Christmas Movies and Shorts The Insects' Christmas Mog's Christmas Ziggy's Gift A Walt Disney Christmas Mickey's Christmas Carol Santa and the Three Bears The Bear Arthur Christmas Christmas Candle Review Trader Joes' Crackling Red Fruits in the Forest Scented Candle Merry Christmas! Give the gift of your support by joining All Things Cozy's Patreon and following us on Facebook, Instagram, and Bluesky. Also, be sure to check out Alonso and Dave's Christmas decoration Instagram account: @dxaxtree.