Podcasts about Pla

La Capital del Vallespir és a punt per acollir el 68è Festival de Sardanes de la vila, una trobada anual de músics i dansaires d'arreu del país. Els carrers de Ceret sonaran des del divendres 17 fins el diumenge 19 al ritme de les cobles i s'organitzaran diverses activitats relacionades amb la dansa tradicional catalana. Un dels punts àlgids del cap de setmana serà dissabte al vespre amb el concurs de la Copa Catalana de Sardana, que es farà a la Plaça de Braus de Ceret, amb entrada gratuïta. La celebració del concurs torna enguany a les Arenes desprès d'anys al centre de la vila. Segons els organitzadors, aquest retorn és per permetre que el públic pugui veure millor els balladors. 

La Confraria de Sant Elm organitza aquest dissabte un nou assaig del Ball de Plaça de concurrència popular, una activitat pensada perquè els infants coneguin el ball abans de la Festa Major i arribin més preparats al Ball de Plaça del 26 de juliol. L'assaig es farà a les set de la tarda a la plaça de la Vila, el mateix escenari on tindrà lloc el Ball de Plaça. Segons explica l'obre major de la Confraria de Sant Elm, Ignasi Riera, això facilita que els nens interioritzin l'espai i puguin participar amb més confiança el dia de la festa. “L'any passat va ser un èxit perquè és un assaig del Ball de Plaça en el lloc on es farà. Els nens ja ho interioritzen i el dia del Ball de Plaça és molt més fàcil tornar-hi a ballar.”Ignasi Riera L'activitat és oberta a tots els infants, sense necessitat d'inscripció prèvia, i tampoc és obligatori haver participat en l'assaig per poder ballar el dia 26. L’important és participar, expliquen. La Confraria destaca que l'assaig també serveix per fer el Ball de Plaça més ordenat. Durant l'activitat i també el dia de la festa, diversos monitors ajudaran els nens i nenes a col·locar-se i seguir el desenvolupament del ball. “Les dues coses que estem treballant més són el control a la plaça i l'ordre. Tenim persones que ajuden els nens a posar-se bé al seu lloc i els van guiant durant tot el Ball de Plaça.”Ignasi Riera A més d'aprendre els passos, la iniciativa busca també fomentar que els més petits facin seva una de les tradicions més emblemàtiques de la Festa Major de Santa Cristina.

Avui al Voltant i Girant Estiu: - A la primera part del Voltant i Girant Estiu parlem amb Andreu Curto, tinent d'Alcaldia de #DeltebreEficient sobre la candidatura amb què el consistori tornarà a optar al Pla de Barris i Viles de Catalunya. - A la segona part del programa connectem amb Ricardo González, propietari de La Taverneta, restaurant de l'Ampolla, per saber-ho tot sobre el seu negoci.

A la primera part del Voltant i Girant Estiu parlem amb Andreu Curto, tinent d'Alcaldia de #DeltebreEficient sobre la candidatura amb què el consistori tornarà a optar al Pla de Barris i Viles de Catalunya.

Avui dimarts avancem l’inici de la Festa Major de Santa Cristina. Aquesta setmana es dona el tret de sortida de la Festa Major de Santa Cristina i serà amb una novetat: un Vespreig amb el grup Viva la Pepa! L'activitat és gratuïta i arriba aquest dijous, a les set de la tarda, a la Roca d'en Maig. De cara a divendres, serà el torn d'una de les activitats de més èxit: el correfoc. A partir d'aquí, comencen uns dies carregats d'activitats molt variades pensades per a tots els públics. El tancament de la Festa Major es farà la diada de Sant Elm, diumenge 26, amb el castell de focs artificials. De tot plegat, en fem un repàs amb la regidora de Cultura i Festes, Vereda López. Altres temes d'interès: Santa Cristina: Encara en clau de Festa Major, entrevistem l'Obrer Major, Francesc Batlle, perquè l'Obreria de Santa Cristina posarà a la venda aquest dijous els tiquets per anar en vaixell a Santa Cristina. Sant Elm: I d'un obrer major a un altre, perquè també parlem amb el representant de la Confraria de Sant Elm, Ignasi Riera, per saber com es presenta l'assaig del Ball de Plaça de concurrència popular que l'entitat organitza aquest dissabte. Cultura: L'Ajuntament ha programat un nou espectacle de dansa titulat Dafne i inspirat en el mite d'Apol·lo i Dafne. Un espectacle que es podrà gaudir durant el mes d'agost i els detalls ens els dona la regidora de Patrimoni Cultural, Cristina Aymerich. Festes: Parlem amb el president de l'associació de veïnes i veïns de Lloret de Dalt, Lluís Cruz, perquè el barri organitza un concert aquest dissabte i en volem tota la informació.

A Lloret, avui mateix hi ha una nova oportunitat per donar sang. El bus del Banc de Sang serà a la Plaça de la Vila de cinc de la tarda a nou del vespre. La campanya continuarà dijous, en horari de matí i tarda al Teatre, i divendres a la tarda al Centre Cívic del Rieral. Sota el lema «Perquè la necessitat no fa vacances. Dona sang«, el Banc de Sang i Teixits fa una crida a la ciutadania perquè participi en la campanya d’estiu. I és que, tot i que la necessitat de sang es manté durant tot l’any, les reserves acostumen a baixar prop d’un 20% durant els mesos d’estiu, quan disminueixen les donacions. Ens en dóna més informació Mireia Blanco, representant del Banc de Sang i Teixits. «A l’estiu baixen les donacions pel canvi d’hàbits, per la calor i perquè la gent fa vacances i diu, bé, ja ho faré quan torni».Mireia Blanco En total, seran tres jornades amb horaris diferents per facilitar la participació dels lloretencs. També hi podran donar sang els visitants, sempre que siguin majors d’edat i entenguin el català, el castellà o l’anglès. Abans de cada donació es farà una analítica de la sang, i al cap d’uns dies cada donant podrà consultar-ne els resultats a l’àrea privada del web del Banc de Sang. En cas que es detecti algun valor fora dels paràmetres habituals, el mateix Banc es posarà en contacte amb la persona. Des del Banc de Sang animen a tothom a donar sang i a menjar bé i mantenir-se ben hidratat abans de fer-ho. Poden donar sang les persones majors d’edat, de fins a 70 anys, que pesin més de 50 quilos, estiguin en bon estat de salut, no estiguin embarassades i presentin un document oficial amb fotografia. «M’agradaria animar a la gent a que vingui a donar sang, és un petit gran gest solidari que salva vides». Mireia Blanco Recordem els horaris de la campanya a Lloret: avui, de cinc de la tarda a nou del vespre, al bus del Banc de Sang situat a la Plaça de la Vila; dijous, matí i tarda, al Teatre de Lloret; i divendres, a la tarda, al Centre Cívic del Rieral.

Ines Cergol: A fresco, Jure Detela; Plačilo za moje stoletje, Andrej Capuder: Nedokončani spisi. Recenzije so napisali Jože Štucin, Sanja Podržaj in Marija Švajncer.

Piše Sanja Podržaj, bereta Maja Moll in Bernard Stramič. Pesnik, pisatelj, esejist, mislec in aktivist Jure Detela je gotovo eden najbolj zanimivih, edinstvenih in enigmatičnih slovenskih literarnih ustvarjalcev. Morda je njegova neobičajna, tudi tragična življenjska pot v splošni zavesti celo bolj znana kot njegovo delo, a eno z drugim je pravzaprav neločljivo. Prepričanja, ki jih je zagovarjal že v sedemdesetih letih prejšnjega stoletja, se z današnjega vidika zdijo daljnosežna, mnogo pred svojim časom. Z dejanji, vsakodnevnimi odločitvami, si je prizadeval za nenasilje v najširšem pomenu besede. Objavil je pesniški zbirki Zemljevidi in Mah in srebro ter avtobiografski esej Pod strašnimi očmi pontonskih mostov. Umrl je mnogo prezgodaj leta 1992 in za seboj pustil tudi nedokončan roman in številne fragmente, zbrane v pričujoči knjigi, je bilo napisano veliko in marsikaj. Predvsem se lahko zgodi, da ko govorimo o osebnostih, kot je bil Detela, zapademo v psihologiziranje in to, da avtorja obravnavamo kot kurioziteto. Na tem mestu bi se temu skušali izogniti in se posvetili njegovemu literarnemu delu, v katerem se kažeta globina in domet njegove misli. Za razumevanje nedokončanega romana Plačilo za moje stoletje je ključno poznati nekaj dejstev iz avtorjevega življenja, ki predstavljajo tudi osrednje teme v romanu. Detela se je zavzemal za absolutno nenasilje, zanj pa to ni bilo zgolj neko abstraktno načelo, ampak je to tudi živel. Bil je vegetarijanec, kar zanj ni bila samo prehranska izbira, temveč tudi izraz etičnega odnosa do vseh bitij, in to je prenesel tudi v svojo poetiko, saj represije ni želel uporabljati niti v jeziku. Njegov odnos do narave presega zgolj ekološko zavest, ampak se je zavzemal za predrugačenje človekovega zavojevalskega odnosa do nje. Izjemno dejaven je bil kot aktivist in se zavzemal za odpravo smrtne kazni v Jugoslaviji ter nasprotoval mehanizmom policijskega in vojaškega nasilja. Roman Plačilo za moje stoletje je nastajal v prvi polovici osemdesetih let. Miklavž Komelj, tudi sam pesnik, ki ga poznamo tudi kot urednika zbranih del in del iz zapuščine Vojka Gorjana, Jaše Zlobca, Srečka Kosovela, Karla Destovnika Kajuha in Vena Pilona, je svoje tovrstno delo pravzaprav začel z Detelo – leta 2011 so izšli Orfični dokumenti: teksti in fragmenti iz zapuščine, nato leta 2018 Zbrane pesmi v kar dveh delih. Plačilo za moje stoletje je filozofski roman, ki vas bo, če poznate poezijo Jureta Detele, zelo presenetil. Napisan je dokumentaristično, čeprav opisuje stvari, ki se niso zgodile, dogodki pa so uporabljeni kot ozadje za argumentacijo. Sama realističnost romana, njegov neposredni in neokrašeni jezik, se ujemajo z Detelovo poetiko, s katero si je prizadeval, da bi besede osvobodil represivnih funkcij. To pomeni, da je vse, kar je zapisano, mišljeno dobesedno, brez kakršnihkoli metafor. Te so namreč substitut, ki reducira in odstrani stvar ali bitje, to, o čemer pravzaprav govorimo, in so kot take primer nasilja v jeziku. Glavni junak in pripovedovalec romana Plačilo za moje stoletje je Jure Detela sam, v njem pa se prikaže kot morilec. Vse se začne z bojem za to, da v Jugoslaviji ne bi podaljšali služenja vojaškega roka in da bi razmere v vojašnicah postale bolj humane. Jure Detela si je s peticijami res prizadeval za različne cilje, vendar ni imel nobenega stika s politiko in politiki, kot je prikazano v romanu. V njem prijatelj Peter Glogovec romanesknega Jureta prepriča, da se udeleži večerje s politično elito – izmišljenimi osebami, ki nimajo povezave z resničnimi političnimi akterji tistega časa. Ti politiki naj bi bili Juretu naklonjeni in bi jih lahko nagovoril, da delujejo v smeri njegovih ciljev, s tem pa bi veliko mladim vojakom prihranil marsikatero bolečino in trpljenje. Jure se vda in v imenu doseganja dobrega cilja popusti glede svojih strogih etičnih načel – na večerji jé gamsje možgane, da ne bi naredil slabega vtisa s svojim vegetarijanstvom, in to sproži učinek snežne kepe, saj se drobni kompromisi hitro sprevržejo v vse hujše in hujše. Nazadnje se s sprijeno politično elito zaplete v utilitaristično logiko sveta, ki temelji na umoru – nasilje vedno utemeljujejo z višjim ciljem. Njihovi argumenti Jureta prepričajo s tem, ko trdijo, da bo z ubojem ene živali ali človeka, pred trpljenjem rešil množice drugih bitij. Nasilje v imenu nenasilja torej oziroma v imenu doseganja višjega cilja, ki je nenasilna družba. Roman govori o nasilju, lahko slutimo, kaj se dogaja, čeprav nasilna dejanja niso nikoli opisana. V ospredju so argumenti za ta dejanja, prave filozofske razprave za in proti, ki predstavljajo glavnino besedila prvega dela romana. Ta doseže vrhunec, ko Jure sodeluje v skrivnostnem karmično očiščevalnem postopku, s katerim naj bi duše tistih, ki so predmet tega postopka, rešili pred neskončnim ciklom rojstev in smrti, ki prinaša trpljenje. Karmično očiščevalni postopek izvajajo na političnih disidentih, jih mučijo in nazadnje ubijejo. Vse v imenu višjega dobrega. Enega od disidentov živega zakopljejo in Jure pri tem sodeluje, nato pa ga pred nadaljnjimi zablodami reši prijatelj Simon, ki predstavlja ideal absolutnega nenasilja. Skupaj disidenta odkopljeta a prepozno. Jure se s Simonovo pomočjo zave, da ga je elita izkoristila za svoje nemoralne cilje, in se v drugem delu romana očiščuje svojih okrutnih dejanj. Prvemu in drugemu delu romana v knjigi sledi dodatek, v katerem je objavljena še druga verzija romana, skupaj z zapisi in fragmenti, ki so bili ohranjeni med rokopisom, a niso njegov del, se pa z njim vsebinsko povezujejo. V uvodu Miklavž Komelj pojasnjuje, kako se je lotil sestavljanja romana iz kaotičnosti rokopisa na premešanih listih in lističih, Detela je roman pisal po fragmentih, nekateri odlomki pa so ohranjeni v dveh verzijah. Delo, ki je brez dvoma zahtevalo veliko študija, potrpežljivosti in poznavanja pesnika ter njegovega kroga, je Miklavž Komelj dopolnil še z detajlno in obsežno spremno študijo, s katero je vzpostavil kontekst, ki je za bralke in bralce v tem primeru nujno potreben. Roman namreč nima velike literarne vrednosti in res ni primerljiv z Detelovo poezijo po slogovni dovršenosti. Njegova največja vrednost so filozofski pogovori, argumenti za nasilje in proti nasilju, v katerih se pokaže avtorjeva intelektualna širina. Romana, ki je obstajal zgolj v fragmentih, avtor seveda ni končal niti ni šel skozi uredniški proces. Tudi Komelj v besedilo ni posegal, objavljeno je takšno, kot je bilo, z vsemi napakami in lapsusi, na katere je kot urednik opozoril v opombah. V spremni študiji predstavlja ne le čas in prostor Detelovega ustvarjanja, temveč se temeljito opira na njegova druga dela, predvsem esejistična, korespondenco, pričevanja tistih, ki so ga poznali, in tako skuša rekonstruirati tudi tisto, kar je pisatelja gnalo pri ustvarjanju, zakaj je želel napisati roman, tako zelo drugačen od vsega, kar je napisal poprej, in tako zelo nasilen. Je sploh želel z njim kaj sporočiti ali ga je pisal zase, da bi si prek njega prišel do dna? Tega zagotovo ne bomo nikoli izvedeli in roman lahko beremo na več načinov, kar izpostavlja tudi Komelj. Po eni strani gre lahko za čisto transgresijo, ali pa za eksperiment, v katerem avtor preizkuša samega sebe in kaj bi se zgodilo z njim, če bi opustil svojo moralno integriteto. Lahko da gre za eno samo veliko halucinacijo, rezultat vseh strahov o tem, da bi povzročal trpljenje. Morda pa gre za grotesko in parodijo, saj je v romanu tudi veliko črnega humorja. Komelj zapiše: »Mučni občutek, ki ga lahko pusti tekst, je – ob tem, da se v njem sijajne pasaže izmenjujejo z osupljivimi bizarnostmi – prav v tem, da ni jasno, kdaj gre za fikcijo in kdaj za resničen dokument o notranjem stanju; in kar je najbolj osupljivo: videti je, da za Detelo med obojim pri pisanju tega teksta sploh ni razlike.« Vsaka izdaja, kot je ta, je v veliki meri tudi delo tistega, ki je naredil izbor, sestavil odlomke ter jih kontekstualiziral s spremnim besedilom. Miklavž Komelj je velik Detelov poznavalec, zato ne dvomimo o tem, da je svoje delo opravil strokovno in korektno. Bolj zanimivo je v tem primeru dejstvo, da je knjiga Plačilo za moje stoletje izšla pri manjši založbi in da se za izdajo še neobjavljenega dela pesnika, ki je pustil trajno sled v slovenskem kulturnem prostoru, ne samo kot pesnik temveč tudi kot prodoren mislec in aktivist, niso odločili pri kateri od večjih založb, ki redno izdajajo tudi dela slovenskih klasikov. Vsekakor je knjiga Plačilo za moje stoletje pomemben prispevek k domači literarni zgodovini in poznavanju opusa Jureta Detele. Njegova dela je danes vredno brati, saj spodbujajo vizijo drugačnega odnosa do sveta – nekaj, kar nujno potrebujemo.

Una partida de cartes no combat la solitud. Crítica teatral de l'obra «Solitudes». Autoria i dramatúrgia: Garbiñe Insausti, José Dault, Iñaki Rikarte, Rolando San Martín i Edu Cármaco. Direcció: Iñaki Rikarte. Interpretació: José Dault, Garbiñe Insausti, Edu Cárcamo. Escenografia i vestuari: Ikerne Giménez. Il·luminació: Carlos Samaniego. Música original i espai sonor: Luis Miguel Cobo. Caracterització (màscares): Garbiñe Insausti. Producció executiva: Kulunka Teatro. Ajudantia de direcció: Rolando San Martín. Ajudantia d'escenografia: Almudena Martín. Cap tècnic del teatre: Aleix Arbonès. Tècnic del teatre: Víctor Bartolomé. Construcció d'escenografia: Mambo Decorados. Màrqueting i comunicació de la companyia: María Díaz. Màrqueting i comunicació del teatre: Focus. Reportatge fotogràfic: David Ruiz. Disseny de cartell: Dani Castillo. Una producció de Kulunka Teatro. Finançat per Unió Europea Fons Next Generation, amb el suport de l'INAEM - Instituto Nacional de Artes Escénicas y de la Música (Govern d'Espanya, Ministeri de Cultura), el Pla de recuperació, transformació i resiliència, el Govern basc i l'Instituto Vasco. Recomanat a partir de 14 anys. Festival Grec 2026. Teatre Condal, Barcelona. Del 10 al 19 de juliol 2026. Veu: Andreu Sotorra. Música: Solituds. Interpretació: Joan Chamorro i Andrea Motis. Composició i lletra: Duke Ellington. Àlbum: Feeling good, 2012.

La cobla de La Flama de Farners serà l’encarregada de l’audició de sardanes d’aquest dissabte, en el marc del centenari de cicles de sardanes d’estiu a Lloret de Mar. Com sempre, es començarà amb dues sardanes de concert, seguides de set peces per ballar. L’audició començarà a les deu de la nit, a la Plaça de la Vila, i dos quarts d’hora abans s’oferirà també, un taller per aprendre a ballar sardanes amb l’Esbart Joaquim Ruyra de Blanes. Ens en dona més detalls Jordi Fontanillas, representant de la cobla La Flama de Farners. «Començarem amb dues sardanes per escoltar: La Ballarina i el Soldadet de Plom de Francesc Cassú i La Cavalleresca de Joaquim Serra».Jordi Fontanillas En acabat, continuaran amb un programa molt ballador compost de 7 sardanes. A més, dins del repertori de La Flama de Farners, també trobarem A Lloret 75 estius de Martirià Font, una sardana molt balladora i bonica, diu Fontanillas, dedicada a Lloret quan va fer el seu 75è aniversari de ballades d’estiu. A dos quarts de deu, a la mateixa plaça, s’oferirà un taller per aprendre a ballar sardanes. «A Lloret teniu molta gent i llavors està bé que es faci un concert i després la gent pugui participar en les ballades».Jordi Fontanillas Un cop impartir el taller i dos quarts d’hora més tard, començarà l’audició de la cobla de La Flama de Farners, una de les més reconegudes de la comarca gironina, que busca anar més enllà de la música tradicional. «Considerem que estem en un molt bon moment ara a l’estiu, i a part de les ballades i els concerts també oferim projectes que se’n van una mica de la tradició de les sardanes».Jordi Fontanillas Actualment, la cobla està presentant un projecte trencadís amb la cantant Neus Mar, on expliquen, fan una petita obra musical. D’altra banda, també tenen projectes amb en Marcel Tomàs, director artístic amb qui fan un projecte de música i poesia. «Sempre busquem anar més enllà de la música tradicional per poder portar la música de cobla una mica més lluny».Jordi Fontanillas Tot i l’onada de calor d’aquests darrers dies, durant el cap de setmana baixaran relativament les temperatures, i dissabte tothom qui ho vulgui podrà gaudir d’un vespre de sardanes, a partir de dos quarts de deu amb el taller i més tard amb audició de la cobla de La Flama de Farners a la Plaça de la Vila.

Notes Avui la Sílvia ens proposa un exercici per practicar adjectius: ella diu el començament d'una frase i l'Andreu l'ha de completar amb un adjectiu, el primer que li vingui al cap. Tot seguit, n'han de trobar el contrari. Entremig, comentaran matisos importants dels adjectius que vagin sortint. Episodi en directe Acompanya'ns el pròxim 23 de juliol a les 17 h a la llibreria Ona per al segon episodi amb públic! Podreu remenar llibres en català, protegir-vos de la calor, practicar el català i passar una bona estona amb nosaltres.

Els Bombers estabilitzen els incendis de Navarcles i del Pla de Manlleu. Tamb

On today's show Andrew and Bill begin with Monday's SLBM test from the PLA Navy, including questions surrounding its timing and location, regional angst, and a reminder that the PLA continues to enhance its nuclear triad capabilities. Then: Two new PLA generals are promoted while rectification continues and five CMC seats remain vacant, and reactions to last week's shocking CITIC plane crash and a major security breach in Beijing. From there: An emailer asks about America's interests in maintaining the Taiwan status quo, Beijing considers limiting access to advanced AI models, the knives are out for Jeffery Kessler at BIS, and the White House preps for Xi's visit in September. At the end Questions about the release of pastor Ezra Jin, context for the U.S. sentencing of disgraced tycoon Guo Wengui, and the Washington Wizards get a letter from Rep. John Moolenaar.

• Deltebre presenta una candidatura de 12,5 milions d'euros al Pla de Barris i Viles de Catalunya per transformar el centre de la Cava amb 33 actuacions de millora urbana, ambiental i social. • El Consorci d'Aigües de Tarragona torna a activar les polseres intel·ligents per prevenir els cops de calor entre els treballadors exposats a altes temperatures. • El futbolista de Camarles Pol Pallarès fitxa per l'Atlètic de Madrid després de tres temporades al futbol base de l'RCD Espanyol i continua la seua projecció com una de les promeses del futbol ebrenc.

A l'episodi d'esta setmana, Cel i Diana es posen al dia entre estiu, festes i projectes de futur. Parlen de la nova platja per a gossos de l'Ampolla, de les Festes del Carme, de la candidatura de Deltebre al Pla de Barris i Viles i de la venda d'entrades de les Festes Majors 2026. També fan parada a Sant Jaume d'Enveja, amb el nou curs de monitors de lleure, i a Camarles, que celebra el fitxatge del jove Pol Pallarès per l'Atlètic de Madrid. Les dos amigues t'ho expliquen per telèfon. Sobretot, agafa la trucada!! L'Infopòdcast és un espai coproduït amb @laxarxacat en què repassem la setmana a Delta.cat.

SCHEDULE JBS, 7-7-20261862 NYC  Liz Peek. Revamping Federal Reserve Communications: No More Dot Plots? Liz Peek discusses new FedChair Kevin Warsh's shift away from "forward guidance" and "dot plots". She argues this pragmatic approach requires investors to analyze raw economic data rather than Fed algorithms. Despite past recession fears, the economy remains stable with low unemployment at 4.2%. (1) Liz Peek. The Democratic Party's 2028 Internal Conflict: Socialists vs. Establishment. Peek analyzes the rising tension between the Democratic establishment and radical socialists like New York Mayor Zohran Mamdani. She suggests Governor Newsom faces credibility issues due to "flip-flops," while younger socialist candidates threaten to alienate traditional Jewish and Black voters, potentially wrecking the party's 2028 prospects. (2) Captain James Fanell. China's Nuclear Triad Expansion: Submerged Ballistic Missile Test. Captain Fanellexplains the significance of China's recent submerged ballistic missile launch from a Jin-class submarine. Reaching over 10,000 kilometers, this JL-3 missile flew over U.S. territories like Guam. This rare test signals China's rapid development of a nuclear triad intended to achieve strategic deterrence against the U.S. (3) Captain James Fanell. Countering China's First Strike Strategy in the Pacific. Fanell argues China's SLBM test challenges their "no first use" policy, effectively demonstrating a first-strike capability. He recommends the U.S. bolster its naval force structure in the Western Pacific and utilize B-2 bomber flights to signal resolve against Chinese efforts to drive America out of the region. (4) Mary Kissel. NATO's New Vigor and the European Defense Dilemma. Mary Kissel discusses NATO'srenewed urgency following Russian aggression in Ukraine. While front-line nations like Poland exceed spending targets, many Europeans have historically relied on the U.S. defense umbrella to fund social welfare states. She warns that Putin continues to test NATO's unity at the margins. (5) Mary Kissel. Confronting Beijing's Provocations and the Cost of Appeasement. Kissel critiques the U.S.government for pursuing trade deals while China conducts intimidating missile tests in the Pacific. She urges the administration to recognize the severity of the threat, strengthen regional alliances, and impose actual consequences for Beijing's increasingly hostile behavior to avoid a greater future threat. (6) Joseph Sternberg. Federal Reserve Introspection and Britain's Political Turmoil. Sternberg examines Governor Waller's speech regarding how "forward guidance" may have blinded the Fed to 2021 inflation. Turning to the UK, he notes Prime Minister Keir Starmer's plummeting popularity and argues that British politics is trapped in personality-driven cycles without addressing fundamental policy or welfare state problems. (7) Joseph Sternberg. Cultural Divides: American Earnestness vs. European Cynicism. During the World Cup, Sternberg observes that European visitors are struck by American earnestness regarding God, patriotism, and politics. He notes that while shared history exists, deep cultural divisions persist; Europeans often view patriotism as destructive, whereas Americans continue to view it as a healthy instinct. (8) Gregory Copley. Xi Jinping's Internal Struggles and the Vulnerable 'Boomer' Fleet. Copley views China'smissile test as a move by Xi Jinping to look credible amidst domestic instability and loss of control over the PLA. He notes that while the Jin-class submarines are "noisy" and vulnerable, the test sends a pointed message to the West and Pacific nations. (9) Gregory Copley. Russian Bluster and NATO's Disorganized Response. Copley dismisses Russian threats against Poland and Finland as "agit prop" designed to save face during the NATO summit. He argues Russia is incapable of a major war with NATO and that Putin remains secure despite domestic pressures, petrol rationing, and the West's disorganized attempts to unify. (10) Gregory Copley. Iran's Leadership Vacuum and the Illusion of Nuclear Success. Copley reports a lack of cohesive leadership in Iran, with Ayatollah Khamenei potentially incapacitated. He asserts the West has failed on all metrics, including regime change and securing the Strait of Hormuz. Iran views its nuclear program primarily as a bargaining chip for sovereignty rather than victory. (11) Gregory Copley. The Prodigal Son: Prince Harry's Mounting Legal and Financial Woes. Copley discusses Prince Harry's precarious position after losing a major lawsuit, leaving him with a 50 million pound debt. King Charles III prioritizes his duty to the monarchy over family ties as concerns grow regarding Harry's management of the Invictus Games and his wife's public criticisms of the family. (12) Thaddeus McCotter. Democratic Party Discipline: Managing Candidate Crises and Ideological Rifts.McCotter explores how the Democratic establishment "blew up" problematic candidates like Eric Swalwell to install figures like Xavier Becerra. He describes an ongoing "civil war" between the establishment and the Democratic Socialists of America (DSA), with leadership working to clear out radicals to appeal to mainstream voters. (13) Thaddeus McCotter. The Republican Civil War: MAGA Populism vs. the Establishment. McCotter analyzes the Republican Party's struggle with the MAGA movement, which he defines as populist rather than traditionally Republican. He warns that without a clear programmatic platform beyond Donald Trump, the movement may not survive his leadership, potentially leading to conflict with the revanchist Republican establishment. (14) Grant Newsham. The Shadow of Appeasement: Europe's Unwillingness to Defend Itself. Newsham compares current European hesitation to confront Russia with 1930s appeasement. He argues that many European nations have developed a "pathologic dependence" on the U.S. to fund their social welfare states. He warns that without U.S. backing, Europe lacks the unity to stop Russian aggression. (15) Henry Sokolski. Iran's Nuclear Defiance and the Futility of Unsupervised Deals. Sokolski highlights the disconnect between U.S. and Iranian positions following a recent memorandum of understanding. Iran refuses inspections of bombed enrichment sites, while the U.S. insists on them. He warns that preventing Iran from building a bomb remains an uphill battle without clearer public goals. (16) Corrections applied: Liz Peek (not "Elizabeth Peak"), Zohran Mamdani (not "Zoron Mandani"), Thaddeus McCotter(not "Thaddius Marter"), JL-3 and B-2 (hyphenated).

Gregory Copley. Xi Jinping's Internal Struggles and the Vulnerable 'Boomer' Fleet. Copley views China's missile test as a move by Xi Jinping to look credible amidst domestic instability and loss of control over the PLA. He notes that while the Jin-class submarines are "noisy" and vulnerable, the test sends a pointed message to the West and Pacificnations. (9)

• Deltebre convoca una sessió participativa per definir la candidatura al Pla de Barris i Viles de Catalunya, amb l'objectiu de recollir les aportacions de la ciutadania abans de presentar el projecte. • L'Ampolla estrena una nova zona per a gossos a la platja de l'Arenal, més àmplia i situada en un entorn més tranquil del delta de l'Ebre, per millorar la convivència a la platja. • Camarles dona el tret de sortida als preparatius de la Festa Major 2026 amb el sorteig de carros, carretes i taulats i la presentació oficial del programa de festes.

Un vespreig donarà el tret de sortida a la Festa Major de Santa Cristina. És la principal novetat del programa, que s'ha presentat aquest dimarts i que compta amb un ampli ventall d'activitats variades per a tots els gustos i edats. La regidora de Festes, Vereda López, remarca la novetat del vespreig i també que se segueixi apostant per organitzar activitats per als més petits, per començar a involucrar-los en les tradicions locals. Per tant, per al públic infantil hi haurà la festa de l'escuma i inflables d'aigua, a banda d’un concert de Xiula. «Increïblement seguim amb novetats, encara que mantenim tota la tradició que es té a Santa Cristina, però aquest any arrenquem amb un Vespreig el dia 16»Vereda López El vespreig d'inici de Festa Major es farà dijous de la setmana vinent, 16 de juliol i les activitats s'allarguen fins diumenge 26, Diada de Sant Elm, quan hi haurà el castell de focs artificials a la platja de Lloret i el concert de La Principal de la Bisbal a Sa Caleta. Entremig, hi haurà més de 40 activitats, com una cercavila i correfoc amb Kalatrons i els Diables de Sa Forcanera, concerts de grups locals, les actuacions de 31FAM, l'Orquestra Maribel i un clon a l'Oreja de Van Gogh, una cantada d'havaneres i un bingo musical, entre altres. Sense oblidar els actes més tradicionals, com són la passada dels Obrers, la processó marítima i el Ball de Plaça.

Arriben les festes del barri de Can Carbó i Mas Baell. De divendres a diumenge, la comissió de festes ha preparat un gruix d'activitats pensades per a tots els gustos i edats. Unes activitats que estan obertes a tothom i que es faran a la Plaça Centre Cívic Can Carbó. El tret de sortida el donarà la cantada d'havaneres amb el grup Es Vano aquest divendres, a dos quarts de deu de la nit. Tot seguit, el pregó amb Toni Salvatella, de l'antic Bar Toni. Una persona idònia per donar la benvinguda a la popular celebració d'aquests dos barris, tal com assenyalen dos membres de la Comissió de Festes, César Gómez i Fèlix Fuentes, que recorden que Salvatella va ser membre d’una de les primeres comissions de festes del barri. «El Bar Toni, obert des del 1963, primer amb l’avi Joan i després amb en Toni fins ara que l’ha traspassat, és testimoni de tot el que ha passat en el barri»César Gómez Per tancar la nit, música amb d'Rumbaos i Dj La Bamba. De cara a dissabte, de bon matí botifarrada popular, per seguir amb jocs infantils, zumba i un aperitiu musical. A la tarda, festa de l'escuma, berenar popular i nit de concerts amb el Dúo Ana y Carlos i el grup de versions Four Fiesta. Diumenge, últim dia de les festes, el barri es despertarà amb una xocolatada i jocs populars i jocs d'aigua. Al migdia, arrossada i, a la tarda, playbacks, quina musical i fi de festa amb Dj Aura Events. Un altre representant de la comissió de festes, Josu Díez, remarca que algunes de les novetats d'aquest any són la recuperació dels ‘playbacks’, la quina musical i la sessió de zumba. «Hem recuperat els ‘playbacks’ de diumenge, que fa anys que es feien al barri, i ho fem amb l’ajuda de la Fundació Ser.Gi que estan al barri treballant pel barri i per la gent del poble»Josu Díez A la barra de les festes (Comissió de festes Can Carbó i Mas Baell) Una altra novetat és l'arrossada popular de diumenge, que pel preu de només 2 euros inclou un plat d'arròs, amanida i pa. «L’arrossada popular és una activitat de molta germanor, serà una manera de trobar-nos tots, asseure’ns tots junts a menjar un arròs, gent del barri i gent de fora del barri»César Gómez Els tiquets es poden comprar al Puntet o a les activitats al llarg de les festes. Segons Félix Fuentes, totes les activitats sempre tenen molt èxit, perquè cada cosa està pensada per un públic diferent i destaca la cantada d’havaneres, on repartiran coca i cava per a tothom. «Totes les activitats tenen èxit, perquè van dirigides a un tipus de públic concret»Félix Fuentes Cartell de les festes de Can Carbó i Mas Baell Des de la comissió de festes de Can Carbó i Mas Baell animen a tothom a participar de la celebració, que començarà divendres al vespre i s'allargarà fins diumenge a la nit.

Brian Molko joins Alan for a brilliantly funny flight, from an unforgettable airport encounter with Alan that reminds Brian of David Bowie, to why he finally decided to revisit Placebo's debut album 30 years later. They talk about rebuilding his relationship with those early songs ahead of Placebo's 30th anniversary tour and the band's debut album, newly RE:CREATED, why the Britpop era made Placebo stand out, and reclaiming Nancy Boy. Along the way there's talk of memory tricks, cannibals, Magaluf, airports, sharks in the Maldives, rehab romances, why Brian believes arriving is the best part of travelling, and an unforgettable quick-fire round. Plus, Brian reveals why this anniversary tour he's been able to celebrate Placebo's earliest music with genuine joy. 00:00 Brian's fear of flying and the luxury of Alanair01:08 The Alan airport encounter that reminded Brian of David Bowie08:00 Why Brian recreated Placebo's debut album09:57 Standing apart from Britpop and embracing difference12:11 Rediscovering the debut album after 25 years12:51 The story behind Nancy Boy14:06 Memory, the Mandela Effect and false memories15:13 Alan pitches “Pla-subo" featuring Susan Boyle16:03 Placenta parties, cannibalism and "long pigs"17:18 Forgetfulness, daydreaming and useless knowledge18:13 Loving the destination but hating the journey20:26 Smoking on planes and Brian's airport theories21:53 Placebo's 30th anniversary tour and finding joy again24:14 Brian's holiday nightmare in Magaluf26:06 Rehab romances27:32 Why kindness gets better service than complaining30:02 The Maldives, rabbits and reef sharks32:04 Eating street food in Bangkok33:16 Quick Fire: beach or pool, window or aisle?35:38 Alan's stage fright wee and Brian's bladder training tips37:40 Why everyone should tip their delivery driver #LifesABeach #AlanCarr #BrianMolko #Placebo #Placebo30 #AlternativeRock #RockMusic #DavidBowie #Britpop #NancyBoy #Travel #AnniversaryTour Learn more about your ad choices. Visit megaphone.fm/adchoices

Rīgas Tehniskajā universitātē darbu uzsākusi jauna laboratorija, kas pētīs to, ko ir visai grūti nomērīt, cilvēka uzvedību, lēmumu pieņemšanu un tehnoloģiju ietekmi, jeb mūsu attieksmi, emocijas un reakcijas uz dažādiem ārējiem stimuliem, piemēram, reklāmām vai dezinformāciju. Veicot fizioloģiskus ķermeņa mērījumus, piemēram, sirds darbību vai acu skatienu, laboratoriskais aprīkojums ļaus iegūt objektīvu informāciju par cilvēka reakciju uz informāciju, pakalpojumu, preci vai rīcību. Raidījumā Zināmais nezināmajā plašāk stāsta RTU Inženierekonomikas un vadības fakultātes tenūrprofesors, „HyperLab” dibinātājs un līdzvadītājs Agnis Stibe. Ierakstā uzklausām Latvijas Universitātes profesoru Uztveres un kognitīvo sistēmu laboratorijas vadītāju Jurģi Šķilteru. Zinātnes ziņās par to, kā bites tiek galā ar karstumu Vēstis par karstuma rekordiem mūsu platuma grādos un cilvēku centieniem atvēsināties dzirdam ne pirmo gadu. Bet pētnieki Austrālijā pievērsušies tam, cik lielā mērā karstums skar bites. Plaša mēroga pētījumā, kas publicēts žurnālā "Nature Communications", apsekota 95 vietējo bišu sugu karstuma tolerance. Dati liecina, ka bišu sugas, kas ligzdo augu stublājos, varētu saskarties ar vislielākajiem draudiem no temperatūras paaugstināšanās, kas saistīta ar klimata pārmaiņām. Turpretī bites, kas ligzdo pazemē, šķiet labāk sagatavotas, lai izvairītos no bīstamā karstuma. Cik lielu karstumu bites var izturēt un vai draudi Austrālijas bitēm būtu attiecināmi arī uz mums? To šoreiz skaidro vienīgā bišu veterinārārste Latvijā, kā arī Latvijas Biškopības biedrības pētniece un konsultante Ineta Eglīte.

Fluent Fiction - Catalan: Festival Fashion: Balancing Style and Savings for Sant Joan Find the full episode transcript, vocabulary words, and more:fluentfiction.com/ca/episode/2026-06-30-22-34-02-ca Story Transcript:Ca: El sol d'estiu brillava intensament sobre la Plaça de Catalunya.En: The summer sun shone brightly over the Plaça de Catalunya.Ca: Era un dia perfecte per fer compres.En: It was a perfect day for shopping.Ca: La gent es movia amunt i avall, buscant les últimes ofertes i novetats.En: People moved up and down, searching for the latest deals and trends.Ca: Entre la multitud, en Marcel i la Laia caminaven animadament.En: Among the crowd, Marcel and Laia walked cheerfully.Ca: El festival de Sant Joan s'acostava i en Marcel volia impressionar els seus amics amb una roba espectacular.En: The Sant Joan festival was approaching, and Marcel wanted to impress his friends with spectacular clothing.Ca: "Vull trobar alguna cosa que em faci destacar aquesta nit de Sant Joan," va dir en Marcel amb decisió.En: "I want to find something that will make me stand out this Sant Joan night," Marcel said decisively.Ca: Laia va somriure.En: Laia smiled.Ca: "Sí, però no et gastis tots els diners en una camisa," va advertir amb to assenyat.En: "Yes, but don't spend all your money on a shirt," she warned sensibly.Ca: Van caminar fins a una botiga de moda, on una camisa de disseny va captar immediatament l'atenció d'en Marcel.En: They walked to a fashion store, where a designer shirt immediately caught Marcel's attention.Ca: El teixit era suau i els colors eren vius, però el preu era altíssim.En: The fabric was soft, and the colors were vibrant, but the price was very high.Ca: "És perfecte," va dir en Marcel mentre la mirava amb ulls brillants.En: "It's perfect," Marcel said as he looked at it with bright eyes.Ca: Laia va fer una ganyota divertida.En: Laia made a playful grimace.Ca: "És molt cara, Marcel.En: "It's very expensive, Marcel.Ca: Pensa en la teva butxaca.En: Think about your wallet."Ca: "En Marcel sabia que la Laia tenia raó, però la temptació era gran.En: Marcel knew that Laia was right, but the temptation was strong.Ca: Van sortir de la botiga sense la camisa, però en Marcel no podia deixar de pensar-hi.En: They left the store without the shirt, but Marcel couldn't stop thinking about it.Ca: Mentrestant, van passejar pels carrers plens de paradetes artesanes.En: Meanwhile, they strolled through streets filled with artisan stalls.Ca: Una parada amb roba feta a mà va cridar l'atenció de la Laia.En: A stall with handmade clothing caught Laia's attention.Ca: Els estampats eren únics i els preus, raonables.En: The prints were unique, and the prices reasonable.Ca: "Mira aquesta camisa," va suggerir la Laia, assenyalant una peça colorida.En: "Look at this shirt," Laia suggested, pointing to a colorful piece.Ca: En Marcel la va agafar, indecís.En: Marcel picked it up, undecided.Ca: Era un disseny diferent, però intrigant.En: It was a different, but intriguing, design.Ca: I molt més assequible.En: And much more affordable.Ca: Amb el consell de la Laia encara ressonant a les seves orelles, en Marcel va prendre una decisió.En: With Laia's advice still echoing in his ears, Marcel made a decision.Ca: "Creus que em quedarà bé?En: "Do you think it'll look good on me?"Ca: " va preguntar en Marcel, encara incert.En: Marcel asked, still uncertain.Ca: Laia va somriure de nou, aquest cop amb orgull.En: Laia smiled again, this time with pride.Ca: "Segur que sí.En: "I'm sure it will.Ca: I no et deixaràs el sou.En: And you won't blow your paycheck."Ca: "Finalment, en Marcel va comprar la camisa de la parada artesanal.En: Finally, Marcel bought the shirt from the artisan stall.Ca: A la nit de Sant Joan, la festa va ser un èxit.En: On the night of Sant Joan, the party was a success.Ca: En Marcel se sentia còmode i especial, sense preocupar-se pels diners que havia estalviat.En: Marcel felt comfortable and special, without worrying about the money he had saved.Ca: S'adonà que la roba no només es tracta de disseny, sinó de saber escollir amb saviesa.En: He realized that clothing is not just about design but about knowing how to choose wisely.Ca: En Marcel va aprendre la importància d'impressionar, sí, però sense descuidar les seves finances.En: Marcel learned the importance of impressing, yes, but without neglecting his finances.Ca: Amb el suport de la Laia, va trobar un equilibri perfecte.En: With Laia's support, he found a perfect balance.Ca: I això va fer que aquella nit de Sant Joan fos encara més memorable.En: And that made that Sant Joan night even more memorable. Vocabulary Words:the sun: el solbrightly: intensamentthe crowd: la multitudcheerfully: animadamentimpress: impressionardecisively: amb decisiówarned: advertirsensibly: amb to assenyatthe fashion store: la botiga de modathe designer shirt: la camisa de dissenythe fabric: el teixitvibrant: viusthe price: el preuplayful grimace: ganyota divertidathe wallet: la butxacathe temptation: la temptacióartisan stalls: paradetes artesaneshandmade clothing: roba feta a màprints: estampatsreasonable: raonablesundecided: indecísintriguing: intrigantaffordable: assequiblethe paycheck: el southe party: la festasuccess: èxitcomfortable: còmodesavings: estalviatwisely: amb saviesafinances: finances

1938 Cadılar Bayramında neden insanlar aniden sokağa döküldü? Voyager 1 Altın Plağına koymadığımız fotoğraflar neyi ifade ediyor? Stephen Hawking ile H. G. Wells arasında nasıl bir bağlantı var?  Barış Özcan'la 111 Hz'in bu bölümünde Orson Welles'in ABD'de yarattığı panikten, Azteklerin, Hernán Cortés'i tanrı sanmasına, evrene “biz buyuz” dediğimiz ifadeleri konuşacağız.  Bu bölümde:  (00:00) 1938 Cadılar Bayramı Paniği (05:13) Münih Krizi (06:26) 1519 Aztekler (08:42) H. G. Wells (11:12) Ozma Projesi  (16:05) Voyager 1 Altın Plağı  (18:00) Stephen Hawking  Yaratıcı: Barış Özcan  Yapımcı: Podbee Media  Bu bölüm reklam ve sponsorluk içerebilir. Tüm bölümler, videolar ve daha fazlasına Podbee App ve podbee.com'dan ücretsiz olarak ulaşabilirsiniz.

Una investigación de eldiario.es destacaba hace unas semanas que la familia real de Emiratos Árabes había cobrado hasta 71 millones de euros en subvenciones públicas europeas por cultivar en España, Rumanía e Italia. En el Pla de Lleida, concretamente, casi el 80% de la alfalfa que se produce en este lugar se exporta a Emiratos Árabes para alimentar a sus vacas y camellos. Viajamos hasta allí para conversar con los agricultores de la zona, y reflexionamos sobre el comercio local y global de la mano de Juanjo Martínez, responsable de Comercio Justo de Oxfam Intermón.

Kaip Ukrainos mokytojai dirba karo sąlygomis ir kaip jie moko Lietuvos mokytojus dirbti su karo siaubą patyrusiais Ukrainos vaikais? Plačiau apie tai kalba Odesos srities Velikodolinskės licėjaus istorijos mokytoja Nadija Hotsuliak, Odesos srities Černomorsko licėjaus matematikos mokytoja Inna Loboda ir Odesos srities Velikodolinsko gyvenvietės teritorinės bendruomenės švietimo skyriaus vadovė Valentina Čebanova.

In 2012, China debuted its first aircraft carrier, the Liaoning, a refurbished Soviet-era ship from Ukraine. The debut of the Liaoning was largely thanks to a longtime pressure campaign by Liu Huaqing, the onetime leader of the People's Liberation Army Navy and the man responsible for transforming China's naval strategy. (China now has three carriers, and is building a fourth). When Liu began his career, China saw its military victories as coming primarily via land warfare; Liu, over decades, forced China to take naval combat seriously. Xiaobing Li writes about Liu's life in his book China's Mahan: Admiral Liu Huaqing and the Rise of the Modern Chinese Navy (Naval Institute Press, 2026), from his early career in the aftermath of the Chinese Civil War and finishing with his long push to start China's aircraft carrier program. Xiaobing Li, professor of history and Don Betz Endowed Chair in International Studies at the University of Central Oklahoma, is the author of The Dragon in the Jungle, Attack at Chosin, Building Ho's Army, History of Taiwan, and The Cold War in East Asia. He is the executive editor of the Chinese Historical Review. Li served in the PLA in China. Learn more about your ad choices. Visit megaphone.fm/adchoices Support our show by becoming a premium member! https://newbooksnetwork.supportingcast.fm/new-books-network

In 2012, China debuted its first aircraft carrier, the Liaoning, a refurbished Soviet-era ship from Ukraine. The debut of the Liaoning was largely thanks to a longtime pressure campaign by Liu Huaqing, the onetime leader of the People's Liberation Army Navy and the man responsible for transforming China's naval strategy. (China now has three carriers, and is building a fourth). When Liu began his career, China saw its military victories as coming primarily via land warfare; Liu, over decades, forced China to take naval combat seriously. Xiaobing Li writes about Liu's life in his book China's Mahan: Admiral Liu Huaqing and the Rise of the Modern Chinese Navy (Naval Institute Press, 2026), from his early career in the aftermath of the Chinese Civil War and finishing with his long push to start China's aircraft carrier program. Xiaobing Li, professor of history and Don Betz Endowed Chair in International Studies at the University of Central Oklahoma, is the author of The Dragon in the Jungle, Attack at Chosin, Building Ho's Army, History of Taiwan, and The Cold War in East Asia. He is the executive editor of the Chinese Historical Review. Li served in the PLA in China. Learn more about your ad choices. Visit megaphone.fm/adchoices Support our show by becoming a premium member! https://newbooksnetwork.supportingcast.fm/east-asian-studies

In 2012, China debuted its first aircraft carrier, the Liaoning, a refurbished Soviet-era ship from Ukraine. The debut of the Liaoning was largely thanks to a longtime pressure campaign by Liu Huaqing, the onetime leader of the People's Liberation Army Navy and the man responsible for transforming China's naval strategy. (China now has three carriers, and is building a fourth). When Liu began his career, China saw its military victories as coming primarily via land warfare; Liu, over decades, forced China to take naval combat seriously. Xiaobing Li writes about Liu's life in his book China's Mahan: Admiral Liu Huaqing and the Rise of the Modern Chinese Navy (Naval Institute Press, 2026), from his early career in the aftermath of the Chinese Civil War and finishing with his long push to start China's aircraft carrier program. Xiaobing Li, professor of history and Don Betz Endowed Chair in International Studies at the University of Central Oklahoma, is the author of The Dragon in the Jungle, Attack at Chosin, Building Ho's Army, History of Taiwan, and The Cold War in East Asia. He is the executive editor of the Chinese Historical Review. Li served in the PLA in China. Learn more about your ad choices. Visit megaphone.fm/adchoices Support our show by becoming a premium member! https://newbooksnetwork.supportingcast.fm/military-history

Fluent Fiction - Catalan: Finding Inspiration: A Night of Magic at Plaça del Sol Find the full episode transcript, vocabulary words, and more:fluentfiction.com/ca/episode/2026-06-25-22-34-02-ca Story Transcript:Ca: La música fluïa per tota la Plaça del Sol.En: The music flowed throughout the Plaça del Sol.Ca: Era una nit plena de màgia.En: It was a night full of magic.Ca: Els llums de colors brillaven com estrelles apropant-se a tocar la terra.En: The colorful lights shone like stars drawing near to touch the earth.Ca: L'olor de calçots a la brasa omplia l'aire, barrejant-se amb el ritme de les guitarres.En: The smell of grilled calçots filled the air, mixing with the rhythm of the guitars.Ca: Pere caminava entre la gent amb el seu somriure de sempre.En: Pere walked among the people with his usual smile.Ca: Era músic, i les nits d'estiu com aquella eren el seu moment preferit.En: He was a musician, and summer nights like this one were his favorite time.Ca: No gaire lluny, Júlia interpolava el seu món dins la plaça amb la càmera a la mà.En: Not far away, Júlia was intertwining her world with the plaza, camera in hand.Ca: Venia de Girona per captar l'essència del Sant Joan, les emocions i la vida en cada fotografia.En: She came from Girona to capture the essence of Sant Joan, the emotions and life in every photograph.Ca: Però fins ara, sols havia trobat imatges comunes i gens especials.En: But so far, she had only found common and unremarkable images.Ca: Cada cop que enfocava, veia el mateix: una munió de gent que ballava i riuria.En: Every time she focused, she saw the same: a crowd of people dancing and laughing.Ca: Res captivador.En: Nothing captivating.Ca: Pere, buscant una mica de tranquil·litat, es va apartar del bullici principal.En: Pere, seeking a bit of tranquility, moved away from the main hustle and bustle.Ca: Va trobar un racó menys concorregut, amagat darrere d'uns tendals.En: He found a less crowded corner, tucked behind some awnings.Ca: Allà, al retirat espai, va veure Júlia.En: There, in the secluded space, he saw Júlia.Ca: Els ulls de Pere es van il·luminar en veure com Júlia apuntava la seva càmera cap al cel, capturant els focs artificials que esclataven com flors luminescents.En: Pere's eyes lit up seeing how Júlia pointed her camera at the sky, capturing the fireworks bursting like luminescent flowers.Ca: "Quina foto!" va dir ell sense pensar-ho.En: "What a photo!" he said without thinking.Ca: Júlia va baixar la càmera i va somriure sorpresa.En: Júlia lowered the camera and smiled in surprise.Ca: "Gràcies! És complicat trobar alguna cosa nova aquesta nit," va admetre ella.En: "Thanks! It's complicated to find something new tonight," she admitted.Ca: "Jo també busco inspiració nova, però amb tanta gent... difícil centrar-se," va confessar Pere, assenyalant la seva guitarra.En: "I am also looking for new inspiration, but with so many people... it's hard to focus," confessed Pere, pointing to his guitar.Ca: Llavors van deixar-se portar per la màgia de la plaça.En: Then they let themselves be carried away by the magic of the plaza.Ca: Es van presentar i, sense adonar-se'n, la connexió entre ells va créixer.En: They introduced themselves, and without realizing it, the connection between them grew.Ca: Pere va tocar unes notes suaus, Júlia va fotografiar el seu somriure mentre el sol sonava a la nit estival.En: Pere played some soft notes, and Júlia photographed his smile while the sun played on the summer night.Ca: Van passar la nit explorant junts, compartint música i art.En: They spent the night exploring together, sharing music and art.Ca: Cada racó amagava alguna meravella inesperada que Júlia immortalitzava.En: Each corner hid some unexpected wonder that Júlia immortalized.Ca: Amb cada clic, Júlia trobava noves històries brollant a través de la seva lent.En: With every click, Júlia found new stories blossoming through her lens.Ca: Al final de la nit, mentre el primer llum del dia començava a pintar el cel, Júlia i Pere s'adonaren que havien trobat més que inspiració.En: At the end of the night, as the first light of day began to paint the sky, Júlia and Pere realized they had found more than inspiration.Ca: Es van donar les gràcies mútuament, sabent que el seu camí s'havia creuat per una raó.En: They thanked each other, knowing that their paths had crossed for a reason.Ca: Pere havia trobat la melodia perfecta per a la seva nova cançó, inspirada pel color dels moments compartits.En: Pere had found the perfect melody for his new song, inspired by the color of their shared moments.Ca: Júlia, amb la càmera plena d'imatges úniques, havia capturat l'autèntica essència del Sant Joan, i més del que havia esperat: un nou començament.En: Júlia, with her camera full of unique images, had captured the true essence of Sant Joan, and more than she had expected: a new beginning.Ca: Amb un somriure compartit, es van acomiadar, prometent-se que aquell encontre seria només el principi d'una història molt més gran.En: With a shared smile, they said goodbye, promising each other that this encounter would be just the beginning of a much larger story.Ca: La plaça del Sol, Testimoni silenciós, seguia brillant amb llum pròpia, un símbol de nous començaments compartits.En: The Plaça del Sol, a silent witness, continued to shine with its own light, a symbol of new shared beginnings. Vocabulary Words:flowed: fluïaplaza: la plaçasmell: l'olorgrilled: a la brasarhythm: el ritmeusual: de sempreintertwining: interpolavacapture: captaressence: l'essènciaemotions: les emocionsunremarkable: gens especialscrowd: una munióhustle and bustle: el bullicisecluded: retiratawnings: els tendalslit up: es van il·luminarlowered: va baixaradmitted: va admetretricky: complicatfocus: centrar-sesoft: suauunexpected: inesperadaimmortalized: immortalitzavastories: les històriesblossoming: brollantrealized: s'adonarenunique: úniquesgoodbye: acomiadar-sewitness: el testimonisymbol: un símbol

In 2012, China debuted its first aircraft carrier, the Liaoning, a refurbished Soviet-era ship from Ukraine. The debut of the Liaoning was largely thanks to a longtime pressure campaign by Liu Huaqing, the onetime leader of the People's Liberation Army Navy and the man responsible for transforming China's naval strategy. (China now has three carriers, and is building a fourth). When Liu began his career, China saw its military victories as coming primarily via land warfare; Liu, over decades, forced China to take naval combat seriously. Xiaobing Li writes about Liu's life in his book China's Mahan: Admiral Liu Huaqing and the Rise of the Modern Chinese Navy (Naval Institute Press, 2026), from his early career in the aftermath of the Chinese Civil War and finishing with his long push to start China's aircraft carrier program. Xiaobing Li, professor of history and Don Betz Endowed Chair in International Studies at the University of Central Oklahoma, is the author of The Dragon in the Jungle, Attack at Chosin, Building Ho's Army, History of Taiwan, and The Cold War in East Asia. He is the executive editor of the Chinese Historical Review. Li served in the PLA in China. Learn more about your ad choices. Visit megaphone.fm/adchoices Support our show by becoming a premium member! https://newbooksnetwork.supportingcast.fm/biography

In 2012, China debuted its first aircraft carrier, the Liaoning, a refurbished Soviet-era ship from Ukraine. The debut of the Liaoning was largely thanks to a longtime pressure campaign by Liu Huaqing, the onetime leader of the People's Liberation Army Navy and the man responsible for transforming China's naval strategy. (China now has three carriers, and is building a fourth). When Liu began his career, China saw its military victories as coming primarily via land warfare; Liu, over decades, forced China to take naval combat seriously. Xiaobing Li writes about Liu's life in his book China's Mahan: Admiral Liu Huaqing and the Rise of the Modern Chinese Navy (Naval Institute Press, 2026), from his early career in the aftermath of the Chinese Civil War and finishing with his long push to start China's aircraft carrier program. Xiaobing Li, professor of history and Don Betz Endowed Chair in International Studies at the University of Central Oklahoma, is the author of The Dragon in the Jungle, Attack at Chosin, Building Ho's Army, History of Taiwan, and The Cold War in East Asia. He is the executive editor of the Chinese Historical Review. Li served in the PLA in China. Learn more about your ad choices. Visit megaphone.fm/adchoices Support our show by becoming a premium member! https://newbooksnetwork.supportingcast.fm/chinese-studies

Valois giminė, meistriškai įvaldžiusi intrigų ir diplomatijos įrankius, pravedė rinkiminę kampaniją Geriausių Tautų Respublikoje šiek tiek per gerai. Sužavėti Lenkijos ir Lietuvos bajorai negalėjo atsispirti žavingiems pasiuntiniams ir jų įtkiniamiems argumentams. Nors mylimiausias Kotrynos di Medici sūnus kitaip įsivaizdavo savo ateitį, iš naujos darbovietės jis išspaudė kiek tik galėjo. Henrikas tapo ne tik mados diktatorium. Jis nutiesė Prancūzijos absoliutizmo pamatus, įgalindamas būsimus šalies valdovus pažaboti išsiskeriojusią oligarchiją. Jo progresyvios reformos tėvynėje aštriai kontrastavo su negarbingu elgesiu Krokuvoje. O nepaisant trumpo laiko, praleisto Geriausių Tautų Respublikoje, Henrikas parsivežė didžiulę patirtį ir krūvą technologinių naujovių. Kokią infrastruktūrą Monlucas žadėjo lenkams? Kiek Henrikų dalyvavo epizode? Kokie argumentai patraukė savo pusėn Radvilas ir Chodkevičius? Ir kodėl Henriko gyvenimą apsprendė ne du, bet trys sostai? Geriausių Tautų Respublika tave kviečia... ------- TELE2 Kelionių draudimas. Bet kurioje šalyje tik 2 €/dienai, o pirmoji kelionės diena – visada nemokamai. Plačiau: https://tele2.lt/kelioniu-draudimas ------- SAILY! Gaukite išskirtinę 15% nuolaidą Saily duomenų planams! Naudokite kodą protopemza atsiskaitydami. Atsisiųskite Saily programėlę arba apsilankykite https://saily.com/protopemza ------- Iliustracija: @korinavaicikone Muzika: kissan4, Gregor Quendel, Dredstudio, theromancrow, Emmraan, litesaturation, Denis-Pavlov-music, artarea_studio, geoffharvey, Scott Buckley, Sonican, Emand_edroff, atlasaudio, Krasnoshchok, freesound_community

In 2012, China debuted its first aircraft carrier, the Liaoning, a refurbished Soviet-era ship from Ukraine. The debut of the Liaoning was largely thanks to a longtime pressure campaign by Liu Huaqing, the onetime leader of the People's Liberation Army Navy and the man responsible for transforming China's naval strategy. (China now has three carriers, and is building a fourth). When Liu began his career, China saw its military victories as coming primarily via land warfare; Liu, over decades, forced China to take naval combat seriously. Xiaobing Li writes about Liu's life in his book China's Mahan: Admiral Liu Huaqing and the Rise of the Modern Chinese Navy (Naval Institute Press, 2026), from his early career in the aftermath of the Chinese Civil War and finishing with his long push to start China's aircraft carrier program. Xiaobing Li, professor of history and Don Betz Endowed Chair in International Studies at the University of Central Oklahoma, is the author of The Dragon in the Jungle, Attack at Chosin, Building Ho's Army, History of Taiwan, and The Cold War in East Asia. He is the executive editor of the Chinese Historical Review. Li served in the PLA in China. Learn more about your ad choices. Visit megaphone.fm/adchoices Support our show by becoming a premium member! https://newbooksnetwork.supportingcast.fm/asian-review

On today's episode of the China Global Podcast, we're going to discuss the South China Sea. The past year has been marked by four intersecting dynamics: First, a sharp escalation of Chinese Coast Guard and maritime militia operations, especially against the Philippines. Second, a resumption of large-scale Chinese island construction after nearly a decade-long pause; Third, increasingly sophisticated Chinese legal and administrative moves to consolidate and institutionalize its claims; And fourth, a deepening of the US-Philippines military partnership and the emergence of a broader network involving US allies and partners from Europe and the Indo-Pacific. To discuss these trends, I'm delighted to have as my guest today, Dr. Collin Koh, who is a senior fellow at the Institute of Defense and Strategic Studies in the S. Rajaratnam School of International Studies based in Nanyang Technological University in Singapore. Timestamps: [00:00] Introduction [01:33] Beijing'sObjectives in the South China Sea [06:24] Changes in China's Strategy  [09:13] A Revival of Island Building in Antelope Reef [16:11] Increased Activity in Scarborough Shoal  [20:13] Violating the 2002 Declaration on the Conduct?  [24:21] Pros and Cons to Finalizing the Code of Conduct [28:58] China's Response to US-Philippines Security Cooperation [33:15] Claimant Perceptions of US Policy 

Episode 813 is here! The summer showcases have wrapped up, and we are diving into the aftermath: ? Nintendo Direct destroys the competition to become the most-watched summer showcase! ? Star Fox Developer Revealed – Velan Studios takes the helm for the Switch 2. ? Denshattack Delayed – Pushed back to July 15th, leaving Brandon devastated. ? In Change the System: – Justin is exploring every inch of Mario Kart World, breaking Xenoblade Chronicles X with ChatGPT, and trying to survive the tutorial dialogue in Pokemon Legends: Z-A. – Brandon is racing giant mechas in Forza Horizon 6 and 3D printing in wood PLA. – Eugene is grinding out bones and getting powerful in Mina the Hollower. Episode 813. Let's go.

Tā nav tikai romānos aprakstīta kaite, kas sižetam piešķir papildus biedējošu romantiku un spraigumu. Diemžēl tuberkuloze ir realitāte, ar kuru sabiedrība saskaras joprojām. Kas zināms par šo slimību mūsdienās un kā ar to cīnīties, pētām raidījumā Kā labāk dzīvot. Plašāk stāsta Rīgas Austrumu klīniskās universitātes slimnīcas (RAKUS) stacionāra "Tuberkulozes un plaušu slimību centrs" 7. nodaļas vadītāja, Latvijas Tuberkulozes apkarošanas biedrības biedre ārste Līga Kukša un RAKUS stacionāra "Tuberkulozes un plaušu slimību centrs" ambulatorās daļas virsmāsa un Latvijas Tuberkulozes apkarošanas biedrības biedre Evita Biraua.

El dia gros serà dimarts 23 amb la Revetlla de Sant Joan a la Plaça Catalunya amenitzada per la música de Blu Versions, Dj Miku i Dj XVII però els actes festius arrencaran dissabte dia 20 a les 18.30h amb el II Corre i no et quedis sec que aquest any ha incorporat nous establiments fruit del darrer creixement de cafeteries que ha viscut el barri. Tot seguit serà el torn del Sopar popular del pà amb tomàquet, tota una tradició per a la gent del barri i pels sitgetans, hi ha un aforament de quatre centes cadires, ampliable a cinc centes, i està gairebé ple. Els actes més institucionals arribaran el dia de Sant Joan i abans, diumenge hi haurà torn també pels més menuts. Tot plegat a càrrec de la comissió que lidera Ainara Martínez des de fa dos anys i que treballa fort per mantenir la festa i per aconseguir voluntaris, probablement la tasca més difícil. L'entrada El Poble Sec a punt per les Festes de Sant Joan i calen voluntaris ha aparegut primer a Radio Maricel.

On today's show Andrew and Bill begin with takeaways from Xi's visit to North Korea this week, including the conspicuous silence on North Korea's nuclearization, Kim Jong Un's assistance to Russia's war in Ukraine, Beijing as Kim's top priority, U.S.-Japan dialogue on regional nuclear threats, and an email about the PRC as a communist country. From there: CPPCC Chairman Wang Huning leads an inspection tour of Xinjiang ahead of the July 1st implementation of the national ethnic unity law, plus thoughts on Xinjiang's strategic importance generally and why Beijing sees its recent efforts as successful. At the end: China preps for an AI infrastructure buildout, the Pentagon alleges that Alibaba, Baidu and BYD are linked to the PLA, the Busan truce is being tested by both sides, and two Knicks stars wish students good luck on the GaoKao.

Henrikas III Valois vienas kertinių Geriausių Tautų Respublikos politinės sistemos architektų. Nors eilėje iki gimtosios Prancūzijos sosto jis laukė ne pats pirmas, tačiau motinos širdyje jis nuo pirmų dienų užėmė privilegijuotą vietą. Ši spalvinga asmenybė nepasižymėjo nei kuklumu, nei santūrumu, tačiau už plėvėsiško fasado slėpėsi talentingas, nors kiek netašytas, administravimo deimantas. O talentingų valdovų valstybei reikėjo kaip vandens kupranugariui - sostų žaidime iš visų pusių smūgiavo galios ištroškę didikai, religiniai fanatikai, bei artimiausi šeimos nariai. Kokiu vardu Henrikas buvo žinomas vaikystėje? Kodėl Prancūzijos valdovas keliavo nuo rūmų prie rūmų? Kokios traumos suformavo būsimo GTR karaliaus asmenybę? Ir kuo jis susijęs su pimpačkiukais?   Pasiilgai Geriausių Tautų Respublikos? Nes ji pasiilgo tavęs...   TELE2 5G Namų internetas – greitas ir pigus. Plačiau: https://tele2.lt/namu-internetas Domina karjera Omnisend? Eik į https://www.omnisend.com/katuciaveiki   Iliustracija: @korinavaicikone Muzika: Freesound_community, SoundReality, Wings of Freedom, Alex Grohl, Ashot_Danielyan, Inplusmusic, Petrushkasound, Zec53, Gregor Quendel, nesrality, Iithop, Emand Edroff, Artarea Studio, Denis Pavlov, SamuelFJohanns

L’inquinamento da plastiche passa anche attraverso la produzione di compost di cattiva qualità, inquinato a sua volta da microplastiche se il materiale di partenza è contaminato a monte. A complicare le cose c’è poi il fatto che questi residui sono difficili da distinguere dai residui di polimeri compostabili - bioplastiche come il mater-b o il PLA -, che invece hanno tutto il diritto di trovarsi frammisti al compost. Da qui, il lavoro fatto congiuntamente da Cnr-Isafom e Università degli Studi di Milano: un nuovo protocollo di analisi che permette in modo facile ed economico di quantificare eventuali plastiche “cattive” presenti nel compost, che potrebbe presto diventare un test standard. Ne parliamo con Mirko Cucina, primo ricercatore dell’Istituto per i Sistemi Agrari e Ambientali nel Mediterraneo, del CNR di Perugia.

La Plata Alejandro Dolina, Patricio Barton, Gillespi Introducción • 0:09:57 Presentación en La Plata y agradecimiento al público • 0:12:06 Recuerdo de la primera salida del programa desde Buenos Aires hacia La Plata • 0:12:35 Presentación de Patricio Barton y Gillespi Segmento Inicial • 0:13:21 Qué significa ser romántico hoy • 0:16:06 Regalos románticos recomendados y objeciones • 0:20:37 Desayuno sorpresa a domicilio y sus inconvenientes • 0:27:24 Notas manuscritas como gesto romántico • 0:30:39 Escapadas de fin de semana y paseos románticos • 0:32:23 Regalar cachorros y responsabilidades afectivas • 0:34:44 Cocinar para la pareja como prueba de amor • 0:36:22 Pasacalles, sándwiches en la costanera y otros gestos desaconsejados • 0:40:29 Regalos domésticos, dinero y publicaciones en redes sociales • 0:45:05 Peluches gigantes, mensajes aéreos y límites del romanticismo • 0:52:23 Regalar canciones como gesto amoroso Segmento Dispositivo • 0:54:56 Las plañideras y el llanto profesional en la antigüedad • 0:56:21 Lloronas en hebreos, griegos y romanos • 0:59:28 Rituales funerarios egipcios con plañideras • 1:02:57 Plañideras en Grecia, Roma y la Edad Media • 1:06:06 Función ritual del llanto y reflexión sobre las lágrimas Segmento Humorístico • 1:13:01 Cuidado con la automedicación • 1:14:46 Confusiones entre gotas, dosis excesivas y antibióticos mal usados • 1:20:32 Pastillas por color, medicamentos vencidos y remedios veterinarios • 1:24:15 Interrumpir tratamientos, tragar antisépticos y triturar pastillas • 1:28:14 Intercambio de remedios, curanderos y peligros al tomar cápsulas sin agua • 1:31:15 Mezcla de sedantes con alcohol y cierre sobre el botiquín doméstico Sordo Gancé / Trío Sin Nombre • 1:42:21 Presentación del Sordo Gancé y el Trío Sin Nombre • 1:43:16 "Mañana campestre" ♫ • 1:46:02 "Tu casa ya no está" ♫ • 1:49:04 Ingreso de Gillespi y "Blue Moon" ♫ • 1:51:36 Recuerdo de "Golondrina" • 1:55:15 Homenaje musical a un amigo • 1:56:54 "Todo un palo" ♫ • 1:59:17 "Solo le pido a Dios" ♫ • 2:00:23 Cierre musical y agradecimiento al público (Resumen generado automáticamente con IA, puede contener errores)

Dr. Deb Muth 00:00:09 Hi there, how are you? Bob Miller 00:00:10 Excellent! Pedaling as fast as humanly possible, but doing okay. Dr. Deb Muth 00:00:14 Good, good. Well, I’m looking forward to our conversation today. This should be amazing. Bob Miller 00:00:20 Yeah, it should be a lot of fun. Dr. Deb Muth 00:00:22 Yeah, anything that’s off-limits for you in, our conversation? Bob Miller 00:00:28 No. Dr. Deb Muth 00:00:29 Okay, anything you want me to make sure we cover for you? Bob Miller 00:00:33 Well, I mean, is it okay if we put a little plug-in for our software? Dr. Deb Muth 00:00:35 Absolutely. Bob Miller 00:00:36 Yeah. Dr. Deb Muth 00:00:37 Absolutely. Bob Miller 00:00:36 Yeah. Dr. Deb Muth 00:00:37 Absolutely. Bob Miller 00:00:38 Hey, can we… can we do a screen share? Yes, we can. Yeah, because I want to show you some maps, and… Dr. Deb Muth 00:00:43 Okay. Things like that, yeah, so… Perfect. So just let me know when you want to do screen share. Bob Miller 00:00:48 Okay. Dr. Deb Muth 00:00:49 And yeah, feel free to plug your software wherever you want to. Bob Miller 00:00:53 Okay, well, good. Let me pull up a, a slide for that, and give me one second, I just want to shut the door to my office to get the noise down. Dr. Deb Muth 00:01:01 No worries. Bob Miller 00:01:16 And, how should I refer to you? Dr. Debb? Dr. Muth, what do you like? Dr. Deb Muth 00:01:18 Dr. Deb is great, or Deb, either way, I’m pretty informal, so… Bob Miller 00:01:22 Yeah, and… Bob is fine for me. Okay. Yeah. Yeah, there you go. Why people feel like they need this, son. Special name, it’s like, seriously. Dr. Deb Muth 00:01:33 Right? I agree. Bob Miller 00:01:35 When I work with my clients, it’s like, Dr. Millison, just, just bop, just, just bop. Dr. Deb Muth 00:01:41 Yep, that’s how I am, too. Just call me Deb, it’s good. Dr. Deb Muth 00:01:44 They feel a little awkward with that, you know? They’re not used to that, but… Bob Miller 00:01:48 Alright. And you’re a naturopath, medical doctor. Dr. Deb Muth 00:01:52 A nastropathic doctor and a nurse practitioner. Oh, nice. Yeah, so I got the best of both worlds, right? Bob Miller 00:01:58 Yeah, damn. Okay. Alright, so here we go… There we go. Alright, so I got that ready, and then I will do a, I will do a screen share. I think you’re gonna really, appreciate what we’ve come up with. We’ve come up with the concept of, Cellular CPR. Dr. Deb Muth 00:02:23 Oh, nice! Bob Miller 00:02:24 And that is, construct the cell membrane, Protect the cell membrane. And restore it if it’s damaged. Dr. Deb Muth 00:02:32 Love that. Bob Miller 00:02:34 I love that. Yeah, so that’s what we’re focusing on, and then how, You know, we want to get to the point that, you know, most people think of genetics, they think of, like, 23andMe or Ancestry. Dr. Deb Muth 00:02:44 Yeah. Bob Miller 00:02:45 And then you have the professional geneticists who are looking at, you know, odd things that could create a disease. We’re looking at functional genomics. Dr. Deb Muth 00:02:54 Which is so much better. Bob Miller 00:02:56 Yeah. Are you familiar with what we do here, or… Dr. Deb Muth 00:02:58 A little bit, a little bit. So, it’ll be new to me, too, so I’m excited. Bob Miller 00:03:03 And how much time do we have? Dr. Deb Muth 00:03:04 We have an hour, give or take a little bit on either side. Do you have a hard stop anywhere? Bob Miller 00:03:10 No, no, I put a, I moved my clients around, and I don’t have anybody till, 3.30, so we’re good. Okay. Dr. Deb Muth 00:03:16 Perfect. Alright. Bob Miller 00:03:18 It’s like we’re getting started early as well, so… Dr. Deb Muth 00:03:19 Yeah, we’re getting started a little bit early, so that’s good. Bob Miller 00:03:22 Yeah, I just got my office cleaned up, so… Dr. Deb Muth 00:03:23 Okay, good. All right, are you all set to get started? Bob Miller 00:03:28 I’m good to go, my friend. Dr. Deb Muth 00:03:29 I’m gonna just record a little intro and a little bit of a, hook for people, and then we’ll get started. I’ll ask you to kind of tell us a little bit about yourself, and then we’ll just take this conversation wherever it’s supposed to go. Bob Miller 00:03:39 Okay, you got it. Dr. Deb Muth 00:03:40 Alright, sounds good. So what if the reason you’re not healing isn’t your diet, your supplements, or your labs, but it’s actually your genes? Dr. Bob Miller is uncovering how genetic variants, when combined with modern toxins, explain why some of us stay sick no matter what we try. Today, we’re talking genetic pathways, detox blocks, and the new science every wellness warrior needs to know. Welcome back to Let’s Talk Wellness Now, the show where we uncover the root causes of chronic illness, exploring cutting-edge regenerative medicine, and empower you to heal from the inside out. I’m Dr. Deb, your medical detective, and today, our guest, Dr. Bob Miller, is a true pioneer in functional genomics. He’s a board-certified traditional naturopath and the founder of Neutrogenetic Research Institute. And he’s the leading groundbreaking research on how genetic variants influence chronic illness, inflammation, and detoxification. His work has been recognized on international stages, uncovering links between genetic expression and conditions like Lyme disease, mast cell activation, or MCAS, and mitochondrial dysfunction. I’m so excited to talk to Dr. Bob today. He is gonna reveal some things that even I don’t know about, so I’m excited to learn alongside of you guys. So… Dr. Bob, let’s get started. Tell us a little bit about yourself, and kind of how you got on this journey. Bob Miller 00:05:04 Well, that’s, that’s interesting. I was sort of like a mid-career coming to the natural health field, because in my early 30s, I found myself with a severe case of ulcerative colitis. Bob Miller 00:05:15 And I was in the hospital for 21 days. probably within hours of death, pleading to death. And they told me I’ve got one option, and that is cut out the colon and wear a bag. Didn’t sound like a lot of fun. Dr. Deb Muth 00:05:27 Not an option I would want. Bob Miller 00:05:29 So, you know, the medical folks wasn’t real happy with me, but I said, yeah, I’d like to explore some alternative things.Never thinking that I’d get into this field, and then I just, you know, worked with some herbalists and things that I found absolutely fascinating. So, that’s how I got into this around 30 years ago. And, haven’t looked back since, and just having a… having a blast as we now move into how our genetics impacts things. So, that’s what we’re gonna… that’s what we’re gonna talk about today. Dr. Deb Muth 00:05:58 I’m excited to talk about this genetic thing. When you started over 30 years ago, what kind of patience and problems first inspired you to dig deeper into that root cause healing and kind of get into the genetic piece of it? Bob Miller 00:06:10 Sure. Well, you know, as a… now, I’m in a part of the country called Lancaster County, Pennsylvania, where there’s a lot of Amish and Mennonite, and they gravitate towards these things.So, this is their first thing to do, and that doesn’t work, then they’ll go other routes. So, you know, back then, we just saw typical, you know, a little tired, constipation. You know, a little bit of fatigue, arthritis, those kind of things. But things have changed dramatically over the years, as people are now getting more chronically sick. You know, it’s worse than it’s ever been. And what we’re finding is the, the culprits Primarily is mold exposure and Lyme disease. When people get those two together, they’re just… it’s an inflammatory cascade that nobody can seem to unravel. So that’s where we spend a lot of our time. And we’re also spending a lot of time looking at mental health, like ADD, ADHD. And, we give… this year I’ll be speaking at three autism conferences. And we can dig into that a little bit as to why we think we’re seeing such a dramatic increase. And aside from autism, that used to be 1 out of 1,000, now it’s 1 out of 33, or 23. You know, we’re also seeing dramatic increases in ADD, ADHD. People are stressed out. And today, I think we’ll have the time to actually go through and show how environmental factors combine with genetics to cause that to happen. So we’ll… we should have a fun visit here today. And today, I think we’ll have the time to actually go through and show how environmental factors combine with genetics to cause that to happen. So we’ll… we should have a fun visit here today. Dr. Deb Muth 00:07:37 This should be a fun visit. We can cover lots of topics. I am so excited. So, you founded Nutri Genetic Research Institute in 2015. What did you hope to accomplish, and what kind of surprised you in your findings so far about that? Bob Miller 00:07:51 Well, you know, let’s back up at what, you know, genetics is used for. Everybody’s familiar with 23andMe and Ancestry that, you know, tells you where your ancestors came from. Then you have your professional geneticists. I mean, these are people with a degree in genetics. And they’ll look for, you know, very odd sort of things that are prone to relate to a disease. So there are disease-related genetics. Well, in functional, we don’t look at either of those. We look at For example, how you’re breaking down your fats and utilizing them. How you’re recycling your glutathione. How you might be handling your iron. And none of those are disease-causing on their own.And none of those are disease-causing on their own. But when they pile up on you, and then combine that with environmental factors, that’s when things start to go south on us. So, that’s what we’re doing, we’re looking at patterns. And our first foray into this was, we did studies on Lyme disease. And our first foray into this was, we did studies on Lyme disease. So, we looked at, like, I think 50 people with Lyme disease. We looked at their genome. So, we looked at, like, I think 50 people with Lyme disease. We looked at their genome. And we found patterns that were more evident in those with Lyme. Now, this doesn’t… these genetics don’t mean you get Lyme, it just means if you get Lyme, you react worse to it. And we found patterns that were more evident in those with Lyme. Now, this doesn’t… these genetics don’t mean you get Lyme, it just means if you get Lyme, you react worse to it. So, as you know, some people get Lyme, they go on a round of antibiotics, and they’re done. So, as you know, some people get Lyme, they go on a round of antibiotics, and they’re done. Others have a little more struggle, and then others are struggling terribly for years. So there’s an old adage of genetics loads the gun, environment pulls the trigger. Dr. Deb Muth 00:09:14 Yeah, that is so true, and I think when we’re talking about Lyme and mold and things like that, we forget sometimes that our genetics can predispose us to be more sensitive to those things, and if we have genetic pathways where we don’t clear things properly, it’s harder for us to get them out of the body. And then you add on that whole rain barrel effect that we’ve always used as a functional medicine term, right? If the barrel’s half full, you’re okay. If it’s full, and now it’s spilling over, it’s a bigger problem. Have you guys found, too, that some of these environmental things actually are changing the genetics of people, or how they’re processing their own genetics? Bob Miller 00:09:53 Well, let’s go back to, Genetics 101. But we’ll go back a little bit further. So, what an interesting mechanism, what a miracle the body is. Bob Miller 00:10:03 Fats, carbohydrates, proteins, drink water, breathe air, expose the sunlight, and somehow everything gets made. I mean, when you just step back and think about that, it’s like, It’s pretty darn amazing. Dr. Deb Muth 00:10:15 I always tell women, you know, the fact that we get pregnant and we have healthy pregnancies and births is a miracle, because if we had to try to control that, that wouldn’t work so well. Bob Miller 00:10:25 Right. Well, that’s another miracle. These microscopic sperm and egg, human being, 9 months later, it’s like. But even inside of us. We are making our hair, our skin, our nails, our blood vessels, our ATP, our energy, it’s all being created. Well, that gets created by enzymes. So, enzymes take one substance, combine it with something else, and make something new. Then another enzyme comes along and does the same thing. Your DNA is the instructions on how to make the enzymes. So, when we are conceived. If it’s a, if it’s a female, of course, it’s the XX, the two chromosomes. You know, we’ve… everybody’s seen those… the genetics that… Listed pair. So, if it’s a female, the father donated the X enzyme. And the mother has no choice but to give the eggs, so that’s female. If the father donates the Y, you have a male that’s in chromosome number 1. Then 2 through 23 is the rest of the instructions on how to make enzymes. So, what can happen? We can get what are called SNPs, single nucleotide polymorphisms. And SNPs just mean that the instructions to make the enzyme’s not quite as good. So, if one parent gives a SNP on the making of an enzyme, The enzyme’s fine. It works. But, general rule of thumb, It may only work at 70-80% of efficiency. Now, a good analogy is think of an 8-cylinder and a 6-cylinder car. If parents give you good information, that’s like having an 8-cylinder car. If one parent gives you that snip, it’s like having a 6-cylinder car. Now, is a 6-cylinder car a fine car? Sure. It’ll get you from point A to point B, but it’s just going to have the power of an 8-cylinder. Then if both parents give you a SNP on the same enzyme, it may be 30-40%, and that’s like having a 4-cylinder car. Sits in the driveway, looks the same, puts gas in it, everything. But if you’ve got a 4-cylinder car. Probably not a good idea to go cross-country pulling a trailer behind you up and down mountains. Dr. Deb Muth 00:12:29 This is true. Bob Miller 00:12:32 So… We can get an 8-cylinder, 6-cylinder, or 4-cylinder enzyme. Now, if it’s not under a lot of stress, if that 4-cylinder car is just taking you to the bank and the grocery store. It’s just as good as an 8-cylinder car. But if you gotta pull that trailer, and there’s a lot of stress on it, being mountains, it’s gonna struggle. Now, there’s one other little caveat to this, and that is some genetic mutations are gain-of-function. They actually work faster. Now, we have enzymes that do all kinds of things. We have enzymes that make and recycle our antioxidants, but we also have enzymes that make inflammation. No, that’s a good thing, because if we get a virus or bacteria, if you didn’t make inflammation to kill it, well, we’d all die of infection. So, you know, we tend to think of free radicals as bad, antioxidants as good. They both play an important role. But interestingly, some of the major enzymes that make inflammation, they can be overactive. They can be turbocharged. And when they’re stimulated by environmental toxins, they overreact. Bob Miller 00:13:40 And therein lies the problem. When they overreact, we have a problem. Bob Miller 00:13:46 So, if we have genes that overreact when stimulated. And then the enzymes that take care of inflammation are underactive. Then you’re gonna be more inflamed. You know, the majority of people that, you know, come for functional medicine Or naturopathic help, or… Inflammation that they can’t seem to get under control. Dr. Deb Muth 00:14:06 Right. Bob Miller 00:14:07 And we will be, you know, during this hour, we’re going to look at some of the pathways that make that happen. So, what we can do then, we can’t change our genetics. When you’re conceived, that’s the hand you’re dealt. When your life would be over, if someone would take some tissue and measure, it’d be exactly the same as conception. Does it change. Bob Miller 00:14:28 The enzyme’s ability to do its job may be compromised. Because remember I said there’s a, the enzyme takes a cofactor. So an enzyme takes substance A, cofactor, make substance B. Well, if that cofactor’s not there, the enzyme’s not going to work either. So, you could have an 8-cylinder car, and if there’s no gas in it, it’s not going anywhere. So… It’s the strength of the enzyme, it’s the cofactor to do the A to B conversion. And that’s what we’re going to get into. So, many people say, well, where did these SNPs come from? Nobody knows for sure. Sometimes they’re what’s just called de novo, when the sperm and egg go together, the instructions get mixed up a little bit. We do believe a lot of it came from a long time ago, when we were almost wiped out by sexually transmitted diseases. And those STDs were altering the genes when the conception, in other words, when the sperm went into the egg, the STDs were interfering. And causing the problem, so… I often joke, if you want to blame somebody. Blame your great-great-great-great-great-great-great-grandparents for, being a bit promiscuous, so… Dr. Deb Muth 00:15:31 Yeah, for being… having a little too much fun, right? Bob Miller 00:15:35 So, we don’t know for sure, but, you know, there are some that, But most of the SNPs that we get inherit from our parents. So, if you look at a child. And you look at the SNPs. 99.9% of the time, it came from one of the parents. Dr. Deb Muth 00:15:50 In identical twins, do they have the exact same identical makeup? Bob Miller 00:15:54 Yep, Dr. Deb Muth 00:15:56 But not in fraternal twins, correct? Bob Miller 00:15:59 No, no, those could be different, Jeff. Dr. Deb Muth 00:16:00 It could be different because they have different sacs, they’re not sharing that same genetic makeup. Bob Miller 00:16:04 Yeah, so keep in mind, both your mother and your father have, you know, the two And so you get one from one parent, one from another. Dr. Deb Muth 00:16:13 So… Bob Miller 00:16:14 Interesting situation. I had, 3, 3 boys. And, we were looking at an enzyme related to breaking down oxalates. Now, the mother and father each had one SNP, and that’s called heterozygous. Three boys, and they all come together, they’re Amish boys, they’re a lot of fun. And I looked at their genomes, and the one boy didn’t have any SNPs at all. And one had won. And the other one had two. Dr. Deb Muth 00:16:41 Interesting. Bob Miller 00:16:42 So, we don’t quite know how these things get handed off, but with the parents each having one, you could have a child with none, one, or two. So, the one, his ability to break down oxalates, which is fine. The other one was slightly impaired, and the other one was dramatically impaired. So, you can have 3 children, and it all depends what the parents have. Now, if a parent has a homozygous, or 2 copies. And the other parent has nothing. Every child will have one. Okay. If both parents are homozygous, that they both have two, Every child will have two. Dr. Deb Muth 00:17:19 too. Bob Miller 00:17:20 Yes, so that’s the way it works, but, you know, but it’s somewhat rare that both parents are homozygous on an enzyme, but it can happen. Dr. Deb Muth 00:17:27 Do we think that infections today, like Lyme disease or mold exposure, things like that, if the parent, the woman, primarily, I’m thinking, is pregnant, and she actively has these infections. Can those infections affect the genetics, kind of like a past sexual transmission did where we thought back in the day? Bob Miller 00:17:47 Yeah, I… I mean, I’m not that much of a geneticist to answer that for sure, but my thought would be no, that at conception, the pattern’s made. Dr. Deb Muth 00:17:55 Okay. And then that’s… that’s the hand you’re dealt. Bob Miller 00:17:58 Yeah. So, I tell people we have good news and bad news. The good news is we can compensate for the weakness. The bad news is we can compensate for the weakness. Dr. Deb Muth 00:18:09 That is so very true. Bob Miller 00:18:11 Yeah, we can’t, because I often get asked, so we’ll do some things now, and we’ll check my genes again, and they’ll be better. It’s like, nope. Dr. Deb Muth 00:18:18 Oh, – – Bob Miller 00:18:19 You gotta play the hands you’re dealt, so… Dr. Deb Muth 00:18:21 That’s right. Bob Miller 00:18:22 You can test your genetics… if you’re looking at the same enzyme, you can test it every year. It’s not gonna change. It’s like the blueprint. Dr. Deb Muth 00:18:30 It’s good and bad, right? It’s the one test you only have to do once in your lifetime. Bob Miller 00:18:34 No, unless, you know, like, our. Dr. Deb Muth 00:18:36 All the time. Bob Miller 00:18:37 Yeah, now our test looks at, called the Functional Genomic Analysis Test of your genomic Resource. We look at 220,000 steps. Dr. Deb Muth 00:18:46 Wow, that’s a lot. Bob Miller 00:18:47 That’s not all of them. Dr. Deb Muth 00:18:49 Right. Bob Miller 00:18:50 So, maybe in the next year, we’re gonna come out with our third version of the chip. And then, if someone wants to get those new things that weren’t on it, they’d have to repeat. But whatever we measured is gonna stay the same. Dr. Deb Muth 00:19:03 That’s a lot of SNPs to look at. Bob Miller 00:19:05 Keeps us busy. Dr. Deb Muth 00:19:06 But there’s still, but there’s still SNPs that we. Bob Miller 00:19:09 That we’d like to have that we don’t have, so… Bob Miller 00:19:11 We started out with version 1 on our genetic test, then we worked with version 2, and we’re already compiling a list of what version 3 would look like. So if somebody has our version 2, And we’re saying, you know what, it’d be nice if we could see these, well, then you’d repeat, but it won’t change what you already know, so… Dr. Deb Muth 00:19:29 Got it, got it. So, when you started out, and you started looking at the research of Lyme disease and chronic infections, which detox pathways are most important for people who struggle with those conditions? Bob Miller 00:19:43 Okay. You know what might make sense as we do a screen share, and I’ll actually show you the pathway. Does that make sense? Bob Miller 00:19:48 Alright, so… let’s see if I… let me just press the share… Dr. Deb Muth 00:19:52 Yep, you should just be able to press share. Bob Miller 00:19:54 And… number 2. Okay. Are we seeing the screen there? Bob Miller 00:20:01 Okay. Dr. Deb Muth 00:20:02 So, this is a map that we made. Bob Miller 00:20:05 And by the way, this is not… All-inclusive of all the things we look at, but we believe this is a core issue. So, where we’re going to start here, there’s something called the microglia. And the microglia are glial cells. They’re in the brain and the central nervous system. And they’re very interesting little creatures, because most of the time, and this is just a drawing of what they sort of look like. Most of the time, they’re in what’s called the M2 anti-inflammatory mood. What that means, these little guys pick up dirt, debris, Recycle them. Turns on an enzyme called interleukin-10 that’s anti-inflammatory. And just kind of does general housekeeping. And just kind of does general housekeeping. However, when a trigger comes along. However, when a trigger comes along. They… it’s the same glial cell, but it moves over to a very pro-inflammatory enzyme. A pro-inflammatory glial cell. And it triggers these 3 enzymes, Actually, these four. That are pro-inflammatory. Tumor necrosis vector alpha, Interleukin-6. NF Kappa B, Inos. Now, these create inflammation. So you might think, well, why is that good? Well, if you have some foreign invader, virus, bacteria coming in, parasite. If you didn’t have these guys coming to the rescue, you would just die of infection. So, these guys are your friend unless they’re your worst enemy. Because TNFA, and we’ll show you when we actually do a demo account, TNFA can be overactive. So, in other words, it over-responds. Interleukin-6 can be overactive. And if Kappa-B can be overactive. The INOS, and I’ll explain each of these as we go through a demo, can be overactive. Now, what that means is, you’re very good at killing virus and bacteria. But this is where autoimmune disease comes in, and just inflammatory conditions. Now, this is just speculation, but we think what happened is, as you know. Thousands of years ago, we didn’t have refrigeration, we didn’t have sewer, we didn’t have pure water, and we didn’t have antibiotics. So, if you made it to 40, you were an old-timer, because everybody was dying of infection. So, what we believe happened is, by what’s called natural selection, Having these overactive. A thousand years ago was to your advantage. Dr. Deb Muth 00:22:31 Hmm. Bob Miller 00:22:32 But now… We have pure water, we have refrigeration, we have sewers, we have antibiotics. But now we have environmental factors that are stimulating them. Now it’s to our disadvantage. And we’ll talk about that a little bit as it relates to the hemochromatosis genes and maybe the G6PD. Dr. Deb Muth 00:22:48 Yep. Bob Miller 00:22:49 Now, why are we becoming so inflamed? Let’s look at the triggers. Now, one of my, favorite expressions is. I was born all the way back in 1954. Dr. Deb Muth 00:23:01 And it was a different world back then. Bob Miller 00:23:05 These are some of the triggers. And we’ll get into these, but right now, high fructose corn syrup, And the high-fat diet. High fructose corn syrup only came about in 1968. So now we’re being exposed to high fructose corn syrup. Then… we didn’t have these, these viruses like COVID. Dr. Deb Muth 00:23:26 Yeah. Bob Miller 00:23:27 Now, there’s now pretty strong evidence that COVID Was actually, you know, made as a gain of function. It’s debated, and I’m not taking an opinion on it, but there’s some people who believe Lyme disease was also a part of experimentation. Dr. Deb Muth 00:23:40 Go. Bob Miller 00:23:41 Then we have molds, and it appears as though mold is getting stronger. you know, 20 years ago, when I was seeing folks, mold wasn’t on the radar. I would say 7 out of the 10 folks we speak to today have mold problems. Yeah, 20 years ago, we talked more about mold allergy being an issue versus mold toxicity being an issue. Right. So… I know some folks are, you know, speculating what’s happening, but one of the theories out there is that EMF is strengthening mold. I don’t know if you ever heard that theory, and I don’t… Dr. Deb Muth 00:24:13 I have. Bob Miller 00:24:14 I’m not claiming it’s true, but it’s an interesting theory. Then even, you know, your black mold from water-damaged buildings. Then our air pollution is getting worse. We’re getting more toxic metals. Dr. Deb Muth 00:24:26 You know, if we have a… Bob Miller 00:24:27 You know, we’re gonna look back someday and say, what were we thinking, smearing aluminum into our armpits? The, what were we doing putting mercury in our teeth? Then, you know, glyphosate. When I was a kid, there was no glyphosate. So, all of these herbicides and pesticides. Polychlorinated biphenols, And then EMF. So, we love our cell phones, you know, and I think unless you, or in the middle of the desert, or down in a cave, you’re being exposed to EMF somewhere. So, you know, we have our cell phones with us, we have, We have Wi-Fi, the towers are everywhere. And we don’t know long-term, but we may find that this can… this creates some inflammation. And I don’t know if you get any folks, but do you have any folks that have… are they EMF sensitive? Dr. Deb Muth 00:25:16 Oh yeah, we have a whole bunch of them. Bob Miller 00:25:18 Yeah, and then if you have any TBIs, So, plenty of things here. that will stimulate into the microglia, M1. Now, you could say, well. We’re all pretty much exposed to the same thing. Why do some people get hit harder than others? So here’s where we’re gonna start. There’s an enzyme called Nrf2 and RF2. And Nrf2 is the enzyme that senses when there’s inflammation. And turns on hundreds of anti-inflammatory enzymes. We’ll show when we do the demo, you can have genetic weakness on NERF2. And NERF2 inhibits and slows down microglia M1. supports M2. Now, if it’s not complicated enough, there’s an enzyme called KEEP1. And KEEP1 inhibits NRF2. And you can actually have gain of function on keep 1, that makes Keap 1 stronger. So… A lot of the people who land on my doorstep So… A lot of the people who land on my doorstep Both parents gave a mutation on KEEP1, making it overactive. Both parents gave a mutation on KEEP1, making it overactive. Dr. Deb Muth 00:26:31 Hmm. Dr. Deb Muth 00:26:31 Hmm. Bob Miller 00:26:32 Suppressing Nrf2, nerve 2 might be weak. So, nobody’s putting the brakes on, M1. And by the same token, Nerve 2 supports M2. Then there’s a process called mTOR and autophagy. mTOR stands for mammalian tard of rapamycin, the growth of new cells. And then autophagy, taking our dead cells and recycling them. We need a balance between the two of them. If we didn’t have mTOR, the sperm and the egg would never become the baby, the baby would never become the adult, we wouldn’t make new cells. But our cells are constantly, you know, the old cells dying off. Autophagy is where we take that debris from the cell and recycle it, just like a farmer Plows the crop under at the end of the year. The dead plant then becomes the fuel for the spring, your dead cell becomes the fuel for the spring, and that’s autophagy. So we’re gonna look back someday and say, what were we thinking? We give our animals growth hormones so they get fatter faster. Oh my. So, we consume those animals, and inventory runs faster. Now, for anybody who’s, You know, maybe above 40, 45 years old. Think back when you were 12, and what did girls look like? They were primarily flat-chested little girls. Now they look like 16-year-olds. Because environmentally, we’re jacking up mTOR. So, mTOR stimulates microglia M1, suppresses microglia M2. Probably 80% of the folks we visit with. This is the part of the problem. NRF2 is weak. mTOR is strong. Environmental factors come along. And this guy gets carried away. He doesn’t do that burst and move back. Stays here. We’re calling that How environmental factors create a locked-in, pro-inflammatory. and neurotoxic phenotype. In other words, once it starts, it just keeps… Feeding upon itself. Alright, so what happens now when microglia is overactive. it triggers these 3 enzymes, TNFA, N of kappa B, And interleukin-6. Each one of these can have genetics that make them run stronger. Then it stimulates an enzyme called NLRP3, Which makes what are called inflammasomes. Now, guess what inflammasomes can be? Your best friend or your worst enemy? Because they will, if you’ve got, again, a virus or bacteria, or possibly even some bad cells in the body. They will zap them. Well, that’s good. Unless it’s overactive. Unless it’s overactive. And then what it does, through interleukin-1 beta, makes excess glutamate. And then what it does, through interleukin-1 beta, makes excess glutamate. Anxiety, gut inflammation, OCD, ADD, autism. And, you know, glutamate, we’ll talk about that a little bit, but glutamate makes you intelligent, highly motivated go-getter. but can also be excitatory. And then, look what it does. Let’s see, do I have the drawing tool here? Yes, I do. Okay. So, it comes down through here, Makes the glutamate. Comes back up through here. through the ADORA 2A enzyme, Then we’ve got a feedback loop that feeds upon itself. Then, through interleukin-18, we make histamine. and mast cells. And then through histamine receptor site number 1, we come back and spin it. And now you’ve just got this spinning feedback loop. So, the glutamate will make you anxious, the histamine will give you allergies and make you anxious. And you’re allergic to everything, and you’re feeling horrible. Now, it doesn’t end there, Dr. Dad. It then goes on to make something called gast dermins that creates pyroptosis, where it actually starts punching a hole in the cell membrane. And you’re only going to be as healthy as your cells are. Just a little background. You know, we’re made up of trillions of cells, and each one of them has what’s called a lipid bilayer, made from lipids, which comes from fats. And you’re only going to be as healthy as those membranes are. So that’s why we coined an interesting phrase. Cellular CPR. Construct the cell. Protect the cell. And restore the cell membrane. And we believe that’s going to be revolutionary in the functional medicine world. So… It’s not hard to figure out that if you start punching holes in the cell membrane, that’s not a good thing, okay? Bob Miller 00:31:22 Now… There’s an interesting molecule called NAD. Thicotide adenoside dinucleotide. And anybody who’s in the, you know, listening to the health podcasts and things, they’re… They’re, they’re learning about NAD. And I’m going to show you a chart later, all the good things that NAD does, but For the most part, it helps what’s called sirtuins. And sirtuins are quite interesting. If anybody’s looking at longevity. The sirtuins is where they’re looking at.Because sirtuins turn on good things. Turn off bad things. And I’ll show some charts on that later. So for right here, this sirtuin uses NAD, to slow down NF-kappa-B. CERT 2 uses NAD to slow down an ORP3. So, if we’ve got genetic weakness on these, or we don’t have enough NAD, We don’t hold this pathway back. Make sense? Dr. Deb Muth 00:32:24 Yeah, makes perfect sense. Bob Miller 00:32:25 Now, I’ll show this a little bit later. So, people are like, oh, well, I’m gonna start taking some NAD. Dr. Deb Muth 00:32:31 Right. Bob Miller 00:32:32 And there’s functional doctors who give NAD intravenous. It was just this morning, I was talking to a woman who said, Oh my gosh. I went and got intravenous NAD, and it took me a month to recover from that. Dr. Deb Muth 00:32:45 Hmm. Bob Miller 00:32:46 what happens is, and I’ll show this in a little more detail, there’s an enzyme called CD38, that’s stimulated by NF-kappa-B. And it takes NAD, To make intracellular calcium. that stimulates NLRP3 and actually makes things worse. So, if we have this guy upregulated, and I’ll show a chart what does that. taking NAD will make you worse. Again, when I go into the software, I’ll show you that whole pathway, so… I would encourage people, you know, just don’t go out and start taking massive amounts of NAD, you know, stick your toe in the water, see how you do. Because everything you’ve heard about, how good it is, is true, unless this guy says, oh, thank you very much, let me make more inflammation. Now, this might be part of our innate immune system, that if we have some pathogen that’s gonna kill us. By golly, we want that to happen. But if this is happening by environmental factors, Then it’s detrimental. So the immune system that protected us a thousand years ago now might be turning on us because of the environmental factors that we showed earlier. All right. Then there’s an enzyme called PARP that’s NAD-dependent, and that actually repairs strain breaks in your DNA. Now, the next thing that happens… is there’s an enzyme called NADPH oxidase that gets stimulated. and something called INOS. Now, I’m sure most people know about nitric oxide. It’s a gas that dilates your blood vessels. That’s why sometimes they’ll even give people drugs, nitroglycerin, to boost their nitric oxide. That’s why people are doing beetroots and other things to boost their nitric oxide. But there’s an OS3 enzyme that makes the nitric oxide that’s good for blood flow. But there’s an INOS That makes nitric oxide to kill pathogens. probably might be the third or fourth time I’ve said this. That’s a good thing, unless it isn’t. So, if it’s killing some pathogen, great. It was just misfiring. it combines… With superoxide that’s made by this enzyme, and makes something called peroxynitrite, which is one nasty free radical that chews you up and spits you out. So, the NOx enzyme, NADPH oxidase, uses NADPH, To make this free radical called superoxide. If we have time, we’ll get into it. NADPH is what your body needs to recycle your antioxidants.So, I coined the phrase, the NADPH steel. Where the NOX enzyme takes this very important NADPH, And rather than being useful, makes superoxide. Now, again, is that fine if you’ve got some bacteria to kill? Of course. But if it’s just chronically running, it’s just making all this chronic inflammation. Then it makes something called hydrogen peroxide. And we need to clear hydrogen peroxide by 3 enzymes, catalase, thyroid reduction. And glutathione peroxidase. If we have genetic issues on here, or we don’t have the cofactors. There’s something called the Fenton reaction, discovered in 1895 by Dr. Fenton. Where hydrogen peroxide combines with iron to make what are called hydroxyl radicals. And guess what they do? They create lipid peroxides, That damages your cell membranes. Now, again, the body’s pretty darn amazing. We have glutathione, And here’s where your body’s taking glutathione and recycling it. But look who’s needed to recycle it. NADPH. So, if this guy up here is chewing it up, We don’t recycle our glutathione. And then an enzyme called glufon peroxidase 4, Takes this damaged lipid and repairs it. So, here we’ve got this protecting, we want to protect it by not having this happen. But then we also need this guy to do the restoration. So, there’s a lot that can go wrong in here, Dr. Deb. Dr. Deb Muth 00:37:07 There’s a lot that could go wrong. And I can imagine some of my listeners are thinking that lipid peroxidase, is that the same thing as what they’re thinking of when we talk about lipids and cholesterol? Is that the same process that’s happening there? Bob Miller 00:37:22 Well, no, no, the lipids can be used to make cholesterol, but here we’re talking about where they’re going to build the cell membrane. And they’re being… and they’re being, destroyed. If anybody would like to see a visual representation of this, just go on YouTube. And type in, ferrooptosis Animation. cool little video, it’s about 3 minutes long, and it shows the lipids coming over, being oxidized, and now GPX4 fixes them, so… YouTube, Pharaoptosis Animation, cute little video. It’s just that really… Shows vividly what we’re… what we’re talking about here. Now, this is… Dr. Deb Muth 00:37:59 And so this is very common, too. Like, a lot of people do hydrogen peroxide IVs. Dr. Deb Muth 00:38:04 And so, if somebody doesn’t know their genetics, they could have a problem with doing those, just like they could doing the NADHIVs, correct? Bob Miller 00:38:13 Sure, yeah, yeah, yeah. So, I’ve talked to so many, you know, of course, the hydrogen peroxide kills pathogens. I mean, that’s what it does. So… but I’ve spoken to so many people that said. I had one client that said they’ve never been the same after having one hydrogen peroxide infusion. Dr. Deb Muth 00:38:30 Interesting. Bob Miller 00:38:31 Yeah. So… it can be… I see why people use it, because it. Bob Miller 00:38:36 pathogens, But on the other hand. And now’s a good time to speak about… I don’t have it on here, but there’s a, there’s an enzyme called the HFE gene. And that is what causes you to absorb iron. And there’s mutations in it that cause something called hemochromatosis. Were you overabsorb iron? Now, true hemochromatosis is when both parents give you a mutation. But there’s now growing evidence even a heterozygous can cause a little bit more iron absorption, not to the human chromatosis point, but overabsorption. So, if you overabsorb iron, And you have too much hydrogen peroxide that’s not cleared, All kinds of inflammation. Now, what’s happened is sometimes this inflammation Will damage the red blood cells. And some well-meaning doctor says, oh, you need some iron. And they take iron and it makes it worse. So, can’t tell you how many people I’ve said, you’ve got the overabsorption of iron, and they say, well, that can’t be right, because I’m low in iron. Well, that could be because it’s being chewed up here. Dr. Deb Muth 00:39:40 Sure. GPX1 and TXN turn it into, to water. The, catalase turns it into water and oxygen. Dr. Deb Muth 00:39:58 Now, I see a lot of my clients who have mutations or SNPs on that GPX gene, on that glutathione gene. And they really struggle to clear a lot of their toxins. Bob Miller 00:40:12 Sure. Dr. Deb Muth 00:40:14 Yeah, absolutely. Well, GPX4. Bob Miller 00:40:18 is what, repairs, but you can see GPX1 Is what uses glutathione. To turn hydrogen peroxide. So, but it all depends upon having enough glutathione. Dr. Deb Muth 00:40:30 Yeah. Bob Miller 00:40:31 Well, guess who controls making a glutathione? Dr. Deb Muth 00:40:34 Nerf 2. Bob Miller 00:40:37 So, if you have a keep one weakness, or strength to two… I’m sorry, keep one is too strong. Nrf2 is too weak. You don’t make glutathione. So, when a lot of people do that, it’s like, well, I’m gonna take glutathione. Dr. Deb Muth 00:40:51 Right. Bob Miller 00:40:52 And some do great, and some do poorly. You know, because… and I’ll show this on one of the other charts. You can see here that the, The glutathione has to be recycled. And if we don’t recycle it, it actually turns into superoxide free radical. So… NADPH are the cofactors, For taking the oxidi… here’s oxidized glutathione, here’s reduced. So, this is a good glutathione. After it does its job, you can see it becomes oxidized.We need to recycle it. Well, if we have weakness on the enzyme that does that, or a weakness in Nrf2, or not enough NADPH. The oxidized glutathione never gets recycled. So, I’ve talked to a lot of people who said, oh, glutathione made me so sick, and say, well. Dr. Deb Muth 00:41:43 Yeah. Bob Miller 00:41:44 You need it, but you need to recycle it. Dr. Deb Muth 00:41:46 Can you speak for just a brief moment, too, about MTHFR? That is a very popular gene, it’s all over social media as the major gene, but can you speak to a little bit about that, and how that fits into this whole process of things? Because it is just such a small piece. Dr. Deb Muth 00:42:04 understanding genetics. Bob Miller 00:42:06 Yeah, to be honest, it drives me nuts. Dr. Deb Muth 00:42:08 Me too. Bob Miller 00:42:11 Alright, so… You know, there are people on social media I won’t say what I think, I’ll be kind. But… But the, And, you know, they might mean well. But they talk about, if you have MTHFR and COMT and PEMT, that’s… oh my goodness, that’s horrible, and we’ll fix that for you, and you’ll be fine. Bob Miller 00:42:36 it just irritates me to no end. And it really could get anybody who’s doing this legitimately in trouble. I mean, I’m afraid someday, you know, there might be some cracking down on this kind of nonsense. Now, to answer your question about MTHFR. Dr. Deb Muth 00:42:51 I mean, it really is, but I’ll tell you what, why don’t we hold that thought until I go to another map and I can actually… Okay. Bob Miller 00:42:56 But the real… the cliff notes is the MTHFR puts a methyl group on your folate, which is needed, but it has gotten way, way, way too much attention. And people learn they have MTHFR, and they start taking a multivitamin with methylfolate, then they take a B vitamin with methylfolate. Dr. Deb Muth 00:43:13 And they’re pushing it too hard. Bob Miller 00:43:15 Yeah. So I can’t tell you how many people I’ve helped by saying, stop it. Dr. Deb Muth 00:43:20 Yeah, take less of it. Bob Miller 00:43:21 Take less of it, yeah. So, yeah. Yeah, there’s a… If somebody, say, ranked the enzymes at their level of importance, MTHFR might be 40 or 50 on a scale of 100, you know. Keep one Nerf two. big deals. Dr. Deb Muth 00:43:40 deals. Bob Miller 00:43:41 NQO1 that I didn’t even talk about yet, NQO1, takes your, NA… your NAD goes into NADH, To make electrons for the electron transport chain. you need NQ01 to bring that back. If that’s not working, and I’ll show you on the NAD map how disastrous that can be. Now, the next piece is here, and I think You know, if you talk to any school teachers and say, if you’ve taught for more than 10 years, how are the kids today? Every one of them says, more ADD, ADHD, more autism. Just look at human beings, we’ve never been so agitated. You know, everybody, and it might be a social media thing, but people take a position on something, and if anybody doesn’t share that position, they view them as the enemy. Dr. Deb Muth 00:44:29 And it’s kind of scary what’s happening to us. Bob Miller 00:44:33 So, we can’t agree to disagree anymore. We see anybody who has a differing opinion as the enemy. And, you know, there was… there’s people that didn’t have Christmas dinners together, because they had political differences, like… Dr. Deb Muth 00:44:44 Excuse me. Bob Miller 00:44:45 can’t you put your political differences aside to have Christmas together, you know? Dr. Deb Muth 00:44:49 Right? Bob Miller 00:44:50 become that, you know, no matter what your position is, and I’m not saying anyone’s right or wrong, I’m just saying. You know, in the old days, they used to say that the Republicans and Democrats in Congress would argue policy and then go have dinner together. And now everybody’s all up in arms, angry. Dr. Deb Muth 00:45:05 Yeah. Bob Miller 00:45:06 So… There’s likely multiple reasons for that. But let me show you one of them. That, you know, to what degree this is… very important, we don’t know, but I think We’re beginning to believe this is very important. So, there’s something… there’s a neurotransmitter called GABA. And God buys the don’t worry, relax, be happy. Chill. Okay. Dr. Deb Muth 00:45:31 Nobody has enough of that anymore. Bob Miller 00:45:33 Well, yeah, you’ll be surprised what I’m gonna show you. So, let me see if I can find a, Let me see if I can find the right slide here. Let me look for it here. So, there’s something called a GABA receptor site. And here you can see… This is a neuron, and this is where you, The neuron normally is excitatory. However, there’s normally low chloride in the neuron. Dr. Deb Muth 00:46:09 Hmm. Bob Miller 00:46:10 So, GABA itself is neither relaxing. For excitatory, all GABA does, it opens up what’s called a chloride channel. And then chloride, which has a negative charge, will flow into the neuron. Follow me there? Dr. Deb Muth 00:46:26 Yep. Bob Miller 00:46:27 And as it does, it changes this from a positive charge to a negative charge, And it’s relaxing. and inhibitory. Dr. Deb Muth 00:46:34 Hmm. Bob Miller 00:46:36 Now, on the other hand, there’s enzymes called NKCC1, That will push chloride in. and KCC2 that will bring chlor… oops and bring chloride out. And then there’s a sodium channel. And, sodium has a positive charge. And glutamate will push that in. So, as long as this is happening. And GABA says, receptor sites, open, chloride goes in, Chill. However, If NKCC1 Pushes extra chloride in. KCC2 doesn’t pull it out. and GABA hits the receptor site, the GABA comes flowing out, Sodium comes in, And now it’s excitatory. So Gabba didn’t change. GABA just opened the receptor site, that’s all it does. Dr. Deb Muth 00:47:33 Yeah. Bob Miller 00:47:34 But it’s the chloride balance that’s going to determine whether this is relaxing or not. Now, these are the things that go along with when they lose that KCC2 or gain NKCC1. Pain and sensitivity, burning electrical, neuropathic pain. Normal touch hurts. Sound and light sensitivity. Tinnitus can flare. Headaches and migraines. Seizure tendency. Body jolts. Spasticity, cramps, stiffness, startle reflex. Trouble falling asleep, non-restorative sleep. Anxiety, stress, reactivity, that’s what we have now. Hyperarousal, panic-like surges, irritability, racing thoughts. Brain fog, slowed processing, working memory slip-ups. Mental fatigue. Episodes of racing hearts, sweaty palms, guts on edge. Those are all the things that happen when this GABA switch occurs. Now, here’s what happens, and this is what I’m going to be presenting at an autism conference. When you have a newborn, they need that NKCC dominant to develop. By early childhood, it should… or, sorry, early adulthood. we should move over to the KCC dominant, that’s the taking the chloride out. Nice-looking 25-year-old boys, functioning very well. However, when we get microglia M1 upregulated. Because of environmental toxins, processed foods, Tylenol, aluminum. they stay in NKCC1 dominant, and there’s ADD, ADHD, Autism, the whole spectrum. because… They’ve not moved over to the… They’ve not moved over to the KCC2. And again, this is caused by… Environmental factors. Stimulating the microglia. And then, interleukin-1, interleukin-18 weakens KCC2, interleukin-1 beta, Strengthens NKCC1. high chloride. We open up the chloride channel, In Rebell Excitatory. So, I think when, When the pediatricians get ahold of this, they’re going to be very excited to know that This could be why we’re seeing such a rise, and not just autism, but ADD, ADHD, anxiety, the whole shit mess. Dr. Deb Muth 00:49:58 thing. Bob Miller 00:49:59 Yeah, so… and you can see NF-kappa-B stimulates that. These stimulate it, and I think that’s why everyone’s getting so anxious. Now, there’s a little bit more to it, and we’ll get into this when we look at some of the maps, but… The, the glutamate, Which is excitatory. will stimulate the NMDA receptor, make more glutamate, And glutamate will inhibit KCC2. And then we also need an astrocyte To, take both ammonia And glutamate, and… Turn them back into glutamine. And I’m going to talk to you a little bit about arachidenic acid, and if we have too much arachidenic acid. or TNFA is upregulated, that doesn’t happen. Ammonia goes up, and there may be multiple reasons for this, but this is a reason why some of the autistic kids do flapping. Dr. Deb Muth 00:50:49 Hmm. Bob Miller 00:50:50 Because they’re not clearing their ammonia. And you can tell if somebody has high ammonia by… they get that old person smell, you know. Dr. Deb Muth 00:51:00 Yup. Bob Miller 00:51:01 your vehicle cycle’s not taking out the, the ammonia. Now, last pathway here. There’s growing interest in mast cell activation. So, back here, we talked about peroxynitride. And that will stimulate mast cells, and those are white blood cells that are your best friend, unless they’re your worst enemy. Then it’ll make histamine. And there’s enzymes called histidine decarboxylase that’ll make more. Dr. Deb Muth 00:51:28 I’m sure everybody’s heard of DAO, the enzyme that degrades histamine. Yep. Bob Miller 00:51:31 We can have genetic weakness, we don’t make that. There’s an enzyme called histamine and methyltransferase, That, That breaks down the histamine. Then if we don’t do that, it’ll get stuck in the histamine receptor site. And then it’ll make something called, renin. Which will cause angiotensinogen to turn into angiotensin. One, that turns into angiotensin II,And that’s where people make aldosterone, where they’ll get the, The swollen ankles and high blood pressure. But interestingly, there’s an enzyme called ACE2, that takes this guy and turns it into angiotensin 1-7, Which is anti-inflammatory and also inhibits… TNFA. Now, you can have weakness on ACE2, But… and anybody’s saying, that sounds familiar? Dr. Deb Muth 00:52:25 That’s where COVID comes in, using ACE2. Bob Miller 00:52:28 And now we just found there’s literature that if you get COVID long enough, it can actually make ACE2 not be able to work as well. So look what it does. It comes down here, stimulates the NADPH oxidase, More superoxide. More peroxynitrite. And we’re on a cycle here. We’ve actually named this the Home Cycle Hypothesis, the proposed feed-forward loop. That just keeps feeding on itself. All being caused by… Primarily, The environmental factors. But hitting those who have genetic weakness the hardest. That’s why. Dr. Deb Muth 00:53:08 To the people. Bob Miller 00:53:09 Don’t live in a moldy house. One person is sick as can be, and the other person says, well, you must be imagining things, because I don’t feel anything. Dr. Deb Muth Yeah. Same thing with long haul, right? Two people can both get sick, one gets sick and never seems to recover, and somebody else gets sick, and they have absolutely no problems with it at all. Bob Miller 00:53:30 Sure. Well, think about it, if you get COVID, and ACE2 is weak, and some of this other stuff is going on. This thing just starts feeding upon itself. Dr. Deb Muth 00:53:38 Keep creating more inflammation, more complications, nothing’s calming down. Bob Miller 00:53:43 Yeah. Now, you, you ask about, MTHFR. So, this is the, this is the, the software called Functional Genomic Analysis. There’s a demo report we have. So, let’s talk a little bit about, MTHFR. So, we actually have a map called a methylation map. Now, what happens is, when you do your saliva test, you, you know, you spit, you put some saliva. in a collection kit, goes to a lab, takes out the DNA data, sends it to the computer, and now you can actually see it visually. Okay. So, it’s gonna take a second for this, data to load up, it’s, and each of these Circles, each of these ovals, is an enzyme. And the data gets loaded up to see where it is. So, until it gets loaded up here, I didn’t preload this. There it goes. So… The primary thing about methylation is There’s a nasty substance called homocysteine that, if it’s too high, can really be detrimental. The body takes methylfolate, and combines with methyl B12, To bring this back up to methionine. And then through the MAT genes, we make SAMI, S-adml methionine. Which is involved in so many processes. Then after it does its thing, it turns back into homocysteine. And this thing needs to keep spinning around. That’s why, you know, it’s a good idea to keep homocysteine at, do you have a number that you’d like? 7, 8? What do you like for a number? Dr. Deb Muth 00:55:24 Yeah, I like mine below 7. Bob Miller 00:55:26 Yeah. So if the homocysteine goes too high. It, caused all kinds of problems. So, here’s where you ask about the MTHFR. So, here you can see on this individual. I click on MTHFR, and you can see it comes up here, here’s the C677. And you can see here where it says, variants. I’ll… I’ll draw in case somebody’s having a hard time seeing that. So, you can see there’s nothing in there. That means there’s no genetic mutations. If one parent would have given a mutation, there’d be a 1. If both parents did, there’d be a 2. Now, here’s why Yes, methylation is important, I’m not saying it isn’t important, but look at this MTHFRC677. In my software. Only 42.5% of the population does not have a mutation. 44.7% have won. 12.9 have 2. So, this isn’t some rare, oh my god, I’m gonna die… Kind of thing, yeah. Dr. Deb Muth 00:56:27 Right. Bob Miller 00:56:28 So, And then what happens is that, and again, I’m not dismissing methylation, I… we could do a whole show on methylation. Bob Miller 00:56:36 get it. But I think that what people are doing is they’re, they’re learning about MTHFR, they get it measured, they panic. They start taking massive amounts of methylfolate, which many times is to their detriment. Dr. Deb Muth 00:56:50 Well, it’s… and isn’t it true, too, with MTHFR, like, you have to also look at MTR, MTRR, and the more we stack up of those, the more complicated than MTHFR can be. It’s not… it’s not as simple as just saying MTHFR 677 versus 1298. It’s more complex than that, kind of like what you’ve already shown with some of the other things. There’s more to it than just that one little sliver. Bob Miller 00:57:17 Oh, sure, well, let’s take a look. So, remember I said there’s a cofactor? One of the cofactors is called FAD. Just a Bob Miller observation, that’s all. But when people have trouble with their riboflavin and they don’t have enough FAD, They’re doing much worse than people who have just a C677. So, right here, you could have perfect C677th. And if you don’t have the cofactor, it’s not gonna work, okay? Dr. Deb Muth 00:57:48 And as you said, there’s an MTR enzyme. Bob Miller 00:57:51 that takes methylfolate and methyl B12, to spin it around. So, here on this individual. here’s your… here’s your B vitamins, or I’m sorry, your B12s. There’s an enzyme called TCN1 that takes it from the stomach into the blood. Then there’s other enzymes that take it from the blood into the tissue. And if you’re having trouble here. Well, then you’re not going to have this working, so… Even if you don’t have MTHFR, And you have MTR, like this, no, I’m sorry, this person doesn’t. But they have the MTRR, and then they don’t have enough B12, this isn’t gonna work, aside from that. And then there’s a middle pathway. And then there’s enzymes called the MAT1. they take the methionine to the salmon. If that’s not working, we stick… we get stuck in methionine. So, it’s, it’s not just an MTHFR. And then, one of the things that people forget about. is through these CBS enzymes and CTH, We make cysteine, which is needed to make glutathione. The master antioxidant. So, it really is that… I call it the, The 3D chess game played underwater. Dr. Deb Muth 00:59:07 It really is. I mean, I see people who have CVS, COMT, glutathione, MGHFR genes. And some of them function just fine. Like, they have Like, I look at this person and I’m like, oh my gosh, I don’t know how they’re functioning because they’re double mutated on so many pathways, but yet they don’t have a lot of symptoms, they don’t have a lot of complications. Somehow their body has figured out a way to adapt to what it has so it can stay alive and it can function at a high functioning level. Bob Miller 00:59:36 Yeah, and they may be, you know, eating right? Yeah. Staying out of a moldy house. reducing stress. So, it’s diet, it’s stress, it’s genetics, environmental factors. So, yeah, we can’t just say somebody’s gonna be good or somebody’s gonna be bad. You know, some people get scared, oh, I got all these, it’s like, well… Bob Miller 00:59:56 Are you living in a moldy house? You know, and if you live in a moldy house and your glucuronidation pathway doesn’t do well, or if you’re, you know, a smoker, or you’re constantly eating junk food, I mean, all. Bob Miller 01:00:07 things come together. Although, you know, when we focus on genetics, we’re well aware that this is just a piece of it. You know, you could have identical twins, Genetically, and if one… Is exposed to mold and smokes and drinks and stressed out. They’re gonna be a whole lot sicker than their sibling. Bob Miller 01:00:28 Yep. Dr. Deb Muth 01:00:29 Yeah, it’s that concept of taking twins, and one gets raced with one family, and one gets raced with another family, and they don’t have the same… problems that… that each other have, you know? It’s a very unique situation, we don’t think about that enough. Bob Miller 01:00:44 Alright, so again, genetics loads the gun, environment pulls the trigger. So, if you’ve got a loaded gun, but you don’t have the triggers, you’re okay. Dr. Deb Muth 01:00:53 Yeah. Bob Miller 01:00:54 Yeah. So, remember I said I was going to talk about NAD? So, here’s NAD, and what it does, it turns into NADH. And what NADH does, it, Comes down this pathway, what’s called the electron transport chain. And that makes your ATP, that’s your energy. So, if this wasn’t working, we wouldn’t be alive, because we wouldn’t have energy. So it donates an electron, that’s why it’s called electron transport chain. So, we need NAD, To make this, to make the energy. But remember I said that NQ01, this would probably be, like, on my top 10 list of… Bob Miller 01:01:36 Much more important than MTHFR. This one takes NADH back to NAD. If we’re stuck over here, We’re low in this NAD+, But what happens is, NQO1 also provides CoQ10. And CoQ10 Is what’s needed for the electron transport chain to flow. So if we get too many electrons up here. And they don’t turn them into energy. They make a nasty free radical called superoxide. Okay. Now, NAD plus also makes NADPH, And that is needed. Remember I said we need to recycle our antioxidants. So, if we have a problem with FAD from riboflavin. Yeah, we don’t have enough NADPH, Glutathione’s not getting recycled, and you’re gonna be inflamed. And you take glutathione, you’ll feel worse. There’s another enzyme called thimoredoxin. Same thing, needs NADPH and FAD. And same way with your nitric oxide, there’s an enzyme called NOS3, That makes the nitric oxide that dilates your blood vessels. And if we don’t have enough NADPH or fat, You’re gonna make superoxide. Rather than nitric oxide. Now, remember

Garrett Chaffin-Quiray and Ed Rosa wonder if bears prefer eating old or young white dudes. Bon appétit, Bart!***Referenced media:“The Silence of the Lambs” (Jonathan Demme, 1991)“First Blood” (Ted Kotcheff, 1982)“Glengarry Glen Ross” (James Foley, 1992)“Once Were Warriors” (Lee Tamahori, 1994)“The Texas Chainsaw Massacre 2” (Tobe Hooper, 1986)“Road House” (Rowdy Herrington, 1989)“The Game” (David Fincher, 1997)“LA Confidential” (Curtis Hanson, 1997)“The Ice Storm” (Ang Lee, 1997)“U Turn” (Oliver Stone, 1997)“Boogie Nights” (Paul Thomas Anderson, 1997)“The Sweet Hereafter” (Atom Egoyan, 1997)“The Devil's Advocate” (Taylor Hackford, 1997)“Prometheus Rising” (Robert Anton Wilson, 1983) Audio quotation:“The Edge” (Lee Tamahori, 1997), including “End Title”, “The Edge”, “Rich Man”, and “Deadfall/Bear Fight” by Jerry Goldsmith, https://www.youtube.com/playlist?list=PLoTgadYyOMmYIku-y2NBhrY1nJE4WdBt_“Campfire by the Lake Ambience with Crickets, Owls, Water, & Night Sounds for Relaxation & Sleep” (2021), posted by Calmed by Nature, https://www.youtube.com/watch?v=9nBFKH3qhGE“First Blood” (Ted Kotcheff, 1982), including “Escape Route” by Jerry Goldsmith, https://www.youtube.com/playlist?list=PLA_6nw_SiTT23YKnzHA24tICcBsYJH-b1“Glengarry Glen Ross” (James Foley, 1992)“bolt action rifle sound effects” (2011), posted by MasterHand125, https://www.youtube.com/watch?v=STbDaAgcvsU“Glasses clinking sound #glass #cheers” (2025), posted by @sound_magic73, https://www.youtube.com/shorts/4VuUSk3xGos“Dersu Uzala” (Akira Kurosawa, 1975), including “Journal” by Isaak Shvarts, https://www.youtube.com/watch?v=6zNtQVYyC4M&list=RD6zNtQVYyC4M&start_radio=1

Naujausiame „Basketnews.lt podkasto“ epizode Jonas Miklovas, Karolis Tiškevičius ir Tomas Purlys aiškinosi, kuris pralaimėjo Eurolygos prognozių lažybas ir kokia bausmė vieno iš jų lauks sąskrydyje. Trijulė taip pat aptarė lūžtančias tribūnas Utenoje, „Žalgirio“ skolininkus rūbinėje, NBA finalą pasitikančio Wembanyamos fenomeną bei Šarūno Jasikevičiaus sūnų 14-mečių rinktinėje. Tinklalaidės partneriai: Jon-Chedar – čederio gabaliukai, priversiantys skonio receptorius šokti. Svajonių užkandis ieškantiems kažko gardaus kelionėms, vakarėliams ar vakarui su krepšiniu.  Telia Play. Krepšinis, filmai, serialai – viskas vienoje vietoje. O dabar Samsung televizorius tik 69€ su Telia Play planu MIX. Plačiau. Nealkoholinis alus „Gubernija“.  Tėčiams, mylintiems krepšinį – BN+ narystė dovanų! Įsigyk čia.Temos: Vyrai, paskaičiuokime Eurolygos finalo ketverto pavasario viščiukus (0:00); LOGIN konferencijoje – įstrigę Pauliaus Motiejūno žodžiai (09:17); Milžiniškas anšlagas Utenoje ir istorinis šansas finalo link (16:41); Nekuklios Eglinsko frazės ir filmas apie „Juventus“ (24:30); Europos taurės renesanse – skambūs vardai ir naujas formatas (26:42); Augantys savivaldybių pinigai klubams ir gėda Panevėžiui (31:30); Keisti Čanako priekaištai teisėjams (41:45); „Žalgirio“ skolininkai ir nestebinančios kauniečių pergalių atkarpos (46:10); Kitų Europos grandų atkrintamųjų situacija vietiniuose čempionatuose (48:50); Išspręstas Atamano ateities galvosūkis ir grįžtantis Željko? (51:29); LKL sezono finišo datos, padėsiančios rinktinei (54:06); Pasiteisinęs į ACB atkrintamąsias įšokusio Margo sprendimas? (55:04); Intriguojantis NBA finalas, bilietų kainos Niujorke ir antžmogiško Wembanyamos branda (58:11); Lukui Jasikevičiui – kvietimas į 14-mečių rinktinę ir tėčio aikštės matymas (1:10:56); Aplodismentai „Auksinio proto“ finalą užtikrintai laimėjusiam BN pliusui Benjaminui (1:14:46).

Kanto: “Ni kunvenas”,de Kaj Tiel plu el la kompaktdisko PLaĉas al mi Legado: Heather el Gazetara komuniko “ La 113a Universala kongreso en Kaŭnas en 2028″. Parolado : Brendan pri la trajnsistemo en Melburno kaj Viktorio. Kanto: “La blondulineto” de ĴoMo el la kompaktdisko   Liberecanoj . Legado: Heather 1) el la revuo Esperanto “ Kvaronjarcento […]

Today I do some number swapping, some late night metal detecting, and I talk to an entire family of psycho bitches. This show is all thanks to Billio Dillio and the billions of others who support my shows on Patreon and Spotify and Tim Apple. The opening song is by BarberShopJon on Fiverr. The background music is Black Mages by Emergency Pizza Party. The end song is Wheels by Ghost Rappy. You know, I just watched a trailer for La Brea and it looks kind of cool. I doubt I'll ever watch it, but I would probably like it if I did.LEARN MORE ABOUT THE SHOW: To find out more about the music you hear on this show, visit our page of artists. For a bit of history and a studio tour, this is a good starting page. Request a prank call and find links related to shows at snowplowshow.com. If you're searching for a specific thing said in a show, shitbradsays.com is a great resource for that.SUPPORT THE PLA: For extra weekly shows, subscribe on Patreon, Spotify, or Apple. Get our t-shirts and stickers at our TeePublic store. Get coins, vinyl records, CDs, and more on our Bandcamp page. We also have thing in our Zazzle store in our Spreadshirt store. Buy important things for us at PLA's wishlist or Brad's wishlist, but most importantly, please tell your friends, family, and strangers about all about us.JOIN THE COMMUNITY: Add PLA on Prankcast for live shows, add PLA on Facebook, add Snow Plow Show on Facebook, add PLA on X, add PLA on Tik Tok, add PLA on Bluesky, add PLA on Tumblr, add PLA on YouTube, add Snow Plow Show on YouTube, PLA on Twitch, PLA on Instagram, join a Prank Call Discord, the PLA Reddit, add RBCP on Instagram, add RBCP on X, add RBCP on YouTube, and leave a voice message for the show at 814-422-5309.PLA FRIENDS AND STAFF: Nik Caesar from scary-art.com is the unofficial PLA artist.  Buy PLA designs from Nik's Spreadshirt store.  You might also like the cactus and PLA designs in Laugh Track Matt's store.  Clownsec does a lot of cool things for PLA so go honk the PLAnet.  Watch JIAD's Calls of Mass Confusion and listen to a few of the prank call shows over at World of Prank Calls. Joe DiVita and Vista Blue do lots of music for us, but so do lots of other people, so visit the SPS music page for a very incomplete list.GAME WITH PLA Join us Animal Crossing addicts by becoming our friends on Switch. If you're into GTA5, join the PLA Radio crew.

The Approach Angle Nate Schwartz (@_nateschwartz) and Kyle Bland (@blandalytics) about ERA estimators and how to apply them. The discussion starts by talking about why ERA needs to be estimated. There are so many factors that go into run prevention that make it hard to value a pitcher just on ERA. They first dive into FIP, breaking down why it makes sense to remove balls in play from the equation entirely. This starts the focus on strikeouts and walks as the main identifer across the board. The chat moves to xFIP, which adjusts for league-average home run rate. Next, the two talk about SIERA, and how it's complex compared to the others and is the most predictive. After covering the main ERA estimators, they shift to how xERA is powered by Statcast data, but that doesn't make it more predictive. Finally, they wrap up by mentioning PLA, Pitcher List's scaled stat for pitch level value (PLV) and the players that stand out across these estimators. Articles discussed: The Relative Value of FIP, xFIP, SIERA, and xERA Pt. II, Dan Richards; pFIP: Pitch Height, Launch Angle, and the FIP Framework, Alex Chamberlain; Predictive Classified Run Average, Connor Kurcon; What is PLV?, Nick Pollack Join Our Discord & Support The Show: PL+ | PL Pro - Get 15% off Yearly with code PODCASTProud member of the Pitcher List Fantasy Baseball Podcast Network Hosted by Simplecast, an AdsWizz company. See pcm.adswizz.com for information about our collection and use of personal data for advertising.

Trump heads to Beijing this week for one of the most consequential U.S.-China meetings in years — with trade wars, Taiwan, AI, rare earths, and the fallout from the Iran conflict all hanging over the talks. Alice Han and James Kynge break down what Trump and Xi really want from the summit, why China may have more leverage than many in Washington realize, and how Beijing quietly used globalization to accelerate its technological rise. They also unpack a striking new study showing Chinese investors heavily targeted research-intensive firms across Europe and North America — raising a bigger question: did the West help build the competitor it's now trying to contain? Plus, Xi Jinping's military purge is intensifying. China has handed suspended death sentences to two former defense ministers as Xi continues reshaping the PLA ahead of a more dangerous geopolitical era. They discuss why Xi is trying to build a world-class fighting force while simultaneously hollowing out large parts of its leadership. Also: China Decode will be LIVE this Friday at 10AM ET on Prof G Plus with Kevin Xu to break down the first day of the Trump-Xi talks and what comes next. Subscribe to China Decode on Substack for weekly analysis, livestreams, and deep dives into the biggest story shaping the global economy: chinadecode.profgmedia.com Learn more about your ad choices. Visit podcastchoices.com/adchoices

An island nation only one-third the size of Virginia, Taiwan produces more than 90 percent of the world's most advanced chips and more than 90 percent of the servers powering the AI revolution. And last year, Taiwan became the United States' fourth-largest trading partner—after Mexico, Canada, and China.More than one-fifth of global maritime trade goes through the Taiwan Strait, according to a Center for Strategic and International Studies analysis, and any conflict over Taiwan would be devastating for the global economy—and likely far worse than the economic disruptions caused by the Iran War.Chinese leader Xi Jinping has told the People's Liberation Army (PLA) to be ready for a successful Taiwan invasion by 2027, the PLA's 100th anniversary.In this episode, I sit down with Taiwan's representative to the United States, Ambassador Alexander Yui, to understand why Taiwan matters and what's at stake as the Chinese Communist Party has ramped up its campaign to isolate, intimidate, and encircle Taiwan in recent years.Taiwanese President Lai Ching-te's recent visit to Eswatini—Taiwan's only African ally—had to be abruptly postponed when Seychelles, Madagascar, and Mauritius revoked overflight permissions—presumably due to pressure from Beijing.“They are constantly harassing our naval and air surroundings, trying to create panic and uneasiness,” Yui says.Since 2013, Beijing has built more than two dozen militarized outposts in disputed waters in the South China Sea and has recently been militarizing yet another artificial island known as Antelope Reef.Views expressed in this video are opinions of the host and the guest, and do not necessarily reflect the views of The Epoch Times.