Podcasts about ENAC

Un primer resumen del ENAC (Encuentro Nacional de Arquitectura Comunitaria) en La Rioja, del 21 al 24 de mayo, con fotos, reportajes y comentarios sobre esas valiosas jornadas que compartimos con estudiantes y profesionales de varias provincias.Continuaremos sobre este tema y otros, en los próximos programas.Te invitamos a sumarte a nuestra campaña: 1000X1000! Mil pesos, mil personas.1000x1000 Por la batalla cultural! Sumate y ayudanos a seguir brindándote la mejor programación: https://www.mercadopago.com.ar/subscriptions/checkout?preapproval_plan_id=2c93808495b859210195e9f01ca91b2c

Die italienische Zivilluftfahrtbehörde ENAC hat eine Änderung ihrer Bestimmungen zur Mitnahme von Haustieren in Flugzeugen bekanntgegeben: Ab sofort dürfen Hunde und Katzen in der Kabine mitfliegen – wenn für sie ein eigener Sitzplatz gebucht wird. Das müssen wir direkt mal in der Praxis ausprobieren...

Come scegliere la misura corretta per un trasportino?Viaggiare con un cane grande in aereo, sicurezza e gestione del cane quando siamo malati.Ecco di cosa abbiamo parlato in questo episodio del podcast.Guarda il podcast quihttps://youtu.be/zXJ7rNfN2qESe avessi la possibilità di partecipare al podcast di Dog Cafe Academy, cosa vorresti chiedere?

Entrevistamos a compañeras y compañeros de la Comisión Organizadora del ENAC (Encuentro Nacional de Arquitectura Comunitaria) que este año se realizará en La Rioja, del 21 al 24 de mayo.Nos cuentan como viene el preparativo para recibir a arquitectos/as y estudiantes, en el que se expondrán las distintas experiencias académicas y territoriales de varias provincias y localidades. Tambien entrevistamos a jóvenes profesionales y estudiantes a punto de recibirse en la FADU (Facultad de Arq. Diseño y Urb. de la UBA), que nos cuentan sobre su carrera, sus sueños, espectativas y su situación laboral.1000x1000 Por la batalla cultural! Sumate y ayudanos a seguir brindándote la mejor programación: https://www.mercadopago.com.ar/subscriptions/checkout?preapproval_plan_id=2c93808495b859210195e9f01ca91b2c

Pastor Richard shares ENAC's vision for 2025 and beyond

ROMA (ITALPRESS) - "Ci stiamo lavorando, penso che tra 6-8 settimane sarà pronto. Parliamo di quello a 5 anni. L'integrazione è già cominciata, con una serie di progetti". Così l'Ad di ITA Airways, Joerg Eberhart, a margine di un convegno organizzato dall' Enac, parlando di piano industriale e integrazione con Lufthansa. xb1/ads/mrv

In this episode, Sam Munda, Managing Director for Kenya and VP of Africa at Travisory, delves into the evolving landscape of Africa's border security and digital travel solutions. With over 30 years of experience in aviation ICT and transport security, Sam shares insights on seamless border management, visa accessibility, and the future of hassle-free travel across the continent. Sam Munda joined Travizory in 2020 and is the Managing Director for the Kenya Office. He leads the company's commercial strategy across Africa, supporting governments in digitizing borders to enhance security, efficiency, and traveler experience. His work also enables real-time data access for better decision-making. With over 30 years of experience in ICT, aviation, and transport security, Sam has held leadership roles in Africa with a major global aviation ICT provider. He is an Electronics Engineer, having graduated from ENAC (École Nationale de l'Aviation Civile) in Toulouse, France, and holds an MBA from the University of South Africa (UNISA).

WASHINGTON (STATI UNITI) (ITALPRESS) - All'Ambasciata Italiana di Washington va in scena la terza edizione della Giornata Nazionale dello Spazio, grande occasione di confronto tra le aziende italiane dell'aerospazio e la Nasa. Il programma ha previsto l'allestimento di un'area espositiva che ha ospitato 20 aziende Italiane, garantendo incontri tra gli operatori italiani e statunitensi.Un evento che punta a rafforzare ulteriormente la partnership tra Nasa, ASI e INAF. Per l'occasione ENAC e Aeroporti di Puglia hanno annunciato la firma di uno studio di fattibilità per le operazioni suborbitali commerciali di Virgin Galactic in Italia, utilizzando lo spazioporto di Grottaglie. xp6/sat/gsl

WASHINGTON (STATI UNITI) (ITALPRESS) - All'Ambasciata Italiana di Washington va in scena la terza edizione della Giornata Nazionale dello Spazio, grande occasione di confronto tra le aziende italiane dell'aerospazio e la Nasa. Il programma ha previsto l'allestimento di un'area espositiva che ha ospitato 20 aziende Italiane, garantendo incontri tra gli operatori italiani e statunitensi.Un evento che punta a rafforzare ulteriormente la partnership tra Nasa, ASI e INAF. Per l'occasione ENAC e Aeroporti di Puglia hanno annunciato la firma di uno studio di fattibilità per le operazioni suborbitali commerciali di Virgin Galactic in Italia, utilizzando lo spazioporto di Grottaglie. xp6/sat/gsl

WASHINGTON (STATI UNITI) (ITALPRESS) - All'Ambasciata Italiana di Washington va in scena la terza edizione della Giornata Nazionale dello Spazio, grande occasione di confronto tra le aziende italiane dell'aerospazio e la Nasa. Il programma ha previsto l'allestimento di un'area espositiva che ha ospitato 20 aziende Italiane, garantendo incontri tra gli operatori italiani e statunitensi.Un evento che punta a rafforzare ulteriormente la partnership tra Nasa, ASI e INAF. Per l'occasione ENAC e Aeroporti di Puglia hanno annunciato la firma di uno studio di fattibilità per le operazioni suborbitali commerciali di Virgin Galactic in Italia, utilizzando lo spazioporto di Grottaglie. xp6/sat/gsl

In questa puntata di Motto Podcast affrontiamo un viaggio tra sfide quotidiane e grandi innovazioni!

MILANO (ITALPRESS) - Amazon ha svolto con successo il primo test per le consegne con i droni in Abruzzo, nell'area di San Salvo, sulla base dell'autorizzazione operativa rilasciata da Enac. L'azienda continua a collaborare con le autorità italiane per soddisfare tutti i requisiti necessari al lancio del servizio il prossimo anno. I droni per le consegne di Amazon hanno volato per la prima volta nei cieli italiani il 4 dicembre 2024. Il volo di prova è stato realizzato con il nuovo drone MK-30, sistema automatizzato di droni che utilizza il programma di computer vision Amazon. Il test è stato svolto grazie all'autorizzazione e ai processi di certificazione posti in essere da Enac in coordinamento con Enav. sat(fonte video ufficio stampa Enav/Amazon)

MILANO (ITALPRESS) - Amazon ha svolto con successo il primo test per le consegne con i droni in Abruzzo, nell'area di San Salvo, sulla base dell'autorizzazione operativa rilasciata da Enac. L'azienda continua a collaborare con le autorità italiane per soddisfare tutti i requisiti necessari al lancio del servizio il prossimo anno. I droni per le consegne di Amazon hanno volato per la prima volta nei cieli italiani il 4 dicembre 2024. Il volo di prova è stato realizzato con il nuovo drone MK-30, sistema automatizzato di droni che utilizza il programma di computer vision Amazon. Il test è stato svolto grazie all'autorizzazione e ai processi di certificazione posti in essere da Enac in coordinamento con Enav. sat(fonte video ufficio stampa Enav/Amazon)

MILANO (ITALPRESS) - Amazon ha svolto con successo il primo test per le consegne con i droni in Abruzzo, nell'area di San Salvo, sulla base dell'autorizzazione operativa rilasciata da Enac. L'azienda continua a collaborare con le autorità italiane per soddisfare tutti i requisiti necessari al lancio del servizio il prossimo anno. I droni per le consegne di Amazon hanno volato per la prima volta nei cieli italiani il 4 dicembre 2024. Il volo di prova è stato realizzato con il nuovo drone MK-30, sistema automatizzato di droni che utilizza il programma di computer vision Amazon. Il test è stato svolto grazie all'autorizzazione e ai processi di certificazione posti in essere da Enac in coordinamento con Enav. sat(fonte video ufficio stampa Enav/Amazon)

durée : 00:02:42 - ENAC, Centre européen en intelligence artificielle par l'innovation - 67 millions d'Euros seront dépensés sur 5 ans dans plusieurs universités et institutions du Grand Est. L'Alsace est bien sûr très concernée et entend attirer des personnes très compétentes dans le domaine.

I numeri li snocciola il sindaco Michelusi: "In Veneto mancano 3.500 operatori socio sanitari e a Thiene da qui al 2050 gli ultraottantenni passeranno da 3.800 a 7.900: questo progetto è previdente e lungimirante per il nostro territorio".

RIMINI (ITALPRESS) - "Nonostante non abbiamo una compagnia di riferimento nazionale, il traffico è cresciuto sulla qualità dei servizi offerti. Finalmente si coglie l'idea che i piani nazionali della mobilità debbano partire dal trasporto aereo perché effettivamente è quello che porta ricchezza in un Paese". Così il presidente dell'Enac, Pierluigi Di Palma, a margine del Meeting di Rimini. xb1/ads

L'esponente della Lega Claudio Borghi vorrebbe portare in Parlamento un emendamento con cui togliere l'obbligatorietà vaccinale per lasciare che sia solo una mera raccomandazione sulla falsariga di quanto avviene in alcuni Paesi europei. Ne parliamo in questo appuntamento. Ci occupiamo poi dell'intenzione di intitolare l'aeroporto di Milano Malpensa a Silvio Berlusconi, l'Enac ha già dato il suo sì ma la proposta si sta già rivelando altamente divisiva.

PALERMO (ITALPRESS) - “Il governo su richiesta di Gesap ha deciso di stanziare 18 milioni di fondi Fsc per il miglioramento del terminal. Da un lato la Regione finanzia, dall'altro i soci Gesap non recepiscono l'invito del governo e del sottoscritto in campagna elettorale, ovvero la privatizzazione: Palermo e Catania sono gli unici due scali in tutta Italia ancora a gestione pubblica”. Così il presidente della Regione siciliana, Renato Schifani, a margine dell'inaugurazione della fermata ferroviaria Palermo-De Gasperi. “Sono convinto che il pubblico debba fare il pubblico e il privato altrettanto - prosegue Schifani -. Oggi primeggiano delle attività di partenariato pubblico-privato in moltissimi aeroporti d'Italia: non si tratta di dare tutto in mano ai privati, ma anche di non esporre Gesap a un piano di investimenti da 50 milioni che chiede Enac per il potenziamento. Credo che sia arrivato il momento di fare chiarezza se gli aeroporti di Palermo e Catania andranno privatizzati o meno: in base ai comportamenti altrui, la Regione valuterà se è il caso o meno di investire senza essere ascoltata su quella che è l'idea da discutere. Non c'è stato mai un tavolo: con senso di responsabilità abbiamo accolto la richiesta di Sac di investire 34 milioni sullo scalo di Catania e quella di Gesap sui 18 milioni per Palermo. Tutto va comunque visto in un senso di collaborazione istituzionale e nell'interesse del cittadino”. xd8/vbo/gtr

PALERMO (ITALPRESS) - “Il governo su richiesta di Gesap ha deciso di stanziare 18 milioni di fondi Fsc per il miglioramento del terminal. Da un lato la Regione finanzia, dall'altro i soci Gesap non recepiscono l'invito del governo e del sottoscritto in campagna elettorale, ovvero la privatizzazione: Palermo e Catania sono gli unici due scali in tutta Italia ancora a gestione pubblica”. Così il presidente della Regione siciliana, Renato Schifani, a margine dell'inaugurazione della fermata ferroviaria Palermo-De Gasperi. “Sono convinto che il pubblico debba fare il pubblico e il privato altrettanto - prosegue Schifani -. Oggi primeggiano delle attività di partenariato pubblico-privato in moltissimi aeroporti d'Italia: non si tratta di dare tutto in mano ai privati, ma anche di non esporre Gesap a un piano di investimenti da 50 milioni che chiede Enac per il potenziamento. Credo che sia arrivato il momento di fare chiarezza se gli aeroporti di Palermo e Catania andranno privatizzati o meno: in base ai comportamenti altrui, la Regione valuterà se è il caso o meno di investire senza essere ascoltata su quella che è l'idea da discutere. Non c'è stato mai un tavolo: con senso di responsabilità abbiamo accolto la richiesta di Sac di investire 34 milioni sullo scalo di Catania e quella di Gesap sui 18 milioni per Palermo. Tutto va comunque visto in un senso di collaborazione istituzionale e nell'interesse del cittadino”. xd8/vbo/gtr

ROMA (ITALPRESS) - In questo numero del Tg Ambiente, prodotto dall'Italpress in collaborazione con TeleAmbiente:- Net-Zero Industry Act, via libera dal Consiglio Ue- Trasporto aereo, Eni, Enac e AdR insieme per la decarbonizzazione- Torna la campagna itinerante Mediterraneo da remare- In Italia è sempre più emergenza siccitàabr/gtr/col

El Gobierno destinará un total de 130 millones de euros al Plan Verano Joven 2024 que permitirá viajar a personas de entre 18 y 30 años, en tren, autobús e interrail, con descuentos que llegan hasta el 90%. Como novedad, este año podrán beneficiarse del plan todos los jóvenes con residencia legal en España, independientemente de su nacionalidad. El sector turístico ha pedido una hoja de ruta que permita al sector avanzar en la transformación y la transición sostenible, en una sesión de los desayunos organizados por Foment del Treball y la Barcelona School of Tourism, Hospitality and Gastronomy (CETT-UB). A pesar de que tres turoperadores alemanes, TUI Group, DER Touristik y Schauinsland-Reisen, se han postulado para asumir las reservas afectadas tras la quiebra del turoperador FTI Group, en Canarias, las empresas del archipiélago podrían tener impagos de hasta tres meses. The Fun Lab, firma española de ingeniería y entidad acreditada internacional de inspección por ENAC en parques acuáticos y piscinas lúdicas, ha inaugurado su primera delegación comercial internacional en Cancún (México), desde la que va a ofrecer sus servicios a los clientes de la región del Caribe. Iryo ha presentado la segunda fase de su marca de multimodalidad —bautizada como 'Iryo Conecta Más Destinos'—, con la que apuesta por la interconexión de medios de transporte desde los trenes hasta la llegada al destino final mediante taxis, autobuses, aviones y barcos. Con motivo del Día Mundial del Medioambiente, un estudio de Appinio revela que el 68% de los españoles se siente afectado por las consecuencias del cambio climático, destacando que Andalucía, Valencia, Cataluña y Madrid son las regiones donde más se considera que el cambio climático es un problema importante. El presidente de la Asociación de Líneas Aéreas (ALA), Javier Gándara, ha denunciado que la multa de 150 millones de euros impuesta por el Ministerio de Consumo a Ryanair, Vueling, Volotea y easyJet por cobrar por el equipaje de mano, "atenta" contra "la libertad de edificación tarifaria y la capacidad de elección de los consumidores". El pasado 16 de mayo, Más Turismo Chino recibió el primer premio internacional en la Feria Internacional de Turismo de Guangzhou en la categoría de Internet / Media. Estos premios son organizados por el prestigioso organismo de turismo chino Chinese Outbound Tourism Research Institute.

ROMA (ITALPRESS) - In questa edizione:- A Padova 33enne precipita da cavalcavia, fermato compagno- Funerali Angelo Onorato, per la moglie è un delitto- Delitto Matteotti 100 anni dopo, il ricordo della premier Meloni- Decreto salva-casa, da oggi al via domande ai Comuni- Scoperta maxi frode fiscale con regia a Catania- Allerta dall'intelligence in Europa per i roghi dolosi- Istat, ad Aprile record tasso occupazione, al 62,3%- Trasporto aereo, Eni, Enac e AdR insieme per la decarbonizzazione- Previsioni 3B Meteo 31 Maggiomrv

ROMA (ITALPRESS) - Mettere a confronto istituzioni e aziende, enti e associazioni, per definire un percorso per promuovere l'utilizzo di carburanti sostenibili per l'aviazione, nell'ottica della decarbonizzazione del trasporto aereo. Questo l'obiettivo di “SAF, the bet to win”, conferenza promossa da Eni, Aeroporti di Roma ed Enac. spf/fsc/gtr

PALERMO (ITALPRESS) - “Credo che sia realmente un giorno importante e un merito va sicuramente al professor Riggio per aver nel suo mandato realizzato questi investimenti infrastrutturali che effettivamente riescono a restituire qualità nei confronti dei passeggeri di un aeroporto che sta crescendo in maniera assolutamente importante”. Così Pierluigi Di Palma, presidente di Enac, a margine della conferenza stampa sulla conclusione dei lavori del primo lotto dell'aeroporto internazionale Falcone Borsellino di Palermo. “Fa parte di una policy dell'Enac, quella di verificare la capacità infrastrutturale oltre a quella operativa e se nel caso limitare l'operatività di un aeroporto se non sono soddisfacenti questi requisiti. Al contrario vediamo che un aeroporto come Pademo insiste sulla qualità e quindi potrà crescere rispetto proprio a questa capacità di coniugare capacità operativa e capacità infrastrutturale con investimenti molto rilevanti da un punto di vista economico, quasi totalmente in autofinanziamento”.Fonte: ufficio stampa Gesap xd6/pc/gtr

PALERMO (ITALPRESS) - “Credo che sia realmente un giorno importante e un merito va sicuramente al professor Riggio per aver nel suo mandato realizzato questi investimenti infrastrutturali che effettivamente riescono a restituire qualità nei confronti dei passeggeri di un aeroporto che sta crescendo in maniera assolutamente importante”. Così Pierluigi Di Palma, presidente di Enac, a margine della conferenza stampa sulla conclusione dei lavori del primo lotto dell'aeroporto internazionale Falcone Borsellino di Palermo. “Fa parte di una policy dell'Enac, quella di verificare la capacità infrastrutturale oltre a quella operativa e se nel caso limitare l'operatività di un aeroporto se non sono soddisfacenti questi requisiti. Al contrario vediamo che un aeroporto come Pademo insiste sulla qualità e quindi potrà crescere rispetto proprio a questa capacità di coniugare capacità operativa e capacità infrastrutturale con investimenti molto rilevanti da un punto di vista economico, quasi totalmente in autofinanziamento”.Fonte: ufficio stampa Gesap xd6/pc/gtr

In questa puntata: Mustafa Suleyman, fondatore di DeepMind e ora alla guida dell'IA di Microsoft, ha un ruolo cruciale nel plasmare il futuro della tecnologia che trasforma il mondo.Conosciamo meglio la sua prospettiva sui rischi e le opportunità dell'IA. Da possibili guadagni milionari in pochi mesi a sfide etiche e di sicurezza, Suleyman ci invita a riflettere su come gestire questa potente tecnologia per il bene dell'umanità. Google DeepMind e Isomorphic Labs hanno svelato oggi AlphaFold 3, un rivoluzionario modello di intelligenza artificiale che predice la struttura e le interazioni delle molecole della vita con una precisione senza precedenti. AlphaFold 3 migliora del 50% le previsioni delle interazioni tra proteine e altre molecole, raddoppiando la precisione per alcune interazioni cruciali.Ma non è tutto: la prossima generazione di AlphaFold è in grado di prevedere le strutture di quasi tutti i tipi di biomolecole, offrendo una visione senza precedenti delle interazioni cellulari e accelerando la nostra comprensione delle macchine molecolari che sostengono il corpo umano.Inoltre, Google DeepMind ha lanciato AlphaFold Server, uno strumento gratuito che consente ai ricercatori di accedere alle capacità di AlphaFold 3 per generare strutture biologiche complesse.  Un passo avanti cruciale per la ricerca scientifica.In tutto il mondo, gli aeroporti stanno abbracciando il riconoscimento facciale per offrire viaggi più fluidi e sicuri. Da Singapore a Madrid, da Tokyo a Dubai, questa tecnologia sta rivoluzionando il modo in cui viaggiamo. In Italia dopo Linate, anche Catania sperimenterà il sistema.Come funziona? I passeggeri dovranno "caricare" il proprio documento ai chioschi in aeroporto o sull'app, e poi "registrare" il proprio volto. A quel punto senza mostrare carta d'identità o biglietto i viaggiatori potranno avere accesso all'aereo. "Con questa tecnologia sicura, semplice e rapida, il Faceboarding sviluppato in collaborazione con Enac e Polizia di Stato, oltre a offrire una maggior velocità dei controlli ne aumenta l'efficacia e garantisce la tutela della privacy e dei dati dei passeggeri" dichiara la Società Esercizi Aeroportuali (Sea). Intelligenza Artificiale Spiegata Semplice è il podcast che ti offre un approccio chiaro e accessibile a questa nuova tecnologia.Ogni lunedì, Pasquale Viscanti e Giacinto Fiore ti guideranno alla scoperta di quello che sta accadendo grazie o a causa dell'Intelligenza Artificiale, spiegandola semplice.Puoi iscriverti anche alla newsletter su iaspiegatasemplice.it

CATANIA (ITALPRESS) - L'Aeroporto di Catania taglia il traguardo dei 100 anni. Un'occasione importante che SAC, la società che gestisce lo scalo etneo e quello di Comiso, ha celebrato insieme alle istituzioni locali, ai rappresentanti del settore, agli stakeholder e ai cittadini. Un anniversario festeggiato anche con lo sblocco dell'iter per la demolizione e ricostruzione del terminal B.col/sat/gtr

CATANIA (ITALPRESS) - L'Aeroporto di Catania taglia il traguardo dei 100 anni. Un'occasione importante che SAC, la società che gestisce lo scalo etneo e quello di Comiso, ha celebrato insieme alle istituzioni locali, ai rappresentanti del settore, agli stakeholder e ai cittadini. Un anniversario festeggiato anche con lo sblocco dell'iter per la demolizione e ricostruzione del terminal B.col/sat/gtr

CATANIA (ITALPRESS) - L'Aeroporto di Catania taglia il traguardo dei 100 anni. Un'occasione importante che SAC, la società che gestisce lo scalo etneo e quello di Comiso, ha celebrato insieme alle istituzioni locali, ai rappresentanti del settore, agli stakeholder e ai cittadini. Un anniversario festeggiato anche con lo sblocco dell'iter per la demolizione e ricostruzione del terminal B.col/sat/gtr

CATANIA (ITALPRESS) - "C'è stata la conferenza di servizi che finalmente supera un blocco di carattere burocratico. Siamo arrivati a definire la possibilità di abbattere il Morandi. Nei prossimi giorni sarà pubblicato il bando che renderà sempre più questo come un hub del Mediterraneo". Lo ha dichiarato il presidente dell'Enac, Pierluigi Di Palma, in occasione della celebrazione per i cento anni dell'aeroporto di Catania, in merito alla demolizione e ricostruzione del terminal B dello scalo.xn5/sat

CATANIA (ITALPRESS) - "C'è stata la conferenza di servizi che finalmente supera un blocco di carattere burocratico. Siamo arrivati a definire la possibilità di abbattere il Morandi. Nei prossimi giorni sarà pubblicato il bando che renderà sempre più questo come un hub del Mediterraneo". Lo ha dichiarato il presidente dell'Enac, Pierluigi Di Palma, in occasione della celebrazione per i cento anni dell'aeroporto di Catania, in merito alla demolizione e ricostruzione del terminal B dello scalo.xn5/sat

Le prime pagine dei principali quotidiani nazionali commentate in rassegna stampa da Davide Giacalone. L'allarme debito, Lega e mercato dei voti, scuola e voto in condotta, le armi all'Ucraina. L'attualità commentata dall'inviato speciale di Panorama, Antonio Rossitto. Parliamo di Cucina. È tornato a trovarci il Professor Alberto Grandi, docente di Storia del cibo all'Università di Parma. Firma il libro “La cucina italiana non esiste” edito da Mondadori. Don Antonio Mazzi, fondatore della comunità Exodus, regala ogni giorno un pensiero, un suggerimento, una frase agli ascoltatori di RTL 102.5. Il Salone del Mobile, manifestazione che sta attirando visitatori da tutta Italia e dal mondo. Qui passano i progetti e le nuove tendenze delle nostre case. Ci ha raggiunti Giulio Cappellini, architetto e art director. Molti italiani hanno già prenotato le ferie e non è semplice muoversi senza spendere una fortuna. In particolare, concentriamoci sul traffico aereo: l'ultimo rapporto ENAC testimonia il netto predominio delle low cost, in particolare di una compagnia. Ne abbiamo parlato con Matteo Rainisio, fondatore di The Flight Club. L'attualità, commentata dal direttore di Italia Oggi, Pierluigi Magnaschi. All'interno di Non Stop News, con Massimo Lo Nigro, Enrico Galletti e Giusi Legrenzi.

Welcome aboard Episode 7 of the “Aerospace Ambition Podcast,” featuring our esteemed guest Rémi Chevallier! Get ready for an engaging conversation!In today's episode 7, we're excited to introduce Rémi Chevallier, a doctoral candidate at ENAC and AIRBUS. With expertise in aviation, data science, optimization, and avionics, Rémi has recently made waves with his paper on detecting contrails using satellite and air traffic data. His work, which he showcased at the Sustainable Skies Conference, promises intriguing insights. A warm welcome to Rémi on the podcast!Discussion Highlights:• Rémi's innovative method for observing contrails: What sets it apart?• How does Rémi's approach differ from the methods of DLR & Google?• The limitations of satellite-only observations for contrail analysis.• The influence of weather conditions on predicting contrails.• Is it possible to assess contrails' climate impact from space?• The role of collaboration among aviation stakeholders in enhancing accuracy.• Debating if contrail avoidance is a comprehensive solution for aviation sustainability.LinksRémi: https://www.linkedin.com/in/remi-chevallier/Marius: https://www.linkedin.com/in/mariuswedemeyer/Kieran: https://www.linkedin.com/in/kieran-t-7b9952102/AAMBITION Newsletter: https://mailchi.mp/55033eb444bd/aambition-newsletter

BRUXELLES (BELGIO) (ITALPRESS) - Pierluigi di Palma, presidente dell'Enac, parla di sostenibilità del trasporto aereo a margine di un incontro organizzato a Bruxelles da Aeroporti 2030 a Bruxelles sul tema "Il sistema aeroportuale italiano - Investimenti green, innovazione digitale e qualità del servizio".xf4/sat/gtr

BRUXELLES (BELGIO) (ITALPRESS) - Pierluigi di Palma, presidente dell'Enac, parla di sostenibilità del trasporto aereo a margine di un incontro organizzato a Bruxelles da Aeroporti 2030 a Bruxelles sul tema "Il sistema aeroportuale italiano - Investimenti green, innovazione digitale e qualità del servizio".xf4/sat/gtr

BRUXELLES (BELGIO) (ITALPRESS) - Pierluigi di Palma, presidente dell'Enac, parla di sostenibilità del trasporto aereo a margine di un incontro organizzato a Bruxelles da Aeroporti 2030 a Bruxelles sul tema "Il sistema aeroportuale italiano - Investimenti green, innovazione digitale e qualità del servizio".xf4/sat/gtr

ROMA (ITALPRESS) - Nel Padiglione italiano alla Conferenza delle Nazioni Unite sui cambiamenti climatici (COP28) in corso in questi giorni a Dubai, Aeroporti di Roma ed Eni hanno organizzato per contro del Patto per la Decarbonizzazione del Trasporto Aereo il side event "The Pact for the decarbonisation of air transport: the Italian ecosystem for a roadmap to Net-Zero". Selezionato dal Ministero dell'Ambiente e della Sicurezza Energetica tra un elevato numero di candidature ricevute, la partecipazione del Patto per la Decarbonizzazione del Trasporto Aereo - il tavolo promosso da Aeroporti di Roma con il patrocinio del MIT, del MASE e di ENAC che riunisce player industriali, stakeholder istituzionali e associazioni per favorire il raggiungimento dei target di sostenibilità del comparto - rappresenta una best practice internazionale per affrontare la sfida della decarbonizzazione.abr/gtr(Fonte video: Adr

ROMA (ITALPRESS) - Nel Padiglione italiano alla Conferenza delle Nazioni Unite sui cambiamenti climatici (COP28) in corso in questi giorni a Dubai, Aeroporti di Roma ed Eni hanno organizzato per contro del Patto per la Decarbonizzazione del Trasporto Aereo il side event "The Pact for the decarbonisation of air transport: the Italian ecosystem for a roadmap to Net-Zero". Selezionato dal Ministero dell'Ambiente e della Sicurezza Energetica tra un elevato numero di candidature ricevute, la partecipazione del Patto per la Decarbonizzazione del Trasporto Aereo - il tavolo promosso da Aeroporti di Roma con il patrocinio del MIT, del MASE e di ENAC che riunisce player industriali, stakeholder istituzionali e associazioni per favorire il raggiungimento dei target di sostenibilità del comparto - rappresenta una best practice internazionale per affrontare la sfida della decarbonizzazione.abr/gtr(Fonte video: Adr

Da qualche mese continua la diatriba tra Ministero delle imprese e del Made in Italy Adolfo Urso ele compagnie aeree Low Cost. In particolare, l'amministratore Delegato Michael O'really (link: https://www.ttgitalia.com/stories/trasporti/187240_laffondo_di_ryanair_sul_nodo_dei_prezzi_di_palma_sbaglia_dovrebbe_dimettersi/) segnala come il rerport presentato dal presidente di ENAC sia pieno di errori e come il Ministro, dopo l'approvazione del decreto Asset, stia deliberatamente trasgredendo il regolamento europeo 1008/2008 (link: https://www.ttgitalia.com/stories/trasporti/187217_ryanair_risponde_a_urso_rispetti_il_diritto_ue_e_ritiri_il_decreto/). Al netto dello scontro si registra ormai da anni un declino strutturale del comparto aereo domestico (link: https://www.ttgitalia.com/stories/commento_del_direttore/187216_una_strada_segnata/). Ryanair ha intrapreso un braccio di ferro, non nuovo per chi segue la vicenda dal lontano 2020, anche con Booking.com. Secondo il vettore Aereo l'OTA e la sua controllata Etraveli per accedere direttamente al portale di vendita biglietti di Ryanair creando una danno economico alla compagnia aerea (link: https://www.ttgitalia.com/stories/tour_operator/187263_ryanair_contro_le_ota_bookingcom_nel_mirino_del_vettore_low_cost/) Al via le domande per sostegni economici a fondo perduto da parte del mInistero del Turismo per agenzia di viaggio e tour operator (link: https://www.ttgitalia.com/stories/agenzie_viaggi/187234_sostegni_per_adv_e_to_si_ampliano_i_beneficiari/). È possibile ancora presentare domanda fino al prossimo 2 ottobre (link: https://www.ttgitalia.com/stories/tour_operator/187269_sostegni_per_agenzie_e_to_la_scadenza_slitta_al_2_ottobre/) l'UNESCO salava Venezia dalla classifica sei siti a rischio. Buona notizia (link: https://www.ttgitalia.com/stories/incoming/187268_italia_e_overtourism_lunesco_salva_venezia/), ma permangono tutte le perplessità relative all'overtourism (link: https://www.romatoday.it/politica/piazza-di-spagna-scalinate-vuote-regolamento-polizia-urbana.html). Nel frattempo i turisti si accontentano sempre più di souvenir immateriali da condividere sui social creando false aspettative ed alimentando ancora di più l'overtourism (link: https://www.theguardian.com/commentisfree/2023/apr/22/as-la-dolce-vita-turns-sour-thanks-to-overtourism-hotspots-are-turning-away-their-visitors) #marketingterritoriale #marketingturistico #agevolazioni #sviluppoterritoriale #destinazionituristiche #aeroporto #strategia

Primeira Leitura: Números 13,1-2.25-14,1.26-30.34-35 Leitura do livro dos Números – Naqueles dias, 1o Senhor falou a Moisés no deserto de Farã, dizendo: 2“Envia alguns homens para explorar a terra de Canaã, que vou dar aos filhos de Israel. Enviarás um homem de cada tribo, e que todos sejam chefes”. 25Ao fim de quarenta dias, eles voltaram do reconhecimento do país 26e apresentaram-se a Moisés, a Aarão e a toda a comunidade dos filhos de Israel, em Cades, no deserto de Farã. E, falando a eles e a toda a comunidade, mostraram os frutos da terra 27e fizeram a sua narração, dizendo: “Entramos no país ao qual nos enviastes, que de fato é uma terra onde corre leite e mel, como se pode reconhecer por estes frutos. 28Porém, os habitantes são fortíssimos e as cidades, grandes e fortificadas. Vimos lá descendentes de Enac; 29os amalecitas vivem no deserto do Negueb; os hititas, jebuseus e amorreus, nas montanhas; mas os cananeus, na costa marítima e ao longo do Jordão”. 30Entretanto Caleb, para acalmar o povo revoltado, que se levantava contra Moisés, disse: “Subamos e conquistemos a terra, pois somos capazes de fazê-lo”. 31Mas os homens que tinham ido com ele disseram: “Não podemos enfrentar esse povo, porque é mais forte do que nós”. 32E, diante dos filhos de Israel, começaram a difamar a terra que haviam explorado, dizendo: “A terra que fomos explorar é uma terra que devora os seus habitantes: o povo que aí vimos é de estatura extraordinária. 33Lá vimos gigantes, filhos de Enac, da raça dos gigantes; comparados com eles, parecíamos gafanhotos”. 14,1Então, toda a comunidade começou a gritar e passou aquela noite chorando. 26O Senhor falou a Moisés e Aarão e disse: 27“Até quando vai murmurar contra mim esta comunidade perversa? Eu ouvi as queixas dos filhos de Israel. 28Dize-lhes, pois: ‘Por minha vida, diz o Senhor, juro que vos farei assim como vos ouvi dizer! 29Neste deserto ficarão estendidos os vossos cadáveres. Todos vós que fostes recenseados, da idade de vinte anos para cima, e que murmurastes contra mim 30não entrareis na terra na qual jurei, com mão levantada, fazer-vos habitar, exceto Caleb, filho de Jefoné, e Josué, filho de Num. 34Carregareis vossa culpa durante quarenta anos, que correspondem aos quarenta dias em que explorastes a terra, isto é, um ano para cada dia; e experimentareis a minha vingança. 35Eu, o Senhor, assim como disse, assim o farei com toda essa comunidade perversa, que se insurgiu contra mim: nesta solidão será consumida e morrerá'”. – Palavra do Senhor. Salmo Responsorial: 105(106) Lembrai-vos de nós, ó Senhor, / segundo o amor para com vosso povo! 1. Pecamos como outrora nossos pais, / praticamos a maldade e fomos ímpios; / no Egito nossos pais não se importaram / com os vossos admiráveis grandes feitos. – R. 2. Mas bem depressa esqueceram suas obras, / não confiaram nos projetos do Senhor. / No deserto deram largas à cobiça, / na solidão eles tentaram o Senhor. – R. 3. Esqueceram-se do Deus que os salvara, / que fizera maravilhas no Egito; / no país de Cam fez tantas obras admiráveis, / no mar Vermelho, tantas coisas assombrosas. – R. 4. Até pensava em acabar com sua raça, / não se tivesse Moisés, o seu eleito, / interposto, intercedendo junto a ele, / para impedir que sua ira os destruísse. – R.

ReferencesWe considered the complexity of the machinery to excrete ammonium in the context of research on dietary protein and how high protein intake may increase glomerular pressure and contribute to progressive renal disease (many refer to this as the “Brenner hypothesis”). Dietary protein intake and the progressive nature of kidney disease: the role of hemodynamically mediated glomerular injury in the pathogenesis of progressive glomerular sclerosis in aging, renal ablation, and intrinsic renal diseaseA trial that studied low protein and progression of CKD The Effects of Dietary Protein Restriction and Blood-Pressure Control on the Progression of Chronic Renal Disease(and famously provided data for the MDRD eGFR equation A more accurate method to estimate glomerular filtration rate from serum creatinine: a new prediction equation. Modification of Diet in Renal Disease Study GroupWe wondered about dietary recommendations in CKD. of note, this is best done in the DKD guidelines from KDIGO Executive summary of the 2020 KDIGO Diabetes Management in CKD Guideline: evidence-based advances in monitoring and treatment.Joel mentioned this study on red meat and risk of ESKD. Red Meat Intake and Risk of ESRDWe referenced the notion of a plant-based diet. This is an excellent review by Deborah Clegg and Kathleen Hill Gallant. Plant-Based Diets in CKD : Clinical Journal of the American Society of NephrologyHere's the review that Josh mentioned on how the kidney appears to sense pH Molecular mechanisms of acid-base sensing by the kidneyRemarkably, Dr. Dale Dubin put a prize in his ECG book Free Car Prize Hidden in Textbook Read the fine print: Student wins T-birdA review of the role of the kidney in DKA: Diabetic ketoacidosis: Role of the kidney in the acid-base homeostasis re-evaluatedJosh mentioned the effects of infusing large amounts of bicarbonate The effect of prolonged administration of large doses of sodium bicarbonate in man and this study on the respiratory response to a bicarbonate infusion: The Acute Effects In Man Of A Rapid Intravenous Infusion Of Hypertonic Sodium Bicarbonate Solution. Ii. Changes In Respiration And Output Of Carbon DioxideThis is the study of acute respiratory alkalosis in dogs: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC293311/?page=1And this is the study of medical students who went to the High Alpine Research Station on the Jungfraujoch in the Swiss Alps https://www.nejm.org/doi/full/10.1056/nejm199105163242003Self explanatory! A group favorite! It Is Chloride Depletion Alkalosis, Not Contraction AlkalosisEffects of chloride and extracellular fluid volume on bicarbonate reabsorption along the nephron in metabolic alkalosis in the rat. Reassessment of the classical hypothesis of the pathogenesis of metabolic alkalosisA review of pendrin's role in volume homeostasis: The role of pendrin in blood pressure regulation | American Journal of Physiology-Renal PhysiologyInfusion of bicarbonate may lead to a decrease in respiratory stimulation but the shift of bicarbonate to the CSF may lag. Check out this review Neural Control of Breathing and CO2 Homeostasis and this classic paper Spinal-Fluid pH and Neurologic Symptoms in Systemic Acidosis.OutlineOutline: Chapter 11- Regulation of Acid-Base Balance- Introduction - Bicarb plus a proton in equilibrium with CO2 and water - Can be rearranged to HH - Importance of regulating pCO2 and HCO3 outside of this equation - Metabolism of carbs and fats results in the production of 15,000 mmol of CO2 per day - Metabolism of protein and other “substances” generates non-carbonic acids and bases - Mostly from sulfur containing methionine and cysteine - And cationic arginine and lysine - Hydrolysis of dietary phosphate that exists and H2PO4– - Source of base/alkali - Metabolism of an ionic amino acids - Glutamate and asparatate - Organic anions going through gluconeogenesis - Glutamate, Citrate and lactate - Net effect on a normal western diet 50-100 mEq of H+ per day - Homeostatic response to these acid-base loads has three stages: - Chemical buffering - Changes in ventilation - Changes in H+ excretion - Example of H2SO4 from oxidation of sulfur containing AA - Drop in bicarb will stimulate renal acid secretion - Nice table of normal cid-base values, arterial and venous- Great 6 bullet points of acid-base on page 328 - Kidneys must excrete 50-100 of non-carbonic acid daily - This occurs by H secretion, but mechanisms change by area of nephron - Not excreted as free H+ due to minimal urine pH being equivalent to 0.05 mmol/L - No H+ can be excreted until virtually all of th filtered bicarb is reabsorbed - Secreted H+ must bind buffers (phosphate, NH3, cr) - PH is main stimulus for H secretion, though K, aldo and volume can affect this.- Renal Hydrogen excretion - Critical to understand that loss of bicarb is like addition of hydrogen to the body - So all bicarb must be reabsorbed before dietary H load can be secreted - GFR of 125 and bicarb of 24 results in 4300 mEq of bicarb to be reabsorbed daily - Reabsorption of bicarb and secretion of H involve H secretion from tubular cells into the lumen. - Thee initial points need to be emphasized - Secreted H+ ion are generated from dissociation of H2O - Also creates OH ion - Which combine with CO2 to form HCO3 with the help of zinc containing intracellular carbonic anhydrase. - This is how the secretion of H+ which creates an OH ultimately produces HCO3 - Different mechanisms for proximal and distal acidification - NET ACID EXCRETION - Free H+ is negligible - So net H+ is TA + NH4 – HCO3 loss - Unusually equal to net H+ load, 50-100 mEq/day - Can bump up to 300 mEq/day if acid production is increased - Net acid excretion can go negative following a bicarb or citrate load - Proximal Acidification - Na-H antiporter (or exchanger) in luminal membrane - Basolateral membrane has a 3 HCO3 Na cotransporter - This is electrogenic with 3 anions going out and only one cation - The Na-H antiporter also works in the thick ascending limb of LOH - How about this, there is also a H-ATPase just like found in the intercalated cells in the proximal tubule and is responsible for about a third of H secretion - And similarly there is also. HCO3 Cl exchanger (pendrin-like) in the proximal tubule - Footnote says the Na- 3HCO3 cotransporter (which moves sodium against chemical gradient NS uses negative charge inside cell to power it) is important for sensing acid-base changes in the cell. - Distal acidification - Occurs in intercalated cells of of cortical and medullary collecting tubule - Three main characteristics - H secretion via active secretory pumps in the luminal membrane - Both H-ATPase and H-K ATPase - H- K ATPase is an exchange pump, k reabsorption - H-K exchange may be more important in hypokalemia rather than in acid-base balance - Whole paragraph on how a Na-H exchanger couldn't work because the gradient that H has to be pumped up is too big. - H-ATPase work like vasopressin with premise H-ATPase sitting on endocarditis vesicles a=which are then inserted into the membrane. Alkalosis causes them to be recycled out of the membrane. - H secretory cells do not transport Na since they have few luminal Na channels, but are assisted by the lumen negative tubule from eNaC. - Minimizes back diffusion of H+ and promotes bicarb resorption - Bicarbonate leaves the cell through HCO3-Cl exchanger which uses the low intracellular Cl concentration to power this process. - Same molecule is found on RBC where it is called band 3 protein - Figure 11-5 is interesting - Bicarbonate resorption - 90% in the first 1-22 mm of the proximal tubule (how long is the proximal tubule?) - Lots of Na-H exchangers and I handed permeability to HCO3 (permeability where?) - Last 10% happens distally mostly TAL LOH via Na-H exchange - And the last little bit int he outer medullary collecting duct. - Carbonic anhydrase and disequilibrium pH - CA plays central role in HCO3 reabsorption - After H is secreted in the proximal tubule it combines with HCO# to form carbonic acid. CA then dehydrates it to CO2 and H2O. (Step 2) - Constantly moving carbonic acid to CO2 and H2O keeps hydrogen combining with HCO3 since the product is rapidly consumed. - This can be demonstrated by the minimal fall in luminal pH - That is important so there is not a luminal gradient for H to overcome in the Na-H exchanger (this is why we need a H-ATPase later) - CA inhibitors that are limited tot he extracellular compartment can impair HCO3 reabsorption by 80%. - CA is found in S1, S2 but not S3 segment. See consequence in figure 11-6. - The disequilibrium comes from areas where there is no CA, the HH formula falls down because one of the assumptions of that formula is that H2CO3 (carbonic acid) is a transient actor, but without CA it is not and can accumulate, so the pKa is not 6.1. - Bicarbonate secretion - Type B intercalated cells - H-ATPase polarity reversed - HCO3 Cl exchanger faces the apical rather than basolateral membrane- Titratable acidity - Weak acids are filtered at the glom and act as buffers in the urine. - HPO4 has PKA of 6.8 making it ideal - Creatinine (pKa 4.97) and uric acid (pKa 5.75) also contribute - Under normal cinditions TA buffers 10-40 mEa of H per day - Does an example of HPO4(2-):H2PO4 (1-) which exists 4:1 at pH of 7.4 (glomerular filtrate) - So for 50 mEq of Phos 40 is HPO4 and 10 is H2PO4 - When pH drops to 6.8 then the ratio is 1:1 so for 50 - So the 50 mEq is 25 and 25, so this buffered an additional 15 mEq of H while the free H+ concentration increased from 40 to 160 nanomol/L so over 99.99% of secreted H was buffered - When pH drops to 4.8 ratio is 1:100 so almost all 50 mEq of phos is H2PO4 and 39.5 mEq of H are buffered. - Acid loading decreases phosphate reabsorption so more is there to act as TA. - Decreases activity of Na-phosphate cotransporter - DKA provides a novel weak acid/buffer beta-hydroxybutyrate (pKa 4.8) which buffers significant amount of acid (50 mEq/d).- Ammonium Excretion - Ability to excrete H+ as ammonium ions adds an important amount of flexibility to renal acid-base regulation - NH3 and NH4 production and excretion can be varied according to physiologic need. - Starts with NH3 production in tubular cells - NH3, since it is neutral then diffuses into the tubule where it is acidified by the low pH to NH4+ - NH4+ is ionized and cannot cross back into the tubule cells(it is trapped in the tubular fluid) - This is important for it acting as an important buffer eve though the pKa is 9.0 - At pH of 6.0 the ratio of NH3 to NH4 is 1:1000 - As the neutral NH3 is converted to NH4 more NH3 from theintracellular compartment flows into the tubular fluid replacing the lost NH3. Rinse wash repeat. - This is an over simplification and that there are threemajor steps - NH4 is produced in early proximal tubular cells - Luminal NH4 is partially reabsorbed in the TAL and theNH3 is then recycled within the renal medulla - The medullary interstitial NH3 reaches highconcentrations that allow NH3 to diffuse into the tubular lumen in the medullary collecting tubule where it is trapped as NH4 by secreted H+ - NH4 production from Glutamine which converts to NH4 and glutamate - Glutamate is converted to alpha-ketoglutarate - Alpha ketoglutarate is converted to 2 HCO3 ions - HCO3 sent to systemic circulation by Na-3 HCO3 transporter - NH4 then secreted via Na-H exchanger into the lumen - NH4 is then reabsorbed by NaK2Cl transporter in TAL - NH4 substitutes for K - Once reabsorbed the higher intracellular pH causes NH4 to convert to NH3 and the H that is removed is secreted through Na-H exchanger to scavenge the last of the filtered bicarb. - NH3 diffuses out of the tubular cells into the interstitium - NH4 reabsorption in the TAL is suppressed by hyperkalemia and stimulated by chronic metabolic acidosis - NH4 recycling promotes acid clearance - The collecting tubule has a very low NH3 concentration - This promotes diffusion of NH3 into the collecting duct - NH3 that goes there is rapidly converted to NH4 allowing more NH3 to diffuse in. - Response to changes in pH - Increased ammonium excretion with two processes - Increased proximal NH4 production - This is delayed 24 hours to 2-3 days depending on which enzyme you look at - Decreased urine pH increases diffusion of ammonia into the MCD - Occurs with in hours of an acid load - Peak ammonium excretion takes 5-6 days! (Fig 11-10) - Glutamine is picked up from tubular fluid but with acidosis get Na dependent peritublar capillary glutamine scavenging too - Glutamine metabolism is pH dependent with increase with academia and decrease with alkalemia - NH4 excretion can go from 30-40 mEq/day to > 300 with severe metabolic acidosis (38 NaBicarb tabs) - Says each NH4 produces equimolar generation of HCO3 but I thought it was two bicarb for every alpha ketoglutarate?- The importance of urine pH - Though the total amount of hydrogren cleared by urine pH is insignificant, an acidic urine pH is essential for driving the reactions of TA and NH4 forward.- Regulation of renal hydrogen excretion - Net acid excretion vary inverse with extracellular pH - Academia triggers proximal and distal acidification - Proximally this: - Increased Na-H exchange - Increased luminal H-ATPase activity - Increased Na:3HCO3 cotransporter on the basolateral membrane - Increased NH4 production from glutamine - In the collecting tubules - Increased H-ATPase - Reduction of tubular pH promotes diffusion of NH3 which gets converted to NH4…ION TRAPPING - Extracellular pH affects net acid excretion through its affect on intracellular pH - This happens directly with respiratory disorders due to movement of CO2 through the lipid bilayer - In metabolic disorders a low extracellular bicarb with cause bicarb to diffuse out of the cell passively, this lowers intracellular pH - If you manipulate both low pCO2 and low Bicarb to keep pH stable there will be no change in the intracellular pH and there is no change in renal handling of acid. It is intracellular pH dependent - Metabolic acidosis - Ramps up net acid secretion - Starts within 24 hours and peaks after 5-6 days - Increase net secretion comes from NH4 - Phosphate is generally limited by diet - in DKA titratable acid can be ramped up - Metabolic alkalosis - Alkaline extracellular pH - Increased bicarb excretion - Decrease reabsorption - HCO3 secretion (pendrin) in cortical collecting tubule - Occurs in cortical intercalated cells able to insert H-ATPase in basolateral cells (rather than luminal membrane) - Normal subjects are able to secrete 1000 mmol/day of bicarb - Maintenance of metabolic alkalosis requires a defect which forces the renal resorption of bicarb - This can be chloride/volume deficiency - Hypokalemia - Hyperaldosteronism - Respiratory acidosis and alkalosis - PCO2 via its effect on intracellular pH is an important determinant of renal acid handling - Ratios he uses: - 3.5 per 10 for respiratory acidosis - 5 per 10 for respiratory alkalosis - Interesting paragraph contrasting the response to chronic metabolic acidosis vs chronic respiratory acidosis - Less urinary ammonium in respiratory acidosis - Major differences in proximal tubule cell pH - In metabolic acidosis there is decreased bicarb load so less to be reabsorbed proximally - In respiratory acidosis the increased serum bicarb increases the amount of bicarb that must be reabsorbed proximally - The increased activity of Na-H antiporter returns tubular cell pH to normal and prevents it from creating increased urinary ammonium - Mentions that weirdly more mRNA for H-Na antiporter in metabolic acidosis than in respiratory acidosis - Net hydrogen excretion varies with effective circulating volume - Starts with bicarb infusions - Normally Tm at 26 - But if you volume deplete the patient with diuretics first this increases to 35+ - Four factors explain this increased Tm for bicarb with volume deficiency - Reduced GFR - Activation of RAAS - Ang2 stim H-Na antiporter proximally - Ang2 also stimulates Na-3HCO3 cotransporter on basolateral membrane - Aldosterone stimulates H-ATPase in distal nephron - ALdo stimulates Cl HCO3 exchanger on basolateral membrane - Aldo stimulates eNaC producing tubular lumen negative charge to allow H secretion to occur and prevents back diffusion - Hypochloremia - Increases H secretion by both Na-dependent and Na-independent methods - If Na is 140 and Cl is 115, only 115 of Na can be reabsorbed as NaCl, the remainder must be reabsorbed with HCO3 or associated with secretion of K or H to maintained electro neutrality - This is enhanced with hypochloridemia - Concurrent hypokalemia - Changes in K lead to trans cellular shifts that affect inctracellular pH - Hypokalemia causes K out, H in and in the tubular cell the cell acts if there is systemic acidosis and increases H secretion (and bicarbonate resorption) - PTH - Decreases proximal HCO3 resorption - Primary HyperCard as cause of type 2 RTA - Does acidosis stim PTH or does PTH stim net acid excretion

Bonjour et bienvenue dans le 128ème épisode de ce podcast ! Aujourd'hui, nous allons parler du seul meeting aérien organisé par des étudiants : Airexpo. Pour en parler avec nous, nos deux invitées sont Tess et Leen. Tess est la présidente de l'association Airexpo et est responsable de l'organisation générale du meeting. Leen est responsable de la communication. Tout d'abord, elle nous expliquerons comment elles ont été amenées à être impliquées dans cette association regroupant des étudiants de l'ENAC et de SupAéro. Ensuite, nous irons en détail sur les différentes étapes de l'organisation du meeting aérien. Nous évoquerons les problématiques de planification du plateau avion, de la sécurité des vols et de l'accueil du public. Avant de conclure, elles nous parlerons plus en détail de leur formation d'ingénieur ENAC. Conclusion Ainsi se conclut donc le 128ème épisode. J'espère qu'il vous a plu et je vous invite à vous abonner sur votre application de podcast favoris. Également, n'hésitez pas à laisser un avis 5 étoiles sur iTunes ce qui permettra à d'autres personnes de découvrir ce podcast. Si vous avez des questions, des remarques ou des suggestions, n'hésitez pas à utiliser le formulaire de contact. Si vous voulez recevoir des notifications lors de la sortie des nouveaux épisodes, vous pouvez m'envoyer directement un email via la page de contact. Vous pouvez également nous suivre sur Twitter sur @ParlonsAviation et sur Facebook sur notre page « Parlons Aviation. » Crédits Ce podcast est proposé sous licence Creative Commons BY-NC-ND 3.0. Mélange et édition audio par Jordan Di Blasi.

ReferencesWe considered the effect of a high protein diet and potential metabolic acidosis on kidney function. This review is of interest by Donald Wesson, a champion for addressing this issue and limiting animal protein: Mechanisms of Metabolic Acidosis-Induced Kidney Injury in Chronic Kidney DiseaseHostetter explored the effect of a high protein diet in the remnant kidney model with 1 ¾ nephrectomy. Rats with reduced dietary acid load (by bicarbonate supplementation) had less tubular damage. Chronic effects of dietary protein in the rat with intact and reduced renal massWesson explored treatment of metabolic acidosis in humans with stage 3 CKD in this study. Treatment of metabolic acidosis in patients with stage 3 chronic kidney disease with fruits and vegetables or oral bicarbonate reduces urine angiotensinogen and preserves glomerular filtration rateIn addition to the effect of metabolic acidosis from a diet high in animal protein, this diet also leads to hyperfiltration. This was demonstrated in normal subjects; ingesting a protein diet had a significantly higher creatinine clearance than a comparable group of normal subjects ingesting a vegetarian diet. Renal functional reserve in humans: Effect of protein intake on glomerular filtration rate.This finding has been implicated in Brenner's theory regarding hyperfiltration: The hyperfiltration theory: a paradigm shift in nephrologyOne of multiple publications from Dr. Nimrat Goraya whom Joel mentioned in the voice over: Dietary Protein as Kidney Protection: Quality or Quantity?We wondered about the time course in buffering a high protein meal (and its subsequent acid load on ventilation) and Amy found this report:Effect of Protein Intake on Ventilatory Drive | Anesthesiology | American Society of Anesthesiologists Roger mentioned that the need for acetate to balance the acid from amino acids in parenteral nutrition was identified in pediatrics perhaps because infants may have reduced ability to generate acid. Randomised controlled trial of acetate in preterm neonates receiving parenteral nutrition - PMCHe also recommended an excellent review on the complications of parenteral nutrition by Knochel https://www.kidney-international.org/action/showPdf?pii=S0085-2538%2815%2933384-6 which explained that when the infused amino acids disproportionately include cationic amino acids, metabolism led to H+ production. This is typically mitigated by preparing a solution that is balanced by acetate. Amy mentioned this study that explored the effect of protein intake on ventilation: Effect of Protein Intake on Ventilatory Drive | Anesthesiology | American Society of AnesthesiologistsAnna and Amy reminisced about a Skeleton Key Group Case from the renal fellow network Skeleton Key Group: Electrolyte Case #7JC wondered about isolated defects in the proximal tubule and an example is found here: Mutations in SLC4A4 cause permanent isolated proximal renal tubular acidosis with ocular abnormalitiesAnna's Voiceover re: Gastric neobladder → metabolic alkalosis and yes, dysuria. The physiology of gastrocystoplasty: once a stomach, always a stomach but not as common as you might think Gastrocystoplasty: long-term complications in 22 patientsSjögren's syndrome has been associated with acquired distal RTA and in some cases, an absence of the H+ ATPase, presumably from autoantibodies to this transporter. Here's a case report: Absence of H(+)-ATPase in cortical collecting tubules of a patient with Sjogren's syndrome and distal renal tubular acidosisCan't get enough disequilibrium pH? Check this out- Spontaneous luminal disequilibrium pH in S3 proximal tubules. Role in ammonia and bicarbonate transport.Acetazolamide secretion was studied in this report Concentration-dependent tubular secretion of acetazolamide and its inhibition by salicylic acid in the isolated perfused rat kidney. | Drug Metabolism & DispositionIn this excellent review, David Goldfarb tackles the challenging case of a A Woman with Recurrent Calcium Phosphate Kidney Stones (spoiler alert, many of these patients have incomplete distal RTA and this problem is hard to treat). Molecular mechanisms of renal ammonia transport excellent review from David Winer and Lee Hamm. OutlineOutline: Chapter 11- Regulation of Acid-Base Balance- Introduction - Bicarb plus a proton in equilibrium with CO2 and water - Can be rearranged to HH - Importance of regulating pCO2 and HCO3 outside of this equation - Metabolism of carbs and fats results in the production of 15,000 mmol of CO2 per day - Metabolism of protein and other “substances” generates non-carbonic acids and bases - Mostly from sulfur containing methionine and cysteine - And cationic arginine and lysine - Hydrolysis of dietary phosphate that exists and H2PO4– - Source of base/alkali - Metabolism of an ionic amino acids - Glutamate and asparatate - Organic anions going through gluconeogenesis - Glutamate, Citrate and lactate - Net effect on a normal western diet 50-100 mEq of H+ per day - Homeostatic response to these acid-base loads has three stages: - Chemical buffering - Changes in ventilation - Changes in H+ excretion - Example of H2SO4 from oxidation of sulfur containing AA - Drop in bicarb will stimulate renal acid secretion - Nice table of normal cid-base values, arterial and venous- Great 6 bullet points of acid-base on page 328 - Kidneys must excrete 50-100 of non-carbonic acid daily - This occurs by H secretion, but mechanisms change by area of nephron - Not excreted as free H+ due to minimal urine pH being equivalent to 0.05 mmol/L - No H+ can be excreted until virtually all of th filtered bicarb is reabsorbed - Secreted H+ must bind buffers (phosphate, NH3, cr) - PH is main stimulus for H secretion, though K, aldo and volume can affect this.- Renal Hydrogen excretion - Critical to understand that loss of bicarb is like addition of hydrogen to the body - So all bicarb must be reabsorbed before dietary H load can be secreted - GFR of 125 and bicarb of 24 results in 4300 mEq of bicarb to be reabsorbed daily - Reabsorption of bicarb and secretion of H involve H secretion from tubular cells into the lumen. - Thee initial points need to be emphasized - Secreted H+ ion are generated from dissociation of H2O - Also creates OH ion - Which combine with CO2 to form HCO3 with the help of zinc containing intracellular carbonic anhydrase. - This is how the secretion of H+ which creates an OH ultimately produces HCO3 - Different mechanisms for proximal and distal acidification - NET ACID EXCRETION - Free H+ is negligible - So net H+ is TA + NH4 – HCO3 loss - Unusually equal to net H+ load, 50-100 mEq/day - Can bump up to 300 mEq/day if acid production is increased - Net acid excretion can go negative following a bicarb or citrate load - Proximal Acidification - Na-H antiporter (or exchanger) in luminal membrane - Basolateral membrane has a 3 HCO3 Na cotransporter - This is electrogenic with 3 anions going out and only one cation - The Na-H antiporter also works in the thick ascending limb of LOH - How about this, there is also a H-ATPase just like found in the intercalated cells in the proximal tubule and is responsible for about a third of H secretion - And similarly there is also. HCO3 Cl exchanger (pendrin-like) in the proximal tubule - Footnote says the Na- 3HCO3 cotransporter (which moves sodium against chemical gradient NS uses negative charge inside cell to power it) is important for sensing acid-base changes in the cell. - Distal acidification - Occurs in intercalated cells of of cortical and medullary collecting tubule - Three main characteristics - H secretion via active secretory pumps in the luminal membrane - Both H-ATPase and H-K ATPase - H- K ATPase is an exchange pump, k reabsorption - H-K exchange may be more important in hypokalemia rather than in acid-base balance - Whole paragraph on how a Na-H exchanger couldn't work because the gradient that H has to be pumped up is too big. - H-ATPase work like vasopressin with premise H-ATPase sitting on endocarditis vesicles a=which are then inserted into the membrane. Alkalosis causes them to be recycled out of the membrane. - H secretory cells do not transport Na since they have few luminal Na channels, but are assisted by the lumen negative tubule from eNaC. - Minimizes back diffusion of H+ and promotes bicarb resorption - Bicarbonate leaves the cell through HCO3-Cl exchanger which uses the low intracellular Cl concentration to power this process. - Same molecule is found on RBC where it is called band 3 protein - Figure 11-5 is interesting - Bicarbonate resorption - 90% in the first 1-22 mm of the proximal tubule (how long is the proximal tubule?) - Lots of Na-H exchangers and I handed permeability to HCO3 (permeability where?) - Last 10% happens distally mostly TAL LOH via Na-H exchange - And the last little bit int he outer medullary collecting duct. - Carbonic anhydrase and disequilibrium pH - CA plays central role in HCO3 reabsorption - After H is secreted in the proximal tubule it combines with HCO# to form carbonic acid. CA then dehydrates it to CO2 and H2O. (Step 2) - Constantly moving carbonic acid to CO2 and H2O keeps hydrogen combining with HCO3 since the product is rapidly consumed. - This can be demonstrated by the minimal fall in luminal pH - That is important so there is not a luminal gradient for H to overcome in the Na-H exchanger (this is why we need a H-ATPase later) - CA inhibitors that are limited tot he extracellular compartment can impair HCO3 reabsorption by 80%. - CA is found in S1, S2 but not S3 segment. See consequence in figure 11-6. - The disequilibrium comes from areas where there is no CA, the HH formula falls down because one of the assumptions of that formula is that H2CO3 (carbonic acid) is a transient actor, but without CA it is not and can accumulate, so the pKa is not 6.1. - Bicarbonate secretion - Type B intercalated cells - H-ATPase polarity reversed - HCO3 Cl exchanger faces the apical rather than basolateral membrane- Titratable acidity - Weak acids are filtered at the glom and act as buffers in the urine. - HPO4 has PKA of 6.8 making it ideal - Creatinine (pKa 4.97) and uric acid (pKa 5.75) also contribute - Under normal cinditions TA buffers 10-40 mEa of H per day - Does an example of HPO4(2-):H2PO4 (1-) which exists 4:1 at pH of 7.4 (glomerular filtrate) - So for 50 mEq of Phos 40 is HPO4 and 10 is H2PO4 - When pH drops to 6.8 then the ratio is 1:1 so for 50 - So the 50 mEq is 25 and 25, so this buffered an additional 15 mEq of H while the free H+ concentration increased from 40 to 160 nanomol/L so over 99.99% of secreted H was buffered - When pH drops to 4.8 ratio is 1:100 so almost all 50 mEq of phos is H2PO4 and 39.5 mEq of H are buffered. - Acid loading decreases phosphate reabsorption so more is there to act as TA. - Decreases activity of Na-phosphate cotransporter - DKA provides a novel weak acid/buffer beta-hydroxybutyrate (pKa 4.8) which buffers significant amount of acid (50 mEq/d).- Ammonium Excretion - Ability to excrete H+ as ammonium ions adds an important amount of flexibility to renal acid-base regulation - NH3 and NH4 production and excretion can be varied according to physiologic need. - Starts with NH3 production in tubular cells - NH3, since it is neutral then diffuses into the tubule where it is acidified by the low pH to NH4+ - NH4+ is ionized and cannot cross back into the tubule cells(it is trapped in the tubular fluid) - This is important for it acting as an important buffer eve though the pKa is 9.0 - At pH of 6.0 the ratio of NH3 to NH4 is 1:1000 - As the neutral NH3 is converted to NH4 more NH3 from theintracellular compartment flows into the tubular fluid replacing the lost NH3. Rinse wash repeat. - This is an over simplification and that there are threemajor steps - NH4 is produced in early proximal tubular cells - Luminal NH4 is partially reabsorbed in the TAL and theNH3 is then recycled within the renal medulla - The medullary interstitial NH3 reaches highconcentrations that allow NH3 to diffuse into the tubular lumen in the medullary collecting tubule where it is trapped as NH4 by secreted H+ - NH4 production from Glutamine which converts to NH4 and glutamate - Glutamate is converted to alpha-ketoglutarate - Alpha ketoglutarate is converted to 2 HCO3 ions - HCO3 sent to systemic circulation by Na-3 HCO3 transporter - NH4 then secreted via Na-H exchanger into the lumen - NH4 is then reabsorbed by NaK2Cl transporter in TAL - NH4 substitutes for K - Once reabsorbed the higher intracellular pH causes NH4 to convert to NH3 and the H that is removed is secreted through Na-H exchanger to scavenge the last of the filtered bicarb. - NH3 diffuses out of the tubular cells into the interstitium - NH4 reabsorption in the TAL is suppressed by hyperkalemia and stimulated by chronic metabolic acidosis - NH4 recycling promotes acid clearance - The collecting tubule has a very low NH3 concentration - This promotes diffusion of NH3 into the collecting duct - NH3 that goes there is rapidly converted to NH4 allowing more NH3 to diffuse in. - Response to changes in pH - Increased ammonium excretion with two processes - Increased proximal NH4 production - This is delayed 24 hours to 2-3 days depending on which enzyme you look at - Decreased urine pH increases diffusion of ammonia into the MCD - Occurs with in hours of an acid load - Peak ammonium excretion takes 5-6 days! (Fig 11-10) - Glutamine is picked up from tubular fluid but with acidosis get Na dependent peritublar capillary glutamine scavenging too - Glutamine metabolism is pH dependent with increase with academia and decrease with alkalemia - NH4 excretion can go from 30-40 mEq/day to > 300 with severe metabolic acidosis (38 NaBicarb tabs) - Says each NH4 produces equimolar generation of HCO3 but I thought it was two bicarb for every alpha ketoglutarate?- The importance of urine pH - Though the total amount of hydrogren cleared by urine pH is insignificant, an acidic urine pH is essential for driving the reactions of TA and NH4 forward.- Regulation of renal hydrogen excretion - Net acid excretion vary inverse with extracellular pH - Academia triggers proximal and distal acidification - Proximally this: - Increased Na-H exchange - Increased luminal H-ATPase activity - Increased Na:3HCO3 cotransporter on the basolateral membrane - Increased NH4 production from glutamine - In the collecting tubules - Increased H-ATPase - Reduction of tubular pH promotes diffusion of NH3 which gets converted to NH4…ION TRAPPING - Extracellular pH affects net acid excretion through its affect on intracellular pH - This happens directly with respiratory disorders due to movement of CO2 through the lipid bilayer - In metabolic disorders a low extracellular bicarb with cause bicarb to diffuse out of the cell passively, this lowers intracellular pH - If you manipulate both low pCO2 and low Bicarb to keep pH stable there will be no change in the intracellular pH and there is no change in renal handling of acid. It is intracellular pH dependent - Metabolic acidosis - Ramps up net acid secretion - Starts within 24 hours and peaks after 5-6 days - Increase net secretion comes from NH4 - Phosphate is generally limited by diet - in DKA titratable acid can be ramped up - Metabolic alkalosis - Alkaline extracellular pH - Increased bicarb excretion - Decrease reabsorption - HCO3 secretion (pendrin) in cortical collecting tubule - Occurs in cortical intercalated cells able to insert H-ATPase in basolateral cells (rather than luminal membrane) - Normal subjects are able to secrete 1000 mmol/day of bicarb - Maintenance of metabolic alkalosis requires a defect which forces the renal resorption of bicarb - This can be chloride/volume deficiency - Hypokalemia - Hyperaldosteronism - Respiratory acidosis and alkalosis - PCO2 via its effect on intracellular pH is an important determinant of renal acid handling - Ratios he uses: - 3.5 per 10 for respiratory acidosis - 5 per 10 for respiratory alkalosis - Interesting paragraph contrasting the response to chronic metabolic acidosis vs chronic respiratory acidosis - Less urinary ammonium in respiratory acidosis - Major differences in proximal tubule cell pH - In metabolic acidosis there is decreased bicarb load so less to be reabsorbed proximally - In respiratory acidosis the increased serum bicarb increases the amount of bicarb that must be reabsorbed proximally - The increased activity of Na-H antiporter returns tubular cell pH to normal and prevents it from creating increased urinary ammonium - Mentions that weirdly more mRNA for H-Na antiporter in metabolic acidosis than in respiratory acidosis - Net hydrogen excretion varies with effective circulating volume - Starts with bicarb infusions - Normally Tm at 26 - But if you volume deplete the patient with diuretics first this increases to 35+ - Four factors explain this increased Tm for bicarb with volume deficiency - Reduced GFR - Activation of RAAS - Ang2 stim H-Na antiporter proximally - Ang2 also stimulates Na-3HCO3 cotransporter on basolateral membrane - Aldosterone stimulates H-ATPase in distal nephron - ALdo stimulates Cl HCO3 exchanger on basolateral membrane - Aldo stimulates eNaC producing tubular lumen negative charge to allow H secretion to occur and prevents back diffusion - Hypochloremia - Increases H secretion by both Na-dependent and Na-independent methods - If Na is 140 and Cl is 115, only 115 of Na can be reabsorbed as NaCl, the remainder must be reabsorbed with HCO3 or associated with secretion of K or H to maintained electro neutrality - This is enhanced with hypochloridemia - Concurrent hypokalemia - Changes in K lead to trans cellular shifts that affect inctracellular pH - Hypokalemia causes K out, H in and in the tubular cell the cell acts if there is systemic acidosis and increases H secretion (and bicarbonate resorption) - PTH - Decreases proximal HCO3 resorption - Primary HyperCard as cause of type 2 RTA - Does acidosis stim PTH or does PTH stim net acid excretion

Dr. Michelle Gumz is an associate professor at the University of Florida. Her research focuses on the kidney's circadian clock and its relationship to cardiovascular health. In this episode, Dr. Gumz details how the circadian clock provides a mechanism for predictive homeostasis that directly impacts cardiovascular and kidney function. She also explains why normal sleep patterns are critical to long-term health outcomes. Dr. Gumz has a long-time interest in the molecular control of renal function. The Gumz laboratory is investigating the role of the molecular circadian clock in the kidney with the long-term goal of determining how the clock in the kidney contributes to the control of blood pressure and overall cardiovascular health. Aldosterone is a mineralocorticoid hormone that regulates sodium balance and blood pressure. As a graduate student, Dr. Gumz was the first to identify the circadian clock gene Period 1 as an aldosterone target. She has subsequently shown that Period 1 regulates the transcription of alpha ENaC, the aldosterone-regulated and rate-limiting subunit of the epithelial sodium channel. New areas of study include cross-talk between the kidney clock and other tissue clocks and sex differences in the function of Period 1 and Bmal1, another critical core clock gene. Follow Dr. Michelle Gumz on Twitter University of Florida Division of Nephrology, Hypertension & Renal Transplantation Sign up for Erik's weekly newsletter - Adaptation Join the AIM7 Beta Community ABOUT THE BLUEPRINT PODCAST: The BluePrint Podcast is for busy professionals and Household CEOs who care deeply about their families, career, and health. Host Dr. Erik Korem distills cutting edge-science, leadership, and life skills into simple tactics optimized for your busy lifestyle and goals.   Dr. Korem interviews scientists, coaches, elite athletes, entrepreneurs, entertainers, and exceptional people to discuss science and practical skills you can implement to become the most healthy, resilient, and impactful version of yourself.   On a mission to equip people to pursue audacious goals, thrive in uncertainty, and live a healthy and fulfilled life, Dr. Erik Korem is a High Performance pioneer. He introduced sports science and athlete tracking technologies to collegiate and professional (NFL) football over a decade ago. He has worked with the National Football League, Power-5 NCAA programs, gold-medal Olympians, Nike, and the United States Department of Defense.   Erik is an expert in sleep and stress resilience. He is the Founder and CEO of AIM7, a health and fitness app that unlocks the power of wearables by providing you with daily personalized recommendations to enhance your mind, body, and recovery. SUPPORT & CONNECT   Instagram - https://www.instagram.com/erikkorem/ Twitter - https://twitter.com/ErikKorem LinkedIn - https://www.linkedin.com/in/erik-korem-phd-19991734/ Facebook - https://www.facebook.com/erikkorem Website - https://www.erikkorem.com/ Newsletter - https://erikkoremhpcoach.activehosted.com/f/  ______________________________________________________________ QUOTES   “The key is using stress and adapting to it and improving. That's what high performance is to me, the ability to adapt rapidly so you can achieve your potential. There are five key pillars to creating the conditions for adaptability: sleep, exercise, mental resilience, nutrition, and community/relationships.” - Dr. Erik Korem   "Stress is your brain and body preparing you to do something effortful." Dr. Alex Auerbach “I maybe have a different concept on leadership. To me, leading is a verb. If you're leading, you're a leader. If you're swimming, you're a swimmer, if you're driving, you're a driver. If you're leading, you're by definition, a leader. I define leading as being looked to in a particular moment to decide or perform an action based on your unique gifts and abilities. So by that definition, everybody is a leader. All rank and role really describe is how many people are hoping you get it right when it's your turn to wear the weight.” - Clint Bruce "Attention is the currency of performance." - Dr. Peter Haberl “That's what I've discovered in the lives of brilliant, prolific, healthy creatives, is that they have networks of people they leverage in the course of their work. That they learn from, that they were challenged by, that they gave great insight and purview into their own life and work, in such a way that they were able to receive feedback that helped them get better at what they do.” - Todd Henry "Restful and fulfilling sleep enables you to grow, adapt, and thrive. It creates the conditions for adaptation, so you can pursue audacious goals and thrive in uncertainty." - Dr. Erik Korem "Most exercise programs fail, not because the reps and sets are poorly designed, but because the program doesn't adjust for how much stress your body can adapt to that day! That's why Dr. Chris Morris' research and practical application of fluid periodization is the key for unlocking your performance potential." - Dr. Erik KoremSee omnystudio.com/listener for privacy information.

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This month on Episode 39 of Discover CircRes, host Cynthia St. Hilaire highlights four original research articles featured in the August 5th and 19th issues of the journal. This episode also features an interview with Dr Annet Kirabo and Dr Ashley Pitzer from Vanderbilt University on their article, Dendritic Cell ENaC-Dependent Inflammasome Activation Contributes to Salt-Sensitive Hypertension.   Article highlights:   Jain, et al. Role of UPR in Platelets   Orlich et al: SRF Function in Mural Cells of the CNS   Xue et al: Gut Microbial IPA Inhibits Atherosclerosis   Wang et al: Endothelial ETS1 on Heart Development   Cindy St. Hilaire:        Hi, welcome to Discover CircRes, the podcast of the American Heart Association's journal Circulation Research. I'm your host, Dr Cindy St. Hilaire from the Vascular Medicine Institute at the University of Pittsburgh, and today I'm going to be highlighting articles from our August 5th and August 19th issues of Circulation Research. I'm also going to have a chat with Dr Annet Kirabo and Dr Ashley Pitzer from Vanderbilt University about their study, Dendritic Cell ENaC-Dependent Inflammasome Activation Contributes to Salt-Sensitive Hypertension.   But before I get to the interview, I first want to share an article from our August 5th issue, and that article is titled, Unfolded Protein Response Differentially Modulates the Platelet Phenotype. The first author of this study is Kanika Jain and the corresponding author is John Hwa from Yale University. Self-stress can lead to protein misfolding, and the accumulation of misfolded proteins can lead to a reduction in protein translation and may alter gene transcription, a process collectively known as the unfolded protein response, or UPR. UPR is well documented in nucleated cells; however, it has not been studied in platelets, which are anuclear, but do have a rapid response to cellular stress. In this study, they investigated the UPR in anucleate platelets and explore its role, if any, in platelet physiology and function.   They found that treating human and mouse platelets with various stressors caused aggregations of misfolded proteins and induction of UPR-specific factors. Oxidative stress, for example, induced the UPR kinase PERK, while an endoplasmic reticulum stressor induced the transcription of the UPR factor XBP1. The team went on to study the UPR in platelets from people with type II diabetes, which is a population in which platelet mediated thrombosis is a major complication. They showed that protein aggregation and upregulation of the XBP1 pathway in diabetic patient platelets correlated with disease severity. Furthermore, treating the diabetic patient platelets with a chemical chaperone that helps to correct protein misfolding reduced protein aggregations and prevented the cells prothrombotic activation. This work confirms that even without transcription, platelets display stress-induced UPR, and that targeting this response may be a way to reduce thrombotic risk in diabetic patients.   Cindy St. Hilaire:        The second article I want to share with you is from our August 5th issue and is titled, Mural Cell SRF Controls Pericyte Migration, Vessel Patterning and Blood Flow, and it was led by Michael Orlich from Uppsala University in Sweden. Blood vessels are lined with endothelial cells and surrounded by mural cells. Vascular smooth muscle cells are the mural cells in the case of veins and arteries, and pericytes are the mural cells in the case of capillaries. In the capillaries, pericytes maintain blood-brain and blood-retina barrier function and can mediate vascular tone, similar to smooth muscle cells. While these pericytes and smooth muscle cells are related, they have distinct roles and characteristics.   To learn more about the similarities and the differences between pericytes and smooth muscle cells, this group examined how each would be affected by the absence of SRF in the other. SRF is a transcription factor, essential for nonvascular or visceral smooth muscle cell function. In visceral smooth muscle cells, SRF drives expression of smooth muscle actin and other smooth muscle genes. Using mice engineered to lack SRF in mural cells, they show that SRF drives smooth muscle gene expression in these pericytes and smooth muscle cells, and its loss from smooth muscle cells causes atrial venous malformations and diminishes vascular tone. In pericytes, loss of SRF impaired cell migration in angiogenic sprouting. In a mouse model of retinopathy, activation of SRF drove pathological growth of pericytes. This work not only highlights the various functions of SRF in mural cell biology, but it also suggests that it has a role in pathological capillary patterning.   Cindy St. Hilaire:        The third article I want to share is from our August 19th issue of Circulation Research and is titled, Gut Microbially Produced Indole-3-Propionic Acid Inhibits Atherosclerosis by Promoting Reverse Cholesterol Transport and its Deficiency Is Causally Related to Atherosclerotic Cardiovascular Disease. The first authors are Hongliang Xue and Xu Chen, and the corresponding author is Wenhua Ling from Sun Yat-Sen University in Guangzhou, China. Recent studies provide evidence that disorders in the gut microbiota and gut microbiome derived metabolites affect the development of atherosclerosis. However, which and how specific gut microbial metabolites contribute to the progression of atherosclerosis and the clinical relevance of these alterations remain unclear. Gut microbiome derived metabolites, such as short-chain fatty acids and trimethylamine N-oxide, or TMAO, have been found to correlate with atherosclerotic disease severity.   This study has now found that serum levels of indole-3-propionic acid, or IPA, are lower in atherosclerosis patients than controls. The team performed unbiased metagenomic and metabolomic analyses on fecal and serum samples from 30 coronary artery disease patients and found that, compared with controls, patients with atherosclerosis had lower gut bacterial diversity, depletion of species that commonly produce IPA and lower levels of IPA in their blood. Examination of a second larger cohort of atherosclerosis patients confirmed this IPA disease correlation. The team also showed serum IPA was reduced in a mouse model of atherosclerosis, and that supplementing such mice with dietary IPA could slow disease progression. Analysis of the macrophages from these mice showed that IPA increased cholesterol efflux, and the team went on to elucidate the molecular steps involved. The results of this study not only unraveled the details of IPA's influence on atherosclerosis, but suggest boosting levels of this metabolite could slow atherosclerotic disease progression.   Cindy St. Hilaire:        The last article I want to share is also from our August 19th issue, and it's titled, Endothelial Loss of ETS1 Impairs Coronary Vascular Development and Leads to Ventricular Non-Compaction. The first author is Lu Wang and the corresponding author is Paul Grossfeld, and they are at UCSD. Congenital heart defects, or CHDs, are present in nearly 1% of the human population. In some cases, the heart defects result from a genetic error, which can give researchers clues to its etiology. Jacobson syndrome is a complex condition caused by deletions from one end of chromosome 11, and the occurrence of a congenital heart defect in this syndrome has been associated with the loss of the gene ETS1. ETS1 is an angiogenesis promoting transcription factor, but how ETS1 functions in heart development was not known.   Wang and colleagues now show that both global or endothelial-specific loss of ETS1 in mice caused differences in embryonic heart development that ultimately led to a muscular wall defect known as ventricular non-compaction. The mice also had defective coronary vasculogenesis associated with decreased abundance of endothelial cells in the ventricular myocardium. RNA sequencing of ventricular tissue revealed that, compared with controls, mice lacking ETS1 had reduced expression of several important angiogenesis genes and upregulation of extracellular matrix factors, which together contributed to the muscular and vascular defects.   Cindy St. Hilaire:        Today I have with me, Dr Annet Kirabo and Dr Ashley Pitzer, both from Vanderbilt University, and we're going to talk about their paper, Dendritic Cell ENaC-Dependent Inflammasome Activation Contributes to Salt-Sensitive Hypertension. This article is in our August 5th issue of Circulation Research. Thank you both so much for joining me today.   Annet Kirabo:             Yeah, thank you so much for having us.   Ashley Pitzer:              Yeah, thank you for having us.   Cindy St. Hilaire:        Yeah, it's a great paper. I think we're all familiar with hypertension and this idea that too much salt is bad for our cardiovascular system. When I was a kid, my grandparents had those salt replacements on their kitchen table, Mrs. Dash and whatever. But, like you said in the start of your paper, the exact mechanism by which salt intake increases blood pressure and also increases cardiovascular risk, it's not really well understood, and you guys are focusing on the contribution of immune responses in this process or in this pathogenesis. Before we dig into the details of your paper, I was wondering if you could give us a little bit of background about what's known regarding the role of inflammation in this salt-sensitive hypertension pathogenesis.   Annet Kirabo:             Yeah. It's difficult to know where begin to from, but the role of inflammation in cardiovascular disease have been known for many, many decades. Right now, Dr David Harrison showed more than 10 years ago that T cells contribute to hypertension, but the mechanisms were not known. Back when I was a post doc in David Harrison's lab, we discovered a new mechanism, how immune cells are activated in inflammation and hypertension, whereby we found that there is increased oxidative stress in antigen-presenting cells. This leads to formation of oxidative products known as arachidonic acid or lipid products known as isolevuglandin, or IsoLGs. These IsoLGs are highly, highly reactive and they adapt to lysines on proteins. This is a covalent binding, which leads to permanent alteration of proteins, and so these proteins act as neoantigens that are presented as self-antigens to T cells, leading to an autoimmune-like state in hypertension.   Annet Kirabo:             We found that these antigen-presenting cells are activated and they start producing a lot of cytokines that paralyze T cells to IL-17 producing T cells that contribute to hypertension. And so, when I started my lab back in 2016, we discovered that excess dietary salt profoundly activates this pathway, and we found for the first time that these antigen-presenting cells, they express ENaC, the epithelial sodium channel, and sodium goes into these antigen-presenting cells and activates the NADPH oxidase, which is an enzyme which produces this reactive oxygen species, leading to this IsoLG formation, which I've talked about, and leading to inflammation.   So, three years ago when Ashley joined my lab, she had extensively studied the inflammasome in her PhD program, and she suggested why don't we look at the role of the inflammasome in this pathway and how IsoLG may contribute to this. In her paper that we are discussing right now, she found that in a dependent manner, sodium enters the cell and activates this pathway, and the NLRP3 inflammasome is involved in this process.   Cindy St. Hilaire:        That's such a wonderful story that fits together so many pieces. One of the things you talk about, which I guess I didn't even appreciate myself is, there are certain individuals out there who are more salt-sensitive than others.   Annet Kirabo:             Yeah.   Cindy St. Hilaire:        What is that difference? Do we know the root cause of that? And then also, how many individuals are we talking about are salt-sensitive?   Annet Kirabo:             Salt-sensitive blood pressure, it is a variable trait and it's normally distributed in the population, but it happens more in some individuals than others. It happens even in 25% of people without any hypertension. These people go to that doctor, that doctor thinks they're normal, they don't have any hypertension, but these people can be at a risk of sudden heart attack or cardiovascular risk or even a stroke, simply because when they eat a salty meal, their blood pressure will go up.   Cindy St. Hilaire:        Yeah, that's one of my questions. How much salt are we talking about here? And not only how much in a meal, but a sustained amount? How bad is a miso soup a day?   Annet Kirabo:             Yes. The American Heart Association and the World Health Organization have recommendations. American Heart Association recommends one spoon per day. We have refused to adapt to this recommendation, but that is the recommendation that they have recommended per day to eat. But this is difficult because most of the salt, as you know, is already in our food through processing in our processed foods and we don't have any control over how much salt we have, and there's also a lot of adding of salt at a table.   Cindy St. Hilaire:        Ashley, your background was more the inflammasome. What were your thoughts entering into this project? Did you have much of a hypertension background?   Ashley Pitzer:              No. My graduate thesis focused mainly on endothelial dysfunction and cardiovascular disease, and so it was a pretty easy segue. But it was just with Annet, so excited about the project and showing me all the data and this robust IL-1 beta production that she was seeing after these immune cells being exposed to high salt, I, with my inflammasome background, was immediately like, this could be playing a role. And so it was, like I said, a pretty easy transition and, as is in the paper, we're doing human studies. All of my research back in grad school was very basic research, so it was very exciting to see how our research was being translated with people having this condition and potentially finding mechanisms where we can target this to help actual people.   Cindy St. Hilaire:        I think a lot of us who are not in the hypertension field, and maybe this was you before you joined Annet's lab, we really only kind of think of the kidneys and the blood vessels when we think about hypertension, but studies like this are changing that. And I think a lot of Annet's earlier work, as well as the work of others, have shown a role for this epithelial sodium channel as an important player in this salt-induced hypertension. New to me, it's not just found in the kidney, which I totally did not appreciate that. And it's this channel sensing the salt that can trigger this IL-1 beta production that does a whole bunch of other things.   Cindy St. Hilaire:        What are those other things? What are those cells that are affected and where is this happening? Obviously it's not just kidney cells, but is it only in the kidney or are these systemic cells? What do we think is happening?   Ashley Pitzer:              That's the question, is, where is this happening? There's been studies at Vanderbilt by Jens Titze and his lab showing, where are these immune cells sensing the salt? And so they've shown that sodium accumulates in the skin, a huge argument is for they're sensing the sodium in the kidney because that's where a lot of it is being processed. But these immune cells travel through the whole body, so they're seeing it where there are the highest amounts of sodium concentration, and so I would argue it's in the kidney.   Annet Kirabo:             Indeed, because we're now collaborating with Tina Kon, and we have recently published with her a paper in the International Journal of Science, where we have done sodium MRI and we find this accumulation of sodium in the kidney even much more than in the skin. And we know that the kidney is where sodium is highly concentrated. So the working hypothesis in the lab is that these immune cells can be activated wherever they are, in the lymph nodes or not, in other tissues, but they can travel to the kidney.   We find that in high salt, if you feed high salt to the mouse, the endothelium in the kidney becomes dysfunctional and it expresses molecules, chemoattractants, that attract these immune cells in the kidney. We think that the high salt accumulation in the kidney can activate these, and then these immune cells are activated and they produce cytokines. Dr Steve Crowley showed that they can produce IL-1 beta, which induces activation of sodium channels that can be induced. We have also actually found that even IL-17 can be produced by these immune cells in the kidney and they can activate sodium channels in the kidney, leading retention of sodium and water and hypertension.   Cindy St. Hilaire:        Very cool. You used a lot of mice in this paper. Can you tell us, I just want to know a little bit about the models you chose to use, but also how similar is hypertension in mouse and humans? Obviously for atherosclerosis, we have to do lots of things to get them to form a plaque. Is hypertension similar in a mouse and do mice also show this salt-sensitive phenotype?   Annet Kirabo:             That is an extremely important point. If you read our paper, we use a slightly different approach. Most people do benchside to bed approach. We did the opposite. We did a bed to benchside approach.   Cindy St. Hilaire:        Always smart.   Annet Kirabo:             Yeah. We first started humans, and then with some references, we went to the mice, because I think when it comes to salt-sensitive blood pressure, mice are different from humans. In fact, if we look in the lab, we find that female mice are protected from salt-sensitive blood pressure, but we find that in the humans, it's the opposite. Females are more prone to salt-sensitive hypertension. Those are studies that we are doing right now. We haven't published. But we know that it can be different.   The model we use most of the time in the lab, the C57 mice, are resistant to salt-sensitive hypertension. These C57 mice would rather die before they raise their blood pressure in response to salt. We can induce salt-sensitivity in these mice like in the paper that we are discussing. When we induce the endothelial dysfunction using L-NAME and we wash it out, then these mice, when you give them, subsequently, salt, suggests that they become salt-sensitive. But we also have a salt-sensitive mouse model that we use, the 129/SV mouse. So we use several models to kind of prove the same thing over and over again with the findings that we found in humans.   Cindy St. Hilaire:        And you used a technique, which I'm a little bit familiar with, but I'd like to hear, A, about it from you, but also your experience in using it, and that is CITE-seq. So, how does that work?   Ashley Pitzer:              That was with our human study where we actually had patients come in, who were hypertensive, took them off medication for 2 weeks. They come in, we get baseline samples, we give them a salt load on one day, and then the next day we completely salt deplete them.   Cindy St. Hilaire:        How much is a salt load? Like a Big Mac? What's a salt load?   Ashley Pitzer:              Yeah, it's pretty much just like eating Lays chips all day. It's a lot of salt. It's a very salty meal.   Annet Kirabo:             And then in addition, we also infuse saline too.   Cindy St. Hilaire:        Oh, wow.   Annet Kirabo:             Because these people, when they come into the hospital, some them have already eating high salt. This approach is to just maximize the whole system so that then when we sort deplete everybody, it's at the same level and it's just to unify the whole process. But sorry, Ashley, you go ahead.   Ashley Pitzer:              With the CITE-seq, we're able to take different patients on different days. So we take samples each day, and we can give each sample a barcode, basically. Give them a barcode, we can pool them all together, process them, and we can sequence their RNA, we can probe for a certain amount of protein expression as well. So then when we analyze, we can look at protein expression, so you get the translation and the transcription for each person on each day, and then you're able to compare. And so you get this huge picture and it's a lot of data.   Cindy St. Hilaire:        How long did it take you to sort through?   Ashley Pitzer:              Well, we have a statistician who does all of that, because my wheelhouse is here and it is on a different planet. So we have somebody who helps us with that who does an unbiased approach. And then once he does an analysis, gives us back what are the things that are changing the most, and one of those was IL-1 beta.   Annet Kirabo:             As you can see, our list is huge, this is a massive input of so many collaborators. We have computational people on there that help us with this. I can't even begin to learn these techniques, but with all this collaboration and the resources at Vanderbilt, these things are possible. And so, this is a really powerful approach where you can combine protein expression and you get the specific cells that express the genes and you couple the channel type to the gene expression.   Annet Kirabo:             We actually found that not all monocytes are the same. There's a specific class that of monocytes, A small class of monocytes that is so angry, and the inflammasome is activated and producing this IL-1 beta, and that is enough to contribute to this phenotype of salt-sensitive hypertension, which dynamically changed according to blood pressure, suggesting that this is a targetable salt-sensitive blood pressure, even in normotensive people, is a targetable trait. And because these monocytes are in blood, can we get a blood sample and routinely diagnose salt-sensitive blood pressure so that doctors are aware and they can appropriately advise patients.   Cindy St. Hilaire:        This was samples obviously taken from a blood draw, right? So they're circulating.   Annet Kirabo:             It was a blood draw, yes.   Cindy St. Hilaire:        What do you think about these immune cells, perhaps, native in the kidney? Do you think the small population of angry cells, like you said, is escaping from the kidney environment? What do you think?   Annet Kirabo:             When I was a post-doc in David Harrison's lab, we found that the most angry dendritic cells that contribute to this inflammation and hypertension are monocyte-derived. So that's why in the human study we focused on monocytes, because there are so many subtypes of dendritic cells, plasmacytoid dendritic, classical dendritic cells. We have studied all of these subtypes, and we have focused on monocyte-derived dendritic cells because they're the ones that seem to be contributing to this phenotype the most.                                     Cindy St. Hilaire:        You guys focused in on the NLRP3 inflammasome, which, obviously it's a really critical component broadly for the innate immune system. Do you think that this is going to be a targetable approach that can be leveraged for hypertension? Or do you think it's too broad? What do you think about that as a therapeutic potential?   Ashley Pitzer:              Even when you look in our paper, and we use a knockout model, where we use a completely global knockout model, put them on high salt, and we give them back only dendritic cells that are from wild-type mice, so they have that NLRP3, that have been exposed to high salt. We were able to increase blood pressure, but I also did, in mice, where I gave them an IL-1 beta neutralizing antibody, similar to canakinumab, which is the CANTOS trial, and there's not much of a difference. There is, but it's minor. It's very minor.   Ashley Pitzer:              So, to be able to target in specific cell types in humans one thing, it's very difficult, and maybe one day we can get there. But I think it at least gives us a better idea of what is the full picture, what's the big mechanism going on with immune cells? In part of our human study, we are looking at something to try and be able to identify who is salt sensitive. So if anything, we're able to sit here and potentially have a way of identifying salt-sensitive patients, where, right now, all we can do is have them come in like we do and do a 3-day study, and not everybody can do that.   Annet Kirabo:             To add onto that, perhaps you know, we are talking about precision medicine. This is an era of precision medicine where you need to really tailor treatments if we can get there, and I think this is one way. CANTOS trial. They had no way of knowing who is salt-sensitive and who is not, it was a global approach, and the lack of differences in blood pressure might be explained that this IL-1 beta pathway is targetable in a specific population whose blood pressure is probably driven by inflammation. There are so many, many mechanisms that drive hypertension, and so perhaps we need to focus this on salt-sensitive people, and maybe we can really use this approach to target. Plus, this is ENaC-dependent.   As you know, amiloride has lost favor in the clinic as a treatment of hypertension, because in the majority, it's not effective. But studies have shown that in Black men, for example, who had been categorized salt-resistant, when they give them amiloride, their blood pressure went down, and yet it's not effective in the majority of the people.   So, can we bring back, can we take another look at amiloride. As our studies indicate that blockade of ENaC is anti-inflammatory and it's also antioxidant agent, can we at least bring back amiloride and look at it again and we focus it for specific populations of people that may be more prone to salt-sensitive hypertension?   Here we have so many targets for potential precision treatment of salt-sensitive potential in this paper. You can target SGK1, which we know is possible, we listed a number of clinical trials that they have used NLRP3 inflammasome inhibitors, you can use amiloride for these people, and you can also potentially scavenge IsoLGs.     Cindy St. Hilaire:        What was the most challenging aspect of this study? There's a lot of moving parts, so what was the biggest challenge? And then, also, what was the most surprising part or the most pleasantly surprising part?   Ashley Pitzer:              You have to think, most of this was going on right when the pandemic hit. And right before that, we had started our human recruitment for the human study. And so that put a little bit of a time damper on it.   Ashley Pitzer:              Other than that, it was just, we were finding one thing, developing a new experiment, doing it again, doing it again. And honestly, what was the most surprising and rewarding was just seeing the same thing in, because we took just PBMCs from normotensive patients, treated them with high salt, and saw the changes that we did with the inflammasome. And to see that exactly again in an in vivo model of giving patients high salt and seeing the same thing, it was very rewarding and confirmed that, okay, we're on the right path. Seeing the same thing over and over and over again, it kind of reaffirms that you had a good idea.   Annet Kirabo:             I might add, one of the most challenging was, initially, the computational. Oh, part of the pandemic I was, the pandemic hit, I had a baby during the pandemic, and it was my time to leave my home, and then all these things were going on. We had a clinical trial where patients had to come in. Vanderbilt was so super supportive ,even checking for COVID-19. Our patients could not have COVID-19. We needed to check them.   Cindy St. Hilaire:        Yeah.   Annet Kirabo:             They also had to check for COVID-19. And so during that time, I realized, wait, I need learn computation analysis. I realized I cannot learn, and then reached out to collaborators that helped. That was extremely challenging. And then the other challenging thing that we faced later during the pandemic is vaccinations. In our criteria, these people cannot be vaccinated for reasons. We've studied inflammation, hypertension, and so vaccination was confounding. And even COVID-19 is even more for confounding. So we had this exclusion criteria where we could not recruit anyone.   Annet Kirabo:             Everybody was having COVID, everybody was being vaccinated, and everybody was in that exclusion criteria, so it was difficult to get people. We have had some slow down, but right now it's beginning to build up.   Cindy St. Hilaire:        So, what's next? What's the next question?   Annet Kirabo:             We have so many.   Cindy St. Hilaire:        That means it was a great study. If you have more, that means it was a great study.   Annet Kirabo:             Yeah. This study and us, it kind of warms. The inside seat just opened up, we have primary data in the genetic regulation of ENaC, we have primary data where we found. We are trying to figure out the specific ENaC channel in these antigen-presenting cells. We don't know. We found that ENaC delta, for example, it's not found in a kidney or you talked about a kidney contribution versus immune cells. ENaC delta is not found in the kidney, but we have primary data that show that ENaC delta is the most correlated with cardiovascular risk, is the most correlated with kidney disease and all forms of hypertension. So now we're like, ENaC delta expressed in the immune cells, not in the kidney, it is the one that is most involved in cardiovascular disease, so how are we going to tell the world that.   Cindy St. Hilaire:        Yeah, very cool.   Annet Kirabo:             Those cells, not necessarily the kidney. The kidney plays a part because the cells are going there, but it's very, very exciting. Plus a number of other lines that we are investigating.   Cindy St. Hilaire:        It's great. Well, congratulations, again, on this publication, on just getting all this done with what sounds like extremely difficult patient recruitment. So, Dr Kirabo and Dr Pitzer, thank you so much for joining me today and I'm looking forward to these next studies on maybe ENaC delta.   Annet Kirabo:             Thank you. Thank you so much.   Ashley Pitzer:              Thank you for having us.   Cindy St. Hilaire:        That's it for the highlights from the August 5th and August 19th issues of Circulation Research. Thank you for listening. Please check out the CircRes Facebook page and follow us on Twitter and Instagram with the handle @CircRes and hashtag Discover CircRes. Thank you to our guests, Dr Annet Kirabo and Dr Ashley Pitzer.   This podcast is produced by Ashara Ratnayaka, edited by Melissa Stoner, and supported by the editorial team of Circulation Research. Some of the copy text for the highlighted articles is provided by Ruth Williams. I'm your host, Dr Cindy St. Hilaire, and this is Discover CircRes, your on the go source for the most exciting discoveries in basic cardiovascular research. This program is copyright of the American Heart Association 2022. Opinions expressed by speakers in this podcast are their own, and not necessarily those of the editors or of the American Heart Association. For more information, visit ahajournals.org.  

Les voy a decir un secreto: el ver óperas primas de estudiantes del CUEC (ahora ENAC) o el CCC es un volado y por eso usualmente trato de evitarlas. Confieso que cuando vi que estaría en programación en el FICG la cinta de Celeste Soledad, era un poco escético de ver la cinta de Alex Argüelles, escrita por él y Emilio Aguilar Pradal, pero debido a que una conocida la estelariza (Michelle Betancourt) y otro conocido la editó (Francisco X. Rivera) decidí darle una oportunidad. Gran acierto. Conocemos a dos hermanas, las que dán título a la cinta, tan dispares como e agua y el aceite. Una tragedia las debe unir, excepto por que una, Celeste (interpretada por Fernanda Echevarría Del Rivero), es una irresponsable de primer nivel, y a pesar de ser la mayor de la casa, prefiere el escapismo y no precisamente como acto de circo para traer dinero a la casa. Por el otro, tenemos a Soledad (Michelle), es la hija menor, dedicada, estudiosa, trabajadora y que quiere entrar a una escuela de artes plásticas... sueño frustrado por la tragedia mencionada. La manera en que ambas hermanas lidian con el fracaso, las responsabilidades y la pérdida es confrontada de maneras ingeniosas e inteligentes, que van desde los comparativos en imágen, en donde ambas comparten lenguaje corporal pero las circunstancias las ponen en extremos opuestos, hasta el manejo de evolución de ellas como personajes y cómo confrontan sus conflictos, en donde el mundo de fantasía y la cruda de ralidad se confrontan, y en donde tristemente hay lugar para el mencionado escapismo.La cinta empieza como una fábula más cercana a la fantasía en la cabeza de una princesa de cuento, con todo y narrador en off de su historia, y de pronto, se vuelve una auténtica historia de terror, en donde nuestra narradora pierde cualquier fiabilidad y es capaz de llevarnos al borde de la locura. Gran trabajo de dirección y realización, y en las actuaciones, Mich se lleva las palmas, mostrando una tremenda versatilidad y muestra que sin problema puede ser una excelente "last girl" de cintas de horror, terror y pánico de ligas mayores. El mismo Alex muestra que, aunque es su ópera prima, puede mostrar este tipo de historias si es que se consolida este equipo de trabajo y continua madurando, ya que su manejo de historia, atmósferas y personajes deja satisfecho al espectador. La cinta se exhibirá el jueves en el Cineforo y el viernes en Cinemex Sania, y si están en Guadalajara, definitivamente vale la pena verla.Este episodio es traído a todos ustedes gracias al apoyo invaluable de:Productora Ejecutiva: Blanca LópezCo-Productor: Dany SaadiaCo-Productor: Juan Carlos Toledo Pérez NúñezCo-Productor: Logan MayerCo-Productor: Miguel HuescaCo-Productor: Óscar CamposCo-Productor: Román RangelAgradecimiento especial a nuestros Patreons: Adriana Fernández, Agustín Galván, Barbas Poéticas, Fernando de Anda, Jaime Rosales, Juan Espíritu, Luiso Uribe, Arturo Manrique, Lau Berdejo, Álvaro Vázquez, Alejandro Alemán, Arturo Aguilar, Emile Rudoy, Enrique Vázquez, Ernesto Diezmartínez, Jorge I. Figueroa, Luis Macías, La Niña Triqui, Marcela Salgado, Mariana Padilla, y Fernando Alonso.Tú también puedes apoyar la creación de este y más programas y recibir crédito (para que aumentes currículum) y otros extras exclusivos en www.patreon.com/churrosypalomitas¿Tienes cuenta de Amazon Prime? ¡Puedes apoyar este proyecto donando el dinero de Jeff Bezos y a ti no te cuesta nada! Instrucciones aquí.https://www.patreon.com/posts/suscripciones-en-40782787¿Quieren continuar la discusión? Tenemos nuestro canal de Discord de Charlas y Palomitas, con distintos temas, unos solo para productores del show y otros para toda la banda.https://discord.gg/gEgCAdC¿Sabías que tenemos playeras bien bonitas con diseños cinematográficos? Los encuentras en nuestra tienda, con envíos a toda la república. ¡Checa el catálogo acá!https://printome.mx/tienda/1/100875fb2c7f3821995.57759414

Les voy a decir un secreto: el ver óperas primas de estudiantes o egresados del CUEC (ahora ENAC) o el CCC es un volado y por eso usualmente trato de evitarlas.Confieso que cuando vi que estaría en programación en el FICG la cinta de Celeste Soledad, era un poco escético de ver la cinta de Alex Argüelles, escrita por él y Emilio Aguilar Pradal, pero debido a que una conocida la estelariza (Michelle Betancourt) y otro conocido la editó (Francisco X. Rivera) decidí darle una oportunidad. Gran acierto.¿Lo quieres en audio? Lo puedes descargar aquí o escuchar en el siguiente reproductor. También puedes escucharnos con tus aplicaciones favoritas como Spotify, Apple Podcasts, Pocket Cast, Spreaker, Stitcher, Tune In, Acast, Player FM, MixCloud, Overcast, iHeart Radio, Hear This At, Podcast Addict, Castbox, y hasta en iVoox.Conocemos a dos hermanas, las que dán título a la cinta, tan dispares como e agua y el aceite. Una tragedia las debe unir, excepto por que una, Celeste (interpretada por Fernanda Echevarría Del Rivero), es una irresponsable de primer nivel, y a pesar de ser la mayor de la casa, prefiere el escapismo y no precisamente como acto de circo para traer dinero a la casa. Por el otro, tenemos a Soledad (Michelle), es la hija menor, dedicada, estudiosa, trabajadora y que quiere entrar a una escuela de artes plásticas... sueño frustrado por la tragedia mencionada.La manera en que ambas hermanas lidian con el fracaso, las responsabilidades y la pérdida es confrontada de maneras ingeniosas e inteligentes, que van desde los comparativos en imágen, en donde ambas comparten lenguaje corporal pero las circunstancias las ponen en extremos opuestos, hasta el manejo de evolución de ellas como personajes y cómo confrontan sus conflictos, en donde el mundo de fantasía y la cruda de ralidad se confrontan, y en donde tristemente hay lugar para el mencionado escapismo.La cinta empieza como una fábula más cercana a la fantasía en la cabeza de una princesa de cuento, con todo y narrador en off de su historia, y de pronto, se vuelve una auténtica historia de terror, en donde nuestra narradora pierde cualquier fiabilidad y es capaz de llevarnos al borde de la locura.Gran trabajo de dirección y realización, y en las actuaciones, Mich se lleva las palmas, mostrando una tremenda versatilidad y muestra que sin problema puede ser una excelente "last girl" de cintas de horror, terror y pánico de ligas mayores. El mismo Alex muestra que, aunque es su ópera prima, puede mostrar este tipo de historias si es que se consolida este equipo de trabajo y continua madurando, ya que su manejo de historia, atmósferas y personajes deja satisfecho al espectador.La cinta se exhibirá el jueves en el Cineforo y el viernes en Cinemex Sania, y si están en Guadalajara, definitivamente vale la pena verla.Este episodio es traído a todos ustedes gracias al apoyo invaluable de:Productora Ejecutiva: Blanca LópezCo-Productor: Dany SaadiaCo-Productor: Juan Carlos Toledo Pérez NúñezCo-Productor: Logan MayerCo-Productor: Miguel HuescaCo-Productor: Óscar CamposCo-Productor: Román RangelAgradecimiento especial a nuestros Patreons: Adriana Fernández, Agustín Galván, Barbas Poéticas, Fernando de Anda, Jaime Rosales, Juan Espíritu, Luiso Uribe, Arturo Manrique, Lau Berdejo, Álvaro Vázquez, Alejandro Alemán, Arturo Aguilar, Emile Rudoy, Enrique Vázquez, Ernesto Diezmartínez, Jorge I. Figueroa, Luis Macías, La Niña Triqui, Marcela Salgado, Mariana Padilla, y Fernando Alonso.Tú también puedes apoyar la creación de este y más programas y recibir crédito (para que aumentes currículum) y otros extras exclusivos en www.patreon.com/churrosypalomitas¿Tienes cuenta de Amazon Prime? ¡Puedes apoyar este proyecto donando el dinero de Jeff Bezos y a ti no te cuesta nada! Instrucciones aquí.¿Quieren continuar la discusión? Tenemos nuestro canal de Discord de Charlas y Palomitas, con distintos temas, unos solo para productores del show y otros para toda la banda.¿Sabías que tenemos playeras bien bonitas con diseños cinematográficos? Los encuentras en nuestra tienda, con envíos a toda la república. ¡Checa el catálogo acá!

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