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54 episodes with m1 m2
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2 episodes with m1 m2
2 episodes with m1 m2
2 episodes with m1 m2
七月新增人民币贷款仅为2600亿元，大幅低于预期的4560亿元，创下2009年以来新低。居民和企业贷款双双减少，消费和投资需求均疲软，消费降级明显，高端消费品销量锐减。虽然宽松货币政策有利于资本市场，但难以提振实体经济。货币宽松无法转化为实际需求，整体经济复苏面临挑战。00:02:01:贷款数据揭示消费趋势：居民贷款减少，企业贷款困难00:04:01:信贷数据揭示经济前景：贷款减少、房产价值下降对信心产生影响00:06:02:实体融资需求低迷，货币宽松对资本市场有利但对实体难有直接影响00:08:03:M1与M2增速放缓，实体经济需求低迷，市场情绪悲观00:10:04:社融数据公布，市场预期平淡，利好出尽是否意味着趋势反转？00:12:09:七月经济数据发布：财政发力不足，需求走弱，对市场形成负面的影响
Send us a Text Message.Welcome to part two of our Season Three Opener! We are joined by five medical students from across the globe, in a two-part episode, to discuss neurology at the medical school level. This is a continuation of our medical student episode. In part one, we covered the preclinical years (M1-M2) of medical school training. In part two, we will cover the clinical years (M3-M4). Listen along to find out more about neurology in medical school!Our Guests:Meera Nair is a rising second-year medical student at Northeast Ohio Medical University. She attended The Ohio State University as an undergrad where she majored in Behavioral Neuroscience. Her academic interests are neuroscience, psychiatry, and sleep medicine. Sean Hergenrother is a rising M3 at Northeast Ohio Medical University. He is originally from the Cincinnati area and attended Marquette University in Milwaukee, Wisconsin to obtain his undergraduate degree. Dr. Andrea Mendez Colmenares is a Venezuelan medical doctor and cognitive neuroscientist. She completed her PhD and a postdoctoral fellowship in Colorado. She recently began her neurology residency at Duke University. Dr. Neha Saini is a recent graduate of Florida State University College of Medicine. Before this, she obtained her undergraduate degree at the University of Flordia and her Master of Public Health Degree from George Washington University. She will start her neurology residency training at UF-Gainesville. She also serves as the social media chair for the Neurophiliia Podcast! Dr. Idha (Joy) Sood, is a new Neurology PGY-1 resident at UTSA. She fell in love with Neurology after watching a Bollywood movie and there was no going back since! Our Hosts:Dr. Nupur Goel is a rising second-year neurology resident at Mass General Brigham in Boston, MA. Follow Dr. Nupur Goel on Twitter @mdgoelsDr. Blake Buletko is a vascular neurologist and program director of the Adult Neurology Residency Program at the Cleveland Clinic in Cleveland, OH. Follow Dr. Blake Buletko on Twitter @blakebuletkoFollow the Neurophilia Podcast on Twitter and Instagram @NeurophiliaPodSupport the Show.
Send us a Text Message.The Neurophilia Podcast is back and better than ever with our Season Three Opener! We are joined by five medical students from across the globe, in a two-part episode, to discuss neurology at the medical school level. Part one covers the preclinical years (M1-M2) of medical school training. Part two covers the clinical years (M3-M4) and is out on 8/19/24. Listen along to find out more about neurology in medical school!Our Guests:Meera Nair is a rising second-year medical student at Northeast Ohio Medical University. She attended The Ohio State University as an undergrad where she majored in Behavioral Neuroscience. Her academic interests are neuroscience, psychiatry, and sleep medicine. Sean Hergenrother is a rising M3 at Northeast Ohio Medical University. He is originally from the Cincinnati area and attended Marquette University in Milwaukee, Wisconsin to obtain his undergraduate degree. Dr. Andrea Mendez Colmenares is a Venezuelan medical doctor and cognitive neuroscientist. She completed her PhD and a postdoctoral fellowship in Colorado. She recently began her neurology residency at Duke University. Dr. Neha Saini is a recent graduate of Florida State University College of Medicine. Before this, she obtained her undergraduate degree at the University of Flordia and her Master of Public Health Degree from George Washington University. She will start her neurology residency training at UF-Gainesville. She also serves as the social media chair for the Neurophiliia Podcast! Dr. Idha (Joy) Sood, is a new Neurology PGY-1 resident at UTSA. She fell in love with Neurology after watching a Bollywood movie and there was no going back since! Our Hosts:Dr. Nupur Goel is a rising second-year neurology resident at Mass General Brigham in Boston, MA. Follow Dr. Nupur Goel on Twitter @mdgoelsDr. Blake Buletko is a vascular neurologist and program director of the Adult Neurology Residency Program at the Cleveland Clinic in Cleveland, OH. Follow Dr. Blake Buletko on Twitter @blakebuletkoFollow the Neurophilia Podcast on Twitter and Instagram @NeurophiliaPodSupport the Show.
本期节目深入解析7月12号央行公布的六月份金融数据，直面新增人民币贷款与社融规模接近预期但仍暗藏信号，特别关注M1和M2同比增速刷新历史新低的问题。从信贷需求下降到金融市场的反响，以及中国经济转型期的融资体系调整，一起探讨当前中国经济面对的挑战与转机。00:02:03:金融数据发布后，市场信心恢复面临困境，我国融资体系将如何调整？00:04:05:未来融资趋势：科技创新与心智生产力主导发展路线00:06:06:战略新兴产业企业的IPO标准：解读中国股市的未来趋势00:08:08:科技创业热情高涨，参与创新的年轻人不断涌现
【文稿：】今天来学一个简单的公式，这个公式可以帮助大家快速了解市场流动性的变化，不要小看流动性对股市的影响，毕竟影响市场的除了经济就是流动性。公式内容非常简单，就是一套减法公式，名字叫M1、M2剪刀差。所谓剪刀差是指M1和M2的增速差，注意、这里说的是增速差，不是数量差。换句话说，你需要知道M1和M2彼此的增速之后、才能求出二者的增速差、也就是所谓的剪刀差。举个例子：每个月统计局都会公布上个月的宏观数据，当然也包括M1、M2等货币供应量数据，我们假设上个月M1的金额同比去年增长了8%，而M2同比去年增长了6%，这时候M1、M2的剪刀差就是2%，也就是用M1的增速8%-M2的增速6%=2%。算法很简单、相信大家都能记住。学会剪刀差是为了让我们更直观的看到流动性的变化。还记得M1和M2的统计范畴吗？M1统计的是社会中的现金+活期存款，而M2统计的是社会中的现金+活期存款+定期存款。了解这些之后我们就能得出一下结论：当M1、M2剪刀差为正数时，说明社会中的“活钱”在变多，所谓的“活钱”是指流动性较好的资金，比如现金和活期存款。剪刀差为正数，说明大量资金是以现金和活期存款的形式存在，而这些资金的流动性很好，随时可以用于消费和投资，这将有利于经济增长、当然也有利于股市上涨。相反，当M1、M2剪刀差为负数时，说明资金更多是以定期存款的形式存在，定存的流动性很差，说明市场中的“活钱”在变少，带来的后果自然不利于经济扩张和股市上涨。你会发现这套结论其实在上期内容也都讲过，当时我说的很清楚：分析时不能只盯着一个数据看，相互之间对比之后你才能看出流动性的变化，只不过有些同学不太擅长举一反三，而公式的意义就是将灵活的东西刻板化，死记公式虽不利于变通，但在套取结果方面确实很方便。另外，公式虽好但也要学会适当变通，M1、M2剪刀差为正数也并不意味着绝对的利好，你需要观察剪刀差趋势的变化，也就是剪刀差在扩张还是在收缩？举个例子：假设1-3月份，M1、M2的剪刀差为3%，2%，1%，三个月的剪刀差均是正数，但是差值正在缩小，也就是剪刀差在收缩。这时候我们要活学活用、不能死记公式、认为剪刀差为正就是流动性强的表现。趋势告诉我们，虽然流动性不错，但不错的程度正在放缓，这就好比1、2、3、4、5这串数字，虽然一直在增长，但增速一直在下降。股市的交易都是在交易未来的预期，当市场看到某一种趋势的时候，一定会提前去交易未来，比如现在看到衰弱的趋势时，市场会提前认定未来会衰弱，进而朝着该方向交易、反之亦然。所以看数据要学会看数据变化的趋势，趋势向好才值得给出积极的评价，仅通过的单一结果下定论过于片面。（内容已登记版权，翻版必究！）
【文稿：】股市基本面分析中，离不开对流动性的分析，而在流动性分析中必然少不了对货币供应量的分析。上期我们了解了何为货币供应量？而今天我们就来详细了解一下有关货币供应量的具体数据，也就是通过哪些数据能看到货币供应量的具体变化？今天要学的数据有三个，分别为M0，M1和M2，别看是三个数据，但数据之间都有一定的联系，理解起来并不难。按照顺序我们先来了解第一个，也就是M0，M0指的就是社会流通中的现金，其反映的是货币的数量，也就是社会中有多少纸币或硬币，把这些现金加起来就是M0。举个例子：社会中有100元现金在流通，这时M0就等于100元，如果此时又多出了100元现金，那么M0就变成了200元。然后再来了解一下M1的概念，M1指的是狭义货币供应量，它统计的是社会中的现金和银行的活期存款，也就是在M0的基础上加银行中的活期存款。假设社会中的现金是100元，银行体系中的活期存款为100元，此时M0就是100元，而M1则是200元。对比M0和M1你就会发现一个问题，二者反映的都是货币的总量，但由于考量的流动性不同，所以数值上有一些差异。流动性最好的一定是现金，而反映现金的是M0。银行的活期存款虽然可以随时支取，但流动性不比现金，M1统计的是现金+活期存款，统计的范围更广了，对流动性的要求也更低了。最后再来学学M2，M2指的是广义货币供应量，它统计的是现金+活期存款+定期存款得来的，也就是M1+定期存款=M2。假如社会中有100元现金在流通，同时银行体系中的活期存款有100块，定期存款也有100块，此时M0=100元，M1=200元，M2=300元。不难发现，相比M1而言M2对流动性做出了进一步的放宽，把银行中的定期存款也计算在内，所以三个数据虽然都是反映货币量的数据，但彼此之间的数值相差甚远。这时候有人会有疑问，既然都是反映货币量的数据，那平时分析流动性的时候分析哪个较好呢？这个问题没有正确答案，要看你对流动性的要求有多高，流动性最好的一定是现金，所以最能反映流动性的一定是M0，其次是M1、最后是M2。当你了解了三个数据的统计方式后，可以从每个月的数据中看出细微的变化。比如这个月M0的增幅很大，而M1的增幅很小，请问这意味着什么？意味着社会中流通的现金明显变多，而变多的这些钱大多选择在社会中流通，并没有再以活期存款的形式流回到银行体系中。如果多出的现金中，有一部分人选择将钱再存到银行的活期存款中，那么M1的数值也必然大幅会增长。对比M1和M2也是同样的道理，M1增幅明显变大，而M2却没有变化，这又意味着什么？M2比M1多统计了定期存款的部分，M2没有变化，说明更多的人要么选择手里拿着现金，要么选择将钱存入活期存款，可唯独没什么人去存定期存款，所以M1增幅非常明显，而M2却没啥变化。M0，M1，M2都代表货币供应量的变化，它们的增长都意味着社会中的“钱”在变多，但由于三个数据反映流动性的程度不一样，所以你可以根据数据增速的变化了解流动性的变化。M0的大幅增长意味着社会流动性是最宽松的，说明大家都将现金拿在手里，钱只要都拿在手里就容易消费、容易投资，也是最容易刺激经济增长的状态。比M0略差的是M1，M1增长较大说明是现金+活期存款带来的结果，活期存款不如现金的流动性好、但也不算太差，所以M1的增长也能在很大程度上刺激经济、刺激股市。三者中M2对流动性的统计是最宽泛的。如果M2增幅较大，除了现金和活期存款变多的可能性之外，还有可能是定期存款变多的缘故，这一点可以与前两个数据对比后得出相应的结论，如果M0和M1增幅都很小，唯独只有M2在大幅增长，那就说明大量的钱都是以定期存款的方式存在，虽然这在一定程度上对股市也形成了利好，但利好程度相对有限，毕竟定期存款流动性很差。所以分析货币供应量的时候不能只看单一数据，三个数据都去看看，根据彼此的增幅变化，你可以简单得出钱在朝哪个方向流动。（内容已登记版权，翻版必究！）
News On Apple #177 - Gurman: Apple explora 'robô móvel' que 'segue os usuários em suas casas' com o projeto skunk-works; Chips das linhas M1, M2 e M3 têm falha em hardware que pode vazar dados privados dos usuários; Spatial Personas, ainda em fase beta, chegam ao Apple Vision Pro; entre outros assuntos, sempre com muitas dicas e um bate papo descontraído com as curiosidades do mundo Apple. Apresentação: Rafael de Angeli (@rafangeli), Pedro Celli (@pcelli) e Marcelo Dada (@marcelodada88). Edição/mixagem: Guilherme Celli (@mestilinski). Oferecimento/Parceiro: Grupo “Apple Brasil iPhone, watch, macbook, ipad” no Facebook (com mais de 188k membros). Saiba todos os rumores e novidades do mundo Apple em www.newsonapple.com
In this week's episode, the gang discusses the DOJ antitrust lawsuit against Apple, the upcoming WWDC 2024 in June, Apple's chip vulnerability, and Tim Cook's goodwill tour in China. The panel also shares their thoughts on NAB 2024, Nikon's acquisition of RED, Canva's purchase of Affinity, and a recent auction of vintage Apple memorabilia. US Department of Justice and 18 state attorneys general sue Apple for violations of the Sherman Antitrust Act, alleging that Apple maintains an unlawful monopoly. The panel breaks down the DOJ's 88-page complaint, discussing its merits, challenges, and potential outcomes Apple announces the dates for WWDC 2024 (June 10-14), with the panel speculating on potential AI announcements and updates to iOS 18 and iPadOS 18 Mark Gurman's reports on the delay of new iPads due to software issues An unpatchable vulnerability in Apple Silicon chips that can leak secret encryption keys, with the panel discussing its implications and mitigations EU announces investigations into Apple, Meta, and Alphabet under the Digital Markets Act, focusing on the App Store and restrictions on developers Nikon acquires RED Digital Cinema, with Alex Lindsay providing insight into the camera industry and the potential impact of the acquisition Canva acquires Serif, the makers of Affinity Photo, Designer, and Publisher, raising questions about the future of the Affinity suite Tim Cook's visit to China to announce a new Shanghai store and meet with developers and companies, as well as his commitment to launch the Vision Pro headset in China by the end of the year Steve Jobs and Apple memorabilia fetch high prices at auction, including a signed business card and a handwritten check Picks of the Week: Andy: STEVE! (martin) a documentary in 2 pieces - a two-part documentary about the comedian's life and career, premiering on Apple TV+ on March 29th Jason: HomeControl Menu for HomeKit - a Mac menu bar app that allows users to control their home devices without opening the Home app Alex: Nuphy Air96 - a mechanical keyboard which offers a great typing experience and customization options Hosts: Leo Laporte, Alex Lindsay, Andy Ihnatko, and Jason Snell Download or subscribe to this show at https://twit.tv/shows/macbreak-weekly. Get episodes ad-free with Club TWiT at https://twit.tv/clubtwit Sponsors: zscaler.com/zerotrustAI Download StressFace robinhood.com/boost zocdoc.com/macbreak cachefly.com/twit
In this week's episode, the gang discusses the DOJ antitrust lawsuit against Apple, the upcoming WWDC 2024 in June, Apple's chip vulnerability, and Tim Cook's goodwill tour in China. The panel also shares their thoughts on NAB 2024, Nikon's acquisition of RED, Canva's purchase of Affinity, and a recent auction of vintage Apple memorabilia. US Department of Justice and 18 state attorneys general sue Apple for violations of the Sherman Antitrust Act, alleging that Apple maintains an unlawful monopoly. The panel breaks down the DOJ's 88-page complaint, discussing its merits, challenges, and potential outcomes Apple announces the dates for WWDC 2024 (June 10-14), with the panel speculating on potential AI announcements and updates to iOS 18 and iPadOS 18 Mark Gurman's reports on the delay of new iPads due to software issues An unpatchable vulnerability in Apple Silicon chips that can leak secret encryption keys, with the panel discussing its implications and mitigations EU announces investigations into Apple, Meta, and Alphabet under the Digital Markets Act, focusing on the App Store and restrictions on developers Nikon acquires RED Digital Cinema, with Alex Lindsay providing insight into the camera industry and the potential impact of the acquisition Canva acquires Serif, the makers of Affinity Photo, Designer, and Publisher, raising questions about the future of the Affinity suite Tim Cook's visit to China to announce a new Shanghai store and meet with developers and companies, as well as his commitment to launch the Vision Pro headset in China by the end of the year Steve Jobs and Apple memorabilia fetch high prices at auction, including a signed business card and a handwritten check Picks of the Week: Andy: STEVE! (martin) a documentary in 2 pieces - a two-part documentary about the comedian's life and career, premiering on Apple TV+ on March 29th Jason: HomeControl Menu for HomeKit - a Mac menu bar app that allows users to control their home devices without opening the Home app Alex: Nuphy Air96 - a mechanical keyboard which offers a great typing experience and customization options Hosts: Leo Laporte, Alex Lindsay, Andy Ihnatko, and Jason Snell Download or subscribe to this show at https://twit.tv/shows/macbreak-weekly. Get episodes ad-free with Club TWiT at https://twit.tv/clubtwit Sponsors: zscaler.com/zerotrustAI Download StressFace robinhood.com/boost zocdoc.com/macbreak cachefly.com/twit
This week's crypto and tech sphere highlights Apple's crypto-threatening chip flaw, a Binance executive's dramatic escape in Nigeria amidst tax evasion charges against the company, and Nigeria's legal actions. A significant NFT sale sees a loss for Kevin Hart's Bored Ape, and Binance discontinues USDC on Tron. GBTC faces a Bitcoin shortage threat, while Polygon's zkEVM chain encounters a 10-hour downtime, underscoring vulnerabilities in tech and shifts in the crypto landscape.________https://substack.com/@dcndailycryptonewsNews Links
1, 2부 (09:05 ~ 10:00) * 편지 1 : 해외여행 가는 그날까지 ( 당당이 / 경상북도 ) * 편지 2 : 외상값 갚고 남은 외상 *손편지 ( 정선자 / 서울시 관악구 ) #M1 : 커피향 가득한 거리 _ 신형원 (이은영 님의 신청곡) 아침 창가에서 #M2 : 축복합니다 _ 들국화 미담 디톡스, 쓰담쓰담- * 편지 3 : 나를 살려준 친구 은주를 찾아봅니다 ( 문갑순 / 경상남도 진주시 ) * 편지 4 : 붕어빵 아주머니 ( 이은자 / 세종특별자치시 다정북로)
1, 2부 (09:05 ~ 10:00) * 편지 1 : 밤을 잊은 그대에게 ( 강나영 / 대구 수성구) #M1 : 행복한 사람 _ 이문세 (강나영 님 신청곡) 아침창가에서 #M2 : 그대가 있음에 _ 양희은 미담 디톡스, 쓰담쓰담 * 편지 2 : 나를 깨워준 또 다른 삶이 정 ( 송기문(남) / 경기 용인시 ) * 편지 3 : '동입'에서 '밥약'을 아시나요? ( 박영옥 / 경기도 시흥시 은계남로 )
1, 2부 (09:05 ~ 10:00) * 편지 1 : 황당했던 일 ( 당당이 ) #M1 : 가을에 만나 _ 윤건 (김미숙 님 추천곡) 아침창가에서 #M2 : 그대 발길 머무는 곳에 _ 조용필 미담 디톡스, 쓰담쓰담 * 편지 2 : 내 성격~~~ ( 김명화 / 인천광역시 서구 ) * 편지 3 : 제가 진짜 오지랖이 넓은 건가요? ( 당당이 / 경기도 오산시 )
1, 2부 (09:05 ~ 10:00) * 편지 1 : 어머니와의 마지막 데이트 ( 백경택 (남) / 서울 광진구 ) #M1: 엄마의 프로필 사진은 왜 꽃밭일까 _ 김진호 아침 창가에서 #M2: 아파트 _ 윤수일 미담디톡스, 쓰담쓰담 * 편지 2 : 서글픈 날 아빠 면목 세워주신 같은 아빠에게 감사합니다 ( 차동수(남) / 충북 충주시 ) * 편지 3 : 꼰대 단상 ( 양용모(남) / 전북 전주시 )
1, 2부 (09:05 ~ 10:00) * 편지 1 : 딸의 행복을 응원하며 ( 당당이 / 경기도 ) # M1: 행복 _ 인순이 아침 창가에서 # M2: 물어본다 _ 이승환 미담디톡스, 쓰담쓰담 * 편지 2 : 지금이닷~! *손편지 ( 김경하 / 전남 순천시) * 편지 3 : 냉장고를 바꾸고 ( 정금희 / 경북 봉화군 )
1, 2부 (09:05 ~ 10:00) * 편지 1 : 심야 여성시대 ( 당당이 ) #M1: 그대에게 _ 신해철 아침 창가에서 #M2: 라디오를 켜봐요 _ 신승훈 미담디톡스, 쓰담쓰담 * 편지 2 : 이런 코너가 생겨 정말 반갑습니다! (권해숙 / 경상북도 경산시 옥산로) * 편지 3 : 결혼 후 14년만에 내 집 마련! (안새미로 / 경기도 화성시)
1, 2부 (09:05 ~ 10:00) * 편지 1 : 광복절에 든 생각 ( 신양옥 / 서울 금천구 두산로 ) #M1 : 한계령 _ 양희은 아침창가에서 #M2 : 그대에게 _ 신해철 * 편지 2 : 남자의 양산 *손편지 ( 박한목 / 서울시 구로구) * 편지 3 : 닭과 백조 ( 윤성원 / 경기 고양시 일산서구 )
1, 2부 (09:05 ~ 10:00) * 편지 1 : 고마운 구급대원님께 *손편지 ( 당당이 / 경기도 광명시 ) # M1: 이젠 나만 믿어요 _ 임영웅 아침 창가에서 # M2: 젊은 그대 _ 김수철 * 편지 2 : 어느 통장의 하루 ( 당당이 / 대전 유성구 유성대로 ) # M3: 출발 _ 김동률 (1458님 신청곡)
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.08.01.550767v1?rss=1 Authors: Martins-Ferreira, R., Calafell-Segura, J., Leal, B., Rodriguez-Ubreva, J., Mereu, E., Pinho e Costa, P., Ballestar, E. Abstract: Dysregulated microglia activation, leading to neuroinflammation, is currently considered to be of major relevance in the development and progression of neurodegenerative diseases. The initial M1/M2 dual activation classification for microglia is now considered outdated. Even the "disease-associated microglia" (DAM) phenotype, firstly described in mice, has proven insufficient to precisely represent the multitude of microglia phenotypes in pathology. In this study, we have constructed a transcriptomic atlas of human brain immune cells by integrating single-nucleus (sn)RNA-seq datasets from multiple neurodegenerative conditions. Sixteen datasets were included, comprising 295 samples from patients with Alzheimer's disease, autism spectrum disorder, epilepsy, multiple sclerosis, Lewy body diseases, COVID-19, and healthy controls. The integrated Human Microglia Atlas (HuMicA) dataset included 60,557 nuclei and revealed 11 microglial subpopulations distributed across all pathological and healthy conditions. Among these, we identified four different homeostatic clusters as well as pathological phenotypes. These included two stages of early and late activation of the DAM phenotype and the disease-inflammatory macrophage (DIM) phenotype, which was recently described in mice, and is also present in human microglia, as indicated by our analysis. The high versatility of microglia is evident through changes in subset distribution across various pathologies, suggesting their contribution to the establishment of pathological phenotypes. Our analysis showed overall depletion of four substates of homeostatic microglia, and expansion of niche subpopulations within the DAM and DIM spectrum across distinct neurodegenerative pathologies. The HuMicA is an invaluable resource tool used to support further advances in the study of microglia biology through healthy and disease settings. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC
Join Jem and Justin as they discuss new ChatGPT tricks, challenges in AI and Fusion 360's improved performance on Apple silicon chips. Expect laughter, NSFW anecdotes, and an exploration of shop happiness.Watch on YoutubeDISCUSSED:✍️ Send Comments on this EpisodePlease note: Show notes contains affiliate links.Hiring CornerEverything I want to talk about is NSFW
1, 2부 (09:05 ~ 10:00) * 편지 1 : 비행기 타고 만나러 갈게, 그때 꼭 내 사과 받아줘! ( 엄영미 / 전라남도 여수시 ) #M1 : 아버지 _ 인순이 아침 창가에서 #M2 : 동행 _ 김동률 * 편지 2 : 아름다운 세상 *손편지 ( 김도연 / 울산시 남구 ) * 편지 3 : 매일 백년을 돌봅니다 ( 오현숙 / 서울 노원구 )
1, 2부 (09:05 ~ 10:00) * 편지 1 : 지난 시간은 소환하지 않아야 해요 ( 김용태(남) / 경상남도 양산시 ) #M1: 편지 _ 김광진 아침 창가에서 #M2: 일어나 _ 김광석 * 편지 2 : 어머니의 유효기간 ( 황인원(남) / 경기도 부천시 ) * 편지 3: 평행선에 서서 인생 개척기 ( 송인식(남) / 인천광역시 남동구)
3, 4부 (10:05 ~ 11:00) * 최수연 리포터 연결 * 전화2: 한국 환경 연구원, 이승수 부연구위원 이례적인 물폭탄 원인과 한반도 기후 전망 * 편지2: 반지하 가족 이야기 (김지혜 / 서울 은평구 갈현로) #M1: 이 또한 지나가리라_신승훈 (박미경님 신청곡) #M2: 나의 꽃, 너의 빛 _ 양희은, 첸
1, 2부 (09:05 ~ 10:00) * 편지 1 : 내 남편을 위한 변명 ( 이승일 / 서울 서대문구 홍제3동 ) # M1: 당신만이 _ 이치현과 벗님들 아침 창가에서 # M2: 기도 _ 윤하 * 편지 2 : 인생은 마치 대용량 로션 같다 ( 장윤석(남) / 서울 강동구 양재대로 ) * 편지 3 : 아빠의 직밍아웃! 어떻게 해야 할까요? ( 당당이 )
1, 2부 (09:05 ~ 10:00) * 편지 1 : 나의 불안장애 극복기 ( 당당이(남) / 서울 광진구 ) * 편지 2 : 사람을 지적하지 않기로 했다 ( 남영우 / 강원도 강릉시 ) #M1: 마음 _ 아이유 (김봉수 님 신청곡) 아침 창가에서 #M2: 환희 _ 정수라 * 편지 3 : 펫티켓을 꼭 지켜주세요 ( 오진희 / 전북 익산시 ) * 편지 4 : 잊혀가는 부업방, 지켜주고 있는 고마운 분들 ( 당당이(남) / 경기 남양주시 별내면 )
1, 2부 (09:05 ~ 10:00) * 편지 1 : 어느날 갑자기 *손편지 ( 당당이 ) #M1: 당신만이 _ 이치현과 벗님들 아침 창가에서 #M2 : 상록수 _ 양희은 * 편지 2 : 양귀비 사건 ( 이주원 / 경남 사천시 ) * 편지 3 : 누군가의 경조사 ( 유소영 / 서울 강북구 도봉로 )
1, 2부 (09:05 ~ 10:00) * 편지 1 : 챗팅을 했다 ( 당당이 / 경기도 시흥시 ) * 편지 2 : 어른이 된다는 것 ( 박미연 / 대전광역시 서구) #M1 : 오락실 _ 한스밴드 아침창가에서 #M2 : 아버지 _ 양희은 * 편지 3 : 품앗이는 오씨남매처럼 ( 오현미 / 전라북도 고창군 )
1, 2부 (09:05 ~ 10:00) * 편지 1 : 나는 아직도 아프다 ( 당당이 / 경남 양산시 ) # M1 : 어느날 문득 _ 정수라 아침 창가에서 # M2 : 너의 꽃, 너의 빛 _ 양희은, 첸 * 편지 2 : 미리미리 에어컨 관리 ( 당당이 (남) / 서울 성북구 ) # M3 : 하늘 바라기 _ 정은지
1, 2부 (09:05 ~ 10:00) * 편지 1 : 그림을 그리다 ( 오현주 / 경남 창원시 ) #M1 : 혜화동 _ 박보람 아침창가에서 #M2 : 꽃밭에서 _ 정훈희 * 편지 2 : '한우농장 박은숙'과 '미용실 박은숙' ( 당당이) #M3 : 사랑비 _ 김태우 (7613 님 신청곡)
1, 2부 (09:05 ~ 10:00) * 편지 1 : 다시 태어났습니다 ( 전영기(남) / 충청남도 광주시 ) #M1: 고맙소 _ 김호중 아침 창가에서 #M2: 쇼 _ 김원준 * 편지 2 : 이걸 붙여 말아? ( 이수일 (남) / 경기도 안산시 ) * 편지 3 : 무서운 동남아 모기 ( 이호남 (남) / 경기 파주시 )
1, 2부 (09:05 ~ 10:00) * 편지 1 : 엄마가 된 그 아이 ( 임유미 / 인천광역시 연수구) #M1 : 고마워요 _ 임현정 아침창가에서 #M2 : 출발 _ 어떤 날 * 편지 2 : 여보! 고마워요 ( 김영수(남) / 전북 전주시 )
1, 2부 (09:05 ~ 10:00) * 편지 1 : 내 아들 진효 *손편지 ( 배승희 / 인천 서구 ) # M1 : 나침반 _ 이적 아침 창가에서 # M2 : 풀잎사랑 _ 최성수 * 편지 3 : 그 아이의 40년 *신춘 지원작 ( 김진영(남) / 경남 거제시 ) * 편지 4 : 보고싶다 설화야 *신춘 지원작 ( 조아영 / 경기 과천시 )
1, 2부 (09:05 ~ 10:00) * 편지 1 : 나를 보고 웃어주는 아이 ( 이외숙 / 부산 해운대구 ) #M1 : 너의 의미 _ 아이유 아침창가에서 #M2 : 강남 스타일 _ 싸이 * 편지 2 : 슬기로운 퇴직생활 - 역전의 용사들이 다시 뭉쳤다 ( 지창명(남) / 경북 김천시 ) #M2 : 우린 제법 잘 어울려요 _ 성시경
1, 2부 (09:05 ~ 10:00) * 편지 1 : 초짜배기 베이비시터 ( 장성균 (남) / 경기도 용인시 ) * 편지 2 : 아버지 ( 유성호 (남) / 세종특별자치시 다솜로 ) #M1: 라구요 _ 강산에 아침 창가에서 #M2: 사람이 꽃보다 아름다워 _ 안치환 * 편지 3 : 보이스피싱을 막은 훌륭한 젊은이 *청원 경찰 박주원 님 전화연결 ( 박영진 / 부산 해운대구 )
1, 2부 (09:05 ~ 10:00) * 편지 1 : (신춘 응모작) 봄비 ( 당당이 / 경기 하남시 ) #M1 : 사랑은 늘 도망가 _ 임영웅 아침창가에서 #M2 : 단발머리 _ 조용필 * 편지 2 : 아버지의 여자친구 ( 당당이 / 경남 양산시 하북면 ) * 편지 3 : 초등학교 급식실 풍경 *손편지 ( 임순향 / 울산시 남구 )
1, 2부 (09:05 ~ 10:00) * 편지 1 : (신춘 응모작) 봄비 ( 당당이 / 경기 하남시 ) #M1 : 사랑은 늘 도망가 _ 임영웅 아침창가에서 #M2 : 단발머리 _ 조용필 * 편지 2 : 아버지의 여자친구 ( 당당이 / 경남 양산시 하북면 ) * 편지 3 : 초등학교 급식실 풍경 *손편지 ( 임순향 / 울산시 남구 )
1, 2부 (09:05 ~ 10:00) * 편지 1 : 뇌풀기 퀴즈를 기다리며 ( 남승희 / 경기도 수원시 영통구 ) * 편지 2 : 돌대가리 ( 강미선 / 서울 종로구 ) #M1 : 버터 플라이 _ 러브 홀릭스 아침창가에서 #M2 : 사랑 일기 _ 시인과 촌장 * 편지 3 : 형용사로 남은 봄나물 누이 ( 김명호 (남) / 부산 연제구 ) * 편지 4 : 특수학교 생활 ( 김윤진 / 인천광역시 서구 )
1, 2부 (09:05 ~ 10:00) * 편지 1 : 때려, 때리라니까 ( 김정희 / 서울 중랑구 ) * 편지 2 : 칭찬하고 싶어요 ( 당당이 / 경기도 ) # M1 : 내게도 사랑이 _ 함중아 아침 창가에서 # M2 : 나무야 (동요) * 편지 3 : 할머니의 영상통화 ( 이민희 / 경북 경주시 ) * 편지 4 : 내 나이 50에 혼자가 되었다 ( 당당이 ) # M2 : 밤안개 _ 현미
1, 2부 (09:05 ~ 10:00) * 편지 1 : 부족한 엄마여서 미안해 ( 당당이 / 서울시 ) * 편지 2 : 49년 만에 벚꽃이 눈에 들어왔어요 ( 표경숙 / 경기 평택시 ) #M1: 아모르 파티 _ 김연자 아침 창가에서 #M2: 기쁜 우리 사랑은 _ 최성수 * 편지 3 : '시.스.템.오.류' 다섯 글자에 곤란해진 생활 ( 당당이 )
Au programme de cet épisode de LCDJ : News : Base de données massive de modèles 3D gratuits : https://objaverse.allenai.org/ Un guide pour créer un GDD efficace : https://300mind.studio/blog/game-design-document/ Sortie de la version Android de GDevelop : https://gdevelop.io/ Blender 3.5 disponible avec la prise en charge de puces M1/M2 du Mac : https://www.blender.org/ L'E3 2023 est annulé quelques explications ici : https://www.gamesindustry.biz/e3-2023-is-cancelled-esa-tells-us-why Personne ne se soucie de votre jeu, et pourquoi il faut bien communiquer dessus : https://www.gamedeveloper.com/gdc2023/the-golden-rule-of-game-promotion-no-one-cares-about-your-game Infos : - Soutenez-nous : https://www.patreon.com/lcdj Animé par Anton Monjon Suivez-nous sur twitter : https://twitter.com/coulissesdujeu Youtube: https://www.youtube.com/@coulissesdujeu Twitch : https://www.twitch.tv/coulissesdujeu
1, 2부 (09:05 ~ 10:00) * 편지 1 : 예순 넷의 도보라이더, 두 번째 이야기 ( 당당이 / 서울 ) #M1 : 오늘도 참는다 _ 배기성 아침창가에서 #M2 : 키 작은 하늘 _ 장혜진 * 편지 2 : 주인 찾아간 전동 요양 침대 ( 심혜원 / 강원 홍천군 ) * 편지 3 : 공부방을 접으며 ( 박계령 / 인천 연수구 )
Découvrez le portrait de Lucila Modebelu, directrice d'hôpital dans trois hôpitaux différents, aujourd'hui directrice du site Louise Michel à Clermont-Ferrand, et présidente depuis 3 ans de l'association Fonction Publique du 21ème siècle. Partie 1 - (1'27) Après avoir étudié à Montpellier (2 ans de médecine, 3 ans d'AES) et suivi un M1/M2 droit de la santé à Rennes, Lucila réussit l'un des concours du secteur sanitaire et devient directrice d'hôpital après une formation de 2 ans à Rennes. Partie 2 - (20'01) Directrice d'hôpital dans 3 sites différents et sur des missions stratégiques et de gestionnaire, elle nous raconte l'ambiance unique dans le secteur hospitalière et l'approche managériale nécessaire. Partie 3 - (47'34) Lucila nous livre quelques conseils pour appréhender les concours et le milieu hospitalier ! Pour plus d'informations sur l'association FP21, retrouvez leur site fp21.fr N'hésitez pas à partager autour de vous, à noter le podcast et à follow la chaîne sur les réseaux sociaux pour rester informé (Instagram, Facebook, LinkedIn) Soutenez-nous sur Tipeee !
Meta, lancé à fond de train dans son « année de l'efficacité », a annoncé une nouvelle et impressionnante charrette de licenciements. On y revient dans le flash info, dans lequel il sera aussi question de cette fonction des Pixel qu'Apple serait bien avisée de copier, et aussi évidemment de l'iPhone 14 jaune !Meta va licencier 10 000 personnes supplémentaires, un quart de l'effectif global envolé en six moisMeta met au placard ses NFT moins d'un an après leur lancementApple propose à ses clients américains d'obtenir des conseils avec un vendeur en vidéoGoogle améliore ses Pixel avec des minuteurs synchronisés, la gomme magique pour tous et d'autres progrès logicielsAperçu de l'iPhone 14 jaune sous toutes les facettesEn deuxième partie d'émission, Pierre fait le point sur la virtualisation de Windows sur les Mac équipés M1 ou M2. C'est possible, mais ce n'est pas tout à fait pareil qu'avec les Mac Intel. Windows 11 sur un Mac Apple Silicon : le grand test avec Parallels DesktopWindows 11 sur un Mac Apple Silicon : VMware Fusion 13 à la ramasseBonne écoute ! Et rendez-vous demain matin pour un nouvel épisode de Sortie de veille. Soutenez votre site préféré et bénéficiez d'une version sans pub ! https://plus.acast.com/s/sortie-de-veille-un-podcast-de-macgeneration. Hébergé par Acast. Visitez acast.com/privacy pour plus d'informations.
iPhoneの写真をWindows PCにバックアップして整理する方法/Apple M1/M2でのWindows 11稼働を正式に承認 アンケート 第3回 今回のゲスト回どうでしたか? アンケート 第2回 Surface […]
Catch up on the cybersecurity and tech news of the week with Don, Dan, and Sophie as they cover the latest. This week in tech, Microsoft created support for users running Windows 11 on Macs, and Microsoft’s email customers were reporting inboxes flooded with spam despite email filtering. Meanwhile, Linux dropped systemd 253, introducing a new tool to create Unified Kernel Image (UKI) files. This week in cybersecurity, Microsoft is patching 76 security issues in Windows and OS components, sounding the alarm that some are already being exploited. And finally, in this week’s “Who Got Pwned?” section of the show, GoDaddy revealed that the same group of hackers had access to their networks for 3 years, even though each breach had been detected, and the Scandinavian Airlines website was hacked, compromising the personal information for some customers.
Catch up on the cybersecurity and tech news of the week with Don, Dan, and Sophie as they cover the latest. This week in tech, Microsoft created support for users running Windows 11 on Macs, and Microsoft’s email customers were reporting inboxes flooded with spam despite email filtering. Meanwhile, Linux dropped systemd 253, introducing a new tool to create Unified Kernel Image (UKI) files. This week in cybersecurity, Microsoft is patching 76 security issues in Windows and OS components, sounding the alarm that some are already being exploited. And finally, in this week’s “Who Got Pwned?” section of the show, GoDaddy revealed that the same group of hackers had access to their networks for 3 years, even though each breach had been detected, and the Scandinavian Airlines website was hacked, compromising the personal information for some customers.
1, 2부 (09:05 ~ 10:00) * 편지 1 : 겹경사 축하해주세요 (김규린 / 경남 창원시) * 편지 2 : 중학교 입학식 날 (김응숙 / 경북 영천시) #M1 : 그리움만 쌓이네 _ 노영심 아침 창가에서 #M2 : 바람과 나 _ 한대수 * 편지 3 : 대상포진 이야기 (정현숙 / 경기 용인시) * 편지 4 : 응원합니다 (최은주 / 경기 연천군)
1, 2부 (09:05 ~ 10:00) * 편지 1 : 나는 아빠가 될 자격이 있는가.... (당당이) * 편지 2 : 인생의 선물 (당당이) #M1 : 인생의 선물 _ 양희은 아침창가에서 #M2 : 자기성찰 _ 느티나무 언덕 * 편지 3 : 나는 한 번도 가장이 아니었다 (당당이 / 경기 의정부시) * 편지 4 : 이혼을 고민하고 있습니다 (당당이 / 경기 시흥시)
1, 2부 (09:05 ~ 10:00) * 편지 1 : 친구 아버님의 환상을 깨지 않게 해주세요! (송지원 / 강원 태백시) * 편지 2 : 이렇게 낚인 사람들 (이지연 / 경기 화성시) *루피실내바다낚시터 #M1 : 울릉도는 나의 천국 _ 이장희 아침창가에서 #M2 : 좋아 _ 박재범 * 편지 3 : 늦은 나이에 시작한 간호학도의 임상실습 (공다미 / 경남 사천시) * 편지 4 : 너, 내 딸 맞지? (윤수정 / 경기 안양시)
Bienvenue dans cet épisode 122 d'iWeek (la semaine Apple), le podcast. M1, M2, RAM, SSD : quel Mac choisir en ce début 2023 ? Enregistré le mardi 31 janvier 2023 à 18h00. Présentation : Benjamin Vincent. Intervenants : Elie Abitbol, Gilles Dounès, Fabrice Neuman. Production : OUATCH Audio. Pour soutenir iWeek : patreon.com/iweek. Cette semaine : le choix d'un Mac s'est complexifié, en ce début 2023, avec la sortie des Mac mini M2 / M2 Pro et des MacBook Pro 14 et 16“ à processeur M2 Pro et M2 Max. Dans la gamme, ces nouveaux Mac cohabitent avec des machines encore sous processeur M1. Ajoutez les variables que sont la lenteur de certains SSD, le prix de la RAM et du stockage, le nombre de coeurs CPU et GPU... cette semaine, nous vous aidons à y voir clair et à faire le bon choix ! Une semaine marquée par l'annonce, par Samsung, de sa nouvelle gamme de smartphones Premium : la gamme Galaxy S23 avec notamment le Galaxy S23 Ultra, ses 200 millions de pixels et sa capacité à filmer en 8K à 30 images par seconde. Quels sont les arguments de ce nouveau fer de lance face à l'offre d'Apple ? Le géant coréen a-t-il rattrapé son retard ou repris une longueur d'avance en attendant l'iPhone 15 en septembre ? Autre sujet : le lancement d'une nouvelle gamme de PC portables Samsung qui font immanquablement penser... aux MacBook Pro 14 et 16“. C'est une semaine qui nous tient particulièrement à coeur parce que nous vous présentons notre nouvelle présence sur Patreon ! Fini, le soutien à l'épisode : place aux abonnements mensuels (5, 8 ou 12 € par mois + TVA) et annuels (50, 80 et 120 € par mois + TVA), plus simples pour vous, plus avantageux aussi puisque pour le prix de l'ancien premier niveau (1,50 € par épisode + TVA), vous obtenez l'accès au nouveau deuxième niveau en version annuelle ! Les abonnements annuels vous permettent d'ailleurs de gagner des cadeaux Collector : un jeu d'autocollants "iWeek (la semaine Apple)" et "la quotidienne iWeek" dans le cas du deuxième niveau (80 € par an + TVA) ; ces mêmes stickers + un mug Collector "iWeek (la semaine Apple) avec le troisième et dernier niveau (120 € par an + TVA). Des cadeaux que vous recevrez, par la Poste, sous 7 à 10 jours, uniquement si vous optez pour les abonnements annuels (2e et 3e niveau), pour vous remercier de votre engagement et de vous fidélité. Du côté des avantages immatériels, outre les épisodes sans publicité pour tous, nrnche, sur la chaîne YouTube d'iWeek ! eek (la semaine Apple) et des bonus hebdos. Autre privilège de ce 2è niveau : l'accès au Twitter Space mensuel (audio) pour échanger avec nous. Mais la cerise sur le gâteau, avec le 3èr niveau d'abonnement, c'est l'accès - en streaming, et donc pendant qu'ils se déroulent - aux enregistrements du podcast hebdo, le mardi en fin d'après-midi, et la possibilité d'interagir avec nous, pendant l'enregistrement, via le chat associé. - Premier niveau ("Je soutiens") : 5 € par mois, 50 €$ par an (+ TVA). - Deuxième niveau ("J'aime") : 8 € par mois, 80 €$ par an (+ TVA). - Troisième niveau ("J'adore") : 12 € par mois, 120 €$ par an (+ TVA). Précision importante : nous attendons que Patreon mette en place l'outil de migration pour nos soutiens actuels. Il vous permettra, concrètement, de quitter votre offre de soutien actuel pour choisir l'un des trois nouveaux niveaux d'abonnement. Dès que cet outil sera accessible, les nouvelles offres d'abonnement le seront aussi.
1, 2부 (09:05 ~ 10:00) * 편지 1 : 난방비 폭탄 (당당이 / 경기도) #M1 : 우리의 밤은 당신의 낮보다 아름답다 _ 코나 아침창가에서 #M2 : 보고싶은 얼굴 _ 민해경 * 편지 2 : 어찌하면 좋을까요 (울산 당당이) #M3 : 그때 그 순간 그대로 (그그그) _ WSG 워너비
1, 2부 (09:05 ~ 10:00) * 편지 1 : 소년공 (이영민(남) / 경기 안양시) * 편지 2 : 덕담쟁이 (임유미 / 인천 연수구) #M1 : 늘 지금처럼 _ 이예린 아침 창가에서 #M2 : 사랑은 받는 것이 아니라면서 _ 해오라기 * 편지 3 : 아빠가 남긴 여성시대 CD (김예지 / 충남 아산시) * 편지 4 : 미워할 수도, 좋아할 수도 없는 엄마 (당당이 / 경기 화성시)
1, 2부 (09:05 ~ 10:00) * 편지 1 : 버스 속의 그 손 (김주희 / 경기 수원시) # M1 : 그 사나이 _ 이희문 아침 창가에서 # M2 : 아득히 먼 곳 _ 이승재 * 편지 2 : 어른 노릇 힘들어 (전미정 / 경기 수원시 영통구) * 편지 3 : 얘들아! 몰카범이야~~! (당당이(남))
1, 2부 (09:05 ~ 10:00) * 편지 1 : 잔소리 대마왕 (강민경 / 인천 연수구) * 편지 2 : 공사장 알바 간 아들 (박상희 / 울산 남구) #M1 : 귀거래사 / 김신우 아침 창가에서 #M2 : 못다한 노래 / 양희은 * 편지 3 : 3년만에 다시 산타를 하면서 (의정부 당당이) #M3 : 다시 만난 너에게 / 피노키오
1, 2부 (09:05 ~ 10:00) * 편지 1 : 수고했어 올해도~ (당당이 / 경기 평택시) 아침 창가에서 # M1 : 으라차차 / 럼블피쉬 # M2 : 다 잊어 / 박예나 * 편지 2 : 서울 중흥초 선생님들 소개합니다. (장서빈 / 서울 중랑구) * 편지 3 : 장애 아들을 키우며 (서지연 / 경기 구리시)
1, 2부 (09:05 ~ 10:00) * 편지 1 : 대설 위의 하얀 천사들 (당당이) #M1: 로맨틱 겨울 / 김진표 아침 창가에서 #M2 : 연 / 라이너스 * 편지 2 : 따뜻한 서울 1일 (이주원 / 경남 사천시) * 편지 3 : 커피 인심 (허현석 / 전남 여수시)
1, 2부 (09:05 ~ 10:00) * 편지 1 : 산타버스 이야기 (권도현 / 부산시) # M1 : 울면 어때 / 바버렛츠 - 아침창가에서 # M2 : 무인도 / 김춘자 * 편지 2 : 다낭 국제병원 응급실에서 (김선승 / 경기도 부천시)
3, 4부 (10:05 ~ 11:00) - 주말엔 밥이 되는 시 - (신아랑님 추천시, 김지하 시인 '무화과') #M1: 거위의 꿈 / 인순이 --------------------------------------------------------------- 여성살롱 *겨울에도 꽃이 피는 나무 #M2 : 풀들의 이야기 / 양희은
1, 2부 (09:05 ~ 10:00) * 편지 1 : 1회용품 금지 사연을 듣고 (공간사) * 편지 2 : 늦은 숙제 (최성욱 / 인천 연수구) # M1 : 모두가 천사라면 / 전영 - 아침창가에서 # M2 :질풍가도 / 유정석 ( 만화 '쾌걸 근육맨' ost) * 편지 3 : 생각이 바뀌면 세상도 달라진다 (이종완 / 강원 강릉시) * 편지 4 : 엄마 (양원식 / 부산 영도구)
1, 2부 (09:05 ~ 10:00) * 편지 1 : 흑역사로 남은 첫 수능감독 이야기 (이정희) #M1 : 꽃길만 걷게 해줄게 / 데이브레이크 아침 창가에서 #M2 : 아름다운 세상 / 유리상자 * 편지 2 : 나의 2022년은 (김보라 / 서울 은평구) * 편지 3 : 아빠, 곱창은 이제 식당에서 먹는걸로 해요. (민선희 / 경기 파주시)
1, 2부 (09:05 ~ 10:00) * 편지 1 : 나의 결혼 원정기 (김장가(가명) / 경상남도) #M1 : 화려하지 않은 고백 / 이승환 (김장가님 신청곡) 아침 창가에서 #M2 : 꿈 / 조용필 * 편지 2 : 임신 어려운 딸을 보며 (이인용 / 경기도 수원시) * 편지 3 : 기억하겠습니다 (백혜민 / 서울 구로구)
Le salarié en CDD ou interim qui refuse deux CDI perd ses allocations au chômage. La loi impose même à l'employeur une délation du salarié à Pôle emploi. C'est l'abjection juridique absolue - on n'était jamais tombé aussi bas - mais on n'a sans doute pas encore atteint le fond ... Lien de téléchargement de la présentation https://docs.google.com/document/d/1igMhi8Zlo1fUl8GAsi6b9yzEmIQWsXPiqnwblM97Rnw/edit?usp=sharing Lien du texte de la commission mixte paritaire https://www.senat.fr/leg/pjl22-112.html PROJET DE LOI portant mesures d'urgence relatives au fonctionnement du marché du travail en vue du plein emploi #droit #travail #juridique #avocat #RH #droitdutravail #licenciement #etudiant #etudes #droit #facdedroit #etudiantendroit #etudesdedroit #licencededroit #L1 #L2 #L3 #master #M1 #M2 #td
la cessation d'activité de l'entreprise peut caractériser l'impossibilité de maintenir le contrat de travail pour un motif non lié à l'accident du travail ou à la maladie professionnelle quand elle est réelle et emporte la suppression de tous les postes de travail vidéo https://youtu.be/4hLYYEgmU4M Soc. 26 octobre 2022 n° 20-17.501 B https://ia-droit.fr/?q=20-17.501 Confirmation de jurisprudence Soc. 15 septembre 2021 n° 19-25.613 B https://ia-droit.fr/?q=19-25.613 Soc. 14 avril 2010 n° 08-45.547 https://ia-droit.fr/?q=08-45.547 Soc. 15 mars 2005 n° 03-43.038 B n° 87 https://ia-droit.fr/?q=03-43.038 #inaptitude #cessation #activité #droit #travail #juridique #avocat #RH #droitdutravail #licenciement #etudiant #etudes #droit #facdedroit #etudiantendroit #etudesdedroit #licencededroit #L1 #L2 #L3 #master #M1 #M2 #td
1, 2부 (09:05 ~ 10:00) * 편지 1 : 시원하게 재채기 하고 싶어요 (박용혁 / 경기도 용인시) #M1 : 아츄 / 러블리즈 [ 아침 창가에서 ] #M2 : 사계 / 노래를 찾는 사람들 * 편지 2 : 유치원 선생님을 응원합니다 (* 손편지) (박정숙 / 충남 천안시) * 편지 3 : 버킷리스트를 정해 실천하자고 제안합니다 (*손편지) (고영화 / 부산 사하구)
We talk to the boys about there week and some other things. We also listen to a song released by HALES. If you like it you can listen to it on Spotify or follow him on insta @musicbyhales and don't forget to follow us on @just2grownmen
1, 2부 (09:05 ~ 10:00) * 편지 1 : 밥 잘 먹는 남편 (조영숙 / 경기도 시흥시) # M1 : 밥만 잘 먹더라 / 옴므 아침창가에서 # M2 : 코뿔소 / 한영애 * 편지 2 : 중년 사내의 일장춘몽 (박정도 / 부산 사하구) * 편지 3 : 여름 휴가 이야기 (*손편지) (김기홍 / 부산 영도구)
1, 2부 (09:05 ~ 10:00) * 편지 1 : 폐를 이식 받다 (애청자) # M1: 천하장사 / 김연자 아침 창가에서 # M2: 행복이란 / 조경수 * 편지 2 : 잘못 송금한 돈 돌아오다 (정진선 / 경기도 부천시) (* '예금보험공사'는 잘못 송금한 돈을 받은 사람이 자진반환하지 않을 경우, 법원의 지급명령을 통해 회수를 진행해드립니다.) ▶ 예금보험공사 사이트 https://www.kdic.or.kr/main.do * 편지 3 : 추석이 지나고 (박윤정 / 경기도 화성시)
Guests Matt Hodson (MATTHS) artist, performer, educator Rich Hilton - Nile Rodgers Studio guy, keyboards for Chic Youtube video version: https://youtu.be/OQ1qJNu5J8g For pre-show, ad free and other great benefits, check our Patreon.com/sonicstate Sign up for iZotope's Music Production Suite Pro for 24.99 a month, or Producers Club for $19.99 a month, and you get access to the most up-to-date versions of our plug-ins as well as the latest features and updates as they are released. No upgrade fees. And, you can tap into iZotope's expert knowledge with exclusive product tutorials and videos on mixing, mastering, and more. Head over to iZotope.com now to get a 7-day free trial. Babyaudio.com - save 15% on any purchases of their range of creative effect plugins, designed to add color and depth to your mixes. When checking out, use the code ST15 00:00:15 SHOW START 00:10:09 Yamaha MODX+ 00:24:02 AD: Baby Audio - Save 15% With ST15 Code 00:24:59 Native Instruments Komplete 14 00:37:18 AD: iZotope Music Producers Club 00:40:26 Nicholas Bryant asks via - [youtube] - QQ All. If you were moving house would studio/music space play a big role in your choice? 00:46:53 bo heem asks via - [youtube] - QQ What is your oldest piece of technology used in your music making? 00:47:14 bo heem asks via - [youtube] - QQ What is your oldest piece of technology used in your music making? 00:51:17 Nick Howes asks via - [youtube] - QQ With the M1 M2 processors now being so ridiculously fast capable of running a Motorola M563XX emulator easily will cloning synths become more of a thing? (rather than emulations) 00:55:00 JHVE asks via - [irc] - QQ hiltonius what OS are you on Rich or what OS Everybody....I'm on Mojave think I have to go to Catalina very very soon 01:01:30 Echo Kraft asks via - [youtube] - QQ-how do you feel about Roland purchasing DW? Where to Watch/Listen - We now stream the live show to Youtube Live, Facebook Live as well as at Sonicstate.com/live every Weds at 4pm UK time- please do join in. Preshow available on Twitch. You can also download the audio version from RSS FEED
3, 4부 (10:05 ~ 11:00) ☎ 열린 사서함: 문숙 '나만 생각하는 남편, 잘 부탁해' - 위로의 토닥토닥세트 [ 이별준비노트 with 한국장례문화진흥원 ] * 편지 1 : 안녕, 죽음아 (신솔이 / 경북 안동시) * 편지 2 : 이별 노트 (이수정 / 경남 함양군) #M1 : 꿈을 꾼다 / 서영은 #M2 : 고맙소 / 조항조
This week, please join author Kory Lavine and Associate Editor Thomas Eschenhagen as they discuss the article "Donor Macrophages Modulate Rejection After Heart Transplantation." Dr. Carolyn Lam: Welcome to Circulation on the Run, your weekly podcast summary and backstage pass to the journal and its editors. We're your co-hosts. I'm Dr Carolyn Lam, associate editor from the National Heart Center and Duke National University of Singapore. Dr. Greg Hundley: I'm Dr. Greg Hundley, associate editor and director of the Pauley Heart Center at VCU Health in Richmond, Virginia. Well, Carolyn, this week's feature, we are going to the world of preclinical science and we are going to learn about a very important new finding pertaining to heart transplant rejection, and macrophages may modulate this, but before we get to that feature, how about we grab a cup of coffee and go through some of the other articles in the issue? Dr. Carolyn Lam: I got mine. Would you like to go first, Greg? Dr. Greg Hundley: You bet, Carolyn. Well, my first study comes to us from Dr. Michael Pencino from Duke University. Carolyn, this study was performed to understand the predictive utility of a previously derived polygenic risk score for long-term risk of coronary heart disease and its additive value beyond traditional risk factors and how that might be able to inform prevention strategies. To accomplish this, data from adults aged 20 to 59 free of cardiovascular health disease from the Framingham Offspring Study and the Atherosclerosis Risk in Communities, or ARIC Study, were analyzed. Now, since the polygenic risk score was derived from people of predominantly European ancestry, individuals who self-reported white race were those that were included. Dr. Carolyn Lam: Oh, interesting, so what did they find, Greg? Dr. Greg Hundley: Right, Carolyn. Somewhat surprisingly, they found that, among 9,757 participants, both the traditional risk factor score and the polygenic risk score where significantly associated with incident cardiovascular heart disease in young, early midlife, and late midlife. Now, the delta C index, when the polygenic risk score was added to the traditional risk factor, score was 0.03, 0.02, and 0.002 in the young, the early midlife, and the late-midlife participants, respectively. Carolyn, despite a statistically significant association between the polygenic risk score and the 30-year risk of cardiovascular heart disease, the C index improved only marginally with the addition of the polygenic risk score to the traditional risk factor model among young adults and did not improve among midlife adults and, thus, Carolyn, the polygenic risk score, an immutable factor, has limited clinical utility for long-term cardiovascular heart disease prediction when added to a traditional risk factor model. Dr. Carolyn Lam: I really like that, Greg, because I think it also tells us that the traditional risk factors, which we can do something about, are still very important. Isn't that great? Well, the next paper is about POTS. Remember what that is? Should I give you a quiz? All right. It's okay. POTS, or Postural Orthostatic Tachycardia Syndrome, is a disorder of orthostatic intolerance that primarily affects females of childbearing age. While the underlying pathophysiology of POTS is not fully understood, it has been suggested that autoimmunity may play a role. Now, the aim of this study was to compare concentrations of autoantibodies to cardiovascular G protein-coupled receptors between 116 POTS patients and 81 healthy controls, and they were from Calgary, Canada, and Malmo, Sweden. Dr. Greg Hundley: Carolyn, really interesting, so what did they find here? Dr. Carolyn Lam: The investigators, led by Dr. Raj from University of Calgary in Canada, found that commercially available autoantibody concentrations to G protein-coupled receptors were not increased or altered in POTS patients relative to healthy controls as assessed using ELISA. Now, while this study suggests that these G protein-coupled receptor autoantibody concentrations alone cannot explain the pathophysiology of POTS, autoantibody activity and signals not picked up by ELISA should still be explored as these results may provide more insights into the pathophysiology of POTS. Dr. Greg Hundley: Very nice, Carolyn. Well, my next study comes to us from the world of pulmonary arterial hypertension. Carolyn, clinical worsening is commonly used as an endpoint in pulmonary arterial hypertension trials. These authors, led by Dr. Steeve Provencher from the Institut Universitaire de Cardiologie Pneumologie de Quebec, aimed to assess the trial-level surrogacy of clinical worsening for mortality in pulmonary artery hypertension trials and whether the various clinical worsening components were similar in terms of frequency of occurrence, treatment-related relative risk reduction and importance to patients. Dr. Carolyn Lam: Okay, so what did they find? Dr. Greg Hundley: Right, Carolyn, so they searched MEDLINE, Embase and the Cochrane Library for trials evaluating the effects of pulmonary arterial hypertension on clinical worsening and, among 35 independent cohorts, so 9,450 patients, the effects of pulmonary arterial hypertension-specific therapies on clinical worsening modestly correlated with mortality. Additionally, study-level clinical worsening was not found to be a surrogate for mortality in pulmonary arterial-hypertension trials. Moreover, components of clinical worsening largely vary in frequency, response to therapy and importance to patients and, thus, are not necessarily interchangeable. Dr. Carolyn Lam: Thank you, Greg. Can I tell you about some other papers in today's issue? There's a Research Letter from Dr. Cosentino on cardiorenal outcomes with ertugliflozin by baseline metformin use, and this is a post hoc analysis of the VERTIS CV trial. Dr. Greg Hundley: Oh, very good, Carolyn. Well, I've got an exchange of letters from Professors Boriani and Steinberg regarding the article “Driving Restrictions and Early Arrhythmias in Patients Receiving a Secondary Prevention Implantable Cardioverter-Defibrillator, the DREAM-ICD-II Study.” There's also an ECG Challenge from Professor Gao entitled “Syncope in a 3-Year-Old Child During the Perioperative Period. What is the diagnosis? What Signs Point Toward Impending Life-threatening Event?” Then, finally, there's a nice, On My Mind piece from Professor Greenland entitled “Insurance Payers Should Cover Selective Coronary Artery Calcium Testing in Intermediate Risk Primary Prevention Patients.” Well, Carolyn, how about we get on to that feature discussion and dive into the world of rejection after heart transplantation? Dr. Carolyn Lam: Yay. Here we go. Dr. Greg Hundley: Welcome, listeners, to this feature discussion on August 23rd. We have a very interesting article today to discuss with our author and associate editor pertaining to preclinical science and cardiac transplant rejection. Our author today is Dr. Kory Lavine from Washington University in St. Louis and our associate editor today is Dr. Thomas Eschenhagen from Hamburg, Germany. Welcome gentlemen. Kory, we'll start with you. Can you describe for us some of the background information pertaining to the construct of your study and what was the hypothesis that you wanted to address? Dr. Kory Lavine: Well, thank you for having me. Our study focused on heart transplant rejection, which remains a major clinical challenge that limits both the survival of heart transplant recipients as well as availability of donor hearts. Current clinical practice really focuses on suppressing the immune system in a global way, and that is somewhat effective, but carries important risks that include infection and life-threatening malignancies. Many studies have appropriately focused on immune cells that infiltrate the transplanted heart that come from the recipient to search for new ways to suppress the immune system safely. What we've understood and learned over the past several years is that the donor heart has its own immune system and its own immune cells, and the majority of those immune cells that come with the donor heart are macrophages that can be broadly divided into two distinct lineages with different functions, tissue-resident macrophages, which lack the cell surface receptors CCR2, and monocyte-derived macrophages with expressed cell surface receptors CCR2. We tested the hypothesis in this study that these macrophages that come with the donor heart remain active for a period of time after transplantation and play important roles in either suppressing or accelerating heart transplant rejection. Dr. Greg Hundley: What was the hypothesis that you wanted to address with your study? Dr. Kory Lavine: Yeah, so our prior work and others' work within this field had suggested that tissue-resident macrophages, CCR2-negative macrophages, are inflammatory, and CCR2-positive macrophages have the opposite functions being inflammatory and play roles in potentiating and initiating inflammation in the heart. In this study, we hypothesized that CCR2-negative macrophages would protect from rejection, while CCR2-positive macrophages may promote heart transplant rejection and could serve as a new therapeutic target to prevent rejection in transplant recipients. Dr. Greg Hundley: Excellent. Kory, can you describe for us the study design that you used to test your hypothesis? Dr. Kory Lavine: Yeah. The study design and approach we used involved a mouse model of heart transplantation where we transplant a donor heart into a recipient mouse that's fully mismatched at all the MHC loci, and this serves as a nice model for both cellular and antibody-mediated rejection. To facilitate tracking these donor macrophages, we used various genetic lineage tracing systems and, to study their phenotypes, we used single-cell RNA sequencing and, to understand their function, we used mouse models that allow us to specifically deplete each of the donor macrophage populations as well as genetic models to manipulate their activation and signaling. Dr. Greg Hundley: The outcome measures were going to be what? Dr. Kory Lavine: Yeah. The outcome measures for transplant rejection in this mouse model are allograph survival, so the survival of the transplanted heart. We're able to directly look at how much rejection is present by histopathology, and then we're able to observe various mechanistic features using detailed phenotyping such as single-cell RNA sequencing and T-cell activation assays. Dr. Greg Hundley: Very nice, Kory. Well, all, our listeners, we're very excited to hear what were your study results? Dr. Kory Lavine: We learned that donor macrophages are dynamic and they survive for a period of time after transplantation or eventually lost due to transplant rejection. When we phenotyped the macrophages that came from the donor heart, we learned that they remained transcriptionally distinct from immune cells that enter the heart that were derived from the recipients, and they had important and distinct functions. If we depleted the tissue-resident macrophages that were CCR2-negative, we observed reduced allograph survival and increased rejection. If we depleted CCR2-positive macrophages that came from the donor heart, we observed improved allograph survival and reduced rejection. Mechanistically, we learned that CCR2-positive macrophages are activated through a MyD88-dependent pathway and, if we inhibited MyD88 cytokines which controls the expression of pro-inflammatory cytokines and chemokines, we could prolong the survival of the donor heart for a very significant period of time, reduce rejection and prevent the development of T-cells that would attack the donor heart. From a mechanistic aspect, what we uncovered is that this signaling pathway in CCR2-positive macrophages regulated the recruitment of an activation of antigen-presenting cells which played important roles in generating T-cells that would target the transplanted heart. Dr. Greg Hundley: It sounds like a really informative and leap forward in the whole sphere of transplant rejection. Well, listeners, now we're going to turn to our associate editor, Dr. Thomas Eschenhagen. Thomas, you have many papers come across your desk. What attracted you to this particular paper and then, secondly, how do you put the results of this study really in the context of other research examining heart transplant rejection? Dr. Thomas Eschenhagen: Yeah, thanks for having me. I mean, first, we got attracted by this paper because it's somewhat an out-of-the-box approach. It's not the standard approach to improve the systemic immunosuppression as many studies did and with actually a lot of success over the last 30 years, survivor got much better. There had been a lot of progress in the field of transplantation medicine as we all know, but as Kory said already, we still have 30% rejection, and these immunosuppressions come at a price. Having this study which turns around somehow the argumentation and looks at the donor organ was something which really attracted us. It uses advanced methods and it applies somewhat in a practical way a concept which emerged over the last, I don't know, maybe decade this concept that macrophages are really very different kind of cells. They're all called macrophages, but they're quite different and even maybe in certain respects having opposing effect. I think many people know about this M1/M2 concept. It's CCR2 receptor positive and negative. It's criticized by some people, but here we see that it really seems to be really important and, of course, then the third argument why we really like the story is that it has a specific, clear translation impact. I mean, looking at the heart, the donor heart, and potentially even treating the donor heart before transplanting it is something which comes immediately out of the story, and that's something which we found super attractive. Dr. Greg Hundley: Really interesting, so really understanding the mechanism and focusing on donor hearts. Well, listeners, let's circle back with Kory. Kory, given that, what do you think is the next study that really needs to be performed in this sphere of research? Dr. Kory Lavine: I think Thomas said it exactly as we're thinking about it, so the next area that we're really excited to attack and we're hopeful that the field will focus on is ways to build methods and technologies to treat the donor heart between the time of procurement and the time of transplant, when it's being transported and potentially even being perfused for a period of time. We're really interested in finding approaches to identify small molecules and other potential biologic therapies that could be used to prevent the activation of donor CCR2-positive macrophages. It's a really attractive approach because treating the donor heart ex vivo decreases the risk of adversely affecting other organs that may be transplanted if you're treating the donor, for instance, and it may decrease the risk of immunosuppression and infection by not having to treat the recipient and we're catching the heart in this window where the risks are much lower. The other area that we're really excited to focus on is trying to identify the exact mediators that are generated from donor CCR2-positive macrophages that mediate the recruitment and activation of antigen-presenting cells because that would represent another potential therapeutic target. Dr. Greg Hundley: Very nice. Thomas, what are your thoughts about what might be the next study to be performed really in this sphere of research? Dr. Thomas Eschenhagen: It's obviously something rather a question to Kory than to me, but I agree to what he said. I think it is pretty obvious what are the next steps mechanistically on the one hand, but practically on the other hand. I mean, at this point, we are at the mouse level, so the question is to which extent can this concept be translated into larger animals and then finally in humans? I was wondering, given these newer methods to keep donor hearts alive for long, extended periods, I was wondering which extent you are already collaborating with the respective groups who develop this approach because that obviously would increase the window of opportunity here for drugs. I think it's really an exciting and pretty visible next steps which we see here, and I can just hope that you're going this path and that it will be successful. Dr. Greg Hundley: Kory, any thoughts on those collaborations that Thomas just spoke of? Dr. Kory Lavine: We're definitely establishing collaborations to focus on ex vivo profusion of donor hearts because that's, as Thomas mentioned, is a perfect window to manipulate the immune populations that are within the donor heart. Those studies have to be team science, they have to be collaborative and they have to have a focus on large animals and then moving into clinic. We're definitely forming those collaborations and excited to work as a group. Dr. Greg Hundley: Very nice. Well, listeners, what an exciting paper to discuss here as part of this feature discussion from the world of preclinical science. We want to thank Dr. Kory Lavine from Washington University in St. Louis, Missouri, and also our own associate editor, Dr. Thomas Eschenhagen from Hamburg Germany, for really bringing us this research study highlighting that distinct populations of donor and recipient macrophages coexist within the transplanted heart, and donor CCR2-positive macrophages are key mediators of allograph rejection and deletion of MyD88 signaling in donor macrophages is sufficient to suppress rejection and extend allograph survival. Well, on behalf of Carolyn and myself, we want to wish you a great week, and we will catch you next week on the run. Dr. Greg Hundley: This program is copyright of the American Heart association, 2022. The opinions expressed by the speakers in this podcast are their own and not necessarily those of the editors or of the American Heart Association. For more, please visit ahajournals.org.
1, 2부 (09:05 ~ 10:00) * 편지 1 : 다둥맘이 출산 장려합니다 (고지연 / 경남 밀양시) * 편지 2 : 상담원을 기다리며 (이현애 / 울산광역시 북구) # M1 : 통화중 / 소방차 아침창가에서 # M2 : 내 나라 내 겨레 / 송창식 * 편지 3 : 귀하고 소중하게 (정소라 / 경기도 시흥시) # M3 : It's alright, It's all good / 윤미래 & 바비킴
3, 4부 (10:05 ~ 11:00) ☎ 열린 사서함 : 박미나 '입원한 엄마에게 편지 써준 딸, 사랑해' - 천하장사 세트 # M1 : 미소천사 / 성시경 # M2 : 여성시대 / 씨야, 다비치, 티아라 # M3 : 아름다운 나라 / 송소희
♤マッサージフリークスの全キャラ名前が日向坂46に似てるか調査！法的措置で発売延期？ | 鯖ログ https://hirokoba051.com/massage%e2%80%90freaks%e2%80%90character%e2%80%90name-5778 ♤M2 MacBook Air、いいんだろうけど高すぎる問題を考える ならばM1 MacBook Airを買う選択はアリなのか？ https://www.itmedia.co.jp/news/articles/2207/22/news115.html ♫ エンディング曲 : キミーは俺らよりアホやったのやから2 ┈┈┈┈┈┈┈┈┈┈┈┈┈┈┈┈┈ Instagram https://www.instagram.com/tomitotimes/ YouTube https://www.youtube.com/channel/UCTYNU2f-t4KZBV-4Wc1apRQ Tomito Times Podcast (Season1) https://anchor.fm/tomito-times
Mac向け「Microsoft Teams」アプリがApple Siliconにネイティブ対応 M1／M2 Macでのパフォーマンスを改善。 Microsoftは8月3日（米国太平洋夏時間）、Apple Silicon（M1チップ／M2チップ）に最適化されたMac向け「Microsoft Teams」アプリの配信を開始した。今後数週間に渡り、段階的に展開される予定だ。
Welcome to The Nonlinear Library, where we use Text-to-Speech software to convert the best writing from the Rationalist and EA communities into audio. This is: Ten experiments in modularity, which we'd like you to run!, published by TheMcDouglas on June 16, 2022 on The AI Alignment Forum. This is the third post describing our team's work on selection theorems for modularity, as part of a project mentored by John Wentworth (see here for the earlier posts). Although the theoretical and empirical parts of the project have both been going very well, we're currently bottlenecked on the empirical side: we have several theories and ideas for how to test them, but few experimental results. Right now, we only have one empiricist coding up experiments, so this overhang seems likely to persist. The purpose of this post is to outline some of our ideas for experiments. We hope that this will provide concrete steps for people who are interested in engaging with empirical research in AI safety, or on selection theorems in particular, to contribute to this area. Experiments 1. Investigate (randomly) modulary varying goals in modern deep learning architectures. In our previous post, we discussed the idea of modularly varying goals in more detail. We conjectured that rapidly switching between a small set of different goals might fine-tune the network to deal with this specific switch, rather than providing selection pressure for modularity. One possible solution to this is RMVG (randomly-sampled modularly varying goals), where we switch between a large set of random goals, all still with the same subtasks, but have a large enough set that we never show the network the same task twice. For example, one could build a CNN to recognise two MNIST digits M1,M2, then perform some algebraic operation on the recognised digits (e.g. addition), and measure the modularity of the zero-training-loss solutions found by ADAM (e.g. using the graph theory measure of modularity with the matrix norm of the CNN kernels as weights - see these CHAI papers for more ideas and discussion). To introduce RMVG, you might switch the task during training from calculating M1+M2 to a×M1+b×M2, where a,b are real numbers, varied periodically after some fixed number of epochs. The network wouldn't get a and b as direct inputs; it could only access them indirectly via their effect on the loss function. This task is modular in the sense that it can be factored into the separate tasks of “recognising two separate digits” and “performing joint arithmetical operations on them”, and we might hope that varying the goal in this way causes the network to learn a corresponding modular solution. Questions you might ask: Does this way of varying goals lead to more modular solutions than the fixed goal of a×M1+b×M2? Can you think of any other modular goals which you could run a similar test for? Are there some types of modular goals which produce modularity more reliably? Does switching training methods (e.g. ADAM to SGD or GD) change anything about the average modularity score of solutions? 2) Measure the broadness of modular and non-modular optima in deep learning architectures. We have some theories that predict modular solutions for tasks to be on average broader in the loss function landscape than non-modular solutions. One could test this by making a CNN and getting it to produce some zero training loss solutions to a task, some of which were more modular than others (see experiment (1) for more detail on this, and (4) for another proposed method to produce modularity), then vary the parameters of these optima slightly to see how quickly the loss increases. We've recently done experiments with simple networks and the retina problem, and this intuition seems to hold up. But more replications here would be very valuable, to examine the extent to which the hypothesis is borne out in different situations / task / network sizes. Questions you might ask: Is there a relationship between bro...
欢迎收听雪球和喜马拉雅联合出品的财经有深度，雪球，国内领先的集投资交流交易一体的综合财富管理平台，聪明的投资者都在这里。听众朋友们大家好，我是主播匪石-34，今天分享的内容名字叫无序的市场，房企的处境，来自朱酒。去年年底的时候，银行有过一阵资产荒，原因是房地产相关贷款，一直占了银行贷款总额的近3成。随着房企们融资受限，下游的很多企业出现周转问题，这是有钱拿不回来；而对上游的银行来说，则是面临资产荒，也就是有钱放不出去。世界第二大经济体，114万亿的庞大市场，有钱放不出去？从数字上来看有些不可思议，但这就是现实。缺钱的很多，但不敢放或者是不能放；有些企业手上的钱太多，银行就拼命想让它们再多借点，大家都不容易。一月份M2增速大涨，看起来资产荒解决了，可M1却和M2形成了巨大的剪刀差，表明资金还没有大量进入实体，对市场的支持并没到位。银行的日子要好过些了，企业的日子依然如故。我们在过去这两年，总能看到一些令人瞠目结舌的高估值，很多个股都在这段时间，把自己的市盈率推到了历史级别的高点。其背后的原因有很多，除了基金抱团这一直接原因外，深层次的原因还是疫情以来，很多行业都遇到了阶段性困难，业绩缺少保证。资本便尽可能抓住那些增长确定性比较好的股票，越抱越紧，直到抱碎了为止。在2021年消费股崩盘之后，从去年年底开始，新能源板块也在大幅回撤。同时一批过去一年多时间里，被不断推高市值的股票，也出现了明显的回落。高处不胜寒，谁也逃不离，这是规律，只有没经过股市洗礼的人，才会相信树能长到天上去。一年多前，赛道两个字金光闪闪，现在都快成骂人话了。可另一方面，疫情又在反复，而且从去年下半年开始，地产、教育、互联网同时受到重创，能赚钱的企业越来越少，不仅仅是银行遇到了难题，对于资金来说也是个难题。有成长的太贵，便宜的又缺少成长，可谓进退两难。当下的市场，处于一个无序状态。所有的资金看起来都像是游资，打几枪就跑。偏偏又遇上了大洋彼岸一直喊加息，大陆深处不断扔炸弹，波动就成了阶段性主题。去年年初的时候，市场还是比较活跃的，在春节后指数大幅回落前后，成交量一直居高不下。去年前两个月，上证指数成交额为16.17万亿，而今年就回落到14.5万亿，整整少了10%。重要原因，在于去年1月有122只新基金成立，发行总规模为4901.4亿元，而今年同期虽然有148只新基金成立，但合计募集规模仅仅1188.2亿元。即便算上春节因素，这个下滑也是断崖式的。现在的市场，可以说是供需两不旺，没有方向，没有主题，没有热情，没有领队。大家都在等，等下周末的会。虽然有些说法已经提了两个月了，但落地的声音仍然是很小，这让一些已经形成的趋势又出现了大回落。在对房地产的尺度不明朗之前，什么事都很难确定。一年中最重要的决策时间到了，解铃还须系铃人，看看会议过后有什么具体措施吧。未来半个月，多看少动，等。
< 1, 2부 > (09:05 ~ 10:00) * 편지 1 : 세상사 마음먹기에 달렸다 ( 애청자 / 강원도 춘천시 후석로 ) * 편지 2 : 마지막 사진 ( 애청자 / 충북 ) ※ 주말엔 투유 ※ * 편지 3 : 엄마에게 ( 오영미 / 경북 경산시 강변서로 ) #M1 : 엄마 / 박창근 #M2 : 보이네 / 나미
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(09:05 ~ 10:00) * 편지 1 : 딸이 아빠에게 드리는 위로 ( 고정은 / 충남 천안시 서북구 ) * 편지 2 : 어디서부터 얘기를 꺼내야 할까요 ( 애청자 ) 아침 창가에서 #M1 : 첫 눈이 온다구요 / 이정석 * 편지 3 : 아내를 보내고 ( 권재두 / 대구 달성군 다사읍 ) #M1 : 동백아가씨 / 이미자 #M2 : 사랑했나봐 / 윤도현
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Dr. De'Broski Herbert is an Associate Professor of Immunology at the University of Pennsylvania. The Herbert lab is exploring the immunoregulatory and regenerative mechanisms operating at the mucosal interface. He discusses his recent paper on IL-33 sources and secretion, his postdoctoral fellowship in South Africa, and the M1/M2 macrophage paradigm.
一週財經聚焦 一、台積電表示，將在11月8日截止日前，提交美國要求的相關資料。美國商務部也已經表示，英特爾、英飛淩、SK 海力士等公司，都表示將在期限內提供數據，並鼓勵其他公司跟進。大企業在地緣政治的夾縫中生存越來越不容易，我們怎麼解讀？ 國際媒體相關報導 ●Economist經濟學人：「The geopolitics of money is shifting up a gear｣(金錢的地緣政治正在轉變之中) ●South China Morning Post南華早報：「HSBC boss Noel Quinn: Complex geopolitical landscape a ‘fact of life' for global banks｣(匯豐銀行總裁 Noel Quinn：複雜的地緣政治格局是全球銀行的「生活事實」) ●CNBC：「As Wall Street sees a Chinese stock market 'on sale,' others warn 'that game is over'｣(當華爾街看到中國股市「拋售」時，其他人警告說「遊戲已經結束」) 分析解讀 我們該如何解讀全球地緣政治對金融市場的影響？ 不知道大家還記不記得2005年出版的一本由Thomas L. Friedman所寫的暢銷書《世界是平的》（The World Is Flat: A Brief History of the Twenty-first Century），書中分析了21世紀初期全球化的過程。書中主要的論題是「世界正被抹平」，這是一段個人與公司行號透過全球化，得到權力的過程。 時過境遷，最近地緣政治未來學者Abishur Prakash出版新書《世界是垂直的》（The World Is Vertical），他認為在地緣政治利益、意識形態和新結盟架構下，世界不再像過去那樣開放和容易接入，基於科技的圍牆和壁壘越築越高，世界變成「垂直」的。 我想，不應該說全球化已經結束，但我們曾經看過的全球化正在結束。我們可以從以下幾個面向觀察： 一、地緣政治： 現在當我們討論這一全球脫鈎時，大多數時候，我們實際上是在談論美國和中國，而這其實掩蓋了其他扮演這一角色的國家。 印度也扮演著重要角色，它在迫使外國科技公司向印度消費者銷售印度產品。印度不希望自己國家的消費者接觸到世界各地的產品，尤其是來自中國的產品。它的意思是，如果一家類似像亞馬遜這樣的外國公司想在印度經營，它也必須得變成一個中間商，才能接觸印度的消費者。 以色列更特別。一直以來以色列都相當注重創新，例如，它是海水淡化技術的世界領導者之一，通過海水淡化使其可以飲用，這讓以色列不再那麼受氣候變化的影響。 至於歐洲，歐盟實際上也在推動與美國的科技脫鈎。當美國和中國在進行脫鈎的同時，美國和歐洲的關係其實也不是太好。 與此同時，大型科技公司也在被迫推動垂直世界的發展，就像tsmc。這是一個似非而是的矛盾命題（paradox），這種矛盾在全球已將開始發生。 在某一時刻，大型科技公司開始被不同的國界所限制。它們過去能夠跨越國界。現在他們被世界各地的邊界所限制。但與此同時，科技公司在支配、推動和影響世界的權力方面與政府平起平坐。在某些方面，科技公司正在創造自己的領地。 二、意識形態： 在過去的20年間，政府忽視了大型科技公司的作用，直到現在他們現在才意識到這些科技公司所扮演的角色。當這些科技公司在選舉和外國干涉中發揮作用時，政府才猛然驚醒。這些公司現在的作用與政府本身一樣大，甚至更強大。因此，他們希望回到過去，回到可以控制科技公司的時代。 我想說的真正一點是，現在各國政府正在利用科技公司來保護它們的主權。 所以，如果你看看中國對滴滴公司的做法，中國政府幾乎是在向所有快速成長的中國初創企業發出的信號：你們不要在美國的證券交易所上市，而是要在中國的證交所上市，這樣，中國才可以保護其有關科技的主權，以更有力的方式保護經濟部門。 因此，現在我們看到科技公司幾乎成為各國保護其地緣經濟實力的工具。 三、新結盟架構： 現在各國只想與志同道合的國家建立聯繫。你看看日本提出的建議--日本提出了一條連接日本、印度和東南亞的人工智慧走廊。這是軟銀集團創始人提出的。現在的狀況是，日本最具標誌性的領導者並不想把日本和所有地區相連接，只想連接世界的某些部分。 再比如「D10」（一個由10個民主國家組成的聯盟），這是一個由英國發起的，為5G制定全球規則的新架構，它只由10個國家組成。這也很有趣，因為英國是全球化的建築師之一，現在它自己想要建立一種「垂直」機構，一個只由少數幾個國家組成的機構。 所以你現在看到的是，因為科技，世界分裂成了各個部落。這將導致巨大的分裂，給企業的運作運作帶來巨大混亂，衝突的風險也會增加。當世界的各個部分彼此分裂、彼此斷開連接時，發生衝突的風險會呈指數級上升。 這會帶來三大嚴重後果： 第一，過去因為全球化，所有國家都朝著同一個方向前進、大家都在部署同樣的科技、都在採用同樣的協議，因為科技讓各國能夠在世界上建立自己的獨立存在。但現在大家會開始思考：我們為什麼要使用別人的軟體？為什麼要使用別人的貨幣？為什麼要使用別人的生態系統？為什麼我們使用別人的互聯網？ 第二，現下的每一個跨國公司，都在全球化的背景下得到了擴展和成功，例如，iPhone在美國設計的，在中國製造，但它的組件來自世界各地。 但是現在的跨國公司，必須適應這種「垂直世界」。我們開始思考：我為什麼要用來自其他國家的東西？這不僅僅是如何應對失去原材料來源的問題、供應鏈的問題，也是如何獲取人才的問題。比如台灣的提議，它不想讓某些高科技行業的工作人員前往中國。 所以現在你看到了真正的圍牆--這些垂直的壁壘阻擋了人才的獲取、阻擋了消費者市場，這是第二大後果。 第三的嚴重後果，是各國的合縱連橫。如果世界如此分散，如果各國在各自的勢力範圍內運作，如果每個聯合國存在的機構都有多種選擇，如果從一個聯合國變成了三、四個聯合國、從一個SWIFT(環球銀行金融電信協會)變成了三四個SWIFT……這些不同的「部落」要如何合作和共存呢？他們會試圖共存嗎？還是會導致某種衝突，某種緊張局勢的出現？ 除此之外，在過去幾年，當西方引領的支持全球化運作的背後基礎設施陷入年久失修之際，中國一直在想方設法建立另外一個可供替代的選擇方案。當世界貿易組織WTO陷於四分五裂，國際貨幣基金組織IMF和世界銀行World Bank醜聞纏身，這個世界，竟然沒有一個組織能夠就達成全球共識，好好管理科技產業。 但在這個令人沮喪的全球拼圖中有那麼一個例外：SWIFT環球銀行金融電信協會，這個支撐西方貨幣主導地位，特別是美元的這個全球支付系統。在過去一年，SWIFT完成了140兆美元的資金交易，這個新高記錄相當於全球GDP的150％。 當全球資金的流動仍然在西方民主國家的控制下的今天，跨境支付更多的在美元體系中發生，只有極小程度擴展到歐元、英鎊或日元。平心而論，能夠提供一個明確法律管轄的可靠系統對全世界的是好的。它對西方國家當然更好，因為這可以鞏固與提升屬於他們的法律規範以及企業的影響力。 但今天，它也面臨了威脅。主要原因主要來自幾個方面： 首先，它的過往記錄令人難以想像。2016年，北韓的駭客使用了偷來的SWIFT憑證，成功竊取了孟加拉央行的81億美元。 另外，美國對美元系統過度的自以為是，所以它使用SWIFT推動了政治的制裁，這促使其他國家有了尋求其他替代方案的想法。此外，美國對位在美國的支付系統升級過慢，對發展中央銀行的數位貨幣無動於衷，國會更對美國聯準會穩定全球的作用頻頻干預。 其次，對SWIFT的威脅來自更大的巨頭。例如信用卡巨頭VISA就正在構建新的基礎設施，來處理零售的「推送」支付，這將在很大程度上與 SWIFT展開並行。10月19日Facebook也推出了它自己的數位錢包，它可以讓跨境支付變得更便宜。 第三，大型銀行也正在開發自己的支付網絡，來服務它的大型客戶。今年早些時候，佔據 1/4美元付款的JPMorgan就與新加坡的DBS銀行，以及新加坡主權財富基金淡馬錫展開了合作，他們準備推出Partior。這是一個通過區塊鏈技術，來繞過代理銀行業務缺陷的支付網絡系統，只有成員之間才能彼此驗證交易。這個網絡將允許即時、透明和「可編程」的支付（也就是，只有滿足某些條件才能移動資金）。 最後一個威脅，是由國家資助推動的。全球許多的中央銀行正在開發自己的數位貨幣（稱為 CBDCs），隨著時間的推移，它們可能會允許銀行間進行海外的匯款交易，從而進一步削弱 SWIFT。 中國就正在建造新的支付匯款管道。2015 年，中國就建構自己的付款系統，稱為CIPS，該系統已經成功在2020年處理了7兆美元。中國也在力推人民銀行的數位貨幣，它才剛剛要求麥當勞在中國的分支機構，必須採用數位貨幣的支付。 我的想法是，眾所周知，美元體系仍然掌控著全球金流以及資本市場的運作，但即使西方世界仍然有著主導的力量，隨著垂直世界的可能變化，其它區域，尤其中國正在虎視眈眈疫情過後的新一輪部署。 國際貨幣基金組織IMF的前官員Eswar Prasad就表示，隨著中國積極在宣傳CIPS(人民幣匯款)的資訊傳遞功能，雖然SWIFT可能不會立即就面臨了危險，但下一個十年，其實充滿著各種垂直世界的不確定性。 一場關於資金如何流動的史詩般的戰鬥才剛要展開，就像是一棟房子需要翻新，最適合開始地方，肯定是房子的管路系統。因此，隨著全球化與地緣政治的改變，這是我們將面臨的新世界。 二、10月20日，德國央行行長Weidmann宣佈辭職，他的辭職正值歐元區的一個微妙時刻--10/17英國央行總裁Andrew Bailey都忍不住暗示，英國為因應創了十年新高的英國通膨，有可能升息。這個動作除了表示對量化寬鬆的鷹派退場，更代表大撒錢的時代仍在繼續，我們怎麼看待後續？ 國際媒體相關報導 ●Bloomberg彭博新聞社：「Weidmann Exits as Chief ECB Hawk With QE Future Unresolved｣(歐洲央行鷹派魏德曼，因未能解決量化寬鬆的問題而退出) ●New York Times紐約時報：「The Fed Cannot Control Its Easy-Money Monster｣(美國聯準會無法控制它的寬鬆貨幣怪物) ●CNBC：「Here's what will happen when the Fed's 'tapering' starts, and why you should care｣(當美國聯準會開始「縮減」時，會發生什麼事？以及為什麼你應該關心？_ 分析解讀 眾所周知，2012年在南歐諸國頻頻發生破產危機之際，時任歐洲央行 (ECB) 行長的Mario Draghi德拉吉曾發誓，要「不惜一切代價」保持歐洲單一貨幣的統一。 在這項努力中，他最大的敵人就是一位持懷疑態度的同事--Jens Weidmann。Jens Weidmann身為德國央行行長，是歐洲央行管理委員會中最強有力的聲音之一，他對德拉吉的策略做出了回應，他認為QE或印鈔是非常危險的，他並因此威脅要辭職。九年後，他做到了。 10月20日，在他擔任德國央行行長的第二個八年任期僅兩年後，Weidmann先生出人意料地宣佈他將在年底卸任。他在即將離任的聲明裡，警告了寬鬆貨幣政策的副作用，暗示他對歐洲央行不停的購買債券是不滿意的。Weidmann先生長期以來一直擔心該銀行的激進主義淡化了通脹風險，並減輕了負債累累的南歐國家進行改革的壓力。 歐洲央行可能會在12月確認其疫情過後的購買計劃，並決定2022年3月到期之後該怎麼做，但目前為止他們尚未有定論。除此之外，在如何解釋通貨膨脹方面存在更深層次的分歧，目前歐元區的通膨率為3.4%，加息並非迫在眉睫，但不安情緒正在加劇，尤其是在德國，能源價格飆升更將通膨率進一步推升至5%。 事實上，2020年以來大家都不好過，疫情肆虐下，有些行業生意慘淡，全球各地更有無數人失業。然而奇怪的是，各地股市卻「漲」聲響亮，從美國道瓊工業指數，到台灣加權股價指數，甚至接連創下有史以來的新高。不是說「股市是經濟的櫥窗」嗎？為何在景氣慘澹、未來更充滿不確定性的同時，資本市場的表現卻恰恰相反？ 答案恐怕正在「印鈔」兩個字上。 每當百業蕭條，民眾怨聲載道，國家自然要「體民所苦」、想辦法「振興經濟」，這時政府可用的手段有二，一是財政/經濟政策和貨幣政策。主要透過減稅、增加公共支出、投資特定產業、增加或刪減福利津貼⋯⋯等方式，調整國家的經濟體質。這個方法的代表性案例，是美國經濟大蕭條時，羅斯福總統推出的「新政」，它多半相對能夠「治本」，卻也往往需經過一定的立法程式、因而需要一段時間方能見效。 另一個方法就相對「簡單粗暴」許多，即中央銀行降低基準利率，或直接擴大資產負債表，即俗稱的「印鈔票」，針對特定對象「紓困」。好聽一點的講法叫量化寬鬆（QE），直白點講就是「大撒幣」。它並不能直接解決經濟體質的問題，卻往往能透過讓市場上流動的資金增加，達到「短期治標」的效果。 但「大撒幣時代」下，儘管可能在短期間解決了市場信心、消費不振等問題，卻也同時帶出大量的新問題。 不可否認的，我們是史上最「有錢」的一代。根據各國央行的公開資訊，從2020年3月(疫情爆發開始)至今，全球主要經濟體（美國，歐盟，日本，中國⋯⋯）等的通貨（即「鈔票」），總量，若單純以名目價值來看，已經超過2008年之前人類歷史5千年中，各國所有貨幣加總的總值（這邊指廣義M1+M2的貨幣總量）。 也就是說，過去一年不到，各國就「印了」超過5千年來的貨幣總值！各位可以想想這規模有多麽可怕。 而這之中更以美國為主。美國在新總統拜登還沒正式上任時，就宣佈的1.9兆美元的「印鈔計畫」，佔所有已開發國家之最。對比2008年的金融危機，聯準會可是用了3年時間，透過 4輪的QE，才把1兆美元發放到市場；但單單2020年以來，至今18個月，美國就已印了高達3.2兆美元的鈔票；現在，還有1.9兆美元的熱錢蓄勢待發。 學過基礎經濟學的人都知道，大規模濫印鈔票，可是會造成貨幣貶值、通貨膨脹的，在生產力不變，供需曲線維持標準的情況下，市場上的產品與能提供的勞動力就是這麼多，一旦貨幣的流通快速增加，按正常推論，原本 100 塊能買到的商品，現在可能要 150 元或更高。辛巴威就是個例子，從 2000 年開始政府不負責任的印鈔，導致物價瘋狂飆漲。我們最近看到能源、大宗商品，甚至勞動力嚴重不足，這都是資金太過寬鬆的後遺症。 然而，觀察目前大行QE政策的國家，嚴重的通膨問題尚未發生，這是因為打入市場的資金在「短期內」抵銷了通貨緊縮的問題。若只看印鈔最狠也最粗暴的美國，則甚至「根本不用擔心通膨問題」，畢竟美元是全球通用貨幣，絕大部分的商品、勞務、國債、黃金，乃至外匯儲備與GDP，都是以美元計價。美國可以輕易地用美元收購全球人民辛勤勞動的果實，近一步把本應在國內引發的嚴重通膨，順理成章的讓全球貿易夥伴「一起分擔」。 聽起來是否很「邪惡」？但現實就是如此：自從美國在二戰、冷戰後成為世界獨強，就等於保障了美元在國際市場的獨霸地位。二戰後美國就挾勝利國之姿，逼迫各國加入布列敦森林協議；接著又片面宣佈放棄美元與黃金的固定匯率，並透過廣場協議搞垮日本，動輒祭出 301條款，無視WTO的自由貿易體制；近年則跟中國大打貿易戰。在國家利益至上的考量下，美國挾美元影響全球經濟之舉，可謂「罄竹難書」。 大撒錢時代，人類看似擁有史上最多的「錢」，但並非人人都能從中受惠，甚至受益的人越來越少。在疫情影響下能維持基本的生活水準，不至於被無薪假、裁員、失業，但只能靠紓困，不過，貧窮的陷阱該怎麼處理？ 即便美國可以轉嫁自身的通膨壓力，但於國際貿易戰場上，價格早已做出反應。明明疫情尚未退去，但主要國家的股匯市、大城市的房價皆再度上漲；大宗商品也不遑多讓，原油價格回到相對高點，玉米，小麥每噸的價格也都有40-50%的漲幅。再看到金屬、銅、鋁、鐵礦，以及稀土等，無論現貨期貨，價格都像發了瘋似的，也連帶影響到生產鏈與供應鏈。 治重症要下猛藥，但就跟所有藥物一樣，用久也會產生「抗藥性」的。當整體經濟已經對「QE上癮」，未來只能用更大的幅度、透支更多未來子孫的財富，來拯救當下一塌糊塗的世界。 事實上各國政府推行QE的目的，都是希望「人人都有基本的保障，一起捱過疫情寒冬」。然而，放眼所及，世界上沒有任何一個國家真正實行了「全民基本收入」（UBI）的政策。 政府大量印製的鈔票，很大比例是用於企業紓困、購入公債與「非投資等級的債券」，講白了，就是先救企業與老闆，目的是避免企業裁員、進而希望消費動能夠維持，並帶動經濟成長。但，老百姓怎麼辦？ 在疫情下的無限 QE、市場近乎零利率的環境下，人們卻不一定敢消費。長此以往，經濟是可能有風險的。 如今，普通工薪階級紛紛勒緊褲帶過日子，還得小心翼翼面對突如其來的風險。然而對前 1% 的資產階級富人來說，這卻是「最好的時代」：眾所周知，當資金大量湧入資本市場、房地產市場時，永遠是資本越大者越能獲取更多利益。舉例來說，台股漲幅100%，是擁有100 張台積電的人賺得多，還是只有零股的人賺得多？ 從現實面來看，有錢人也更容易掌握資訊與工具，懂得如何全球配置資產、並利用QE 與低利率營造出來的環境，創造更多得資本利得。 資本市場（股市）與房地產市場和實體經濟脫鉤，早已如今全球不爭的事實。當資本集中在少數人手裡，股市與房市的收益率，長期高於經濟成長率，而經濟成長率又高於實質生產力，將成為越來越普遍的現象。 從微觀經濟（microeconomic）的角度來看，這是一國之內貧富不均越來越極端的徵兆。而從宏觀經濟（macroeconomic）的角度，則是增加了「有能力印鈔」的強國，與開發中國家之間的不平等。 因此我們看到許多新興市場國家，如俄羅斯、巴西、墨西哥等國，近期之內紛紛升息，因為他們面臨越來越大的經濟壓力。另一方面，美元霸權則讓美國坐享美元紅利，根本就像是最肥的資本家，藉由印出超越過去幾千年人類貨幣總和的鈔票，變相掠奪全世界的財富。 這個我們從未見識過的新世界，未來將是我們必須嚴肅面對的問題。 《經濟學人》總評 《經濟學人》的封面設計很粉亮。在粉色系的封面上，看見的是一款我們非常熟悉的泡麵（Instant Noodle），泡麵盒上面的文字非常有創意，包括了中文的「即時經濟」，下面標注了「GDP-ENHANCING」(GDP增強版)；以及小紅圈裡面的「NO ADDED THEORY」(不再強加理論)。封面設計上面的主標題正是「Instant economics」(即時經濟學)；補充標題則是「The real-time revolution(這個實時革命)。 本週《經濟學人》的全球版本封面故事，報導了經濟學界正在進行中的實時革命。因為信息量太少以及變數太多，過往被慣常使用的數學方程式和理論基礎，似乎讓經濟學家在黑暗中摸索不到方向，他們再也提不出可以提高就業或促進經濟增長的有效政策。 隨著資訊質量和及時取得的轉變，這個世界正處於一個經濟學上的實時革命邊緣。這次疫情促使著各國政府和中央銀行不得不開始推進各式實驗，從監控餐廳的預訂到跟蹤網路上的移動支付。整個結果雖然仍是剛剛啟動，但隨著數位設備、傳感器和即時支付越來越無處不在，準確而快速觀察經濟變化的能力將會大大提高，這為公共部門決策提供了美好的前景，也為政府大膽干預提供了極大的誘惑。 《經濟學人》最後認為，目前的數據仍然不足以可靠的預測到未來，複雜難測又充滿各種變化的經濟體，不可能只依賴大政府的運作，它們必須依賴的是那些數以百萬計的中小企業，以及消費者的各種自發行為。即時經濟學不是萬能的神奇預測者，它帶來的美好未來並不引人側目，但充滿變革特色，那就是一個更好更快、而且更理性的決策變化。 我本身也是經濟學背景，我非常同意經濟學人的觀點。過去我們分析未來的經濟，常常會說「在其他條件不變的情況下分析供需」，但在這個時代，因為real-time、因為數據，這種分析方式已經變得不可能。所以，即便透過微積分數學方程式、透過畫圖、透過理論，都無法百分百準確預測，但大數據的出現，有可能是第三波的經濟學浪潮。這也是經濟學人想提醒我們的。 Powered by Firstory Hosting
This episode is also available as a blog post: http://confoundedinterest.net/2021/05/28/the-fed-velocityraptors-money-velocity-m1-m2-measures-are-still-historically-abysmal-poor-bang-for-the-buck/
Gillyanne and I have some more best bits we'd like to share with you, this time from Series 1 Episodes 6-9 and Series 2 Episodes 1, 3 & 5.Episode 6 - The Singer in the Room. Industry sounds, why my belt isn't your belt, and at what point a singer needs to be "fixed" in their technique. And we answer Joanna's question about students and "when do you give up?"Episode 7 - Stories Behind the Stories Part 2. Behind the scenes on the Oxford Handbook of Singing, Jeremy's transcriptions of classic recordings, and the sometimes tricky business of collaborative writing.Episode 8 - Turning Points. How we've changed what Vocal Process does for us over the last 21 years, what it's like to create voice training resources in different formats, and how the biggest turning point of all changed the way we teach for good.Episode 9 - Making it work. The two things that help us create new resources for entirely different audiences - context and purpose.Series 2 Episode 1 - What's in Your Mug? Gillyanne explains what sparked the idea, and Jeremy describes two staples of every course we teach - the WOW Card and the Lionel Card.Series 2 Episode 3 - Analysing Voices and Relationships. What we listen for, how we use reverse engineering, how to sound the same as someone else without "cloning", and Jeremy demonstrates one of our signature vocal techniques in a line from "South Pacific".Series 2 Episode 5 - Registers, What's in a Name? We tackle one of the biggest cans of worms in vocal training, Vocal Registers. M1/M2, Chest/Head, Modal/Falsetto. We talk about Mixing, and Jeremy demonstrates a whole heap of mixes in M1 and M2, featuring and disguising his primary gearchange.Mentioned in this episode:Our brand new Vocal Process Learning Lounge: 15 years of groundbreaking voice training resources (over 500 training videos) available in full for less than the price of one singing lesson https://vocal-process-hub.teachable.com/p/the-vocal-technique-learning-loungeThe Online Singing Teacher Training https://store.vocalprocess.co.uk/singing-teacher-training-onlineHow to Accompany Your Singing Students ebook https://www.amazon.co.uk/How-accompany-your-singing-students-ebook/dp/B07DPTDWHXOxford Handbook of Singing https://www.amazon.co.uk/Oxford-Handbook-Singing-Library-Psychology/dp/0199660778Why Do I Need A Vocal Coach https://www.amazon.co.uk/dp/B084QDLT7C/
Gillyanne and Jeremy tackle the controversial topic of vocal registersM1 and M2 - what the M words actually meanThe difference between M1 and chest voiceThe only way to find out where the mechanisms change (according to the research)Why registers help us navigate our pitch range (with examples)Why key is vital to registers in different genresWhy mixing is not about the vocal folds!And Jeremy makes a sweeping statement about THE MIXWith live demonstrations of M1 and M2 singing from both Gillyanne and JeremyThe original article from Jeremy https://vocalprocess.co.uk/modal-falsetto-everything-between/The M1/M2 popup Workshop https://store.vocalprocess.co.uk/m1-m2-workshopTeacher Other Genders popup Workshop https://store.vocalprocess.co.uk/teach-genderThe Vocal Process Hub with all our published training resources for the last 15 years will be available from World Voice Day (April 16th) 2021
Video on BitChute: https://www.bitchute.com/video/WR3i6uelhTle/ PLAYLIST: Current Events https://soundcloud.com/chycho/sets/current-events-news-politics-1 PLAYLIST: Julian Assange & WikiLeaks https://soundcloud.com/chycho/sets/wikileaks-julian-assange PLAYLIST: Investing & Personal Finance https://soundcloud.com/chycho/sets/investing-and-personal-finance ***SUPPORT*** ▶️ Patreon: https://www.patreon.com/chycho ▶️ Paypal: https://www.paypal.me/chycho ▶️ Subscribe Star: https://www.subscribestar.com/chycho ▶️ Streamlabs at: https://streamlabs.com/chycholive ▶️ YouTube Membership: https://www.youtube.com/channel/UCe4HBBAeK0CYoir4LjXU8fA/join ***WEBSITE*** ▶️ Website: http://www.chycho.com ***LIVE STREAMING*** ▶️ Twitch: https://www.twitch.tv/chycholive ***VIDEO PLATFORMS*** ▶️ YouTube: https://www.youtube.com/user/chychochycho ▶️ BitChute: https://www.bitchute.com/channel/chycho ▶️ Rumble: https://rumble.com/c/c-508765 ▶️ Odysee: https://odysee.com/@chycho:9 ▶️ Twitch: https://www.twitch.tv/chycholive ***FORUM*** ▶️ Discord: https://discord.gg/MXmS7B9 ***SOCIAL MEDIA*** ▶️ Minds: https://www.minds.com/chycho ▶️ Gab: https://gab.ai/chycho ▶️ Ello: https://ello.co/chycho ▶️ Vk: https://vk.com/id580910394 ▶️ Twitter: https://twitter.com/chycho ▶️ Parler: https://parler.com/profile/chycho ***AUDIO/PODCASTS*** ▶️ SoundCloud: https://soundcloud.com/chycho ***MARKETPLACE*** ▶️ Ebay Page: https://www.ebay.ca/usr/chycho ***CRYPTO*** ▶️ As well as Cryptocurrencies: Bitcoin (BTC): 1Peam3sbV9EGAHr8mwUvrxrX8kToDz7eTE Bitcoin Cash (BCH): 18KjJ4frBPkXcUrL2Fuesd7CFdvCY4q9wi Ethereum (ETH): 0xCEC12Da3D582166afa8055137831404Ea7753FFd Ethereum Classic (ETC): 0x348E8b9C0e7d71c32fB2a70DcABCB890b979441c Litecoin (LTC): LLak2kfmtqoiQ5X4zhdFpwMvkDNPa4UhGA Dash (DSH): XmHxibwbUW9MRu2b1oHSrL951yoMU6XPEN ZCash (ZEC): t1S6G8gqmt6rWjh3XAyAkRLZSm9Fro93kAd Doge (DOGE): D83vU3XP1SLogT5eC7tNNNVzw4fiRMFhog Peace. chycho http://www.chycho.com
In this episode we walk through a discussion of money supply, Fed policy, and velocity, to find out if inflation is coming to the dollar. This is an important concept for bitcoin because many people believe bitcoin's fate is tied to a weak dollar, which it is not. Website: https://bitcoinandmarkets.com/e218 Twitter: https://twitter.com/btcmrkts https://twitter.com/ansellindner Links M0: https://fred.stlouisfed.org/series/BOGMBASE M1: https://fred.stlouisfed.org/series/M1 M2: https://fred.stlouisfed.org/series/M2 GDP: https://www.investopedia.com/terms/g/gdp.asp
Mogens fortæller sandheden om M1/M2 & M3, og fortæller samtidig, hvordan man løser trængselsproblemerne på M1/M2.
Dr. Klaus Ley discusses Charles Mills' 2000 article, published in The JI, describing the M1/M2 polarization axis of macrophages.
On this episode of Next on the Tee my guests are: PGA Master Professional Paul Rudeen, Golf Digest Top 100 Instructor Tom Stickney, and TaylorMade Golf CEO David Abeles. Paul Rudeen - Paul shard his tips for how to warm up before your round of golf, tips for how to pitch and chip the ball closer to the hole, how to read the grain on the green and one swing tip to keep in mind as you play. Tom Stickney - Tom shared stories about some of the players he got to be around when he was a Golf Instructor at Big Horn Golf Club in Palm Desert, California. He also shared tips for how to hit better shots from uphill lies, how to use the slope of the green to our advantage plus hitting a safety flop shot to help you not walk away with making a double or triple bogey when we miss the green with our second shots. David Abeles - David shared his story from graduating with a finance degree from the University of Connecticut to catching on at TaylorMade. He also talked about having two TaylorMade guys battle it out at the Masters, the disappointment of Dustin Johnson's injury, the science and technology behind their M1 & M2 golf clubs and TP5 golf balls plus Tiger's future with the brand.
Dr Carolyn Lam: Welcome to Circulation on the Run, your weekly podcast summary and backstage pass to The Journal and its editors. I'm Dr. Carolyn Lam, associate editor from the National Heart Center and Duke National University of Singapore. Today's issue features two exciting papers regarding heart failure in patients with breast cancer. We will be discussing this right after these summaries. Are we any closer to improving survival in Eisenmenger syndrome? Well, today's first original paper looks at contemporary trends and presents a multivariable mortality risk stratification model based on five simple noninvasive predictors of death in this population. Dr. Kempny and colleagues from Royal Brompton Hospital in London in the United Kingdom preform a large multicenter study in 1098 patients with Eisenmenger syndrome followed up between years 2000 and 2015. At the end of the study almost two-thirds of patients were on advance therapy for pulmonary arterial hypertension, while only six patients underwent lung or heart and lung transplantation. The study showed that despite advances in management, there was significant mortality amongst contemporary adults with Eisenmenger syndrome and 25.3% of patients died over a median follow up period of 3.1 years. Mortality was higher in older patients, those with a pre-tricuspid shunt, lower oxygen saturation, absence of sinus rhythm, or with a pericardial effusion. This important study is accompanied by an editorial by Drs. Lange, from Texas Tech University Health Sciences Center El Paso and Dr. Brickner from UT Southwest Medical Center in Dallas, Texas. The editorialists call for a prospective randomized control trials of the effect of current, or future pulmonary vasoactive disease targeting therapies on mortality in Eisenmenger syndrome patients, and say it's time to direct our efforts from improving risk-stratification towards improving survival. The next study provides experimental evidence of tolerogenic dendritic cell therapy as a novel anti-remodeling therapy in myocardial infarction. Tolerogenic dendritic cells are promising, potent, beneficial regulators of the post-infarct healing process via their control of T-regulatory cells and M1 M2 macrophages. Plus they have the advantage of the ease of administration and feasibility of a heart specific tolero-dendritic cell production. In the current paper by co-first authors, Drs. Choo and Lee, and co-corresponding authors, Drs. Chang and Lim, from Catholic University Korea and Chai University in Korea, authors generated tolerogenic dendritic cells by treating bone marrow-derived dendritic cells with TNF-alpha and cardiac lysate from mice with myocardial infarction. They then injected myocardial infarction mice twice with tolerogenic dendritic cells within 24 hours and at 7 days after LAD ligation. In treated animals, in vivo cardiac magnetic resonance imaging and ex vivo histology confirm the beneficial effects on post-infarct LV remodeling. Furthermore, subcutaneously administered tolerogenic dendritic cells near the inguinal lymph node migrated to the regional lymph nodes and induced infarct tissue specific T-regulatory T-cell populations in the inguinal and mediastinal lymph nodes, spleen, and infarcted myocardium, all of which elicited an inflammatory to reparative macrophage shift. The altered immune environment in the infarcted heart resulted in better wound remodeling, preserved left ventricular systolic function, and an improved survival following myocardial infarction. Thus, this study shows that tolerogenic dendritic cell therapy in a preclinical model of myocardial infarction may be potentially translatable into an anti-remodeling therapy for ischemic repair. The final paper reports results of cell therapy on exercise performance and limb perfusion in peripheral artery disease from the PACE trial, which is an NHLBI-sponsored randomized double-blind placebo-controlled phase two clinical trial, designed to assess the safety and efficacy of autologous bone marrow-derived aldehyde dehydrogenase bright cells in peripheral artery disease, and to explore associated claudication physiological mechanisms. In this paper from corresponding author Dr. Moye from UT School of Public Health in Houston, Texas and colleagues of the Cardiovascular Cell Therapy Research Network, a total of 82 patients with claudication and infrainguinal peripheral artery disease were randomized at nine sites to receive alcohol dehydrogenase bright cells or placebo. All patients underwent bone marrow aspiration and isolation of aldehyde dehydrogenase bright cells followed by 10 injections into the thigh and calf of the index leg. Results showed that there were no significant differences in the change over six months between study groups for the co-primary endpoint of peak walking time, collateral count, peak hyperemic popliteal flow, and capillary profusion measured by magnetic resonance imaging. Additionally, there were no significant differences for the secondary endpoints including quality of life measures. There were no adverse safety outcomes. Interestingly, a post-hoc exploratory analysis suggested that aldehyde dehydrogenase bright cell administration might be associated with an increase in the number of collateral arteries in participants with completely occluded femoral arteries. In summary, cell therapy did not improve peak walk time or magnetic resonance outcomes, and the changes in peak walk time were not associated with the anatomic or physiologic MRI endpoints. However, future peripheral artery disease cell therapy trial design may be informed by new anatomic and perfusion insights. These and other issues are discussed in an accompanying editorial by Drs. Breton-Romero and Hamburg from Boston University School of Medicine. Well, that wraps it up for our summaries, now for our feature discussion. We are really in the grove here in Washington, D.C. and I am borrowing the words of my very special, star associate editor, guest, Dr. Gregory Hundley, and he's from Wakefield University School of Medicine. We're discussing two very important papers and they deal with the risk of heart failure following breast cancer. Why they're so important? Well, first of all, it's about time we looked at this problem in detail, and secondly, they actually represent papers in a new section of the journal called "Bridging Disciplines," and in this case cardio-oncology. Very, very important topics. We're here with the corresponding authors of both papers, Bonnie Ky from University of Pennsylvania School of Medicine and Dr. Margaret Redfield from Mayo Clinic. Dr Gregory Hundley: Thank you, Carolyn. I really appreciate that wonderful introduction and also the chance to talk with Bonnie about this exciting topic. So, Bonnie, you've got a paper here, now, where you did a study in patients with breast cancer, and it sounds like you acquired echocardiograms over a period of time. Can you tell us a little bit about that? Dr Bonnie Ky: Correct. So this is longitudinal prospective cohort study, it's an NIH-funded R01, whereby we are enrolling patients from the breast cancer clinic who are receiving doxorubicin or trastuzumab or a combination of the two therapies. And we're performing very careful cardiovascular phenotyping, from the time at which they initiate chemotherapy through their chemotherapy and then annually once a year we have them come back, for a total follow up time of 10 years. We took a subcohort, 277 patients, and from their echocardiograms, we analyze them very carefully for various measures of left ventricular size, function, not only systolic function but also diastolic function. We also looked at measures of contractility such as strain in multiple dimensions, and then also measures of ventricular arterial coupling, as well as arterial loads, so how the ventricle interacts with the arterial system. And what we found was that over a 3.2 period time period, on population average, these modest declines in left ventricular ejection fraction, and even across all three treatment groups, and even at three years there were persistent LVF declines. Dr Gregory Hundley: So, I understand, Bonnie, that you also collected some information as to whether or not these patients were experiencing symptoms associated with heart failure. How did the imaging markers relate to the symptomatology associated with heart failure? Dr Bonnie Ky: What we found was that early changes in arterial stiffness or total arterial load, as well as early changes in EF were associated with worse heart failure symptoms at one year. A lot of our other analysis was focused on defining what echo parameters of remodeling, size, function are driving or associated most strongly with LVF decline, as well as LVF recovery. Dr Gregory Hundley: And then at two years, what happened? Did the echo parameters, were they still associated with heart failure or was there a little discrepancy there? Dr Bonnie Ky: Interestingly, at two years ... no, there was no significant association with changes in arterial load and heart failure symptoms at two years. Dr Gregory Hundley: So there might be something transient that's occurring that is associated with heart failure early, and then the patients still had heart failure late, so maybe something else is operative. What do you think we need to do next? What's the next step in your research and then other investigators around the world; what do we need to do to design studies to look at these issues further? Dr Bonnie Ky: Yeah. What does the field need, the field of cardio-oncology that's really growing and developing at rapid paces. Some of the major findings from the study was that changes in total arterial load were very strongly associated with both LVF decline and LVF recovery. So total arterial load is the measure of blood pressure or total arterial stiffness, it's derived from blood pressure. And to me, that begs the question, or begs the next step is that changes in blood pressure are associated with decline as well as recovery. I think, oh, as cardiologists we've also always recognized the importance of afterload reduction. And to me, this study suggests that we need a study, a randomized clinical trial, looking at blood pressure lowering in this population to help mitigate LVF declines. Dr Carolyn Lam: I'd actually like to turn it back to you. You are world-renowned for your work in cardio-oncology. Where do you think this fits in, and where do you think we need to address most urgently? Dr Gregory Hundley: I think where this fits in wonderfully is a lot of individuals around the world are collecting echocardiographic measures, and all different types. And what Bonnie has helped do is clarify what we would expect to see in this particular patient population. How those measures change over time and that feeds into another block of data, when the measurements head south, do we change therapy, do we add protective agents, and things of that nature. So I think Bonnie's work really contributes on that front. What she has also pointed out is that more research needs to be performed, not necessarily because the patients had heart failure symptomatology at two years, but not necessarily associated with the decline in EF; are there other systems in the cardiovascular realm that are being affected? The vascular system- Dr Carolyn Lam: Yeah. Dr Gregory Hundley: Skeletal muscle, many other areas. So as cardiologists start to work more with oncologists in this space, and we're all working together to make sure that not only patients survive their cancer, but they have an excellent quality of life, I think we'll see, as we have in other heart failure syndromes, a look toward other aspects of the cardiovascular system, body in general, to reduce the overall morbidity associated with the disease. I think what we need to recognize as cardiovascular medicine specialists is that now for many forms of cancer, cardiovascular events, and certainly morbidity are becoming the primary issue that folks have to deal with with survivors. It's not necessarily the cancer recurrence, it's not necessarily a new cancer, it's cardiovascular. So we've got to integrate cardiology earlier in working with oncologists to improve overall survival and create an excellent quality of life from our different perspectives. Dr Carolyn Lam: So, Maggie, let's move on to your paper now. You looked at radiotherapy's effect, whereas Bonnie looked at chemotherapy's effect. Could you tell us what you did and what you found? Dr Margaret Redfield: The rationale for doing this study was, of course, seeing a lot of patients with HFpEF who had had radiation therapy for breast cancer, and I always just sort of assumed that that was because 12% of women over the age of 40 get breast cancer and 20% of women over the age of 40 get heart failure, but it seemed to be somehow more common than that. The other rationale was that radiation therapy does not actually affect the cardiomyocytes; they are very radiation resistant. And what radiation does is cause microvascular endothelial cells damage and inflammation, and that is felt to be fundamental in the pathophysiology for HFpEF. So we thought we should look at this. I collaborated with a radiation oncologist and oncologists, and they were interested in looking at this because there's a lot of techniques now to reduce cardiac radiation exposure during radiation therapy, including proton beam therapy, and they're trying to prioritize who they use this new technology on. So what we did was start with a population-based study, all women who lived in Olmsted county who received radiation therapy for breast cancer in the contemporary era, where they're already using these dose reducing techniques. So we wanted to make it relevant to what's going on today. And so we started with a base cohort of all women. We matched patients' cases, it was a case-control study, so we matched cases and controls according to their age at the time of breast cancer, whether they had heart failure risk factors, like hypertension or diabetes, whether they got adjuvant chemotherapy, and tumor size, because we felt it was important that radiation could affect different parts of the heart, depending on whether it was right- or left-sided tumor. And what we found is that the risk of heart failure increased with the mean cardiac radiation dose. We measured the mean cardiac radiation dose in every case and every control from their CT scans and their radiation plants. And as the radiation dose went up, the risk of heart failure went up, even matching or controlling for chemotherapy, which wasn't used that often in this group, or heart failure risk factors. And the vast majority of these cases were indeed HFpEF. So we then looked at factors that happened in-between the radiotherapy and the onset of heart failure, making sure that this all wasn't just coronary artery disease, 'cause we know radiation can increase the risk of coronary artery disease. And indeed there were, only in about 18% of cases was there a new episode of coronary disease in the interim between the radiotherapy and the breast cancer. So, basically found that the mean cardiac radiation dose, even in today's era, does increase the risk of heart failure with preserved ejection fractions. Dr Carolyn Lam: The things that stuck out to me ... it's population based. You did such a comprehensive study to really answer very key questions: dose of radiation, is it really just mediated by age and age-related risk factors, is it just about MI or could it be more microvascular disease? Congratulations, I really appreciated this paper. Some of the take-home messages are directly related to the treatment of breast cancer, isn't it? And about the importance of minimizing radiation dose if possible. I suppose one of the take-homes is, as well, for screening and watching out for heart failure. One thing though: how were these woman diagnosed with HEpEF? I mean, this is always the questions I get. How do you get diagnosed with HEpEF? Dr Margaret Redfield: Right, well, first we started with looking to see if they had a ICD code for heart failure, and then we looked at each case of heart failure and determined if they either met Framingham criteria at the time of the diagnosis and the majority of them did. If they didn't actually meet the Framingham criteria, we looked to be sure there was a physician diagnosis of heart failure in the record and that they had supportive evidence of heart failure: echocardiographic findings, natriuretic peptide findings, and other clinical characteristics of heart failure. And importantly, in the large control group from where we, you know, got our controls, people, a very large group of patients who did not get heart failure, we'd use natural language processing to look at all those records to make sure we weren't missing anybody who didn't have an ICD diagnosis or code for heart failure to make sure we weren't missing any cases of heart failure. So, we really tried to use very stringent methods to make sure we had true cases and control groups. Dr Carolyn Lam: Indeed, and it actually goes back to Bonnie's paper as well, where we have to remind everyone that the diagnosis of HEpEF really starts with the symptomatology of heart failure in particular, that you so rigorously determined. I think just one last thing, Maggie: what do you think this implies now, for HEpEF? What do we do in general so the non-radiation-associated, do we believe more the Walter Paulus-Carsten Tschope hypothesis, and if so, what do we do? Dr Margaret Redfield: Yes, well I think it really does support that hypothesis. We know that radiation therapy, again, we know what it does to the coronary microvascular endothelial cells and that's been elegantly worked out both in patients and in animal models. I think this really supports the Paulus hypothesis because this microvascular damage was able to produce heart failure, so I think that really supports that hypothesis. And there's been some studies showing decreased coronary flow reserve in HEpEF patients; it's very common. So I think indeed it does support that hypothesis and that the coronary microvasculature is key in the pathophysiology of HEpEF. However it's a little scary to me because that sort of damage, once it's established, may be very hard to treat. You know, proangiogenic strategies in peripheral vascular disease have not yet yielded the benefits that we hoped for, so I think it's a tough therapeutic challenge that'll be very important to try to address in pre-clinical studies to try and figure out once the microvasculature is so damaged how do we treat that? How do we reverse that process? Dr Carolyn Lam: Yeah. Words of wisdom. Maggie, thanks so much for inspiring, just all of us in this field. I just had to say that. You know, you are the reason that I am totally in love with HEpEF. (laughter) Dr Margaret Redfield: (laughter) Dr Carolyn Lam: So thank you so much for joining me today on the show. In fact, thank you to all my three guests. You've been listening to Circulation on the Run. You must tell everyone about this episode, it is full of gems. Thank you, and tune in next week.
M1 홍진영-사랑의 와이파이 M2 서주경-벤치 M3 오혜성-지금 이 순간 M4 박상철-무조건 M5 박구윤-뿐이고 M6 단야-사랑한다고 말해요 M7 김용임-빙빙빙 M8 천송이-한잔해요 M9 김연자-10분내로 10위~1위 소개 (10 정유하-해바라기 9 박상철-무조건 8 양태성-심쿵 7 진성-안동역에서 6 장윤정-초혼 5 박구윤-뿐이고 4 오승근-내 나이가 어때서 3 단야-여기서 살자 2 홍진영-산다는 건 1 단야-사랑한다고 말해요)
M1 박구윤-쾌지나 M2 최훈-변하지 않아요 M3 박현빈-샤방샤방 M4 단야-사랑한다고 말해요 M5 진성-안동역에서 M6 홍진영-산다는건 M7 양태성-심쿵 M8 양태성-다 이뻐 M9 양태성-심쿵 10위~1위 소개(10 최훈-변하지 않아요 9 양태성-심쿵 8 박현빈-샤방샤방 7 장윤정-초혼 6 오승근-내 나이가 어때서 5 단야-사랑한다고 말해요 4 진성-안동역에서 3 단야-여기서 살자 2 정유하-해바라기 1 홍진영-산다는건)
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