모네의 그림 <수련>
모네, 수련.
모네는 많은 양의 수련 연작을 남겼다. 빛의 상태에 따라 미묘하게 변하는 연못을 화폭에 담으려 했다. 그런데 위의 화질이 너무 않좋다.
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대시호탕은 사하제瀉下劑로서 장중경 당시 傷食、食傷에 이용되었다. 증세의 핵심은 “此心下不安，按之滿痛，此為實也”
大柴胡湯，也是古代良方，是瀉下劑，它用於什麼呢？當時張仲景用來治療傷食、食傷，我一直強調張仲景當時可能治療了很多軍人，為什麼呢？因為漢代，軍閥混亂，那個時候是戰亂最多的時期，名醫作為社會的優良資源，當然要治療軍人，張仲景《傷寒論》、《金匱要略》我把它看作是治療軍人疾病的書籍，柴胡牡蠣桂枝湯治療軍人煩心、失眠；桂枝湯軍人用來抗疲勞的，大柴胡湯是慶功宴之後，將軍夜裡肚子痛得哇哇亂叫，並“此心下不安，按之滿痛，此為實也”，怎麼辦，當下之，服用大柴胡湯後，舌苔黃膩好轉，食積退去，腹中不痛也，中國的東西非常簡單。大柴胡湯是很多種功效的良方，解痙、止痛、通便、降脂、降壓、消炎等等，用起來是非常的簡單，關鍵在於“此心下不安，按之滿痛”也，這一定需要摸，但嚴重的話就不需要按。中西醫結合在文化大革命中搞得非常多，其中最好的要數是大柴胡湯經證，張仲景的關鍵處方，這個方證大家一定要搞清楚指征，然後還有許多的或然證，因為大柴胡湯適用面也非常寬，很多疾病都能用。或者發燒、或者便秘、或腹瀉，這裡不要以為大柴胡湯，只是適用於便秘，腹瀉也是能用的。“瀉下則安”，這個很有意思，很多拉肚子一直拉，都不好（轉），一摸肚子痛的，大黃的指征不一定是大便乾結，使用大黃的是痛、硬，所以只要是痛，就可以使用大柴胡湯。或者黃疸、胰腺疾病，膽囊炎，或者頭痛、高血壓的患者，或者支氣管哮喘的患者，像這都是或然證，不是一個症狀，而是一個系統，還有舌苔黃燥、脈滑數的問題。
哪些疾病可以用，我們還要講病症，這個病症很重要的，我們不能忽略。現代診斷對我們安全正確使用經方至關重要，我們還有研究，比如對中國經方論壇的研究，其與日本經方研究的距離就在現代醫學上，人家也很清楚、發現了某個疾病與某張方的關聯，就是一個發明、一個創作，這做得比較好的是大塚敬節，他對古代與現代的漢方作出了很大的貢獻，可惜他的書很多遺失，現存的其中一本《湯本求真》，是很有建設的著作。胡希恕先生是怎麼開悟的呢？他看了這本書才醒過來了，成了我們出名的專家；岳美中先生也看了，他很聰明、他也不多講，牽涉了中日的民族感情。中國的拿來主義，在於劑量，我在日本呆了六個月，我看到東洋學派是怎麼學的？我感到我們中國跟它有很大的差距，日本以前就只有西醫，沒有中醫的課程，可講不講的；但是現代日本教育人，規定醫學生畢業要掌握漢方製劑法，那這樣，所有的醫學院校都要開設漢方課，有的叫東洋醫學課，有的叫漢方和漢藥課；現在各個醫學院校都有講中醫的老師、教授一大堆，而且他們也講授經方，他們經方是一張一張方子地講授的，如大柴胡湯，先把資料錄進去，然後歸納好。日本的清英大學和我們的北京中醫藥大學的中醫課程，中醫生的畢業比例分析發現，日本院校中醫課程與西醫課程的比例很少、一點點，但是畢業的很多中醫學生，大多都能用於臨床，而我們中國中醫院校的學生學的中醫是不少了，但是畢業以後很少真正從事中醫的，這是什麼原因呢？
好，再次回歸到大柴胡湯這裡，膽囊炎、膽石症、膽蛔蟲，它是一個傳統的抑膽藥。那麼膽石症發作期很有效，那靜止期能不能用？只有腹下按壓有抵抗感可以用，我的經驗，有的老師喜歡用大柴胡湯加石膏來排石，還有一點，病人吃藥前先吃油煎雞蛋，然後氣通，再用大柴胡湯，陽胃燥熱證就是這種，這是很值得我們研究的一個證，現在我們這有用附子，也是出現這個證再用藥的，所以大柴胡湯不是用於膽石症，而是用於“心下按之滿痛”的證型，這是非常的重要的。
대시호탕은 췌장염의 효과적인 방제이다.
大柴胡湯可以說是胰腺炎一個必效的方、專方，無論急性、慢性，無論胖瘦都是很好用的，很有效果的。我估計張仲景當時治療的就是一個戰士的急性胰腺炎，喝多了、吃多了，就得了胰腺炎，就用大柴胡湯、大黃的劑量也大。上海有一位醫生，他單用大黃治療胰腺炎，用250g大黃，還有一個經驗是早瀉早緩解、遲瀉遲緩解，嘔吐吃多少就嘔多少，有的就是讓他嘔、吃多少嘔多少，越早越好，早瀉早好，下法為妙，下法是好法？都是好法。我治療很多胰腺炎都有效果，太多的例子我就不一一舉例了。這個反流性膽汁食道炎，現在是非常多，故反流性膽汁食道炎，用大柴胡湯。如果出現大便秘結，用大柴胡湯有效；如果燒心感、難受，可以加梔子，梔子對食管炎是非常有效的，胃炎燒心感、難受，則用大柴胡湯加梔子。
고지혈증
高脂血症，它也是一個高脂血症的脂類調節劑，治療反流性膽汁食道炎、胃炎，我說這個是治療胃腸動力學的。高脂血症，有很多人腹部充實，按壓有力，如果有肝火，煩躁、便秘等症，故治療高脂血症，不要單單是想到山楂、荷葉，那是民間藥、食療，用首烏，這不講究證。高脂血症用大柴胡湯就有效，一般2個月有效，快的一個月就見效，而且能降體重，所以用於高高的、肥胖的人，容易起效。大柴胡湯能降體重、減肥，尤其我發現中年女性，特別是接近更年期的女性，上身特別的飽滿，胃氣、胃部的脂肪也較多，而且月經的量也比較多，並且經前乳房脹痛、食欲旺盛、煩熱、充滿激情者，這個時候可以使用大柴胡湯，枳殼要重用，用量為30g，量少則不起效。所以它有減肥作用。
고혈압, 중풍
高血壓、中風可用，大柴胡湯加黃連，就是大柴胡湯加三黃瀉心湯，對一些體質充實的，三黃合大柴胡湯有效。
유선염, 유선소엽증생에는 대시호탕에 청피 등을 가미한다.
乳腺炎、乳腺小葉增生，大柴胡湯加青皮、陳皮，枳殼、枳實一起用，或者和枳實芍藥散一起用，大柴胡合枳實芍藥散可以緩解症狀、治療確實有效。
기관지효천
支氣管哮喘，原來只是想到麻黃，其實也有柴胡帶，對什麼樣的人起效，對體格健壯的、吐黃痰的、不停地喘氣等起效，對吐黃痰的加黃連，不吐、但嘴唇發涼、發冷的，大柴胡湯桂枝茯苓丸，這是胡希恕先生的經驗，我用過很多例，包括我太太的支氣管哮喘，這個大柴胡湯加桂枝茯苓丸用上就有效果，所以不像其他方法，是可以用得很得手，等到這個環節後，除根就用小青龍湯加梔子，還有一種情況，就是胸脅苦滿，往來寒熱，摸上去兩個脅下繃硬，而且一吃飯就脹得厲害，這個柴胡桂枝茯苓丸湯一用上就能起效。看看這個患者，有支氣管哮喘30多年，近年發作頻繁來看，他中午、晚上出現心慌、濃痰、結塊，自己是中醫，也用了平胃散，後來用血府逐瘀湯，胸悶好轉，但沒有根本解決，我是大柴胡湯合併小建中湯，量不是很重，另外，我用柴胡加白芍、枳殼、桔梗、黃連、瓜蔞皮排痰，另外還有“排痰散“，人家以為是我的經驗、我的經方，其實這也是張仲景的經方，也叫排膿散，這個膿不要以為是我們傷口的膿液，其實不是，古時候粘液發黃、吐痰黏黏都可以歸為膿一類，就用這個白芍、枳殼、桔梗，我就用這個白芍、枳殼、桔梗，按照2 : 2 : 1的比例研末花粉沖服，每次10g，這個很是簡單、很有效果，其功效勝過沐舒坦。枳殼、白芍舒緩平滑肌的痙攣，痰液就易排出，所以張仲景的小方很有意思，我們要把它挖掘，不要局限於字面上。吐痰也就吐膿、排膿也叫排痰，這個患者一周後咳嗽明顯好轉，這個上腹部也不痛了、痰也少了，效果非常地好。這樣的例子實在是太多了。
還有心律不齊，我剛學醫的時候還上過當，以為心律不齊是氣陰虛，喜歡用生脈散，一個老太太平時經常心律不齊，人又瘦，舌苔有光，我給她用了生脈散，第二天，她根本就不找我了，找我對面的老中醫，老中醫問到她大便怎麼樣，她就說大便3天1次，什麼時候開始，她回答說吃了蛋炒飯後開始的，老先生就給她開了大柴胡湯加枳實、枳殼，再過一段時間，她滿臉笑容，心律也齊了，我就覺得我們的教科書上所說的大便不通、肚子硬、很多腹脹的，都可以用大柴胡湯，這些用了之後很舒服，有的快速型心律不齊，全身通紅通紅，加黃連，加梔子，因為黃連抑制心律異常性。
이 모든 질병의 관건은 체질에 있다. 시호탕 체질에 맞아야만 대시호탕이 듣는다.
但是這麼多病，關鍵在於體質，我們治療的是一種體質狀態，只是將我們發現的大柴胡證用到現代醫學的診療疾病裡面去，我們稱之為大柴胡湯體質，另外一種體質，以中老年較多，體格比較壯實，上腹部也是比較充實飽滿的，這些胃口都是好的，就是不敢多吃，多吃後就脹痛，這往往是可以使用大柴胡湯的，按壓伴有硬感，經常有噯氣，同時易患高血壓病、高脂血症、膽囊炎、膽石症、胰腺炎、支氣管哮喘，好多的疾病，大柴胡湯主之。
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전국언론노동조합이 발표한 언론장악 적폐청산을 위한 언론 부역자 3차 명단 41명
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□ SBS ▲하금렬 전 사장 ▲최금락 전 보도본부장
1차 부역자 명단
최성준 방송통신위원회 위원장, 김성우 전 청와대 홍보수석, 박효종 방송통신심의위원회 위원장, 이인호 KBS 이사장, 고영주 방송문화진흥회 이사장, 고대영 KBS 사장, 안광한 MBC 사장, 배석규 전 YTN 사장, 박노황 연합뉴스 사장, 백종문 MBC 미래전략본부장 등 10명
-----------> 이들이 없다면 오늘날 한국의 언론이 북한이나 나치 독일의 선전선동으로 타락한다는 말과 같다. 좌파들은 무엇보다 이들을 자리에서 밀어내기 위해 모든 수단을 다 사용할 것이다. 만일 이들 언론인이 모두 제거된다면, 한국은 희망의 빛을 잃고 만다.
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Kinship Systems, Cooperation and the Evolution of Culture
Benjamin Enke
NBER Working Paper No. 23499
Issued in June 2017
NBER Program(s): POL
친족 구조의 긴밀성과 사회의 특성이 관련이 있다는 논문이다.
조상들의 친족이 느슨하게 연결된 사회는 신(神), 보편적 윤리, 죄책감, 대규모 제도 등의 바탕 위에 상호 협력하고 신뢰하는 사회를 만든다.
이에 반해 역사적으로 친족 구조가 긴밀하게 조직된 사회는 타 집단을 속이고, 타 집단 소속원들을 믿지 못하며, 집단에 대한 연고의식을 보인다.
---> 전라도 지역의 특성 같기도 하다. 문화인류학을 전공하는 사람은 이 논문의 방법을 이용해, 전라도 지역의 친족 관계를 연구해 볼만 하다.
Cultural psychologists and anthropologists argue that societies have developed heterogeneous systems of social organization to cope with social dilemmas, and that an entire bundle of cultural characteristics has coevolved to enforce cooperation within these different systems. This paper develops a measure of the historical tightness of kinship structures to provide empirical evidence for this large body of theories. In the data, societies with loose ancestral kinship ties cooperate and trust broadly, which is apparently sustained through a belief in moralizing gods, universally applicable moral principles, feelings of guilt, and large-scale institutions. Societies with a historically tightly knit kinship structure, on the other hand, exhibit strong in-group favoritism: they cheat on and are distrusting of out-group members, but readily support in-group members in need. This cooperation scheme is enforced by moral values of in-group loyalty, conformity to tight social norms, emotions of shame, and strong local institutions. These relationships hold across historical ethnicities, contemporary countries, ethnicities within countries, and migrants. The results suggest that religious beliefs, language, emotions, morality, and social norms all coevolved to support specific social cooperation systems.
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What If (Almost) Every Gene Affects (Almost) Everything?
Three Stanford scientists have proposed a provocative new way of thinking about genetic variants, and how they affect people’s bodies and health.
Ed Yong
Jun 16, 2017
In 1999, a group of scientists scoured the genomes of around 150 pairs of siblings in an attempt to find genes that are involved in autism. They came up empty. They reasoned that this was because the risk of autism is not governed by a small number of powerful genes, which their study would have uncovered. Instead, it’s likely affected by a large number of genes that each have a small effect. Perhaps, they wrote, there might be 15 such genes or more.
Two decades later, that figure seems absurdly and naively low. If you told a modern geneticist that a complex trait—whether a physical characteristic like height or weight, or the risk of a disease like cancer or schizophrenia—was the work of just 15 genes, they’d probably laugh. It’s now thought that such traits are the work of thousands of genetic variants, working in concert. The vast majority of them have only tiny effects, but together, they can dramatically shape our bodies and our health. They’re weak individually, but powerful en masse.
But Evan Boyle, Yang Li, and Jonathan Pritchard from Stanford University think that this framework doesn’t go far enough.
They note that researchers often assume that those thousands of weakly-acting genetic variants will all cluster together in relevant genes. For example, you might expect that height-associated variants will affect genes that control the growth of bones. Similarly, schizophrenia-associated variants might affect genes that are involved in the nervous system. “There’s been this notion that for every gene that’s involved in a trait, there’d be a story connecting that gene to the trait,” says Pritchard. And he thinks that’s only partly true.
Yes, he says, there will be “core genes” that follow this pattern. They will affect traits in ways that make biological sense. But genes don’t work in isolation. They influence each other in large networks, so that “if a variant changes any one gene, it could change an entire gene network,” says Boyle. He believes that these networks are so thoroughly interconnected that every gene is just a few degrees of separation away from every other. Which means that changes in basically any gene will ripple inwards to affect the core genes for a particular trait.
The Stanford trio call this the “omnigenic model.” In the simplest terms, they’re saying that most genes matter for most things.
More specifically, it means that all the genes that are switched on in a particular type of cell—say, a neuron or a heart muscle cell—are probably involved in almost every complex trait that involves those cells. So, for example, nearly every gene that’s switched on in neurons would play some role in defining a person’s intelligence, or risk of dementia, or propensity to learn. Some of these roles may be starring parts. Others might be mere cameos. But few genes would be left out of the production altogether.
This might explain why the search for genetic variants behind complex traits has been so arduous. For example, a giant study called… er… GIANT looked at the genomes of 250,000 people and identified 700 variants that affect our height. As predicted, each has a tiny effect, raising a person’s stature by just a millimeter. And collectively, they explain just 16 percent of the variation in heights that you see in people of European ancestry. That’s not very much, especially when scientists estimate that some 80 percent of all human height variation can be explained by genetic factors. Where’s that missing fraction?
Pritchard’s team re-analyzed the GIANT data and calculated that there are probably more than 100,000 variants that affect our height, and most of these shift it by just a seventh of a millimeter. They’re so minuscule in their effects that it’s hard to tell them apart from statistical noise, which is why geneticists typically ignore them. And yet, Pritchard’s team noted that many of these weak signals cropped up consistently across different studies, which suggests that they are real results. And since these variants are spread evenly across the entire genome, they implicate a “substantial fraction of all genes,” Pritchard says.
The team found more evidence for their omnigenic model by analyzing other large genetic studies of rheumatoid arthritis, schizophrenia, and Crohn’s disease. Many of the variants identified by these studies seem relevant to the disease in question. For example, some of the schizophrenia variants affect genes involved in the nervous system. But mostly, the variants affect genes that don’t make for compelling stories, and that do pretty generic things. According to the omnigenic model, they’re only contributing to the risk of disease in incidental ways, by rippling across to the more relevant core genes. “It’s the only model I can come up with that make all the data fit,” Pritchard says.
“Pritchard’s a very perceptive investigator, who looks beyond what most people do,” says Aravinda Chakravarti, a geneticist at John Hopkins Medicine. “Do I believe this all correct? No, but it’s very compelling. It’s a serious hypothesis that we’ve got to prove or disprove.”
If Pritchard is right, it has big implications for genetics as a field. Geneticists are running ever-bigger and more expensive searches to identify the variants behind all kinds of traits and diseases, in the specific hope that their results will tell them something biologically interesting. They could show us more about how our bodies develop, for example, or point to new approaches for treating disease. But if Pritchard is right, then most variants will not provide such leads because they exert their influence in incidental ways.
프리차드가 옳다면, 대부분의 변종들은 사소한 방식으로 영향을 미치기 때문에, 질병 치료에 대한 해결을 제공하지는 못한다.
Put it this way: The Atlantic is produced by all of us who work here, but our lives are also affected by all the people we encounter—friends, roommates, partners, taxi drivers, passers-by etc. If you listed everyone who influences what happens at The Atlantic, even in small ways, all of those peripheral people would show up on the list. But almost none of them would tell you much about how we do journalism. They're important, but also not actually that relevant. Pritchard thinks the same is true for our genes. And if that’s the case, he says, “it’s not clear to me that increasing your study size is going to help very much.”
The alternative, he says, is to map the networks of genes that operate within different cells. Once we know those, we’ll be better placed to understand the results from the forthcoming mega-studies. “It is a really hard problem,” says Boyle. “Historically, even understanding the role of one gene in one disease has been considered a major success. Now we have to somehow understand how combinations of seemingly hundreds or thousands of genes work together in very complicated ways. It’s beyond our current ability.”
There are, however, projects that are trying to do exactly that. “I’m very excited about trying to understand whether these network ideas are correct,” says Pritchard. “I think it’s telling us something profound about how our cells work.”
나는 <서구의학은 파산했다>에서 서구의 환원주의와 그에 바탕한 의학은 파산했다고 선언했다. 환원주의의 진면목은 유전자 논란에서 드러난다. 서구의 학자들은 환원주의적 방식에 따라, 유전자 하나가 모종의 질병을 유발한다고 굳게 믿고 있었다. 그래서 그 유전자를 찾으려고 혈안이 되어 있었다.
그런데 이제 와서 보니, 유전자 하나가 아니라, 거대한 유전자 집단이 서로 서로 영향을 미치면서, 미세하게 영향을 미친다는 것이다. 환원주의는 더 이상 신체라는 복잡계에 적용할 수가 없게 되었다. 서구의학은 파산했다.
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