医学考博双语阅读精选16

1、微信公众号：医学博士英语南京医科大学小白老师医学考博双语阅读精选（16） Cancer and the microbiomeA punch in the gutHow microbes promote liver cancer inthe overweightOBESITY brings problemsnotably heart disease, diabetes and cancer. It is not hard to understand its connection with heart disease and diabetes: excess fat clogs arteries

2、and messes around with the metabolism.Its link with cancer is less intuitive. Shin Yoshimoto of the Japanese Foundation for Cancer Research, in Tokyo, and his colleagues suspect this is at least partly because researchers have been looking for that link in the wrong place. Most work in the field is

3、focused on the cells of the human body. But researchers should, Dr. Yoshimoto believes, be at least as interested in the cells of the microbiome, the collection of 100 trillion bacteria that live in the gut.Mostly, the microbiome is beneficial. It helps with digestion and enables people to extract a

4、 lot more calories from their food than would otherwise be possible. Research over the past few years, however, has implicated it in diseases from atherosclerosis to asthma to autism. Dr Yoshimoto and his colleagues would like to add liver cancer to that list. Their paper making this accusation is p

5、ublished in this weeks Nature, and it is a careful, step-by- step analysis of the matter. They start from the facts that fat animals have different gut bacteria from thin ones; that some bacteria produce inflammatory molecules as part of their metabolism; and that inflammation promotes cancer. They

6、began their experiments by feeding laboratory mice a fatty diet, to make them obese. Such mice, they found, are no more likely to develop cancer than those fed an abstemious diet. Obesity alone, then, does not seem to cause tumours. But it might still promote them.Their next experiment therefore sta

7、rted by giving the mice a carcinogen known to trigger tumour formation throughout the body. One group was then fed standard fare while another got the high-fat diet. After 30 weeks, just 5% of the slim group had developed tumours, not in the liver but in the lungs.In the obese group, every animal ha

8、d developed liver cancer.To understand how this happened, the researchers began with the tumours and worked backwards.First, they found that the cancerous liver cells in their mice were generally accompanied by cells that had the symptoms of old age.Such cells also emit chemical signals which promot

9、e inflammation, and thus encourage tumours. The researchers suspected that these cells were being made senescent by something produced by gut bacteria. That suspicion was confirmed when they served some of their mice a cocktail of four antibiotics, to prune the animals microbiomes. This treatment lo

10、wered the number of senescent and cancerous cells, suggesting the microbes were indeed to blame forpromoting cancer.1微信公众号：医学博士英语南京医科大学小白老师Dr. Yoshimoto and his team then started tofocus on which bacteria were causing theproblem. First, they discovered they could get the same cancer-suppressing effe

11、ct using just vancomycin, an antibiotic that kills only “Gram-positive” bacteria. They also observed, as prior research had suggested, that a fatty diet raised levels of a chemical called deoxycholic acid and that antibiotics lowered it. Previous research had demonstrated too that DCA damages DNA in

12、 a way that promotes senescence. Dr Yoshimoto showed that lowering DCA levels in mice did indeed reduce the development of liver cancer. Certain types of gut bacteria, including strains of Clostridium, are known to burp out DCA. And further detective work, including examination of the mices faeces,

13、revealed higher levels of a strain of Clostridium called OUT-1105 in the fat mice than in the thin ones.This strain, Dr Yoshimoto thinks, is the most likely culprit. There is, then, a chain of causation leading from the gut to the liver that promotes tumours in obese mice. And the chances are good t

14、hat something similar pertains in Homo sapiens. Humans are not mice, of course. But the two species microbiomes often do behave in the same way.If cancer does end up being added to the growing list of problems which an upset microbiome can cause, that may stimulate research into ways of tweaking it

15、to stop it causing disease. It will also, once again, emphasise the microbiomes role, for both good and ill, as anadjunct part of the human body.和微生物组肠道里的元凶微生物如何诱发胖人的肝癌肥胖产生了问题尤其是心脏病、糖尿病和。肥胖与心脏病、肥胖与糖尿病的联系不难理解：多余脂肪堵塞血管，使新陈代谢紊乱。但是肥胖与的联系凭直觉就不能理解了。位于东京的日本研究的Shin Yoshimoto 以及他的同事怀疑，这主要是因为研究人员的研究角度错误。此领域的多

16、数工作只是集中在人身细胞的研究。Shin Yoshimoto 认为，研究人员应当留心微生物组，这群生活在肠道的 100 万亿个细菌群。微生物组中的大多数都是有益的。它们帮助消化，让人体从食物中分离出更多的能量。然而，近几年的研究工作认为，微生物组是造成动脉硬化或孤独症等的病因。但是，Yoshimoto 以及他的同事则认为微生物组也是肝癌的病因。他们的论文指出指控，发表2微信公众号：医学博士英语南京医科大学小白老师在本周的自然杂志上。本篇文章进行了仔细、逐步的分析。文章开始便列举了事实，肥胖动物的肠道细菌与瘦的不同；某些细菌在新陈代谢过程中产生一种能引起炎症的分子；炎症诱发。他们通过实验小鼠进行

17、实验，喂养高脂肪食物，让它们长胖。他们发现，吃了脂肪含量高的小鼠患的机率不高于饮食有度的小鼠。因此，单独肥胖一项因素不会引起肿瘤，但是仍然会诱发肿瘤。因此，他们下一步的实验就是喂养小鼠能在全身形成肿瘤的致癌物质。一组实验小鼠喂养标准食物，另一组喂养高脂肪食物。30 个星期后，体形瘦削的那组只有 5%患有肿瘤，不是在肝脏，而是在肺部。体形肥胖的那组，每只小鼠都患上了肝癌。要了解其中的原因，研究人员先从肿瘤入手，采用了反。首先，他们发现，实验小鼠中癌化的肝脏细胞周围的细胞出现了老龄化的症状。这些老化细胞会释放出引发炎症的化学信号，并 进一步诱发肿瘤。研究人员怀疑，细胞出现老化是由肠道细菌产生的某些

18、物质所致。研究 人员混合了四种抗生素，喂养小鼠时，减少小鼠体内的微生物群。此时，他们的怀疑得到了证实。这种喂养方法减少了老化和癌化细胞的数量，表明微生物确实是诱发 素。的因接下来，Yoshimoto 和他和团队开始研究是何种微生物导致问题。首先，他们发现， 用专杀“革兰氏阳性”细菌的抗生素万古霉素进行实验，也能取得相同的抑癌效果。同时， 他们发现，高脂肪饮食会提升化学物质脱氧胆酸的水平，万古霉素会使其降低。先前的研究也发现，DCA 会以一种诱发衰老的方式破坏DNA。Yoshimoto 让人们看到，降低 实验小鼠体内DCA 的水平确实会减少诱发肝癌的机率。某些肠道细菌，包括梭状芽胞杆菌菌株，研究人员进行进一步的工作，包括