从传统木作和酿酒技术看李白《静夜思》之“床”

李白《静夜思》“床前明月光”的“床”有“卧具说”“坐具说”“井栏说”“檐廊说”等说法,否定“卧具说”的认为,不可能在有“卧床”的室内看到地上的月光。其实不然,唐时房屋用的是“隔扇门”,为落地门且上半部透光,因此在“卧床”时看到地上月光是可能的。并且,此床也有可能为“酒榨”,即“酒床”,也称“糟床”——古代酿酒工艺流程中不可或缺的设备。古代家庭酿酒使用小型“酒床”,酒坊使用大型木制“酒床”,酒坊往往前店后坊,店面是可以灵便装卸的木板大排门,早卸晚上。

Effect of lactulose on establishment of a rat non-alcoholic steatohepatitis model

AIM： To explore the relationship between changes of intestinal environment and pathogenesis of non-alcoholic steatohepatitis （NASH）. METHODS： Forty-two Sprague-Dawley rats were randomly dMded into model group （n = 24）, treatment group （n = 12）, and control group （n = 6）. The rats of model and treatment groups were given high-fat diet, and those of the control group were given normal diet. Furthermore, the rats of treatment group were given lactulose after 8 wk of high-fat diet. Twelve rats of the model group were killed at 8 wk of high-fat diet. At the 16 wk the rats of treatment group, control group, and the rest of the model group were killed. The serum levels of aminotransferase were measured and the histology of livers was observed by H＆E staining. RESULTS： The livers of rats presented the pathological features of steatohepatitis with higher serum levels of alanine aminotransferase （ALT） and aspartate aminotransferase （AST） in the model group after 16 wk. Compared to the model group, the serum levels of ALT and AST in treatment group decreased significantly and were close to the normal group, and the hepatic inflammation scores also decreased markedly than those in the model group after 16 wk （5.83±2.02 vs 3.63±0.64, P〈0.05）, but were still higher than those in the model group after 8 wk （3.63±0.64 vs 1.98±0.90, P〈0.05）. However, the degree of hepatic steatosis had no changes in treatment group compared to the model group after 16 wk. CONCLUSION： Lactulose could ameliorate the hepatic inflammation of rats with steatohepatitis induced by fat- rich diet, but could not completely prevent the development of steatohepatitis. It is suggested that intestinal environmental changes such as intestinal bacteria overgrowth, are one of the important factors in the pathogenesis of NASH.

Signaling mechanisms in alcoholic liver injury: Role of transcription factors, kinases and heat shock proteins

Alcoholic liver injury comprises of interactions of various intracellular signaling events in the liver. Innate immune responses in the resident Kupffer cells of the liver, oxidative stress-induced activation of hepatocytes, fibrotic events in liver stellate cells and activation of liver sinusoidal endothelial cells all contribute to alcoholic liver injury. The signaling mechanisms associated with alcoholic liver injury vary based on the cell type involved and the extent of alcohol consumption. In this review we will elucidate the oxidative stress and signaling pathways affected by alcohol in hepatocytes and Kupffer cells in the liver by alcohol. The toll-like receptors and their down-stream signaling events that play an important role in alcohol-induced inflammation will be discussed. Alcohol-induced alterations of various intracellular transcription factors such as NFKB, PPARs and AP-1, as well as MAPK kinases in hepatocytes and macrophages leading to induction of target genes that contribute to liver injury will be reviewed. Finally, we will discuss the significance of heat shock proteins as chaperones and their functional regulation in the liver that could provide new mechanistic insights into the contributions of stress-induced signaling mechanisms in alcoholic liver injury.

Role of transmethylation reactions in alcoholic liver disease

Alcoholic liver disease is a major health care problem worldwide. Findings from many laboratories, including ours, have demonstrated that ethanol feeding impairs several of the many steps involved in methionine metabolism. Ethanol consumption predominantly results in a decrease in the hepatocyte level of S-adenosylmethionine and the increases in two toxic metabolites, homocysteine and S-adenosylhomocysteine. These changes, in turn, result in serious functional consequences which include decreases in essential methylation reactions v/a inhibition of various methyltransferases. Of particular interest to our laboratory is the inhibition of three important enzymes, phosphatidylethanolamine methyltransferase, isoprenylcysteine carboxyl methyltransferase and protein L-isoaspartate methyltransferase. Decreased activity of these enzymes results in increased fat deposition, increased apoptosis and increased accumulation of damaged proteins- all of which are hallmark features of alcoholic liver injury. Of all the therapeutic modalities available, betaine has been shown to be the safest, least expensive and most effective in attenuating ethanol-induced liver injury. Betaine, by virtue of aiding in the remethylation of homocysteine, removes both toxic metabolites （homocysteine and S-adenosylhomocysteine）, restores S-adenosylmethionine level, and reverses steatosis, apoptosis and damaged proteins accumulation. In conclusion, betaine appears to be a promising therapeutic agent in relieving the methylation and other defects associated with alcoholic abuse.

Promoting genetics in non-alcoholic fatty liver disease: Combined risk score through polymorphisms and clinical variables

Non-alcoholic fatty liver disease(NAFLD) has a prevalence of approximately 30% in western countries, and is emerging as the first cause of liver cirrhosis and hepatocellular carcinoma(HCC). Therefore, risk stratification emerges as fundamental in order to optimize human and economic resources, and genetics displays intrinsic characteristics suitable to fulfill this task. According to the available data, heritability estimates for hepatic fat content range from 20% to 70%, and an almost 80% of shared heritability has been found between hepatic fat content and fibrosis. The rs738409 single nucleotide polymorphism(SNP) in patatin-like phospholipase domain-containing protein 3 gene and the rs58542926 SNP in transmembrane 6 superfamily member 2 gene have been robustly associated with NAFLD and with its progression, but promising results have been obtained with many other SNPs. Moreover, there has been proof of the additive role of the different SNPs in determining liver damage, and there have been preliminary experiences in which risk scores created through a few genetic variants, alone or in combination with clinical variables, were associated with a strongly potentiated risk of NAFLD, non-alcoholic steatohepatitis(NASH), NASH fibrosis or NAFLD-HCC. However, to date, clinical translation of genetics in the field of NAFLD has been poor or absent. Fortunately, the research we have done seems to have placed us on the right path: We should rely on longitudinal rather than on cross-sectional studies; we should focus on relevant outcomes rather than on simple liver fat accumulation; and we should put together the genetic and clinical information. The hope is that combined genetic/clinical scores, derived from longitudinal studies and built on a few strong genetic variants and relevant clinical variables, will reach a significant predictive power, such as to have clinical utility for risk stratification at the single patient level and even to esteem the impact of intervention on the risk of disease-related outcomes. Well-structured future studies would demonstrate if this vision can become a reality.

Correlation between Thymidylate Synthase Genotype and Susceptibility to Gastric Carcinoma

OBJECTIVE To investigate the correlation between polymorphism of the 5′-untranslated region （5′-UTR） of thymidylate synthase genes, as well as the lifestyle, and the susceptibility of gastric carcinoma. METHODS A case-control study, with 60 cases of gastric carcinoma and 170 cases of general risk population-based controls from Nantong, Jiangsu province, China, was conducted. The epidemiological data, such as living habits of the cancer patients, were collected. DNA of peripheral blood leukocytes was obtained from all of the subjects. The TS 5′-UTR tandem repeat genotype was detected using polymerase chain reaction （PCR）. RESULTS There were three TS 5′-UTR genotypes in the group of gastric cancer cases （2R/2R, 2R/3R and 3R/3R） and six TS 5′-UTR genotypes in the group of the controls （2R/2R, 2R/3R, 3W3R, 2R/4R, 2R/5R and 3R/4R）. The genotypic frequencies were respectively 5.0%, 43.3% and 51.7% in the gastric cancer group. Compared with the parameters in the control group, i.e., 4.7%, 31.7%, 60.6%, 1.2%, 1.2% and 0.6%. There were no significant differences between the two groups. Compared with the 3R/3R- genotype individuals who where non-smokers, drank alcohol twice or less each week, drank tea and did not intake pickled food （PF）, the risk of gastric cancer significantly went up in the 2R/2R or 2R/3R-genotype people who had habits of smoking, drinking alcohol more than twice each week, no tea drinking but with frequent intake of PF. The adjusted ORs were as follows, 3.79 （95% CI： 2.45-8.64）, 3.41 （95% CI and 3.61 （95% CI： 1.81-8.78）. CONCLUSION There is 1.21-8.47）, 5.99 （95% Ch 3.01-14.7）, an obvious correlation between the polymorphisms of TS 5′-UTR genotypes and the lifestyle of individuals in the development of gastric carcinoma.

Role of alcohol in the regulation of iron metabolism

Patients with alcoholic liver disease frequently exhibit increased body iron stores, as reflected by elevated serum iron indices (transferrin saturation, ferritin) and hepatic iron concentration. Even mild to moderate alcohol consumption has been shown to increase the prevalence of iron overload. Moreover, increased hepatic iron content is associated with greater mortality from alcoholic cirrhosis, suggesting a pathogenic role for iron in alcoholic liver disease. Alcohol increases the severity of disease in patients with genetic hemochromatosis, an iron overload disorder common in the Caucasian population. Both iron and alcohol individually cause oxidative stress and lipid peroxidation, which culminates in liver injury. Despite these observations, the underlying mechanisms of iron accumulation and the source of the excess iron observed in alcoholic liver disease remain unclear. Over the last decade, several novel iron-regulatory proteins have been identified and these have greatly enhanced our understanding of iron metabolism. For example, hepcidin, a circulatory antimicrobial peptide synthesized by the hepatocytes of the liver is now known to play a central role in the regulation of iron homeostasis. This review attempts to describe the interaction of alcohol and iron-regulatory molecules. Understanding these molecular mechanisms is of considerable clinical importance because both alcoholic liver disease and genetic hemochromatosis are common diseases, in which alcohol and iron appear to act synergistically to cause liver injury.

FLASHLAMP- PUMPED PULSED DYE LASER IN TREATMENT OF PORT- WINE STAINS

To assess the effectiveness of the flashlamp- pumped pulsed dye laser (Photogeneca V, Synosure Corp, Boston, United States) in the treatment of port- wine stains. Methods. One hundred and ninety- four consecutive patients with port- wine stains were treated with a flashlamp- pumped pulsed dye laser in Peking Union Medical College Hospital from January 1998 to August 1999. Results. Of 194 patients who completed treatment, 56.2％ had more than 60％ fading of the lesion and only 6.7％ had less than 20％ fading. An average of 3.6 treatments were needed to achieve more than 60％ fading. The response was better in children than in adults, although the difference was not significant. Pigmentary change (usually transient) occurred in 3.1％ of patients. Conclusions. This study confirms the efficacy of the flashlamp- pumped pulsed dye laser in the treatment of port- wine stains in children and adults.

Severe alcoholic hepatitis:Glucocorticoid saves lives and transplantation is promising

Glucocorticosteroids have been used as the only treatment for a long time which significantly reduced the mortality of the patients with severe alcoholic hepatitis.The efficacy of transplantation has been recently addressed in a pilot study.The result seems promising but needs larger multicenter trials.

做爱不作战

有经验的旅行家都认为，只要遇到一张好的床，即便身边没有女人，旅行都不会失色多少。