中国胆毒鱼类的研究

在我国民间相信吞服鱼胆可治目疾 ,然而因吞服鱼胆而引起的中毒 ,危害身体健康事件时有发生。自196 4- 1999年的 35年中 ,据不完全统计吞服有毒鱼胆而中毒的人数达 45 1人 ,其中死亡达 83人 ,死亡率为 18.0 4%。本文主要叙述鱼胆中毒的概况 ,胆汁有毒成分 (鲤醇 ) ,动物实验 ,中毒症状及治疗。经动物实验及多年的调研共发现 12种淡水鱼类的胆汁有毒 ,它们均是鲤科鱼类 ,从理论上阐明吞服任何鲤科鱼类的鱼胆均是危险的。

我国几种常见的胆毒鱼类

鱼胆有毒的鱼类称为胆毒鱼类。我国部分地区民间常有吞服鱼胆治病的习惯，认为胆能“清热解毒”、“明目”、“镇咳”。但若吞服了有毒鱼的较大的鱼胆，就会引起严重的中毒，甚至生命危险。

疏肝利胆排毒汤治疗肝豆状核变性56例

目的:观察中医药治疗肝豆状核变性的临床疗效及治疗前后血铜、尿铜、尿锌的变化。方法:自拟方药疏肝利胆排毒汤口服治疗肝豆状核变性56例。结果:总有效率为78.57%。结论:中药疏肝利胆排毒汤治疗肝豆状核变性有效,且能促进尿铜的排泄,无毒副作用。

疏肝利胆排毒汤对肝豆状核变性患者肝脏功能及肝硬化改善作用的临床研究

目的:观察疏肝利胆排毒汤对肝豆状核变性(HLD)患者肝硬变及肝脏功能的改善作用。方法:61例患者随机分为2组。治疗组40例予基础用药加中药疏肝利胆排毒汤治疗;对照组21例予基础用药加青霉胺治疗。观察2组患者治疗前后肝脏声像图、肝功能改善情况、24h尿铜及角膜K—F环的变化。结果:治疗组肝脏声像图改善率为62.50%,对照组肝脏声像图改善率分别为47.62%(P<0.05);2组患者治疗后肝功能各项指标均有不同程度的改善,但治疗组明显优于对照组。结论:中医药治疗肝豆状核变性可通过减轻肝细胞的铜中毒,促进HLD肝硬变及肝脏功能的改善,有可能扭转肝豆状核变性患者体内的铜代谢运转机制,其疗效优于青霉胺治疗。

海鲜虽美防鱼毒

吃海鲜已成时兴,皆因海鲜味道鲜美营养丰富。据营养学家分析,鱼肉含有丰富的蛋白质、矿物质和维生素。这些,都是人体不可缺少的营养物质。鱼肉的蛋白质比其他肉类的蛋白质更易被人体消化吸收;

谨防有毒鱼和水生动物的伤害(一)

鲜鱼、海味是食中上品．不仅味鲜美。营养丰富，且具有滋补肝、脾，肾，益气升血，降压……等功效。但是，有一些鱼和水生动物的体内含有毒素，能使人中毒，甚至死亡。

疏肝利胆排毒汤治疗肝豆状核变性38例临床观察

目的观察疏肝利胆排毒汤治疗肝豆状核变性(WD)的临床疗效。方法58例WD患者随机分为治疗组(38例)和对照组(20例),治疗组服用中药疏肝利胆排毒汤治疗,对照组服用青霉胺片治疗,30天为1个疗程。3个疗程后观察两组疗效及尿铜、角膜色素环(K-F环)、血清铜、血清铜蓝蛋白、血清铜氧化酶的变化。结果治疗组总有效率为73.68%,对照组为70.00%,两组比较差异无统计学意义(P>0.05),但治疗组无任何不良反应,且相关生化指标均有不同程度的变化。结论中药疏肝利胆排毒汤治疗肝豆状核变性安全有效,有可能改善体内铜浊毒邪运转机制。

饮食保健十二戒(二)

七、不要最后的晚餐。许多人对早餐、中餐不重视,而在时间充裕的晚餐放开肚皮大吃大喝,这是很不科学的饮食方法。晚餐过饱可引起肥胖,增加结石的机会,促升血压,诱发冠心病和糖尿病,更易患肠癌等。正确的饮食观应该是早餐吃好,中餐吃饱,晚餐适量。 八、不要吃得太大胆。动物的胆多数能入药进食,报载台湾每年因患猛爆性肝炎而死亡者众,生吃蛇胆是主要原因之一。鱼胆能入药。但其常含毒胆酸、鹅去氧毒胆酸及胆汁毒素等剧毒,误食会致人死命。

Comparison of murine cirrhosis models induced by hepatotoxin administration and common bile duct ligation

AIM： To build up the research models of hepatic fibrosis in mice.METHODS： Inbred wild-type FVB/N mice were either treated with alpha-naphthyl-isothiocyanate （ANIT）, allyl alcohol （AA）,carbon tetrachloride （CCl4）, 3,5-diethoxycarbonyl-l,4-dihydrocollidine （DDC）, and silica, or subjected to common bile duct ligation （CBDL） to induce hepatic injury. Liver biopsies were performed every 4 wk to evaluate hepatic fibrosis over a period of 6 mo. Cumulative cirrhosis and survival curves were constructed by life table method and compared with Wilcoxon test.RESULTS： Under the dosages used, there was neither mortality nor cirrhosis in AA and silica-treated groups. DDC and ANIT caused cirrhosis within 4-12 and 12-24 wk, respectively.Both showed significantly faster cirrhosis induction at high dosages without significant alteration of survival. The duration for cirrhosis induction by CCl4 ranged from 4 to 20 wk, mainly dependent upon the dosage. However, the increase in CCl4 dosage significantly worsened survival. Intraperitoneal CCl4 administration resulted in better survival in comparison with garage administration at high dosage, but not at medium and low dosages. After CBDL, all the mice developed liver cirrhosis within 4-8 wk and then died by the end of 26 wk.CONCLUSION： CBDL and administrations of ANIT, CCl4, and DDC ensured liver cirrhosis. CBDL required the least amount of time in cirrhosis induction, but caused shortened lives of mice. It was followed by DDC and ANIT administration with favorable survival. As for CCl4, the speed of cirrhosis induction and the mouse survival depended upon the dosages and the administration route.

Effect of mutant p27^(kip1) gene on human cholangiocarcinoma cell line, QBC_(939)

AIM：To investigate the effects of exogenously mutated p27^kip1 （p27） on proliferation and apoptosis of human cholangiocarcinoma cell line, QBC939 in vivo.METHODS： Adenviral vectors were used to transfect mutated p27 cDNA into human QBC939 cell line. Expression of p27 was detected by RT-PCR. Western blot. Cell growth, morphological change, cell cycle, apoptosis and cloning formation were determined by MTT assay and flow cytometry.RESULTS： The expression of p27 protein and mRNA was increased signifi cantly in QBC939 cell line transfected with Ad-p27mt. The transfer of Ad-p27mt could signifi cantly inhibit the growth of QBC939 cells, decrease the cloning formation rate and induce apoptosis. p27 over expression caused cell cycle arrest at G0/G1 phase 72 h after infection with Ad-p27mt.CONCLUSION： p27 may cause cell cycle arrest at G0/G1 phase and subsequently lead to apoptosis. Recombinant adenovirus expressing mutant p27 may be potentially useful in gene therapy for cholangiocarcinoma.

Distribution of Like-muscarinic Acetylcholine Receptor M2 in the Brain of Three Castes of Polyrhachis vicina

The cholinergic system plays an important role in the central nervous system of insects and is closely related to the complex behavior of insects. The immunohistochemical technique was performed to detect the expression of like-muscarinic acetylcholine receptor M2 in the brain of three castes of Polyrhachis vicina. A positive expression of like-muscarinic acetylcholine receptor M2 was observed in the mushroom body, central body and antennal lobes of the ant brain; but there is great diversity in their location and intensity among worker, queen and male ants. It is speculated that like-muscafinic acetylcholine receptor M2 plays a critical role in the central nervous system, in terms of projecting visual information and olfactory information into the protocerebrum and integrating many inputs.

Cholelithiasis associated with haemolytic-uraemic syndrome

Cholelithiasis occurs infrequently in the paediatric age group. Hereditary spherocytosis, sickle cell anaemia and thalassemia are the haemolytic disorders most commonly associated with development of gall stones in paediatric age group. The question is whether an isolated episode of haemolysis can cause gallstones.

Serum bile acid profiling reflects enterohepatic detoxification state and intestinal barrier function in inflammatory bowel disease

AIM： To determine free and conjugated serum bile acid （BA） levels in inflammatory bowel disease （IBD） subgroups with defined clinical manifestations. METHODS： Comprehensive serum BA profiling was performed in 358 IBD patients and 310 healthy con- trols by liquid chromatography coupled to electrospray ionization tandem mass spectrometry. RESULTS： Serum levels of hyodeoxycholic acid, the CYP3A4-mediated detoxification product of the second- ary BA lithocholic acid （LCA）, was increased significantly in Crohn＇s disease （CD） and ulcerative colitis （UC）, while most other serum BA species were decreased signifi- cantly. Total BA, total BA conjugate, and total BA glyco- conjugate levels were decreased only in CD, whereas total unconjugated BA levels were decreased only in UC. In UC patients with hepatobiliary manifestations, the conjugated primary BAs glycocholic acid, taurocholic acid, and glycochenodeoxycholic acid were as signifi- cantly increased as the secondary BAs LCA, ursodeoxy- cholic acid, and tauroursodeoxycholic acid compared to UC patients without hepatobiliary manifestations. Finally, we found that in ileocecal resected CD patients, the unconjugated primary BAs, cholic acid and chenode- oxycholic acid, were increased significantly compared to controls and patients without surgical interventions. CONCLUSION： Serum BA profiling in IBD patients that indicates impaired intestinal barrier function and increased detoxification is suitable for advanced diag- nostic characterization and differentiation of IBD sub- groups with defined clinical manifestations.

Clinicopathologic characteristics of intrahepatic cholangiocarcinoma in patients with positive serum a-fetoprotein

AIM:To explore clinicopathologic characteristics of intrahepatic cholangiocarcinoma (ICC) in patients with positive serum a-fetoprotein (AFP). METHODS:One hundred and thirty one patients who underwent surgical dissection for pathologically confirmed ICC were divided into a positive AFP (> 20 ng/mL) group (n = 32) and a negative AFP group (n = 99), whose clinicopathologic features were analyzed and compared. RESULTS:The positive rate of HBsAg and liver cirrhosis of the positive AFP group was higher than that of the negative AFP group, while the positive rate of CA19-9 (> 37 U/mL) and the lymph node metastasis rate was lower. CONCLUSION:ICC patients with positive AFP share many clinicopathologic similarities with hepatocellular carcinoma.

Acute acalculous cholecystitis in children

Acute acalculous cholecystitis(AAC) is the inflammatory disease of the gallbladder in the absence of gallstones. AAC is estimated to represent at least 50% to 70% of all cases of acute cholecystitis during childhood. Although this pathology was originally described in critically ill or post-surgical patients, most pediatric cases have been observed during several infectious diseases. In addition to cases caused by bacterial and parasitic infections, most pediatric reports after 2000 described children developing AAC during viral illnesses(such as Epstein-Barr virus and hepatitis A virus infections). Moreover, some pediatric cases have been associated with several underlying chronic diseases and, in particular, with immune-mediated disorders. Here, we review the epidemiological aspects of pediatric AAC, and we discuss etiology, pathophysiology and clinical management, according to the cases reported in the medical literature.

Direct-acting antiviral agents against hepatitis C virus and lipid metabolism

Hepatitis C virus (HCV) infection induces steatosis and is accompanied by multiple metabolic alterations including hyperuricemia, reversible hypocholesterolemia and insulin resistance. Total cholesterol, low-density lipoprotein-cholesterol and triglyceride levels are increased by peginterferon and ribavirin combination therapy when a sustained virologic response (SVR) is achieved in patients with HCV. Steatosis is significantly more common in patients with HCV genotype 3 but interferon-free regimens are not always effective for treating HCV genotype 3 infections. HCV infection increases fatty acid synthase levels, resulting in the accumulation of fatty acids in hepatocytes. Of note, low-density lipoprotein receptor, scavenger receptor class B type I and Niemann-Pick C1-like 1 proteins are candidate receptors that may be involved in HCV. They are also required for the uptake of cholesterol from the external environment of hepatocytes. Among HCV-infected patients with or without human immunodeficiency virus infection, changes in serum lipid profiles are observed during interferon-free treatment and after the achievement of an SVR. It is evident that HCV affects cholesterol metabolism during interferon-free regimens. Although higher SVR rates were achieved with interferon-free treatment of HCV, special attention must also be paid to unexpected adverse events based on host metabolic changes including hyperlipidemia.

Hepatitis B virus infection:A favorable prognostic factor for intrahepatic cholangiocarcinoma after resection

AIM： To study the prognostic factors for intrahepatic cholangiocarcinoma （ICC） and evaluate the impact of chronic hepatitis B virus （HBV） infection on survival rate of ICC patients. METHODS： A total of 155 ICC patients who underwent macroscopic curative resections （R0 and R1） were enrolled in this retrospective study and divided into group A with HBV infection and group B without HBV infection according to their chronic HBV infection, represented by positive hepatitis B surface antigen （HBsAg） in serum or in liver tissue. Clinicopathological characteristics and survival rate of the patients were evaluated. RESULTS： All patients underwent anatomical resection. Their 1- and 3-year survival rates were 60.6% and 32.1%, respectively. Multivariate analyses revealed that HBV infection, hepatolithiasis, microscopic satellite lesion, and lymphatic metastasis were the independent prognostic factors for the survival rate of ICC patients. The median disease-free survival time of the patients was 5.0 too. The number of tumors, microscopic satellite lesion, and vascular invasion were the independent prognostic factors for the disease-free survival rate of the patients. The prognostic factors affecting the survival rate of ICC patients with HBV infection and those without HBV infection were not completely consistent. Alkaline phosphatase 〉 119 U/L, microscopic satellite lesion, vascular invasion, and lymphatic metastasis were the independent factors for the patients with HBV infection, while r-glutamyltransferase 〉 64 U/L, microscopic satellite lesion, and poor tumor differentiation were the independent factors for the patients without HBV infection. CONCLUSION： HBV infection is a valuable clinical factor for predicting tumor invasiveness and clinical outcome of ICC patients. ICC patients with HBV infection should be distinguished from those without HBV infection because they have different dinicopathological characteristics, prognostic factors and outcomes after surgical resection.

Pathogenesis of achalasia cardia

Achalasia cardia is one of the common causes of motor dysphagia.Though the disease was first described more than 300 years ago,exact pathogenesis of this condition still remains enigmatic.Pathophysiologically,achalasia cardia is caused by loss of inhibitory ganglion in the myenteric plexus of the esophagus.In the initial stage,degeneration of inhibitory nerves in the esophagus results in unopposed action of excitatory neurotransmitters such as acetylcholine,resulting in high amplitude non-peristaltic contractions(vigorous achalasia);progressive loss of cholinergic neurons over time results in dilation and low amplitude simultaneous contractions in the esophageal body(classic achalasia).Since the initial description,several studies have attempted to explore initiating agents that may cause the disease,such as viral infection,other environmental factors,autoimmunity,and genetic factors.Though Chagas disease,which mimics achalasia,is caused by an infective agent,available evidence suggests that infection may not be an independent cause of primary achalasia.A genetic basis for achalasia is supported by reports showing occurrence of disease in monozygotic twins,siblings and other first-degree relatives and occurrence in association with other genetic diseases such as Down's syndrome and Parkinson's disease.Polymorphisms in genes encoding for nitric oxide synthase,receptors for vasoactive intestinal peptide,interleukin 23 and the ALADIN gene have been reported.However,studies on larger numbers of patients and controls from different ethnic groups are needed before definite conclusions can be obtained.Currently,the disease is believed to be multi-factorial,with autoimmune mechanisms triggered by infection in a genetically predisposed individual leading to degeneration of inhibitory ganglia in the wall of the esophagus.