There are no anatomic or physiologic criteria for the diagnosis of irritable bowel syndrome (IBS) and the disease is defined mainly on exclusion of organic lesions. Therefore, quite a few patients with IBS are not promptly diagnosed and treated. It is important to apply RomeⅡCriteria, instead of its limitation, in those who have abdominal pain with relief by defecation, sensation of incomplete evacation after defacation, passage of rectal mucus and abdominal distention, and to employ endoscope and laboratory studies necessary for those with "red flags" to exclude organic diseases. Recent advances in the research of IBS demonstrated that predisposing factors such as intestinal inflammation may contribute to changes in the intestinal mucosal immune system, resulting in hypersensitivity of afferent nerves and abnormal intestinal motility. Severe life events or/and chronic depression are more likely to associate with the patterns of IBS and its severity, and to have relation with post infection IBS. Behind the above mentioned factors there may exist specific genetic abnormality.

In the past few years,it has been disclosed that identified epigenetic processes and epigenetic changes are involved in human diseases.Disorders of these processes may influence chromatin structure and gene expression,which may result in complicated syndroms,multiple-factor diseases and cancers. The researchprogress of epigenetic processes of several diseases is reviewed in this paper.

Objective To investigate the effects of different doses of angiotensin Ⅱ(Ang Ⅱ) on hepa tic stellate cells(HSC) proliferation and collagen synthesis in rats. Methods The pronase E and collagen Ⅰ were used to isolate HSC, 3H TdR, 3H Leu and 3H Pro incorporation methods were used to evaluate the effects of different doses of AngⅡ on HSC DNA, protein and proline synthesis. Results It showed that 10 -9 ～10 -6 mol/L AngⅡ could significantly increase the 3H TdR incorporation rate of HSC ( P

Tetrandrine (Tet) is a bibenzylisoquinoline alkaloid isolated from Stephania tetrandra S Morr. Lots of studies demonstrated that Tet could: ① act as a calcium antagonist via blocking plasma membrane voltage- or receptor-operating calcium channels, inhibiting extracellular calcium entry and intracellular calcium mobilization, so it could prevent hepatocytes, cardiomyocytes, pancreas cells and neurocytes from toxic or ischemia-reperfusion injuries. However, in HL-60 and leukamia T cells, Tet promoted calcium releasing from mitochondria or/and microsomes and induced these cells death. ② down-regulate T cell protein kinase C signal transduction pathway, inhibit T cell proliferation, interleukin-2 secretion and expression of the T cell activation antigen. It could also interrupted integrity of macrophages, reduced neutrophiles and macrophages respiratory-bursting and proinflammatory cytokines secretion through minimizing nuclear transcription factor kappa B DNA binding activity. ③ induce tumor cells apoptosis. ④ down-regulate P glucoprotein activity and reverse tumor cells multidrug resistance. ⑤ also inhibit platelet-derived growth factor induced hepaticstellate cells and human lung fibroblast proliferation, down-regulete type Ⅰ and type Ⅲ collagen secretion. In this article, we also reviewed the therapeutic effects of Tet on hepatic fibrosis, pulmonary fibrosis, portal hypertension, pulmonary hypertension, anti-inflammation and anti-tumors.

Proton pump inhibitor (PPI) is considered as the standard treatment for acid-related disorders. However, its long-term use, especially in patients with gastroesophageal reflux disease, would cause potential risks, such as hypergastrinemia along with reduced gastric acidity, hyperplasia of enterochromaffin cells (ECL), gastric neoplasms, rebound gastric acid hypersecretion when PPI treatment is stopped, increased oxyntic gastritis in patients with H. pylori infection, and the possible stimulation of growth of non-gastric tumours due to hypergastrinaemia. Each of these trends has led to numerous studies and evaluations on the potential risk-benefit ratio of the long-term use of PPIs, and countermeasures are being proposed for these problems.

Objective The present study was to elucidate whether there was a local renin-angiotensin-aldosterone system (RAAS)in rat hepatic stellate cells(HSC)and the immortalized rat HSC line—HSC-T6. Methods HSC was isolated by perfusion of collagenase and pronase to liver. The renin activity, angiotensin Ⅱ(Ang Ⅱ) and aldosterone(ALD) concentration in the cells were assayed by radio-immunoassay. Angiotensin converting enzyme(ACE) activity was detected by ultra-violet spectrophotography. The expression of angiotensin Ⅱ type 1 receptor(AT1R) was determined by immunohistochemistry. RT-PCR method was used to assay the mRNA expression of renin, angiotensinogen, ACE, AT1R and CYPⅡB2(the critical enzyme of aldosterone synthesis). Results Ang Ⅱ, ALD, renin and ACE activity could be detected in HSC and HSC-T6. Immunohistochemistry showed that both of them could express AT1R. mRNAs of renin, ACE, AT1R and CYPⅡB2 were also detected in both of them. Conclusions Both rat HSC and the immortalized rat HSC line HSC-T6 possessa a local RAAS.

?-Est. Besides,?-Est could promote the expression of ER ? by HSC at the concentration of 10 -7 mol/L but not its metabolites. Conclusion The present results indicate that ?-Est may attenuate hepatic fibrosis and the possible mechanism is via the action of its metabolites.

0.05). There was a higher prevalence of IBS in Heilongjiang province (14.02%) than that in Shanghai (11.72%, P

Objective Recently, a series of studies demonstrated that activation of local renin angiotensin system (RAS) may be related to tissue fibrosis, but the role of RAS in hepatic fibrogenesis has not been evaluated. The present study was designed: (1) to assess the effect of angiotensin converting enzyme (ACE) inhibitor and angiotensin Ⅱ type 1 (AT1) receptor antagonist in preventing hepatic fibrosis induced by CCl 4 administration in rats; (2) to investigate whether or not there are expression of AT1 receptors on hepatic stellate cells. Methods Study was conducted in male Sprague Dawley rats. Except for control group, three treated groups, either enalapril (10 mg/kg), losartan (10 mg/kg) or a combination of enalapril and losartan were given to the fibrotic rats (daily gavage), and saline vehicle was given to the control rats. After 6 weeks, liver fibrosis was assessed directly by hepatic morphometric analysis, which have been considered the gold standard for the quantitative measurement of fibrosis. The expression of AT1 receptors and ? smooth muscle actin (? SMA) in liver tissue were detected by immunohistochemical techniques. Results Compared to the rats of control groups, either enalapril or losartan, or a combination of two drugs can limit the expansion of the interstitium ( P 0.05). Expression of AT1 receptors was found in abundance in hepatic fibrotic interstitium of fibrotic rats, whereas only limited in vasculature in rats of control group to a very slight degree. Conclusions The present results demonstrated that: (1) activation of RAS is related to hepatic fibrosis induced by CCl 4; (2) angiotensin converting enzyme inhibitor and AT1 blocker might slow the propression of hepatic fibrosis; (3) activated hepatic stellate cell expresses AT1 receptors.

Objective Activin A, a member of the transforming growth factor (TGF ?) superfamily, has been reported to overexpress in liver cirrhosis. The aim of this study was to examine the expression changes of activin A in the process of carbon tetrachloride induced rat hepatic fibrosis. Methods Hepatic fibrosis was induced in rats by subcutaneous injections of 40% carbon tetrachloride oily solution for a period of 1 to 7 weeks. 6～10 rats were killed at week 1,2,3,4,5,6 and 7 weeks. The kinetics of activin A messenger RNA expression and its protein localization were assayed by semi quantity reverse transcription polymerase chain reaction (RT PCR) and immunohistochemistry. Results RT PCR and immunohistochemistry showed normal rat liver could express activin A mRNA and protein, and its expression was transiently decreased and became undectable after carbon tetrachloride injections for 2 or 3 weeks, then increased grandually. After carbon tetrachloride injecting for 6 and 7 weeks, activin A mRNA and protein expression were significantly enhanced in rats liver ( P