BACKGROUND:Acute pancreatitis is a common inflammatory disease mediated by pancreatic acinar cel s injury, and is mainly characterized by leukocyte infiltration. N-acetylcysteine can control leukocyte migration and regulate inflammation in some serious inflammatory diseases. OBJECTIVE:To investigate the protective effects of N-acetylcysteine in rat model of acute pancreatitis caused by sodium taurocholate. METHODS:Ninety Sprague-Dawley rats were randomly divided into three groups:normal control group, acute pancreatitis group and N-acetylcysteine group. Except normal control group, acute pancreatitis model was established in the other two groups by retrograde injection of sodium taurocholate into major duodenal papil a. Rats in the N-acetylcysteine group were treated with N-acetylcysteine intravenously through the tail vein. RESULTS AND CONCLUSION:After acute pancreatitis model was established, plasma amylase levels in the models were significantly higher than that in the normal control rats (P<0.05). Interleukin-1β,-6,-10, and tumor necrosis factorαexpression levels were also obviously higher than that in the normal control rats (P<0.05). Immunohistochemical staining demonstrated that N-acetylcysteine was mainly expressed in the islet cel s, and the pancreatic expression of N-acetylcysteine was down-regulated at both the mRNA and protein levels during the course of acute pancreatitis. N-acetylcysteine administration significantly reduced plasma amylase levels, myeloperoxidase activity, pro-inflammatory cytokine production, and pancreas and lung tissue damages. Furthermore, N-acetylcysteine administration did not cause significant inhibition of nuclear factor-κB activation in the pancreas. N-acetylcysteine is capable of improving damage of pancreas and lung, and exerting anti-inflammatory effects in rats with severe acute pancreatitis.

The HER-2/neu gene, also named c-erbB-2 or erbB-2, is proto-oncogene of v-erbB-2 which was firstly discovered in 1985. Many studies have been reported since that amplification of the HER-2 gene in breast tumors is associated with poor prognosis was recognized. The relevant knowledge of HER-2/neu gene is summarized in this article.

Objective To compare the consistency of immunohistochemistry (IHC) and fluorescence in situ hybridization (FISH) in detecting c-erbB-2 status in breast cancer tissues. Methods A total of 50 breast cancer paraffin embedded samples were selected, of which there were 10 cases of c-erbB-2 protein expression (+), 20 cases of (++) and 20 cases of (+++). FISH was used to assess the amplification of c-erbB-2 gene, and SPSS 13.0 software was employed to analyze the difference and consistency between the two methods. Results IHC and FISH methods had a good consistency when detecting c-erbB-2 (+) and (+++) expressions in breast cancer tissues, with the coincidence rate of 89.2%. However, when IHC was used to test c-erbB-2 (++), the result of FISH was quite different, with the coincidence rate of only 35.3%. Conclusion IHC is a preliminary method to detect c-erbB-2 status in breast cancer. IHC and FISH methods have a good consistency in detecting c-erbB-2 (+) and (+++) status in breast cancer tissues. As detection of c-erbB-2 (++) with IHC has a different result from FISH, such patients should receive FISH confirmation for herceptin therapy.

Objective To investigate the clinical manifestations of early postoperative internal hernia. Methods Patients who were diagnosed with early postoperative small bowel obstruction(EPSBO)within 30 days after operation and underwent laparotomy between 1994 and 2006 were included for study.Clinical and radiological findings were analyzed. Results Totally 38 EPSBO patients were identined.among those,9 patients(23.7%)had an internal hera ag the cause of the howel obstruction.Other causes included intestinal adhesions in 27 patients(71.1%),gallstone ileus in 1 patient(2.6%)and stoma obstruction in 1 patient(2.6%).In the internal hernia group,6 cases were male and 3 cases were female witIl a mean age of 53.6 years.The mean time from the primary operation to symptom development was 7.8 d(range,2～17 d)and the mean time of conservative treatment Was 3.4 d(range,1～8 d).The main clinical features included:complete mechanical obstruction with symptoms rapidly progressing and early bowel strangulation.Specific radiologic abnormalities misht be identified,especially by contrast-enhanced CT.In this series,intestinal strangulation was found in 6 patients with bowel necrosis in 4 eases,necessitating howel resection in 5 patients.Wound infection developed in one cage and there was no perioperative death.Conclusion Internal hernia can occur early postoperatively and it bears a high risk of strangulation and bowel necrosis.Prompt operative intervention should be carried out in highly suspicious patients in order to avoid complications and achieve good outcome.

This article was aimed to study the stability of hesperidin in alkaline solution, in order to provide experi-ment evidences for quality control of extraction and purification as well as formulation development. RP-HPLC was applied to determinate content changes of hesperidin in alkaline solution by changing the temperature, pH and heat-ing time. The results showed that hesperidin was degraded in alkaline solution by heating. The content of hesperidin decreased along with the increasing of heating temperature and heating time. The hesperidin appeared to be more stable in a weak base. It was concluded that for the purpose of ensuring of the stability of hesperidin in alkaline so-lution, it should be kept at low temperature (below 50℃), weak base conditions and shorten the heating time during the preparation process.

0.05).Genotype CT frequency in T2DM group was significantly increased when compared with non-DM control group(P=0.012,OR=2.254).Conclusion Pro198Leu polymorphism of GPX-1 gene increases the risk of type 2 diabetes in Han Chinese of Shanghai,while T allele is not a risk factor of diabetic CHD.

OBJECTIVESTo investigate whether antisense Bmi-1 plasmid could inhibit the proliferation of Jurkat cells.

METHODSThe antisense plasmid was constructed by PCR amplification of a 171 bp segment spanning Bmi-1 start codon and zinc finger structure and the PCR product was subsequently inserted reversely to plasmid pLNCX2. The final construct was confirmed through restriction enzyme digestion. G418 was added into the medium after the plasmid was successfully introduced into Jurkat cells by using lipofectin-mediated DNA transfection. The proliferation of Jurkat cells were determined by MTT and colony formation assays. Cell cycle was determined by flow cytometry. The p16 expression of Jurkat cells was studied by immunofluorescent histochemistry.

RESULTSThe growth rate of antisense Bmi-1 transfected Jurkat cells was significantly lower than that of the controls, and the colony forming capacity of the transfected cells decreased significantly (P < 0.01), the colony numbers being (90.7 +/- 9.07)/10(3) cells, (83.3 +/- 6.11)/10(3) cells and (56.0 +/- 5.56)/10(3) cells for control cells, empty plasmid transfected Jurkat cells and antisense Bmi-1 transfected Jurkat cells, respectively. The percentage of G, phase cells was increased and the p16 expression of antisense Bmi-1 transfected cells was significantly upregulated than that of control cells.

CONCLUSIONAntisense Bmi-1 can inhibit the growth and upregulate the expression of p16 of Jurkat cells in vitro.

Cell Cycle ; Cell Proliferation ; Gene Expression Regulation, Neoplastic ; Genetic Vectors ; Humans ; Jurkat Cells ; Nuclear Proteins ; genetics ; Oligonucleotides, Antisense ; genetics ; Plasmids ; genetics ; Polycomb Repressive Complex 1 ; Proto-Oncogene Proteins ; genetics ; Repressor Proteins ; genetics ; Transfection

OBJECTIVETo investigate the role of activated hepatocyte growth factor (HGF) in apoptosis of hepatic stellate cells (HSCs) and in modulating the Rho signaling pathway.

METHODSHSCs were divided into the following groups: blank control, consisting of HSCs without treatment; two treatment controls, consisting of HSCs exposed to exogenous HGF at 50 ng/ml and HSCs exposed to exogenous HGF activator (HGFA) at 70 ng/ml; three experimental groups, consisting of HSCs exposed to both exogenous HGF and HGFA, HSCs pre-incubated with the HGF inhibitor c-met at 500 ng/ml for 6 hours and then exposed to exogenous HGF and HGFA, and HSCs pre-incubated with the Rho pathway inhibitor Y-27632 at 10 ng/ml and then exposed to exogenous HGF and HGFA. Activation status of the cultured HSCs was determined by change in expression of alpha-smooth muscle actin (SMA). The optimal intervention concentration of Y-27632 was determined by MTT assay. The apoptotic status of HSCs was determined by flow cytometry. Expression of the HGF-alpha chain was detected by immunofluorescence. The expression of RhoA was evaluated by PCR (for mRNA) and by immunohistochemical staining and Western blot analysis (for protein).

RESULTSExposure to 10 mumol/L Y-27632 led to obvious growth inhibition of HGF + HGFA-induced HSCs, compared with the other concentrations tested (P less than 0.05). HGF + HGFA induced the expression of the HGF-alpha chain in a time-dependent manner (P less than 0.01); however, the increases in expression of HGF-alpha chain induced by HGF alone and HGFA alone were not significantly different from the level in the blank controls (P more than 0.05). Exposure to HGF alone and HGFA alone led to a time-dependent increase in apoptosis (24 h, 48 h, 72 h) but exposure to HGF + HGFA led to the highest levels of apoptosis (P less than 0.05). Exposure to HGF + HGFA led to a time-dependent decrease in RhoA mRNA and protein expression (P less than 0.01).

CONCLUSIONActivation of hepatocyte growth factor promotes apoptosis of hepatic stellate cells by suppressing RhoA expression and down-regulating the Rho signaling pathway.

Objective To explore the value of intra-voxel incoherent motion diffusion weighted imaging(IVIM-DWI)in brain perfusion of early hypertensive patients. Methods Totally 36 hypertensive patients and 14 volunteers were recruited and scanned using routine MRI sequences including axial T2WI, T1WI, T2FLAIR, TOF-MRA and IVIM-DWI sequence. Perfusion-related diffusion coefficient (D*) values and perfusion fraction (f) values in various regions were measured separately.The independent sample t test was used to analyze the data.Results Compared with the volunteers,both D*values and f values in lenticular nucleus,thalamus,superior frontal gyrus,occipital lobe,genu of corpus callosum(CC)and posterior horns of periventricular WM, were found to be lower (P<0.05) in hypertensive patients. For other regions, there were no significant difference(P>0.05).Conclusion IVIM-DWI has the ability to detect subtle brain perfusion abnormalities at early stages of hypertension.It has an important value to the prevention and treatment of hypertensive encephalopathy.

To explore the angiotensin peptide [Ang (1-7)]-mediated inhibition of Ang II in human hepatic stellate cells (HSCs) and determine the involvement of the ACE2-Ang (1-7)-Mas axis. The human HSC line, LX2, was used in all experiments, and divided into control (unstimulated) and Ang II-stimulated (10-6 mol/L) groups. The Ang II-stimulated cells were further divided among several pre-treatment (prior to Ang II) groups: ROCK-inhibited (Y27632 blocking agent, 10-6 mol/L); irbesartan-inhibited (AT-1 receptor antagonist, 10-6 mol/L); and Mas receptor-inhibited (A779 Mas receptor antagonist, 10-6 mol/L). To explore the potential inhibitory effects of various Ang family members, the Ang II-stimulated and pre-treated LX2 cells were exposed to Ang (1-7) (10-6 mol/L) for 24 h. Western blot, reverse transcription-polymerase chain reaction (RT-PCR), and QuantiGene assay were used to assess changes in protein and mRNA expression levels of RhoA, ROCK, and connective tissue growth factor (CTGF). Compared with the control group, Ang II-stimulated cells showed significantly increased levels of RhoA protein (0.337+/-0.074 vs. 0.870+/-0.093), ROCK2 mRNA (0.747+/-0.061 vs. 0.368+/-0.023), and CTGF mRNA (0.262+/-0.007 vs. 0.578+/-0.028) (all, P less than 0.01). Pre-treatment with irbesartan or Y27632 eliminated these responses. Ang (1-7) inhibited the Ang II-stimulated up-regulation of RhoA, ROCK, and CTGF. Ang (1-7) can inhibit the Ang II-stimulated up-regulation of RhoA, ROCK and CTGF in hepatic stellate cells, indicating that the ACE2-Ang (1-7)-Mas axis, an important branch of the renin-Ang-aldosterone system is involved in the occurrence and development of liver fibrosis.
Angiotensin I ; pharmacology ; Angiotensin II ; pharmacology ; Cells, Cultured ; Connective Tissue Growth Factor ; metabolism ; Hepatic Stellate Cells ; drug effects ; metabolism ; Humans ; Peptide Fragments ; pharmacology ; RNA, Messenger ; genetics ; Signal Transduction ; rho-Associated Kinases ; metabolism ; rhoA GTP-Binding Protein ; metabolism