ObjectiveTo investigate the relationship between the severity of acute pancreatitis and apoptosis of acinar cells. MethodsThe apoptotic ratio of acinar cells was measured in rat acute pancreatitis model by methods of in situ end labeling.ResultsThere was almost no apoptotic acinar cells in the model of acute edematous pancreatitis. With the increase in the severity of the pancreatitis apoptotic cells were more and more common until to the late stage of hemorrhagic and necrotic pancreatitis when the apoptotic ratio of acinar cells dwindled, meanwhile the necrotic acinar cell increased continuously.ConclusionsIn acute simple edematous pancreatitis apoptotic acinar cells is infrequently seen. In acute moderate hemorrhagic and necrotic pancreatitis the ratio is correlated positively with the severity of pancreatitis.In the late stage the ratio was correlated negatively with the severity of pancreatitis.

Objective To investigate the mechanism by which taxol induces apoptosis of pancreatic acinar cells during experimental acute pancreatitis in rats. Methods Intrapancreatobiliary duct injection of sodium deoxycholate was carried out to establish acute pancreatitis model in Wistar rats. Taxol was injected intraperitonealy to induce pancreatic acinar cell apoptosis. The expression of apoptosis associated protein Bcl-2,Bax,Fas,FasL and p53 was detected by immunohistochemistry. Results The expression of Bax(2 506?942),Fas(279?150) and p53(180?56) increased,while Bcl-2(79?42) remained unchanged in pancreatic acinar cells during acute pancreatitis,and the expression of FasL could only be detected in infiltrative inflammatory cells. Conclusions During acute pancreatitis,the acinar cell apoptosis induced by taxol is associated with activity regulation of Bax,Fas/FasL system and p53.

Sphingolipids as an important regulator play a critical role in the cell biological functions. Among them, ceramide (Cer) and sphingosine (Sph) induce apoptosis and inhibit cell proliferation; on the contrary sphingosine 1-phosphate (S1P) promotes cell survival and proliferation. The balance between ceramide/sphingosine and S1P forms a so-called "sphingolipid-rheostat", which decides the cell fate. Sphingosine kinases, which catalyze the phosphorylation of sphingosine to S1P, are critical regulators of this balance. Here, we review the role of sphingosine kinase 1 (SphK1) in regulating fundamental biological processes and tumorigenesis and the potential of SphK1 as a new target for cancer therapeutics.

Objective　To introduce the research trence of the medchnisims of ischemia/reperfusion(I/R) injury in transplanted liver(TL). Methods　Making a literature summarization based on papers review.Results　The main mechnisms of I/R injury in TL as the followings: (1) Production of various cytokines resulted from endothelial cell injury with activation of kupffer cells, which can result in TL injury and induce systemic inflammation syndrom. (2) White blood cells and platelets adhere to the liver sinusoid (LS), which can cause TL injury and obstruct the LS causing “no reperfusion" of TL. (3) Alteration of pH in the cells of TL. After recovery of normal metabolism of the reperfused TL, alteration of pH in the TL can cause damage to TL cells, and cause edema of mitochrondria resulting in decresing of TL function. (4) Reoxygenation injury mainly caused by activated oxygen relsased by white blood cell. Conclusions　I/R injury of TL is caused by combination of muttiple foctors. Improving the activity of hepatocytes and endothelial cells, imhibiting the activation of kupffer cells, decreasing the production of activated oxygen and TNF are the key points in preventing I/R injury of TL.

Liver fibrosis is a pathological process of the excessive accumulation of extracellular matrix, especially collagen al (I) in liver. Ultimately, hepatic fibrosis leads to cirrhosis or hepatic failure. Liver fibrosis and early cirrhosis can be reversed, thus control of the development of liver fibrosis is very important for preventive treatment of cirrhosis and hepatic failure. This is a review of potential targets for anti-hepatic fibrosis based on plenty of publications, including TGF-β1 and integrin α(v) and so on, aimed at providing novel therapeutic targets in liver fibrosis.

BACKGROUND: It has been reported that Angiotensin Ⅱ (Ang Ⅱ) is related to occurrence and development of dermatofibrosis; however, less is explored about the expression and effect of AT1 and AT2 receptors in the fibroblasts of human hypertrophic scar.OBJECTIVE: To observe the expression of Ang Ⅱ type 1 (AT1) and type 2 (AT2) receptors in human hypertrophic scars, and explore their effects on collagen synthesis of fibroblasts.DESIGN, TIME AND SETTING: Randomized control experiment was performed at the Experimental Center, Guangzhou General Hospital of Guangzhou Military Area Command of Chinese PLA between August 2006 and November 2007. PARTICIPANTS: Samples of hypertrophic scare were taken from 18 patients (10 males and 8 females, 19-47 years Old). Seven specimens of normal skin served as control. All of the specimens collected were divided into two parts, one part for immunohistochemical staining after fixated by 4% paraformaldehyde, the other part for culturing fibroblasts.METHODS: The expression of both AT1 and AT2 receptors in fibroblasts of hypertrophic scare was detected with immunohistochemical staining and radioligand receptor binding assay. Collagen synthesis was examined in cultured fibroblasts of hypertrophic scars by measuring [3H]-proline incorporation into collagenous proteins.MAIN OUTCOME MEASURES: The expression of both AT1 and AT2 receptors in human hypertrophic scars; the [3H]-proline incorporation value in cultured fibroblasts.RESULTS: Positive staining signals of both AT1 and AT2 receptors were found in fibroblasts of hypertrophic scars. Similar results were also observed in cultured fibroblasts of hypertrophic scars, expression level of AT1 and AT2 receptors were (10.69±2.15) fmol/106 cells and (4.9±1.05) fmol/106cells, respectively. In cultured fibreblasts, Ang Ⅱ stimulation significantly increased collagen synthesis, which was inhibited by valsartan, an AT1 receptor blocker, but augmented by PD123319, an AT2 receptor antagonist.CONCLUSION: Both AT1 and AT2 receptors were expressee in the fibreblasts of hypertrophic scars, and Ang Ⅱ regulates collagen synthesis in hypertrophic scar fibroblasts through a negative cross-talk between AT1 and AT2 receptors, which might contribute, at least partly to formation and maturation of human hypertrophic scars.

The research on intracellular trafficking of adenovirus has been described mainly through observations of subgroup C adenoviruses in transformed cell lines. The basic elements of the trafficking pathway include binding to receptors at the cell surface, internalization by endocytosis, lysis of the endosomal membrane, escape to the cytosol, intracellular trafficking along microtubules, nuclear pore docking, and viral genome translocation into the nucleus. More than 80% of the adenovirus genome is delivered to the nucleus in a highly efficient manner in approximately 1 h. However, exceptions to this trafficking pattern have been noted, including: variations based on target cell type, cell physiology, and adenovirus serotype. This review summarizes mechanism of adenovirus infection pathway and intracellular trafficking, providinging a foundation for the development of clinical adenoviral vector.
Adenoviridae ; physiology ; Cell Membrane ; virology ; Cell Nucleus ; virology ; Cytoplasm ; virology ; Endocytosis ; Endosomes ; virology ; Genetic Vectors ; Humans ; Microtubules ; Virus Internalization

For screening the potential drugs as anti-liver fibrosis candidates, we established a high- throughput drug screening cell model based on COL1A1 promoter. The activity of COL1A1 promoter and luciferase reporter gene can be elevated by TGF-β1, and inhibited by candidate drugs. We constructed a recombined plasmid with COL1A1 promoter and luciferase reporter gene pGL4.17, the activity of COL1A1 promoter was reflected by fluorescence intensity. COL1A1 promoter activity was detected by Dual-Luciferase Reporter Assay System, it came that the relative luciferase activity of COL1A1 promoter was 15.98 times higher than that of control group induced by TGF-β1, showing the recombined plasmid could be used in cell model. The recombined plasmid was transfected into human hepatic stellate cells LX2, detected the effect of potential drugs, and obtained a stable expression system through stable transfection and monoclonal cell culture. A sample which could reduce COL1A1 promoter activity signally by our cell model, decreased collagen I mRNA and protein expression detected by real-time RT-PCR and Western blotting. It indicates this novel cell model can be used in high-throughput drug screening of potential anti-liver fibrosis drugs.

Objective: To investigate the efficacy of horizontal acupuncture with sticking needles plus plucking manual technique in treating scapular, dorsal and lumbar myofascitis.Methods: One hundred and seventy-eight patients with scapular, dorsal and lumbar myofascitis were randomly allocated to observation group treated by horizontal needling with sticking needles plus plucking manual technique and control group treated by perpendicular acupuncture at the pain point. Results and conclusion: The cure rate, and the total effective rate in the observation group were 69.6%, and 100% respectively and those in the control group were 13.1%, and 82.5% respectively. Statistical analysis showed a very significant difference in curative effect between the two groups (P＜0.01), indicating that the effect was significantly better in the observation group than in the control group.

This study aimed to investigate the synergistic effect of lidamycin (LDM) and rituximab on human B cell lymphoma Ramos cells. Cell proliferation was measured using MTS assay, cell apoptosis was analyzed by Annexin V-FITC/PI assay, the expression of apoptosis related proteins was analyzed by Western blotting, and the in vivo lymphoma inhibition was verified using BALB/c mice inoculated via tail vein using Ramos cells which stably expressed pEGFP-N1 plasmid. The results showed that, after the pretreatment with rituximab for 48 h, rituximab and LDM showed significantly synergistic effects on cell proliferation. Cells in combined treatment group had a higher apoptosis rate than that in LDM treatment group. Compared with the LDM treatment group, the expression of apoptosis-related proteins such as Cleaved caspase-3, Cleaved caspase-7, Cleaved caspase-9 and Cleaved PARP in combined treatment groups increased, and expression of cIAP-2 and Bcl-2 decreased. The result of in vivo experiment showed that, in the combined treatment group, the survival time of BALB/c mice was significantly longer than the mice in control group and LDM treatment group, and the degree of tumor accumulation and metastasis to lymph nodes and spleen was lower.