Objective To improve the effect of reoperation for postoperative upper gastrointestinal rebleeding due to portal hypertension.[WT5”HZ] Method [WT5”BZ] The operative procedure and effect of reoperation in 29 patients in our hospital within the last 7 years were evaluated and reviewed. [WT5”HZ] Results [WT5”BZ] There was no mortality and short term rebleeding; 8 patients had postoperative complications(8/29) including postoperative gastric bleeding in 4. 23 patients received barium meal examination and gastroscopy on follow up of an average of 35 months. 5 of 23 patients were found to have newly developed esophageal varices. Among them, 3 patients with moderate severe varices had had simple pericardial devascularization; 1 patient with slight varices had before had pericardial devascularization plus esophagus transection and reanastomosis. Only one out of 4 receiving mesocaval shunt developed moderate varices. None of the 7 patients receiving lower part esophagus resection plus proximal gastrectomy developed recurrent esophageal varices.[WT5”HZ] Conclusion [WT5”BZ] The result of simple pericardial devascularization was unsatisfactory. Lower part esophagus resection plus proximal gastrectomy had good short and long term result for the treatment of upper gastrointestinal rebleeding due to portal hypertension.

Pancreatic cancer is one of the most malignant tumors with a high mortality rate attributed to its widespread metastasis.A number of cellular signal transduction pathways involved in multiple genes play an important role in regulating this complex metastatic cascade of pancreatic cancer.NF-kappa B is one of the crucial signaling pathways.Studies has indicated that NF-kappa B could modulate a series of biological events relevant to tumor progress by controlling multiple targeted genes expression,such as cell proliferation,anti-apoptosis,angiogenesis,epithelial-mesenchymal transition,inflammation,stress response,etc.Furthermore,it can also up-regulate Hedgehog and MMPs signaling pathways.To help us better understand the potential mechanism and identify more sensitive tumor markers and selective targets,this review will underline the significant roles of NF-kappa B signaling pathway in regulatory network of pancreatic cancer metastasis.

OBJECTIVETo observe the intervention effect of electroacupuncture (EA) at "Weizhong" (BL 40) on rats with bupivacaine-induced multifidus muscle injury, so as to explore the action mechanism.

METHODSA total of 72 rats were randomly divided into a control group, a model group, a Weizhong group and a Shenshu group, 18 rats in each group. Each group was again randomly divided into a 4-day subgroup, a 7-day subgroup and a 14-day subgroup, 6 rats in each subgroup. Rats in the model group, Weizhong group and Shenshu group were treated with intramuscular injection of 0.5% bupivacaine (BPVC) to establish the model of multifidus muscle injury. Rats in the Weizhong group and Shenshu group were treated with EA at "Weizhong" (BL 40) and "Shenshu" (BL 23), 20 min per treatment, once a day. Each subgroup was treated for 4 days, 7 days and 14 days respectively. Rats in the control group and model group were treated with immobilization. The morphology and cross sectional area (CSA) changes of multifidus with HE and Masson staining at different time points were observed; the expression of insulin like growth factor 1 (IGF-1) and myogenic differentiation antigen (MyoD) was measured by immunohistochemical method.

RESULTSAfter the modeling, there were significant morphology changes of multifidus at different time points, which was not fully recovered after 14 days. The morphological observation in the Weizhong group and Shenshu group was superior to that in the model group. At 7th day, the CSA in the Weizhong group was higher than that in the model group (P < 0.05); at 14th day, the CSA in the Weizhong group and Shenshu group was higher than that in the model group (P < 0.01, P < 0.05). At 4th day and 7th day, the expression of IGF-1 in the model group was higher than that in the control group (both P < 0.01); at 4th day, that in the Weizhong group was higher than that in the model group (P < 0.01), and that in the Weizhong group was higher than that in the Shenshu group (P < 0.05), and that in the Shenshu group was as higher than that in the model group (P < 0.05); at 14th day, that in the Shenshu group was higher than that in the model and Weizhong group (P < 0.01). At 4th day, the expression of MyoD in the Weizhong group and Shenshu group was higher than that in the model group (P < 0.01), which was more significant in the Weizhong group (P < 0.01).

CONCLUSIONElectroacupuncture at "Weizhong" (BL 40) and "Shenshu" (BL 23) can both promote the regeneration of multifidus muscle injury. EA at "Weizhong" (BL 40) has a better effect at early phase, which may be related to the up-regulation of IGF-1 and MyoD and the completion of the proliferation of myoblast in advance.

Acupuncture Points ; Anesthetics, Local ; adverse effects ; Animals ; Bupivacaine ; adverse effects ; Electroacupuncture ; Humans ; Male ; Muscles ; injuries ; physiopathology ; Muscular Diseases ; chemically induced ; physiopathology ; therapy ; Rats ; Rats, Sprague-Dawley ; Regeneration

Objective To investigate the effects of emulsified isoflurane on myocardial apoptosis, and the expressions of Bcl-2 and Bax after hypoxia/reoxygenation in cultured myocardial cells of neonatal rats. Methods Myocardial hypoxia/reoxygenation model was established on cultured primary myocardial cells of neonatal rat. The myocardial cells were divided into four groups: the normal group, model group, fat milk group, and emulsified isoflurane group. The cellular morphologic changes and pulsatile frequency of each group were observed under inverted microscope and the ultrastructure of myocardial cells was observed under transmission electron microscope. The apoptotic rate of myocardial cells was determined by flow cytometry, the expression of bcl-2 mRNA and bax mRNA were detected by RT-PCR and the protein expressions of Bcl-2/Bax were observed by Western blot. Results The apoptotic rate were significantly decreased in both emulsified isoflurane and fat milk groups (P0.05). Conclusion Emulsified isoflurane and one of its components, fat milk,can inhibit myocardial apoptosis induced by hypoxia/reoxygenation in cultured myocardial cells. Emulsified isoflurane exerts its anti-apoptosis effect maybe through up-regulating Bcl-2 expressions and down-regulating Bax expressions.

ObjectiveTo investigate the inhibitory effect of all-tram-retinoicacid (ATRA) on HCC cell growth and probe the potential molecular mechanism.MethodsHCC cell lines,HepG2 and SMMC-7721 were treated by ATRA and cell growth was analyzed by using MTT assay.The expression levels of miR-18a were evaluated in HepG2 and SMMC-7721,compared with the normal livers pool by using RealTime PCR analysis.Cell growth analysis by using MTT assay was performed on HepG2 and SMMC-7721 after transfection with anti-miR-18a.Rescued assay was designed to probe the mechanism of ATRA on cell growth by using ATRA with or without miR-18a mimic.ResultsHepG2 cell growth was suppressed about 74％ (P＜0.05,36 h),72％ (P＜0.01,48 h),and 67％ (P＜0.05,72 h) and SMMC-7721 cell growth was inhibited about 68％ (P＜0.05,48 h),and 64％ (P＜0.05,72 h) after treatment with ATRA,compared with the cells treated with Ethanol.MiR-18a expression was up-regulated in HepG2 and SMMC-7721 cell lines about 4.7- and 3.8-fold (P＜0.05),respectively.Endogenous miR-18a levels were down-regulated by ATRA about 67％ and 56％ (P＜0.05).The inhibitory effect of ATRA on HCC cell growth was reversed about 1.2-fold (P＜0.05,48 h) by overexpression of miR-18a in HepG2 cells and cell growth of SMMC-7721 was enhanced about 1.25- and 1.2-fold (P＜0.05,24 and 48 h) with ectopic expression of miR-18a.ConclusionHCC cells growth is suppressed by ATRA through miR-18a mediated network.

Objective To evaluate clinical features of three different gallbladder projective lesions. Methods Statistic analysis was performed for clinical data obtained from 325 cases of gallbladder projective lesions. Results There were 308 patients of benign lesions, including cholesterol polyps in 278 cases, other polyps in 5 cases, and adenomas of 25 cases. Malignant lesions was found in 17 cases, including 2 adenomas with malignant changes and 15 adenocarcinomas. 36. 0% and 32. 0% patients with benign polyps and adenomas were over 50 years of age, while 82.4% patients with adenocarcinomas were over 50 years. Average size of benign polyps, adenomas and adenocarcinomas were 8. 5 mm, 11.7 mm and 31.1 mm in diameter. 1.5% of benign polyps, 0% of adenomas and 52. 9% of adenocarcinomas were of low echo. 42.9% of benign polyps, 68.0% of adenomas and 100% of adenocarcinomas were single polyp. Conclusion The nature of gallbladder projective lesions can be suggested by patient age, size, number, and intensity of gallbladder projective lesions under B-ultrasound.

Objective To investigate the inhibitory effect of 5-fluorouracil (5-FU) on hepatocellular carcinoma (HCC) cell growth and to elucidate its potential molecular mechanism.Methods Real-time PCR analysis was conducted to determine the expression of miR-373 in HCC tissue specimens and HCC cell lines.The expression of miR-373 was also evaluated in HepG2 cells after 5-FU treatment.Western blot analysis was performed to detect the protein levels of PPP6C,a verified target of miR-373,with transfection of miR-373 mimics or 5-FU treatment.A rescue assay was conducted to investigate the cell growth in HepG2 cells by using CCK-8.Results miR-373 expression was up-regulated in both HCC tissues and cell lines.miR-373 expression depicted about 2.94-fold augment in HepG2 cells as compared to normal liver cells control (P ＜0.01).5-FU treatment led to a significant decrease of miR-373 levels (approximately 50％,P ＜0.01,48 h) and resulted in a marked increase of PPP6C protein (approximately 2.1-fold,48 h) in HepG2 cells.The overexpression of miR-373 could prevent the impact of 5-FU treatment on cell growth in HepG2 cells and CCK-8 assay showed that HepG2 cell growth was rescued approximately 81％ and 84％ at 24 h (P ＜ 0.05) and 48 h (P ＜ 0.01),respectively.Conclusion 5-FU can repress endogenous miR-373 level,which activates the expression of downstream targeted gene PPP6C,thereby exerting an inhibitory effect on HepG2 cells.

The aim of this study was to observe whether necroptosis is involved in the process of cardiac hypertrophy induced by pressure overload. SD rats underwent transverse abdominal aortic constriction (TAC) operation for establishing cardiac hypertrophy model. The structure and function of the left ventricle of rats were evaluated via echocardiography, left ventricular mass index, the expression of markers of cardiac hypertrophy and histological detection. Real-time PCR and Western blot were used to measure the gene and protein expression of receptor interacting protein kinase 1 and 3 (RIPK1 and RIPK3, the necroptosis markers) respectively. Four weeks after TAC operation, rat model for cardiac hypertrophy was established. The experimental data showed that the gene and protein expressions of RIPK1 and RIPK3 in the rat heart hypertrophic tissues after TAC for 4 weeks were increased significantly compared with those in the sham group. HE staining showed cardiomyocytes injury and hypertrophy in the hearts of TAC rat models. By transmission electron microscope, we observed that mitochondria of cardiomyocytes were damaged seriously in the TAC models. Treatment with losartan used, the selective antagonist of angiotensin II type I receptor could improve the cardiac function of TAC rats. Moreover, losartan treatment decreased the expression of RIPK1 and RIPK3 in heart tissues of TAC rats. The results suggest that necroptosis occurrs in the process of cardiac hypertrophy with pressure overload, and losartan could alleviate the cardiac hypertrophy and inhibit necroptosis.
Animals ; Apoptosis ; Cardiomegaly ; pathology ; Disease Models, Animal ; Echocardiography ; Heart ; physiopathology ; Losartan ; pharmacology ; Myocytes, Cardiac ; Pressure ; Protein-Serine-Threonine Kinases ; metabolism ; Rats ; Rats, Sprague-Dawley ; Real-Time Polymerase Chain Reaction ; Receptor-Interacting Protein Serine-Threonine Kinases ; metabolism

BACKGROUND: The neurotoxicity and cardiotoxicity of bupivacaine have been reported frequently. However, the studies on bupivacaine-induced muscle toxicity are few.
OBJECTIVE: To establish and evaluate local intramuscular injection of bupivacaine on the changes in histomorphology and ultrastructure of rat multifidus muscle at various time points.
METHODS: A total of 54 male Sprague-Dawley rats weighing 280-320 g were randomly divided into black group (n=18), model group (n=18) and model control group (n=18). Each group was then equal y subdivided into three subgroups according to time points (4, 7 and 14 days) (n=6). Both sides of multifidus muscle of the rats (L4 and L5) were injected with 0.5% bupivacaine. The morphological and ultrastructural changes of multifidus muscle were observed and analyzed with light microscope and transmission electron microscope at 4, 7 and 14 days after model establishment.
RESULTS AND CONCLUSION: (1) A single intramuscular injection of 0.5% bupivacaine induced muscular damage. (2) Hematoxylin-eosin staining results showed fiber necrosis, inflammatory cel infiltration, and a smal amount of macrophages in local skeletal muscle. (3) Under the transmission electron microscope, the structure of myofibrils was destroyed or disintegrated; kinds of bands and lines were indistinct, disrupted or disappeared; the structure of mitochondria was abnormal, the mitochondrial cristae were reduced or disappeared. In the 7- and 14-day groups, multifidus muscle proliferated and repaired. (4) Ultrastructural change scores in skeletal muscle were significantly higher in the model group than in the blank and model control groups (P < 0.05). Above scores were significantly greater in the 4-day group than in the 7- and 14-day groups (P < 0.05), and higher in the 7-day group than in the 14-day group (P < 0.05). (5) Results suggest that a single intramuscular injection of 0.5% bupivacaine can result in pathological changes of skeletal muscle from morphology and ultrastructure. This method can establish a suitable model of skeletal muscle injury.

Objective To investigate the clinical feature and treatment of adenomyomatosis of the gallbladder(GBA).Methods Thirty-three cases of GBA admitted from 1992 to 2007 were reviewed retrospectively and their clinical characters were sununarized. Results These cases were divided into three types grossly:14 cages of diffuse type,10 cases of segmental type and 9 Cages of localized type.Cholelithiasis wag associated in 21 cases and 11 cases with cholecystitis.Main clinical presentations included pain in the upper abdomen,discomfort after meal,nausea and vomit.Preoperative correct diagnosis was achieved in only six cases.Twenty-eight patients underwent laparoscopic cholecystectomy and three did open cholecystectomy.Concomirant exploration of common bile duct with T tube drainage and resection of liver ansioma was performed in one each.Adenomyomatosis of the gallbladder was diagnosed by pathologic examination in all cases. Condusions Due to the high rate of combination with cholelithiasis and cholecystitis,GBA has no specific clinical manifestations.The preoperative diagnosis lies on radiological examinations.Cholecystectomy is an appropriate treatment as adenomyomatesis of the gallbladder has a malignant potential.