Objective To investigate the role of bone marrow mesenchymal stem cells (MSC) in early acute necrotizing pancreatitis (ANP) complicated with multiple organ dysfunction (MODS). Methods Fifty Sprague-Dawley (SD) rats weighing 180 ～ 220 g were randomly assigned into 5 groups (n = 10). Group A was the normal negative control without any treatment, ANP was induced in Group B rats by intraperitoueal injections with L-arginine 2.5 g/kg body weight twice, Group C received Hoechst33258 labeled autologous bone marrow mMSCs one day after ANP model induction, Group D was the group of mMSCs transplantation, in which the mice were given the isolated mMSCs via the tail vein 3 days prior to the ANP induction, Group E was the stem cell mobilized group treated by the injection of granulocyte-colony stimulating factor (G-CSF) into rats 33258 and transplanted into the arigiual cavity or via the tail vein. Three days after the injury was induced, the rats were sacrificed, the tissues of pancreas, liver and intestine were harvested and the morphological changes were examined. A part of samples were snap-frozen and the presence of labeled MSC in the cryostat prepared was examined directly by fluorescence microscopy. The positive sections were chosen for further immunofluorescence assay. Anti-CK19 immunofluorescence staining was performed in pancreatic and liver sections;and Pan Cytokeratin immunofluorescence staining were performed in intestinal sections. The mortality rates within 30 days were recorded. Results The control group had normal tissue structures, with no death. 3 hour after ANP induction, there were mass hemorrhagic ascites, pefi-pancreas saponification, pancreatic disorganization, necrosis, phlogocyte infiltration;liver and intestine involvement and necrosis in rats in Group B and C with a mortality rate 40%. 3 hour after ANP induction, there were less ascites, mild pancreatic edema, intact acinns lobula, no interstitial tissue exudation, less pancreatic hemorrhage and necrosis, less phlogocyte infiltration;less liver and intestine injuries in rats in Group D and E with a mortality rate 10%. The pancreatic, liver, and intestinal sections in the control group and ANP group had no flavo green fluorescence;while the sections in Group C had some flavo green fluorescence but they were negative for immunofluorescence staining;in addition, the sections in Group D and E had plenty of flavo green fluorescence and CK19 (+) cells were present in pancreatic and liver tissues and Pan Cytokeratin (+) cells were present in intestinal tissues. Conclusions MSC played an important role in the process of pathological repair in ANP complicated with MODS, autologous or transplanted MSC had protective effects.

Objective To observe the effects of ganglioside and piracetam in improving the neurological function in patients with hypertensive cerebral hemorrhage.Methods Ninety-six patients with hypertensive cerebral hemorrhage Were randomly divided into 2 groups,ganglioside group(48 patients)and piracetam group(48 patients).Ganglioside group used the amount 40mg ganglioside mixed with sodium chloride injection(100ml,concentration 0.9%),and the piracetam group uesd piracetam(20g)mixed with the same injection.Both the patients of the 2 groups were given intravenous drip once a day,then after continuous 3 weeks,the general information and the improvement of nerve were observed.Results The effective rate and excellent rate of ganglioside group were remarkably higher than piracetam group,there was significant difference between the two groups(P＜0.05).Conclusion Ganglioside was better than pimcetam in improving clinical symptoms and the neurological deficit of the patients with hypertensive cerebral hemorrhage.

Pancreas is an integrated organ with both endocrine and exocrine functions. Insulin is secreted from the pancreas islet B cell and is the only hormone that could reduce blood sugar and play an important role in glucose homeostasis. Pancreatic disease can result in diabetes mellitus in some cases. Although acute pancreatitis is the most common disease of pancreas,the relationship between acute pancreatitis and new-onset diabetes has been ignored. However,many researches have shown recently that acute pancreatitis is associated with new-onset diabetes. Blood glucose monitoring is warranted for patients after acute pancreatitis with important significance.

Acute necro-hemorrhagic pancreatitis (ANHP) was induced in rats by intra-pancreatic duct injection with a mixed solution of bile salt and trypsin. After 6- to 30-hr of operation the increase of plasma lipidperoxidant (LPO) levels from 4.67 to 20.5 nmol/ml and the fall of plasma amylase levels from 6577 to 2629 U were observed in the rats with ANHP. The values of the plasma LPO at 10-,20-,and 30-hr in the rats with ANHP were significantly higher than those in the control (P

Objective To observe the preliminary curative effect of transrectal ultrasound-guided lauromacrogol injection for treating benign prostate hyperplasia in elderly patients.Methods Forty-two patients with benign prostate hyperplasia combined with lower urinary tract symptonms received transrectal ultrasound-guided lauromacrogol injection.Then they were followed up after 3,6,12 months respectively. Prostate volume changes before and after treatment,international prostate symptom score(IPSS),postvoid residual volume (PRV ),maximum urinary flow rate (Qmax ) and features of contrast-enhanced ultrasonography before and after treatment were observed.Complications were analyzed.Results Before treatment,prostate volume,IPSS,PVR of patients were (57.3±1 7.7)ml,(28.3 ±5.2)points,(143.8±82.5) ml respectively,12 months after treatment,they reduced to (44.8 ±6.1 )ml,(8.8 ± 1 .4)points,(28.9 ±9.5 ) ml,there were statistical diffrences between before and after treatment(P <0.05 ).Qmax increased from (5.9±3.2)ml/s to (14.9 ±3.1 )ml/s (P <0.05).Contrast-enhanced ultrasonography showed filling defect sign in prostatic inner gland.No serve complications occurred.Conclusions Transrectal ultrasound-guided lauromacrogol injection for treating benign prostate hyperplasia has the characteristics of minimally invasive,safe,effective and economical.It applies to elderly patients who are unable or unwilling to have surgery.

Background The primary pathologic mechanism of posterior capsular opacification (PCO) is proliferation,migration and epithelial-mesenchymal transition (EMT) of residuary lens epithelial cells (LECs) after cataract extract surgery.Researches showed that MG132,a proteasome inhibitor,can attenuate the proliferation of bovine LECs,but its effect on human LECs remains unclear.Objective This study was to investigate the inhibitory effect of MG132 on proliferation,migration and differentiation of human LECs in vitro.Methods Human lens capsule were collected during the surgery.Human LECs were primarily cultured by explant method and passaged.The second or third generation of cells were incubated to 96-well plates at the density of 5×105/ml (200 μl/well) for 24 hours.Fibroblast growth factor-2 (FGF-2,10 mg/L),MG132 (10 μmol/L) or MG132+FGF-2 was added into the culture medium for 24 hours separately,and regular cultured cells served as the control group.The proliferation value (absorbance,A490) of the cells was assayed by MTT colorimetric method.A bare area was made by a sterile cotton swab in the cell layer,and migrated cell number in the blank zone was counted to evaluate the migration ability of the cells after 24 hours.Transforming growth factor-32(TGF-β2),MG132 or MG132+TGF-β2 was added into the culture medium for 24 hours separately,and the expression of fibronectin (FN) in the cells was detected using immunochemistry.Results The proliferation values (A490) of the cells were 0.582±0.020,0.723±0.010,0.434± 0.011 and 0.465±0.008 in the control group,FGF-2 group,MG132 group and MG132 + FGF-2 group,respectively,showing a significant difference among the groups (F =110.482,P＜0.01).The A value was significantly higher in the FGF-2 group and lower in the MG132 group and MG132+FGF-2 group than that of the control group (all at P＜ 0.05).The migrated cell number was 8.67 ± 1.08,11.58 ± 1.59,2.67 ± 0.09 and 2.75 ± 0.09 in the control group,FGF-2 group,MG132 group and MG132+FGF-2 group,respectively,with a significant difference among the groups (F=34.301,P＜0.01),and more cells in the blank zone were seen in the FGF-2 group and less cells were in the MG132 group and MG132+FGF-2 group in comparison with the control group (all at P＜0.05).Compared with the control group,the proliferative rate and migrating rate of the cells declined by 25.4％ and 75.0％ in the MG132 group as well as 20.1％ and 68.3％ in the MG132+FGF-2 group,but in the FGF-2 group,they increased by 24.2％ and 33.6％.The expressing levels (A value) of FN in the LECs were 1.242±0.023,2.329±0.113,1.043 ±0.021 and 1.163±0.018 in the control group,TGF-β2 group,MG132 group and MG132 +TGF-β2 group,respectively,with a significant difference among the groups (F =113.752,P＜0.01),a considerably increased expressing value was seen in the TGF-β2 group and decreased value was in the MG132 group and MG132+TGF-β2 group when compared with the control group (all at P＜0.05).Conclusions MG132 can effectively inhibit the proliferation,migration and differentiation of human LECs in vitro.

Objective To explore relationships of expression of hypoxia?inducible factor?1α(HIF?1α), vascular endothelial growth factor(VEGF)and protein kinase B(P?Akt)with angiopoiesis and cell apoptosis. Methods Biopsy specimens were collected from skin lesions of 32 patients with lichen planus and normal skin of 20 patients with lipomyoma, and subjected to paraffin embedding. Immunohistochemical staining was performed to measure expression of HIF?1α, VEGF and P?Akt, and TUNEL technique was used to detect apoptosis of keratinocytes in these paraffin?embedded tissue sections. Microvessel density (MVD)was assessed by counting CD34?labeled vascular endothelial cells. Results HIF?1α, VEGF and P?Akt were moderately or strongly expressed in lichen planus lesions, but absent or weakly expressed in normal skin of controls, and the expression of HIF?1α, VEGF and P?Akt was significantly higher in the lichen planus group than in the control group (all P < 0.01). HIF?1α was mainly expressed in nuclei of keratinocytes, while VEGF and P?Akt were expressed in the cytoplasm of keratinocytes. In addition, the lichen planus group showed significantly increased MVD(21.27 ± 6.54 vs. 10.26 ± 1.10 microvessels/high?power(200 ×)field, t = 5.607, P < 0.01)and apoptosis rate of keratinocytes(72.81% ± 9.234% vs. 28.16% ± 3.464%, t = 8.431, P < 0.01) compared with the control group. Pearson correlation analysis showed that there were positive correlations between HIF?1αand VEGF expression, between VEGF and P?Akt expression, and between P?Akt and HIF?1αexpression in the lichen planus group(r=0.625, 0.453, 0.455, respectively, all P<0.01), and expression of HIF?1α, VEGF and P?Akt was all positively correlated with MVD(r=0.721, 0.646, 0.671, respectively, all P<0.01). Conclusion HIF?1αand its downstream target genes VEGF and P?Akt may play a certain role in the occurrence of lichen planus.

Objective To investigate the efficiency and mechanism of differentiation of reprogrammed adipose-derived stem cells (ADSCs) to neurons in vitro.Methods ADSCs from rats were cultured in vitro and then purified and identified.ADSCs at the third passage were divided into three groups:ADSCs without lentivirus-mediated gene transfection (blank group),ADSCs transfected with lentivirus carrying no neurogenin2 (Ngn2) (empty virus group) and ADSCs with lentivirus-mediated transfection of Ngn2 (Ngn2 group).All groups were induced in the medium containing cell growth factor for 15 days.The positive expression of neuron-specific nuclear protein (NeuN) in three groups was detected using immunofluorescence method so as to observe the efficiency of neuron differentiation.Expression variances of Mash1,Hes1 and Dll1 in each group were detected by Western blot analysis and the mechanism of differentiation was also discussed.Results After 15 days of induction,positive expression rate of NeuN in Ngn2 group,empty virus group,blank group was 90.12％,45.34％ and 40.26％ respectively,with significant differences among groups (P ＜ 0.01).Western blot analysis showed that Ngn2 group had a significantly higher expression of Dll1 (P ＜0.01) and obvious lower expressions of Hes1 and Mash1 (P ＜0.01),as compared with empty virus group and blank group.However,there were no significant differences of expression levels of Dll1,Mash1 and Hes1 between empty virus group and blank group (P ＞ 0.05).Conclusions After induction,the ratio of neuron differentiation of reprogrammed ADSCs is increased by almost 99％,as compared with simple ADSCs.The increased dfferentiation of reprogrammedADSCs to neurons may be associated with the inhibition of notch signaling through up-regulating Dll1 and down-regulating Mash1 and Hesl.

ObjectiveTo evaluate the therapeutic effect of endoscopic full-thickness resection (EFTR) for gastric stromal tumors.MethodsA total of 33 patients with gastric stromal tumor orgination from deep muscularis propria layer received EFTR from January 2010 to July 2011.The effectiveness and safety of EFTR were compared with those of other 34 patients with gastric stromal tumor origination from muscularis propria layer who underwent endoscopic submucosal dissection (ESD).ResultsExcept in 2 patients with lesions larger than 3.0 × 3.0 cm,EFTR was successful in others 31 patients,who recovered well and had no recurrence during the follow-up within 12 months.There were no significant differences in resection rate,incidence of complications,body temperature,white blood cell counts or recovery time between 2 procedures (P ＞ 0.05 ).However,the number of clips used in EFTR ( 7.0 ± 3.5 vs.4.9 ± 3.1,P =0.013 ) and postoperative fasting days (3.4 ± 1.5 vs.2.0 ± 1.0,P =0.001 ) were significantly higher than those of ESD procedures.ConclusionEFTR is effective and safe for gastric stromal tumors with no higher risk than ESD,but it is more complex technically.EFTR can be used as an expanding method of ESD in endoscopic treatment of gastric stromal tumors.

Objective To investigate the regional distribution and morphological features of nesfatin-1/NUCB2 in digestive system of the humans, Sprague-Dawley (SD) rats and the institute of cancer research (ICR) mice, so as to lay the foundation for further study of its functions in the digestive system. Methods The specimens were obtained from SD rats and ICR mice as well as 20 patients with digestive disease, who were admitted to the First hospital affiliated to Nanjing Medical University and receired surgercal treatment. The specimens from patients with malignant tumors were obtained 5 cm apart from cancerous tissues and from patients with benign tumors were obtained near the focus. The resected tissues included pancreas, stomach, duodenum, esophagus, liver, small intestine or colon. The distribution of nesfatin-1/NUCB2 was examined with immunohistochemical (IHC) staining and its protein level in each organ was measured using Western blotting. Results The immuinohistocemical study revealed the similar distribution pattern of nesfatin-1/NUCB2 in the digestive system of the patients, SD rats and ICR mice. Nesfatin-1/NUCB2 was found to localize in the center of the pancreatic islets, the lower 1/3 to 1/2 of the gastric mucosal glands, as well as the submucosa of the duodenum. Western blotting examination showed the expression of NUCB2 in all tissues from patients, SD rats and ICR mice, whereas the protein level of the nesfatin-1/NUCB2 was higher in pancreas (0.84±0.03, 0. 84±0.05 and 0. 84±0.04, respectively), stomach (0.86±0.06,0.81±0.02 and 0. 78±0.02, respectively) or duodenum (0.79±0.09,0. 79±0.04 and 0.78±0.05)than that in esophagus (0.43±0.04,0.44 ± 0.02 and 0.47 ± 0.06, respectively), liver (0.42±0.01,0.44±0.04 and 0.43 ± 0.01, objectively), small intestine (0.32±0.04,0. 32 ± 0. 04 and 0.34 ±0.04, respectively) or colon (0. 29±0.01,0.32±0.03 and 0. 28±0.03, respectively)(all P values=0. 000). Conclusion Nesfatin-1/NUCB2 is widely expressed in the pancreatic islets, gastric mucosal glands and duodenum of the patients, SD rats and ICR mice, which indicates that nesfatin-1/NUCB2 may be involved in the regulation of food intake, carbohydrate metabolism and gastrointestinal motility.