Objective To study the significance of S100A12 in patients with acute pancreatitis (AP).Methods 139 patients with AP were divided into the severe acute pancreatitis (SAP) and moderate acute pancreatitis (MAP) groups.61 patients in the SAP group were further subdivided into the infection group (n =32) and the non-infection group (n =29) based on the presence/absence of secondary infection.Serum samples of these patients were collected on the 3rd,7th and 14th day after treatment.ELISA was used to determinate the S100A12,IL-1 β and IL-6 levels in serum.The area under ROC was used to evaluate the predictive role of S100A12,IL-1β,IL-6 and CRP for infection in patients with SAP.Results The S100A12,IL-1β and IL-6 levels in SAP patients were markedly higher than those in MAP patients and normal controls on the 3rd,7th and 14th day after treatment.These levels decreased toward normal range in MAP patients.They were persistently high in SAP patients after treatment for 7 days,but decreased significantly after 14 days.The serum levels of S100A12,IL-1β,IL-6 and CRP were significantly higher in the infection subgroup(647.5 ± 300.1,155.9 ±48.5,95.7 ±25.5,166.8 ±53.0) than the non-infection subgroup(249.0 ± 176.3,108.0 ± 46.1,64.0 ±38.5,117.9 ±34.9) (P ＜0.05).The sensitivity and specificity of serum S100A12 in diagnosing secondary infection in SAP were 96.8％ and 83.3％,which were higher than those of serum IL-1β,IL-6 or CRP.Conclusion The level of S100A12 was associated with systemic inflammatory response syndrome (SIRS) in AP,and it may serve as a new marker in early diagnosis of SAP and in secondary infection in SAP.

Objective To evaluate the correlation between human serum S100A12 level and severity of acute pancreatitis (AP).Methods Serum S100A12 were tested in 64 AP patients in 24 hours after the onset.S 100A12 levels was compared to the severity of AP,and the area under the curve (AUC) of the receiver operating characteristic curve(ROC) of serum S100A12 levels for estimating the severity of AP were made and compared with laboratory parameters and APACHE-Ⅱ,Ranson' s scoring system.Results S100A12 levels in early AP patients were higher than healthy controls (P ＜ 0.05).S100A12 levels increased and correlated with MCTSI scores:patients scored 7-8 ＞ patients scored 4-6 ＞patients scored less than 4 (P ＜ 0.01).S100A 12 levels increased with organ failure (P ＜ 0.01).The AUC of S100A12 in 24 hours after onset for distinguishing MAP between MSAP and SAP was 0.80,cut-off point was 61.83 ng/ml,sensitivity was 70.01％ and the specificity was 73.52％.Serum S100A12 levels were higher in SAP than in MSAP(P =0.01).The AUC of S100A12 in early AP for distinguishing between MSAP and SAP was 0.84,cut-off point was 285.32 ng/ml,the sensitivity was 76.94％ and the specificity was 94.12％,Youden index was 71.00％,positive likelihood ratio was 13.00,negative likelihood ratio was 0.20,the diagnostic performance was better than APACHE-Ⅱ,Ranson and Marshall scoring systems and serum CRP concentration.Conclusions Human serum S100A12 levels elevated at early stage of AP.S100A12 ＞285.32 ng/ml represents high risk of SAP,which is more sensitive and accurate than APACHE-Ⅱ and Marshall scoring system.

Objective To study the risk factors related to the severity of post-ERCP hemorrhage in the patients with choledocholithiasis.Methods Clinical data of 56 patients with choledocholithiasis and post -ERCP hemorrhage from January 2008 to August 2015 were analyzed.Made the occurrence of severe hemorrhage as dependent variable,supposed 18 factors in patients and procedure related aspects as possible covariates,analyzed with univariate and binary logistic regression.Results Severe hemorrhage was occurred in 1 1 patients after ERCP.Among patients related factors,female,history of oral corticosteriod,level of bilirubin,size of stone,periampullary diverticula, prolonged time of bleeding-cruor,acute cholangitis,acute pancreatitis and course of disease were proved to be signifi-cant risk factors by univariate analysis(P<0.01 ).Periampullary diverticula,prolonged time of bleeding-cruor and acute cholangitis were independent risk factors in further multivariate analysis(P=0.023,0.036,0.045).Among procedure related factors,EPBD(P<0.01),EST(P<0.01),residual biliary stones(P=0.029)were proved to be significant risk factors by univariate analysis,and EPBD was found as independent risk factor(P=0.029)by multiva-riate analysis.Conclusion Appearance of periampullary diverticula,prolonged time of bleeding -cruor and acute cholangitis were considered as risk factors related to severity of post-ERCP hemorrhage in patients with choledocholi-thiasis.Moreover,EPBD was also an independent risk factor which might aggravate severity of post-ERCP hemor-rhage.

OBJECTIVE To investigate the causes of fever and risk factors in portal hypertensive patients after combined operation(devascularization+shunt).METHODS Forty five cases of portal hypertension(PHT) after combined operation were retrospectively and prospectively analyzed.RESULTS Complications caused 88% post operational fever.The most common cause was hydrothorax,hematocele or hydrops and infection in splenic recess.Long-term fever was related to liver function(P

Objective:To investigate whether hydrogen sulfide (H 2S) protects against intestinal ischemia/reperfusion (I/R) injury in rats by regulating c-Jun N-terminal kinase/activator protein-1 (JNK/AP-1) signaling pathway. Methods:Thirty male Wistar rats were divided into sham operated group (Sham group), I/R group, and H 2S donor sodium hydrosulfide (NaHS) intervention group (I/R+NaHS group), with 10 rats in each group. The I/R injury model was established by blocking the superior mesenteric artery with a non-traumatic vascular clip, with 60 minutes of ischemia followed by 120 minutes of reperfusion. In the I/R+NaHS group, 100 μmol/kg of NaHS was injected through the tail vein 10 minutes before reperfusion, followed by continuous infusion of 1.07 mmol·kg -1·h -1 until the end of the 120-minute reperfusion period. Plasma H 2S concentration was measured using a sensitive sulfur electrode. Malondialdehyde (MDA) and superoxide dismutase (SOD) levels in the small intestine tissue were assayed spectrophotometrically. Histological sections of the small intestine were stained with hematoxylin-eosin (HE) staining and scored using the Chiu scoring system to assess the degree of intestinal mucosal injury. Western blotting was used to detect the protein expressions of phosphated-JNK (p-JNK), JNK, AP-1, and BCL-2 in the small intestine tissue. Results:Compared with the Sham group, the I/R group exhibited damage to the lamina propria, hemorrhage, and ulceration, with a significantly higher Chiu score (4.80±0.63 vs. 0.70±0.09, P < 0.01); plasma H 2S concentration and SOD activity in the ileum tissue were significantly reduced [H 2S (μmol/L): 17.29±1.40 vs. 34.62±1.48, SOD (kU/g): 5.38±0.93 vs. 20.56±1.85, both P < 0.01], while MDA level was significantly elevated (μmol/g: 16.06±1.71 vs. 4.80±0.92, P < 0.01); expression of BCL-2 protein in the ileum tissue was significantly down-regulated (BCL-2/β-actin: 0.32±0.06 vs. 0.79±0.05, P < 0.01), while expressions of p-JNK and AP-1 proteins were significantly up-regulated (p-JNK/β-actin: 0.69±0.03 vs. 0.10±0.03, AP-1/β-actin: 0.82±0.02 vs. 0.22±0.02, both P < 0.01). Compared with the I/R group, the I/R+NaHS group showed moderate separation between the epithelial and lamina propria layers, with partial damage to the tips of the villi; the Chiu score was significantly lower (2.90±0.56 vs. 4.80±0.63, P < 0.01); plasma H 2S concentration and SOD activity in the ileum tissue were significantly increased [H 2S (μmol/L): 24.48±1.84 vs. 17.29±1.40, SOD (kU/g): 10.29±1.26 vs. 5.38±0.93, both P < 0.01], while MDA level was significantly reduced (μmol/g: 7.88±1.01 vs. 16.06±1.71, P < 0.01); expression of BCL-2 protein in the ileum tissue was significantly up-regulated (BCL-2/β-actin: 0.44±0.06 vs. 0.32±0.06, P < 0.01), while expressions of p-JNK and AP-1 proteins were significantly down-regulated (p-JNK/β-actin: 0.54±0.05 vs. 0.69±0.03, AP-1/β-actin: 0.66±0.04 vs. 0.82±0.02, both P < 0.01). There was no statistically significant difference in the expression of JNK in the ileum tissue among the Sham group, I/R group, and I/R+NaHS group (JNK/β-actin: 0.63±0.02, 0.66±0.02, 0.64±0.02, respectively, P > 0.05). Conclusion:H 2S exerts a protective effect on intestinal I/R injury in rats by down-regulate the expression of the JNK/AP-1 signaling pathway, as well as reducing oxidative stress levels.