Acquired immune deficiency syndrome,or AIDS,has been a major infectious disease that troubles the public health in a global scale. Human immunodeficiency virus type 1(HIV-1)is the causative reagent responsible for AIDS development. Even though the highly active anti-retroviral therapy(HAART,or the cocktail therapy)that has been widely applied could effectively suppress the infection and replication of HIV-1,the infected people suffer from other related diseases,such as the HIV-associated neurocognitive disorder(HAND). This paper mainly focused on the function of an important regulatory protein of HIV-1,trans-activator of transcription(Tat),and its correlation with HIV-1 replication and HAND development,so as to clarify the importance of developing anti-AIDS drugs targeting Tat protein

Objective To explore the regulatory effect of TAK 1 inhibitors on MAPK and NF-κB signaling pathway in diabetic rats and its renal protection mechanism .Methods A total of 48 rats accorded to the random number table method were divided into DN group , TAK1 group and control group ,each group with 16 rats,control group with normal fed , DN group and TAK1 group by the intraperitoneal injection of 1%50 mg/kg STZ DN model rat.8 rats were killed in each group at 4 weeks and 8 weeks respectively ,the pathological changes of renal tissue were observed ,serum TNF-α,MCP-1,IL-1βlevels were detected by enzyme linked immunosorbent assay ,p38MAPK,NF-κBp63 protein expression were detected by Western blotting ,p38MAPK、NF-κBp63 mRNA levels in renal tissue were detected by real time fluorescence quantitative PCR.Results At 4 weeks and 8 weeks, the body weight, blood glucose and UAER of DN group and TAKl group were significantly higher than those in control group (P <0.05).The body weight and UAER of DN group were significantly higher than those of TAK1 group (P <0.05).The serum TNF-α,MCP-1,IL-1βlevels in DN group and TAK1 group were significantly higher than those in control group (P <0.05),and DN group serum TNF-α,MCP-1,IL-1βlevels were significantly higher than those in TAK1 group (P <0.05).The expression levels of p38MAPK,NF-κBp63 protein and mRNA in DN group, TAK1 group were significantly higher than those in control group (P <0.05), and p38MAPK,NF-κBp63 protein and mRNA in DN group was significantly higher than that in TAK 1 group ( P <0.05 ) .Conclusions TAK1 induces inflammation by activating MAPK and NF-κB signaling pathways,and participates in diabetic renal injury . TAK1 inhibitors with anti-inflammatory effect by down regulate the expression of inflammatory factors .

Objective To discuss the expression level of CUEDC2 protein and its connection with 24 h urinary albumin and serum creatinine iu db/db mice with diabetic nephropathy.Methods db/db mice were selected as experimental groups (n =10),and db/m mice as control (n =10).All mice were fed in barrier facilities under the same conditions.At week 24,all were sacrificed and the samples were collected for analyses.The histological changes were assessed by Hematoxylin-Eosin(HE) staining,periodic acid-Schiff (PAS) staining and Masson's trichrome (Masson) staining.The location and expression of CUEDC2 were measured by immunohistochemistry assays.24 h urinary albumin and serum creatinine were quantified by clinic lab in our hospital.Results Immunohistochemistry demonstrated that CUEDC2 was mainly located in the medulla tubules plasma cells.The results of HE staining revealed that there appeared glomerular number decreased,atrophy and inflammatory cell infiltration in the mice kidney of diabetic nephropathy group at the 24th week.The mesangial matrix expansion and renal tissue collagen deposition were significantly up-regulated in db/db mice compared with the normal control.As compared with the control group,the CUEDC2 protein expression and mRNA expression in db/db mice were significantly decreased than that in db/m mice (both P ＜ 0.05),and 24 h urinary albumin and serum creatinine were significantly increased.The correlation analysis showed CUEDC2 was negatively correlated with 24 h urinary albumin and serum creatinine (both P ＜ 0.05).Conclusion The expression of CUEDC2 in diabetic nephropathy mice kidney is significantly decreased and negatively correlated with the levels of 24 h urinary albumin and serum creatinine.

Objective To investigate the relationship between alcohol and smoking and the development of pancreatic calcification in chronic pancreatitis (CP) in China. Methods The patients were divided into two groups according to the presence of pancreatic calcification at admission and the data were analyzed; furthermore, the discharged patients without pancreatic calcification were divided into two groups as newly diagnosed pancreatic calcification group and persistent non-pancreatic calcification group. Logistic regression and Cox proportional-hazards model was used for multivariate analysis of the risk factors for pancreatic calcification. Results From January1997 to July 2007, 449 patients with CP were enrolled and followed up successfully. 248 patients presented with pancreatic calcification at admission; among the 201 patients presented without pancreatic calcification, 13 patients developed pancreatic calcification after discharge. Patients with pancreatic calcification had a young age at onset, long CP history, higher incidence of diabetes mellitus and diarrhea. Age at onset ≤ 40, alcohol intake over 20 g/day, and diabetes mellitus and diarrhea were risk factors for pancreatic calcification. The only risk factor of development of pancreatic calcification after discharge was excessive alcohol intake (OR: 3.2). Conclusions Alcohol intake increased the risk of pancreatic calcifications, suggesting the patients abstain from alcohol intake. Further studies are necessary to clarify the role of smoking.

Objective To investigate the risk factors for failure of percutaneous catheter drainage (PCD) for patients with infective pancreatic necrosis (IPN).Methods A retrospective review of medical records of patients with IPN who received PCD at Pancreatic Intensive Care Unit (PICU) of Changhai Hospital from April 2010 to June 2014 was performed.The patients were divided into 2 groups:(1) PCD success group (n =48) and (2) PCD failure group (n =12).The potential parameters for failure of PCD were recorded,which included age,sex,etiology,length of hospital stay,outcome,MCTSI,APACHE Ⅱ scores,number of organ failure,duration of use of antibiotics,duration of use of PPIs,if delayed fluid resuscitation occurred,start of enteral nutrition,nutrition status,etc,and univariate and multivariate logistic regression analysis was used.Results Univariate analysis showed MCTSI,number of organ failure,malnutrition,use of PPIs (more than two weeks),delayed enteral nutrition,delayed fluid resuscitation,the number of drainage catheter,number of aspiration,multi-drug resistant infections of drainage fluid were risk factors for failure of PCD;while multivariate logistic regression analysis showed that MCTSI (OR =3.33;95％ CI 1.52 ～ 7.29;P =0.003);multi-drug resistant infections of drainage fluid (OR =8.62;95 ％ CI 1.11 ～ 67.19;P =0.040) were risk factors for failure of PCD.Conclusions MCTSI and multi-drug resistant infections of drainage fluid can significantly influence the success rate of PCD.PCD should be carefully considered for patients with high score of MCTSI and multi-drug resistant infections of drainage fluid.

Objective To study the effects of CUEDC2 on renal interstitial fibrosis and inflammation response in rats with unilateral ureteral obstruction (UUO). Methods 30 Balb/c rats were randomly distributed into sham operation group(sham-vector),uuo operation group(uuo-vector) and CUEDC2 treatment group after uuo (uuo-cuedc2). Hematoxylin-eosin and Masson staining were used to measure renal pathology; Inflammation factors were quantified by ELISA; Immunohistochemistry was performed to measure the expression of CUEDC2;Protein expression of CUEDC2, Fibronectin, E-cadherin, Collagen I were detected by Western Blot. Results At 7 and 14d after operation, the area of interstitial fibrosis and expression of ICAM1,MCP1,IL1,IL8, Fibronectin and Collagen I in uuo-cuedc2 showed a marked decrease when compared to uuo-vector (p?0.05),the level of E-cadherin was significantly increased (P < 0.05). Conclusion CUEDC2 can inhibit renal interstitial fibrosis and decrease the expression of inflammation factors and Collagen deposition.

Objective To evaluate the therapeutic effect of percutaneous endoscopic necrosectomy (PEN) in treating infectious pancreatic necrosis (IPN).Methods A retrospective review of clinical data of 6 patients with IPN who received PEN in Changhai Hospital, Second Military Medical University from Dec 2015 to Sep 2016 was performed.Clinical parameters were recorded, including basic information, severity evaluation and therapeutic methods and times.In addition, vital sign parameters and inflammatory marks before and after PEN treatment were compared.Results There were 4 patients with severe acute pancreatitis (SAP) and 2 patients with moderately severe acute pancreatitis (MSAP) in these 6 patients with IPN.Mean APACHEⅡ score was 12 (10~15), and mean MCTSI scores was 9.3(8~10).All 6 patients received a total of 13 times PEN treatments, with a mean of 2.2(1~3) times.Each patient was treated with a mean of 2.5(1~4) drainage tubes placed in the peripancreatic abscess after PEN treatment, and the mean time for drainage was 139 d(106~183 d).Besides, the mean hospitalization time was 116 d (48~223 d).All the patients′ condition was improved significantly after PEN treatment, including reduced heart rate, body temperature and inflammatory markers, without bleeding or other serious complications.Only 1 patient had pancreatic fistula after treatment, and no patients needed open abdominal drainage surgery.Patients with higher MCTSI scores likely required more times of PEN and more drainage catheters, longer length of drainage and hospital stay.Conclusions PEN was safe and effective for treating patient with IPN, but those with higher MCTSI scores were associated with more PEN treatments, more drainage tubes, and longer time of drainage and hospitalization.

Objective:To investigate the predictive value of acute gastrointestinal injury (AGI) score for the severity of acute pancreatitis (AP), infectious pancreatic necrosis and patients′ death.Methods:Clinical data of 719 patients with AP were collected from the AP database of the National Clinical Research Center for Digestive System Diseases from January 2016 to June 2018. According to the severity of the disease, they were divided into MAP group (506 cases), MSAP group (112 cases) and SAP group (101 cases). AGI, APACHEⅡ, MCTSI and BISAP scores were calcululated in the three groups. Receiver operating characteristic curve (ROC) was drawn and the area under the curve (AUC) was calculated. The predictive value of the above four scoring systems for the hospitalization days, disease severity, infectious pancreatic necrosis and death was analyzed, respectively.Results:There were no cases of infectious pancreatic necrosis or death in the MAP group, but there were 9 cases of infectious pancreatic necrosis and 2 deaths in the MSAP group and 19 cases of infectious pancreatic necrosis and 8 deaths in the SAP group. There was a strong correlation between AGI score and AP patients′ hospitalization days ( r=0.619). AUC of AGI, APACHEⅡ, MCTSI and BISAP score in predicting the AP patients′ severity (MSAP+ SAP) was 0.967 (95% CI 0.951-0.982), 0.769(95% CI 0.720-0.899), 0.842(95% CI 0.809-0.875), 0.862 (95% CI0.832-0.893). AUC for forecasting infectious pancreatic necrosis was 0.803, 0.677, 0.692, 0.724, and the 95% CI was 0.724-0.882, 0.573-0.781, 0.582-0.636, 0.801-0.812. AUC for predicting death in patients with AP were 0.915, 0.597, 0.659, 0.812, and the 95% CI were 0.843-0.986, 0.444-0.751, 0.498-0.698 and 0.882-0.926. AGI score had the highest predictive value, followed by BISAP score, and the correlation between these two scores was the closest. The predictive value of AGI combined with BISAP score for infectious pancreatic necrosis and patient death (AUC were 0.837, 0.942, 95% CI were 0.770-0.903, 0.897-0.987) was better than that of AGI and BISAP score alone. Conclusions:AGI score combined with BISAP score is more effective in predicting the severity of AP, the occurrence of infectious pancreatic necrosis or patient death.

Objective To evaluate the value of medical treatment in the management of SAP.Methods From January 2000 to December 2011,a total of 1064 cases out of 931 SAP patients were admitted and retrospectively analyzed.The etiologies,severity score,complication rates,therapies,effectiveness and costs of those SAP cases were summarized.Results There were 559 males and 372 females with a mean age of (51 ± 15)years old.The main cause was biliary tract disease (58.3％),followed by fat-rich diet (31.2％),hyperlipidemia (13.6％) and alcohol (7.1％).At the time of admission,95.5％ of SAP patients presented with level D disease according to Balthazar CT severity index,26.0％ had a Ranson score ≥3 and 30.1％ had an APACHE Ⅱ score ≥ 8.There were 42.7％ cases complicated with systemic inflammatory response syndrome (SIRS).Acute lung injury and acute respiratory distress syndrome (ARDS),acute kidney injury,shock or heart failure,acute liver dysfunction,and diffuse intravascular clotting (DIC)occurred in 24.0％,8.1％,5.4％,3.2％,and 1％ of all patients,respectively.Other complications of SAP included abdominal cavity bleeding (n =17),pseudocyst bleeding (n =9),pancreatic abscess (n =78) and gastrointestinal fistula (n =33).Totally 25 (2.3％) patients died in hospital and 36 (3.4％) patients were discharged against advice,with an overall treatment success rate of 94.3％.The mean hospital stay was (23.7 ± 19.2) d,and the average cost was 52.3 thousands of RMB.Conclusions A comprehensive treatment pathway relying on medical treatment,focusing on organ function support and assisted by miniinvasive intervention may improve the treatment success rate of SAP,which is worth of further application.

BACKGROUNDIt has been known that Kai1 is one of transmembrane 4 superfamily regulating cell proliferation, adhesion and mobility and its down-regulated expression is closely correlated with progression and prognosis of tumor. Fas ligand (FasL) is one of tumor necrosis factor/nerve growth factor family activating caspase-3, a key proteinase in cell apoptosis and leading immune escape in tumor cells. The aim of this study is to investigate the expression of Kai1 and FasL in non-small cell lung cancer (NSCLC) and to explore their roles and relationship in carcinogenesis and progression of NSCLC.

METHODSKai1 and FasL expressions were examined in 79 NSCLC tissues and their adjacent normal lung tissues by SP immunohistochemistry. Their expressions were compared with clinicopathological features of NSCLC. The relationship between Kai1 and FasL expressions was also analyzed in NSCLC.

RESULTSKai1 expression in NSCLC tissue was remarkably lower than that in their adjacent tissue (55.7% vs 82.6%, P < 0.05). However, it was the converse for FasL (73.4% vs 52.2%, P < 0.05). Kai1 expression was not correlated with age and gender of NSCLC patients, tumor location or histological classification (P > 0.05), but negatively with lymph node metastasis and clinicopathological staging and positively with differentiation degree (P < 0.05). FasL expression was not correlated with age and gender of the patients, tumor location or histological classification (P > 0.05), but positively with lymph node metastasis and negatively with differentiation degree (P < 0.05). Kai1 expression was closely correlated with FasL expression in NSCLC (P < 0.05).

CONCLUSIONSDown-regulation of Kai1 expression and up-regulation of FasL may play important roles in carcinogenesis and progression of NSCLC. Kai1 and FasL could be considered as molecular markers to reflect pathobiological behavior of NSCLC. Additionally, close correlation of FasL expression with Kai1 expression in NSCLC provides a novel insight into the regulatory effects of FasL expression on Kai1 expression.