OBJECTIVE:To study risk factors for carbapenem-resistant Acinetobacter baumannii(CRAB)infection,and to provide reference for its clinical prevention. METHODS:In retrospective study,302 A. baumannii(AB)infection patients were collected from our hospital during Dec. 2012 to Jun. 2017. According to the results of drug sensitivity test,those patients were divided into CRAB group(116 cases)and non-CRAB group(186 cases). Risk factors for CRAB infection were analyzed by using univariate analysis. Multivariate Logistic regression analysis was performed for variables with significant difference between 2 groups. RESULTS:Univariate analysis showed that the factors of significant difference in 2 groups including patients suffering from septic shock(P=0.003),sepsis(P=0.000),combined with other infection(P=0.006),diabetes(P=0.029),malignant tumors(P=0.036),patients suffering from infection of other site except for pulmonary infection,intraabdominal infection and skin infection(P=0.009)before AB isolation,patients given carbapenems(P=0.002)and antifungal drugs 28 d before AB isolation(P=0.002). Multivariate Logistic regression analysis showed that the factors of significant difference in 2 groups including patients suffering from sepsis(P=0.033)or diabetes(P=0.011)before AB isolation. CONCLUSIONS:Independent risk factors for CRAB infection include patients suffer from sepsis or diabetes before AB isolation.

OBJECTIVETo investigate the effect of Src kinase inhibitor PP2 on hypoxia/reoxygenation (H/R) injury in rat astrocytes in vitro.

METHODSIn vitro cultured rat astrocytes were exposed to hypoxia for 8 h followed by reoxygenation for 24 h with or without pretreatment with PP2 (10 µmol/L) for 24 h before H/R injury. MTT assay and flow cytometry were used to detect the viability and apoptosis of the exposed astrocytes, respectively, and the protein expressions of Src, Bax, and Bcl-2 in the cells were determined using Western blotting.

RESULTSPP2 pretreatment significantly increased the viability and decreased the apoptosis rate of rat astrocytes exposed to H/R injury (P<0.01). Western blotting showed that H/R injury caused increased expression of Src kinase, which was lowered by PP2 pretreatment. The ratio of Bax/bcl-2 in the astrocytes increased after H/R injury, and was significantly decreased by PP2 pretreatment (P<0.01).

CONCLUSIONPP2 protects rat astrocytes from H/R injury possibly by inhibiting the expression of Src kinase and activating the anti-apoptotic mechanisms in the cells.

Animals ; Apoptosis ; Astrocytes ; pathology ; Cell Hypoxia ; Cells, Cultured ; Flow Cytometry ; Pyrimidines ; pharmacology ; Rats ; src-Family Kinases ; antagonists & inhibitors

OBJECTIVETo determine the expression of connexin 43 (Cx43) protein and explore the functional modulation of gap junction intercellular communication in astrocytes.

METHODSCultured neonatal SD rat astrocytes were divided into normal control group, all-trans retinoic acid (ATRA) group (treated with 10 µmol/L ATRA for 24 h) and oleamide group (treated with 25 µmol/L oleamide for 2 h). Western blotting and immunofluorescence assay were used to detect total cellular Cx43 protein expression and Cx43 expression on the surface of the astrocytes, respectively. Parachute assay was used to evaluate the functional changes of gap junction intercellular communication of the astrocytes.

RESULTSCompared with the normal control cells, ATRA treatment resulted in a significantly increased expression of total Cx43 protein in the astrocytes (P<0.01), and oleamide significantly suppressed its expression (P<0.01). Similarly, ATRA obviously enhanced while oleamide suppressed Cx43 protein expression on the surface of the astrocytes. The gap junction intercellular communication of the astrocytes was enhanced by ATRA (P<0.01) and inhibited by oleamide (P<0.01).

CONCLUSIONATRA and oleamide can modulate gap junction intercellular communication of the astrocytes possibly by regulating the expression of Cx43 protein.

Animals ; Astrocytes ; metabolism ; Cell Communication ; drug effects ; Cells, Cultured ; Connexin 43 ; metabolism ; Gap Junctions ; metabolism ; Oleic Acids ; pharmacology ; Rats ; Rats, Sprague-Dawley ; Tretinoin ; pharmacology

Objective: Incidence of primary liver cancer (PLC) in China is mostly related to chronic infection of hepatitis B virus (HBV). Qidong was one of the endemic areas with high incidence of PLC in China before 2000. We conducted a series of studies regarding on PLC etiological prevention during the past decades to develop better primary prevention strategies for PLC. Methods: Qidong Hepatitis B Intervention Study was conducted in 1983-1990. A total of 41 182 newborns were randomly assigned to vaccination group and 40 211 (97.64%) of them completed the three-dose, 5 µg-plasma-derived hepatitis B (HB) vaccination series at age 0, 1, 6 month. Among them, 28 988 participants received one-dose 10 µg recombinant HB booster vaccination at age 10-14 years. A total of 41 730 newborns were randomly assigned to the control group. When they were at age 10-14 years, 23 368 participants received the catch-up vaccination with three-dose, 10 µg-recombinant HB vaccine. Two cross-sectional HBV serology surveys were conducted in 1996-2000 and 2008-2012. Information on PLC incidence and mortality of chronic liver diseases were collected through cancer registry and vital statistics until December 31, 2016. Cox proportional hazard models were employed to compute hazard ratio (HR) of PLC and other liver diseases for the participants with neonatal HB vaccination or catch-up vaccination, and the protective efficacy was also calculated. Results: During serologic survey in 1996-2000, a total of 22 689 participants in vaccination group and 12 395 participants in control group donated blood samples. The HBsAg seropositive rates in the vaccination group was 2.16% (491/22 689), which is significantly lower than that of control group (9.08%, 1 126/12 395) (χ²=896.61, P<0.001). During serologic survey in 2008-2012, a total of 17 386 participants in vaccination group and 18 060 participants in control group donated blood samples. The HBsAg seropositive rates in the vaccination group was 1.83% (319/17 386), which is still significantly lower than that of control group (6.77%,1 222/18 060) (χ²=518.05, P<0.001). By December 31, 2016, 4 cases of PLC in the vaccination group and 17 cases of PLC were identified in the vaccination and control group, respectively. The estimated efficacy of neonatal HB vaccination on HBsAg seroprevalence in childhood (at age 10-11 years), early adulthood (at age 19-28 years) and incidence rate of PLC at age below 33 years was 79% (95%CI: 76%-81%), 74% (95%CI: 71%-78%) and 79% (95%CI: 36%-93%), respectively. The estimated efficacy of three-dose, 10 µg-recombinant HB catch-up vaccination in early adulthood is 21% (95%CI: 11%-30%), which is significantly lower than that of neonatal HB vaccination. Conclusion HB vaccination to neonates/infants is crucial against chronic HBV infection in childhood through young adulthood, and subsequently reduced the risk of PLC in young adults.

Objective To investigate the effect of Src kinase inhibitor PP2 on hypoxia/reoxygenation (H/R) injury in rat astrocytes in vitro. Methods In vitro cultured rat astrocytes were exposed to hypoxia for 8 h followed by reoxygenation for 24 h with or without pretreatment with PP2 (10 μmol/L) for 24 h before H/R injury. MTT assay and flow cytometry were used to detect the viability and apoptosis of the exposed astrocytes, respectively, and the protein expressions of Src, Bax, and Bcl-2 in the cells were determined using Western blotting. Results PP2 pretreatment significantly increased the viability and decreased the apoptosis rate of rat astrocytes exposed to H/R injury (P<0.01). Western blotting showed that H/R injury caused increased expression of Src kinase, which was lowered by PP2 pretreatment. The ratio of Bax/bcl-2 in the astrocytes increased after H/R injury, and was significantly decreased by PP2 pretreatment (P<0.01). Conclusion PP2 protects rat astrocytes from H/R injury possibly by inhibiting the expression of Src kinase and activating the anti-apoptotic mechanisms in the cells.

Objective To investigate the effect of Src kinase inhibitor PP2 on hypoxia/reoxygenation (H/R) injury in rat astrocytes in vitro. Methods In vitro cultured rat astrocytes were exposed to hypoxia for 8 h followed by reoxygenation for 24 h with or without pretreatment with PP2 (10 μmol/L) for 24 h before H/R injury. MTT assay and flow cytometry were used to detect the viability and apoptosis of the exposed astrocytes, respectively, and the protein expressions of Src, Bax, and Bcl-2 in the cells were determined using Western blotting. Results PP2 pretreatment significantly increased the viability and decreased the apoptosis rate of rat astrocytes exposed to H/R injury (P<0.01). Western blotting showed that H/R injury caused increased expression of Src kinase, which was lowered by PP2 pretreatment. The ratio of Bax/bcl-2 in the astrocytes increased after H/R injury, and was significantly decreased by PP2 pretreatment (P<0.01). Conclusion PP2 protects rat astrocytes from H/R injury possibly by inhibiting the expression of Src kinase and activating the anti-apoptotic mechanisms in the cells.

Domain database is essential for domain property research. Eliminating redundant information in database query is very important for database quality. Here we report the manual construction of a non-redundant human SH2 domain database. There are 119 human SH2 domains in 110 SH2-containing proteins. Human SH2s were aligned with ClustalX, and a homologous tree was generated. In this tree, proteins with similar known function were classified into the same group. Some proteins in the same group have been reported to have similar binding motifs experimentally. The tree might provide clues about possible functions of hypothetical proteins for further experimental verification.
Amino Acid Sequence ; Computational Biology ; Databases, Protein ; Humans ; Molecular Sequence Data ; Sequence Alignment ; src Homology Domains ; genetics

Objective To explore the expression profile of the JAK/STAT pathway in patients with acute myeloid leukemia(AML)and to analyze its impact on the survival prognosis of patients.Methods This study compared differentially expressed genes between AML patients and healthy controls in 2 independent cohorts(n=64,n=121),and these genes were enriched by pathways.The expression levels of JAKs and STATs genes were compared between AML patients and healthy controls.The clinical values of JAK/STAT genes were analyzed using gene expression data,patients'clinical and prognostic information from 2 AML cohorts(n=163,n=403).Results Gene microarray expression results in 26 AML patients and 38 healthy controls showed 1266 genes with significantly differential expression(Padj≤0.05,| log2FC| ≥0.5),of which 426 genes were significantly upregulated in AML patients and 840 genes were significantly downregulated in AML patients.Pathway enrichment of these genes was performed in the JAK/STAT pathway,which was found to be active in AML patients(P＜0.05).Comparison of mi-croarray data from the GSE1159 cohort(n=121)showed AML patients had higher levels of JAK1(P=0.019),J AK2(P=0.047)and STAT4(P＜0.001)gene expression than the healthy controls,and their STAT5A(P=0.028)and STAT6(P=0.022)gene expression levels were lower than those in the healthy controls.Univariate survival analysis identified shorter over-all survival(P=0.02,HR=1.463;P=0.041,HR=1.293)and event-free survival(P=0.01,HR=1.510)in patients with high STAT4 expression than in those with a lower STAT4 expression in the TCGA and GSE6891 cohorts(n=163;n=403).Univa-riate and multifactorial COX analyzes confirmed that high STAT4 expression was an independent prognostic risk factor for AML patients(EFS:P=0.002,HR=1.958;OS:P=0.036,HR=1.556).Conclusion In AML patients,the JAK/STAT path-way is activated,and the STAT4 expression level is higher than that of the healthy controls.High expression of STAT4 suggest poor prognosis,wihich is an independent risk factor for the prognosis of AML patients.

Objective:To evaluate the safety and feasibility of transumbilical single-port transabdominal preperitoneal hernioplasty plus cholecystectomy (SILS-TAPP+LC).Methods:The clinical data of 52 adult patients who underwent [SILS-(TAPP+LC)] from Mar, 2019 to Oct, 2021 at the Affiliated Hospital of Nantong University were retrospectively analyzed.The perioperative indicators, postoperative complications and follow-up data were analyzed.Results:All operations were successfully completed without conversion to open or multi-port laparoscopic surgery.The duration of surgery was (49.2 ± 7.5) min. Three patients experienced gallbladder rupture, and there was no bladder or intestinal injury during the surgery.During the 20-24 months of postoperative follow-up period,4 patient developed seroma in the postoperative period, 4 patients complained foreign body sense in the inguinal region, 3 patients reported chronic pain, but no other complications, such as biliary fistula, recurrence, mesh infection, or trocar hernia, were observed.Conclusion:SILS-(TAPP+LC) was a safe and feasible approach associated with little postoperative pain and rapid recovery.

Vascular malformations, which mainly occur in the head and neck region, are a group of congenital disorders that cannot involute and dilate gradually as patients grow. Traditional therapeutic strategies for vascular malformations include laser therapy, sclerotherapy, interventional embolization, surgical resection, etc. However, for some cases with a relatively larger range of lesions, traditional therapeutic strategies might fall short of the goals. With the development of molecular genetics, gene mutations are currently recognized as the root cause of the occurrence of vascular malformations. The progression of vascular malformation lesions is further promoted by the activation of related pathways. Low-flow vascular malformations mainly involve activation of the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) pathway, whereas high-flow vascular malformations mainly involve activation of the rat sarcoma (RAS)/rapidly accelerated fibrosarcoma (RAF)/mitogen-activated protein kinase kinase (MAPKK)/extracellular-signal regulated protein kinase (ERK) pathway. Targeted drugs against relevant gene mutations and signaling pathways have also been applied in the treatment of vascular malformations, and previous studies have shown that the mTOR inhibitor rapamycin is effective and now widely used in the treatment of low-flow vascular malformations. The PI3K inhibitor alpelisib is also promising in the treatment of venous malformations, and the MAPKK inhibitor trametinib has shown good results in the treatment of arteriovenous malformations. Therefore, traditional therapies supplemented by targeted drugs may bring new breakthroughs to the treatment of vascular malformations.