Objective To investigate the possible mechanism of Nrf2 in sepsis development and its effect in the septic acute liver injury ,and derive the effect of curcumin on Nrf2 expression ,which provide theoretical basis for clinical prevention and treatment of sepsis .Methods Divided putting 72 male Sprague-Dawley rats into 3 groups:control group ,experimental group and intervention group .After operation ,3 groups were further divided into subgroups 6 hours later ,12 hours later ,24 hours later and 48 hours later respectively .The septic rats model with acute liver injury was reproduced by method of cecal ligation and puncture (CLP) .The ex-perimental group and the intervention group took CLP .The rats in the intervention group were rejected with curcumin in the abdo-men at a dosage of 100 mg/kg an hour after operation .Detected the expression of Nrf2 in the livers of each group used Western blot and measure alanine aminotransferase(ALT ) in serum by drawing the rats′heart blood ;observed the pathological changes in the liver with HE coloration .Results ALT :the values of ALT in the experimental group was significantly increased compared with the control group(P<0 .05);while in the intervention group ,it was markedly improved compared with the experimental group (P<0 . 05) .The expression of Nrf2 :Nrf2 exists in control group rat′s hepatic tissue .In the experimental group ,it was progressively in-creased since the 6 h time point and decreased after the 12 h time point which shown significant decreased compared with the control group(P<0 .05) .In the intervention group ,it was gradually increased since the 6 h time point and decreased after the 24 h time point which was obviously higher than the experimental group(P<0 .05) .Pathological changes :There was no obvious abnormalities in the control group rats′liver structure ,while a lot of inflammatory cells gather and liver cells swell in the experimental group .It was obvious improved after curcumin intervention .Conclusion As Nrf2 is generally lower in the experimental group than in the comparative group ,it shows that Nrf2 directly participates in the occurrence and development of sepsis ,while severe infection blow damages the endogenou s protection system .Decreased activity of Nrf2 causes ignificantly inhibition of anti-oxidative stress and nat-ural immune response ,which may exacerbate acute liver injury by oxidative stress in sepsis .In case of sepsis ,curcumin may increase the level of Nrf2 and the antioxidant enzyme′s activity in the hepatic tissues ,enhancing the general antioxidant ability and alleviating the oxidative stress which points out that curcumin prevents the septic acute liver injury .

Objective To investigate antenatal sonographic findings of the fetal isolated callosal hypoplasia and partial agenesis. Methods A retrospective study was performed on the cases of hypoplasia and partial agenesis of the corpus callosum suspected at antenatal sonographic basic examination from 2006 to 2014, all the cases were confirmed by pathology or magnetic resonance imaging(MRI). For the surviving infants, clinical follow-up had been performed to assess the developmental outcome. Results Thirteen fetuses suspected with callosal underdevelopment were identified at a median gestational age of 31 (range, 18~39) weeks. Ten cases were confirmed by autopsy and MRI, including 9 with partial agenesis and 1 with hypoplasia. Among the 10 fetuses confirmed with isolated partial agenesis or with hypoplasia, incidence of the absent cavum septum pellucidum was 20%, the ‘Tear-drop’ lateral ventricles was 40%, the upward displacement of the third ventricle was 80%. Pregnancy was terminated electively in 8 of the cases with partial agenesis or with hypoplasia. Among the 2 surviving infants, apparent normal development was observed in only one case, but we lost the follow-up of this case at two-year-old. Six fetuses received the chromosome identification, almost all of them were normal. Conclusion The basic ultrasonic examination is feasible for the antenatal diagnosis of isolated callosal underdevelopment the. The indirect classical signs of callosal partial agenesis and hypoplasia are different with those of complete agenesis of the corpus callosum. The incidences of the‘Tear-drop’ lateral ventricles and the upward displacement of the third ventricle are higher than the absence of CSP. The chromosome of isolated callosal partial agenesis or hypoplasia is normal, however, the prognosis is uncertain.

BACKGROUNDTo investigate whether autologous lung cancer tissues derived gp96-peptide complex/dendritic cell vaccine could induce peptide specific cytotoxic T lymphocyte (CTL) response in vitro.

METHODSA patient's tumor-derived antigens including gp96-peptide complexes and tumor cell lysate were co cultured with DCs derived from the same patient's bone marrow blood mononuclear cells. The various antigen/DC vaccines were used to stimulate peripheral lymphocytes. Interferon-γ (IFN-γ) level of activated lymphocytes was detected by ELISA method and the Cr51 release test was performed to evaluate the gp96-peptide specific CTL response in three kinds of target cells including the primary cultured tumor cells, PG cells and K562 cells.

RESULTSIFN-γ could be observed from the supernate collected in all antigen groups after the cognate T lymphocytes were stimulated by various vaccines. The concentration of IFN-γ induced by gp96-peptide complexes/DC vaccine was higher than that of other groups. In addition, the killing effect of the activated T lymphocytes on patient's primary tumor cells was higher than that on PG and K562 cells.

CONCLUSIONSAutologous tumor-derived gp96-peptide complexes can induce a peptide complex specific CTL response, and the CTL response is significantly intensified after DCs are pulsed.

Objective To investigate the incidence and potential risk factors of linezolid (LZD) related thrombocytopenia (TP) in patients with liver cirrhosis (LC). Methods Clinical data of LC patients treated with LZD for at least 1 dose (600 mg per 12 h) between January 2013 and May 2017 were retrospectively collected and analyzed to investigate the incidence and risk factors of LZD-related TP defined as platelet count during LZD therapy ≤ 50×109/L or a decline by ≥25％ of the baseline level. Results A total of 52 patients with LC were included in this study. The cumulative incidence of LZD-related TP was 51.9％ (27/52), of which 85.2％ (23/27) was severe TP (decline of platelet count by ≥50％ of the baseline level). Multivariate logistic regression analysis showed that the baseline platelet count ≤110 ×109/L (OR=6.989, 95％ CI: 1.192-40.971, P=0.031), LZD course ≥ 7 d (OR=9.478, 95％ CI: 1.349-66.587, P=0.024) and LZD dose ≥ 17 mg·kg-1·d-1 (OR=0.062, 95％ CI: 0.010-0.383, P=0.003) were independent risk factors of LZD-related TP in LC patients. Kaplan-Meier analysis revealed that the overall median time from the initiation of LZD therapy to in-hospital death was 18 days in TP patients and 13 days in non-TP patients without significant difference (P＞0.05). Cox proportional-hazards regression revealed no significant correlation between the in-hospital mortality and LZD-related TP in LC patients (P＞0.05). Conclusions Patients with LC are at high risk of LZD-related TP, but not associated with organ hemorrhage during LZD therapy and in-hospital mortality. Platelet count should be monitored more closely during LZD therapy for LC patients with lower baseline platelet count and longer LZD course.