AIM To investigate the protective effect of propofol on ischemia-reperfusion (I-R) injury in isolated rat hearts and clarify the possible molecular mechanism from oxidative stress and the apoptosis initiated by mitochondria pathway. METHODS The isolated Langendorff-perfused rat hearts were rendered globally ischemia for 25-min followed by 30-min reperfusion to establish I-R injury model. The cardiac function parameters were recorded. The swelling, integrity of electron transport chain (ETC) and content of malondialdehyde (MDA) in myocardium mitochondria were determined. The percentage of apoptotic cardiomyocytes and the expressions of Bcl-2 and Bax proteins were evaluated by flow cytometry. The expressions of caspases-8, -9 and -3 proteins in myocytes were detected by immunohistochemistry. RESULTS Compared with I-R group, perfusing with 30 and 60 μmol·L-1 propofol from 10 min before ischemia to whole reperfusion period resulted in improvement in cardiac function. The swelling and ETC lesion of mitochondria alleviated, and MDA content decreased. The percentage of apoptotic cardiomyocytes was markedly lower than that of I-R group. The expression of Bcl-2 protein was higher and the expression of Bax was lower than that of I-R group. The expressions of caspase-3 and caspase-9 proteins were obviously lower than those in I-R group. CONCLUSION Propofol confers significant protection against the I-R injury in the isolated rat hearts. Diminishing oxidative stress, protecting mitochondria from peroxidative injury, thus interfering with the mitochondria-dependent apoptotic pathway may be one of the major mechanisms of its cardioprotection.

Objective To evaluate the clinical value of CTPA combined with V/Q imaging to guide the end point of anticoagulant therapy in reducing the recurrence rate of pulmonary embolism. Methods A total of 159 cases of pulmonary embolism diagnosed by CTPA were randomly divided into experimental group(n=80)and control group(n = 79). After the regular low molecular weight heparin and warfarin anticoagulation therapy ,the experimental group used the CTPA combined with V/Q imaging to evaluate the pulmonary embolism absorption ,to guide the end point of anticoagulant therapy and to evaluate the recurrence rate of pulmonary embolism at the end of 1-year treatment. But in control group ,only CTPA was used to guide the treatment and then the recurrence rate in 2 groups was compared. Results The anticoagulant treatment course of experimental group was(5.90 ± 1.80) months,which was significantly longer than that of control group(3.57 ± 1.09)months(P<0.05). The recurrence rate of experimental group was significantly lower than that of control group(7.5%vs. 22.8%)after 1-year treatment (P<0.05). However,there was no significant difference between 2 groups(8.75%vs 3.80%)in the rate of bleed-ing during anticoagulation therapy (p>0.05).Conclusions CTPA combined with V/Q imaging to guide the end point of anticoagulant therapy for pulmonary embolismhas important clinical value in reducing the recurrence rate of pulmonary embolism.

Aim To investigate the protective effects of propofol against tert-butyl hydroperoxide(t-BHP)-induced oxidative injury in cultured rat cardiomyocytes and the possible mechanism.Methods Primary cultured neonatal rat cardiomyocytes was performed.Cultured cardiomyocytes were divided into five groups: control group,t-BHP group,and propofol 1,10,30 ?mol?L-1 group.Cellular Superoxide dismutase(SOD) activity,glutathione(GSH) and malonaldehyde(MDA) content were measured by colorimetric assay.Mitochondrial activity was determined by methylthiazolyl tetrazolium(MTT) test.The mitochondrial membrane potential(??m) was analyzed by Rhodamine123 staining and flow cytometry.The apoptosis of cardiomyocytes was detected by flow cytometry(FCM).The expression of caspase-3 was determined by Western blot.Results Compared with the control group,the MDA content significantly increased in t-BHP-treated group(P

Aim To explore the molecular mechanisms of propofol in cardioprotection,the activation of NF-?B and NF-?B-regulated inflammatory mediator expression was examined with the model of ischemia/reperfusion in rat heart.Methods Rat myocardium I/R injury was induced by occlusion of the left main coronary artery for 30 min and reperfusion for 2 h.Propofol(3,6,12 mg?kg-1?h-1)was intravenously given at 15 min before ischemia.Heart rate(HR),mean arterial blood pressure(MAP) and pressure-rate index(PRI)were recorded under basal conditions,during the occlusion and at the end of reperfusion,respectively.The translocation of NF-?B in the cardiomyocytes was detected by immunohistochemistry,and NF-?B expression was determined by Western blot.The concentrations of TNF-?,IL-1? in serum and myocardium were evaluated by ELISA and radioimmunoassay,respectively.The cardiac amount of mRNA codifying for intercellular adhesion molecule-1(ICAM-1)and inducible nitric oxide synthase(iNOS) was investigated by RT-PCR and in situ hybridization(ISH),respectively.Results At the end of reperfusion,the cardiac function parameters(HR,MAP,pressure-rate index) in I/R group were lower than those of sham group(P

Objective To express Tp0751 laminin-binding adhesion of Treponema pallidum (T. pallidum) ,and assess the immunocompetence. Methods The Tp0751 ORF without upstream non-cod-ing region was ligated into the expression vector pET-28a( + ), and expressed in E. coli R2566. Its immuno-gen was analyzed by Western blot and ELISA. Results A fusion protein with molecular weight about 26×103 was attained after expression and purification. Western blot proved that the recombinant protein can specifically react with T. palliclum IgG positive sera. Specific humoral response were elicited after introducing recombinant protein in Zealand rabbit and the specific antibody titer was above 1:10 2400 detected by indi-rect ELISA. Conclusion The expressed recombinant protein showed excellent immunoeompetence, and the results lay the foundation for the research on its function to T. paUidum infection.

ObjectiveTo investigate the relationship between syndrome differentiation types and the objective indexes of fatty liver.MethodsA cross-sectional study was adopted. Clinical observation table of fatty liver for TCM diagnostic performance was used to collect the data of patients and cluster analysis was adopted for syndrome differentiation. The difference of the objective indexes among different syndromes was studied.ResultsFatty liver showed more severity in spleen Qi deficiency and dampness group compared with heart and liver yin deficiency group(χ2=8.218,P=0.041). Patients in the spleen and stomach Qi deficiency group had less smoking history(χ2=8.416,P=0.038). Patients in the spleen Qi deficiency and dampness group had higher AST, TP, ALP and WHR indexes and lower Alb.ConclusionsDifferences of objective indexes in different fatty liver syndromes can be used for enriching syndrome differentiation contents, and provide the basis for microcosmic syndrome differentiation of fatty liver.

Objective To study the clinical features, effects of therapeutic regimen and prognosis of patents with mantle cell lymphoma (MCL). Methods Clinical data of 27 MCL patients admitted in Tianjin Medical University Cancer Institute&Hospital from January 2008 to December 2014 were retrospectively analyzed. Cox regression analysis was used to analyze influencing factors of prognosis of MCL. Results The median age was 68 years old for 27 patients, and the male-to-female ratio was 4.4∶1. Ann Arbor staging showed that 25 cases were stageⅢ-Ⅳ(92.6%), 8 cases were heptosplenomegaly (29.6%), 7 cases showed extranodal involvement (25.9%). ECOG scoring showed that 4 cases with scores of 2-4 (14.8%), 8 cases were 0-3 (29.6%), 14 cases were 4-5 (51.9%) and 5 cases were 6-11 (18.5%). The Ki-67 index≤30%was found in 9 cases (33.3%), and>30%was found in 18 cases (67.7%). Patients with B symptom was found in 10 (37.0%). The elevated lactate dehydrogenase (LDH) was found in 17 cases (63.0%). The increased Beta 2- microglobulin was found in 8 cases (29.6%). Seven patients were found with bone marrow involvement. The total effective rate (ORR) was 81.8%in group with R-CHOP method, and the ORR was 68.8%in group with CHOP method. Multivariate analysis showed that age, LDH and Ki-67 were independent factors influencing the prognosis of MCL (P<0.05). Conclusion Most patients with MCL are found in advanced stage. Patients with age>60 years, elevated LDH and Ki-67 index>30%are with poor prognosis.

ObjectiveTo investigate the clinical features of drug-induced liver injury (DILI) caused by antitumor drugs during the treatment of malignant tumors. MethodsA retrospective analysis was performed for the clinical data of 56 patients who were diagnosed with malignant tumors in Henan Provincial People′s Hospital from January 2015 to December 2016 and experienced DILI during the treatment with antitumor drugs, including sex, age, type of primary tumor, hepatotropic virus infection, liver function, type of chemotherapeutics, onset time of liver injury, application of liver-protecting drugs, and outcome of liver injury. ResultsAmong the 56 patients with DILI caused by antitumor drugs, 30 (53.6%) had hepatocellular injury, and 45 (80.4%) had mild liver injury. FOLFOX, GP/DP, and CHOP were the most common regimens for DILI, and of all 56 patients, 50 (89.3%) had DILI caused by multiple drugs. Platinum-based drugs, anti-microtubule agents, and alkylating agents were the common drugs causing DILI. Of all 56 patients, 35 (62.5%) developed DILI within 1-2 weeks after medication. ConclusionDILI caused by antitumor drugs mainly has a mild degree and hepatocellular injury type is the most common clinical type. Platinum-based antitumor drugs and related chemotherapeutic regimens are the most common drugs for DILI. A combination of multiple antitumor drugs is more likely to cause DILI, and patients with such DILI often have a good prognosis.

Esophageal squamous cell carcinoma (ESCC) is one of the most aggressive cancers in China, but the underlying molecular mechanism of ESCC is still unclear. Involvement of micro-RNAs has been demonstrated in cancer initiation and progression. Despite the reported function of miR-503 in several human cancers, its detailed anti-oncogenic role and clinical significance in ESCC remain undefined. In this study, we examined miR-503 expression by qPCR and found the downregulation of miR-503 expression in ESCC tissue relative to adjacent normal tissues. Fur-ther investigation in the effect of miR-503 on ESCC cell proliferation, migration, and invasion showed that enhanced expression of miR-503 inhibited ESCC aggressive phenotype and overexpres-sion of CCND1 reversed the effect of miR-503-mediated ESCC cell aggressive phenotype. Our study further identified CCND1 as the target gene of miR-503. Thus, miR-503 functions as a tumor suppressor and has an important role in ESCC by targeting CCND1.

OBJECTIVETo investigate the effects of arsenic trioxide (As(2)O(3)) on the apoptosis and p-glycoprotein (P-gp) expression of multidrug-resistant human leukemia cells.

METHODSHuman multidrug-resistant leukemia cell line K562/ADM overexpressing the MDR1 gene, was used as the target cells. The cell proliferating activity was assessed using the MTT colorimetric assay. Cytomorphology was investigated under light, confocal and electron microscopes. DNA fragmentation was examined using agarose gel electrophoresis, while p-gp expression, cell cycle status and sub-G1 cells were determined using flow cytometry.

RESULTSZero point five to 20 micromol/L As(2)O(3) inhibited the proliferation of K562/ADM cells, and K562/ADM cells were more sensitive to As(2)O(3) than the parental K562 cells. As(2)O(3)-induced apoptosis of K562/ADM cells was determined by the observance of typical morphological changes and the appearance of DNA ladder and sub-G1 cell populations. As(2)O(3) significantly inhibited the P-gp expression of K562/ADM cells, and synergistically enhanced the sensitivity of the drug-resistant cells to adriamycin.

CONCLUSIONSAs(2)O(3) induces growth-inhibition and apoptosis, down-regulates P-gp expression and exerts a synergistic effect in combination with adriamycin in multidrug-resistant leukemia cells.

ATP-Binding Cassette, Sub-Family B, Member 1 ; analysis ; Apoptosis ; drug effects ; Arsenicals ; pharmacology ; Drug Resistance, Multiple ; Gene Expression ; Genes, MDR ; Humans ; Leukemia ; genetics ; metabolism ; Oxides ; pharmacology