To observe the D-dimer levels and the numbers of micro-embolic signals (MES) in atrial fibrillation patients with different thromboembolic risk scores. A total of 216 persistent atrial patients were classified according to their different scores with a range of 0 -6.They were also divided into two groups by ≥2 or ＜ 2 according to the CardiacFailure,Hypertension,Age,Diabetes,Stroke 2 (CHADS2) point system.D-dimer levels and the numbers of MES were detected in all patients.A rising trend of D-dimer level and the number of MES was observed with the increases of CHADS2 score. D-dimer level and the number of MES in group 0 or 1 score were significantly lower than those in other high score groups (P ＜ 0.05).And the number of MES in group 5 or 6 score was significantly higher than those in other low score groups (P ＜ 0.05).D-dimer level and the number of MES in the group of ≥ 2 score were significantly higher than those in group ＜ 2 score ( P ＜ 0.01 ).It suggests that D-dimer level and the nunber of MES may reflect the thromboembolic risks in atrial fibrillation patients.

Objectives To investigate preparation of gemcitabine albumin nanoparticles, and its property of slow-release, the cytotoxic effect on pancreatic cancer cells (PANC1) in vitro, for improving the effect of regional intra-arterial infusion chemotherapy in pancreatic cancer with new medicament in the future. Methods The gemcitabine albumin nanoparticles were prepared with bovine serum albumin and gemcitabine with the desolvation-crosslink method, the concentration of gemcitabine was detected by high performance liquid chromatography (HPLC). The cytotoxic effect on pancreatic cancer cells in vitro were detected with MTT colorimetric assay. Results The mean diameter of gemcitabine albumin nanoparticles was (156.2±2.2) nm, and Zeta potential was (-20.4±1.41)mV, drug loading was 10.8%, drug release time in virto was 3 hours respectively. Gemcitabine albumin nanoparticles (0.01～50 μg/ml) had a 31%～44% inhibitory rate on PANC1 cell, which was similar to the inhibitory rate of same concentration of gemcitabine (26%～47%). Conclusions The new preparation of gemcitabine albumin nanoparticles had obvious drug slow-release effect, which may help improve the effect of regional intra-arterial infusion chemotherapy for pancreatic cancer.

Objective:To investigate the influence and mechanism of stromal interaction molecule 1 (STIM1) in microglia/macrophages M1 activation after cerebral ischemia-reperfusion injury.Methods:(1) Animal experiment: 20 male C57BL/6J mice were randomly divided into sham-operated (Sham) group, middle cerebral artery occlusion and reperfusion (MCAO/R) group, MCAO/R+si-Ctrl group, and MCAO/R+si-STIM1 group ( n=5); MCAO/R models were established in mice of the latter 3 groups; empty vector control virus and STIM1 gene knockout lentivirus were transfected into mice in the MCAO/R+si-Ctrl group and MCAO/R+si-STIM1 group. The transfection efficiency of STIM1 and the expression of microglia/macrophages M1 activation marker cluster of differentiation 86 (CD86) in each group were observed. (2) Cell experiment: primary microglia were divided into Ctrl group, oxygen-glucose deprivation/re-oxygenation (OGD/R) group, OGD/R+si-Ctrl group, OGD/R+si-STIM1 group, OGD/R+solvent group, and OGD/R+4-phenylbutyric acid (4-PBA) group; OGD/R models were established in the later 5 groups; empty vector control virus and STIM1 gene knockout lentivirus were transfected into mice in the OGD/R+si-Ctrl group and OGD/R+si-STIM1 group; cells in the OGD/R+4-PBA group were pre-treated with 1 mmol/L 4-PBA for 1 h at 24 h before OGD/R modelling to inhibit endoplasmic reticulum stress (ERS), and cells in the OGD/R+solvent group were pre-treated with 0.5% dimethyl sulfoxide (DMSO) for 1 h at the same time. Reverse transcription quantitative polymerase chain reaction (RT-qPCR), ELISA, Western blotting and other methods were used to detect the levels of CD86, tumour necrosis factor-α ( TNF-α) mRNA, interleukin (IL)-1β, and ERS-related proteins (transcription factor C/EBP homologous protein [CHOP], activated transcription factor 4 [ATF4]) in these cells. Results:(1) Animal experiment: the STIM1 expression in MCAO/R+si-STIM1 group was significantly lower than that in Sham group, MACO/R group and MCAO/R+si-Ctrl group ( P<0.05); as compared with that in the MACO/R group and MCAO/R+si-Ctrl group, the number of microglia/macrophages co-expressing CD86 and Iba-1 around the ischemic foci of mice in the MCAO/R+si-STIM1 group was significantly decreased ( P<0.05). (2) Cell experiment: as compared with those in the OGD/R group and OGD/R+si-Ctrl group, the expression levels of STIM1, CD86, and TNF-α mRNA, and supernatant IL-1β content in the OGD/R+si-STIM1 group were significantly decreased ( P<0.05); as compared with those in the OGD/R group and OGD/R+si-CTRL group, the ATF4 and CHOP expression levels in OGD/R+si-STIM1 group were significantly decreased ( P<0.05); as compared with those in the OGD/R group and OGD/R+solvent group, the CD86 level, TNF-α mRNA expression level and IL-1β content in the OGD/R+4-PBA group were significantly decreased ( P<0.05). Conclusion:STIM1 affects microglia/macrophages M1 activation after ischemia-reperfusion injury by regulating ERS level.