Implantable Neurostimulators ; Micro-Electrical-Mechanical Systems ; Microelectrodes

Objective: To explore whether resveratrol can reduce intestinal damage in hemorrhagic shock rats and the underlying mechanism. Methods: A total of 24 Sprague-Dawley rats of speciif c pathogen free (SPF) were randomly divided into a control group(n=8), a resveratrol group (SR group,n=8) and a vehicle group (SS group,n=8). hT e mean arterial pressure was recorded. Two hours atf er hemorrhagic shock, 15 mg/kg resveratrol or 0.3 mL equal volume of vehicle and autologous blood were given, respectively. The intestinalspecimens were collected for hematoxylin-eosin (HE) staining and calculated the pathological score. The superoxide dismutase 2 (SOD2) and cytochrome C (Cyt C) protein expression was examined by immunohistochemistry and/or Western blot. ATP level, activities of glutathione peroxidase (GXH-px), catalase (CAT) and SOD were also detected. Results: Two hours atfer autologous blood transfusion, the mean arterial pressure in the SR group was signiifcantly higher than that in the SS group (P<0.01). Compared with the SS group, the pathological injury was signiifcantly alleviated and pathological scores were dramatically reduced in the SR group (P<0.05). hTe activities of GXH-px, CAT, SOD and the ATP levels in the SR group were signiifcantly higher than those in the SS group (allP<0.01). Compared with the SS group, the SOD2 expression was significantly higher while the Cyt C expression was dramatically lower in the SR group (both P<0.01). Conclusion: Resveratrol could alleviate the intestinal injury in hemorrhagic shock rats, which might be associated with its effects on reduction of oxidative stress and protection of mitochondria.

Objective To study the significance of the sample S/Co ratio when using a domestic reagent for anti-hepatitis C virus(HCV)antibody detection and to explore the procedure and standard of anti-HCV antibody diagnosis by using this domestic reagent.Methods Anti-HCV antibody was detected in 295 000 blood donors by a domestic anti-HCV reagent with enzyme-linked immunosorbent assay(ELISA)method and the reactive samples were tested again by ortho anti-HCV antibody reagent.The samples which anti-HCV antibodies were determined as positive by ortho anti-HCV rea- gent were examined by recombinant immunoblot assay(RIBA)reagent and 106 samples of them were also tested for HCV RNA.Results Six hundred and eighty-one samples were reactive in 295 000 samples screened by the domestic ELISA reagent,the reactive ratio was 0.23 %.Among the reactive samples screened by the domestic ELISA reagent,367 samples were determined as positive by ortho anti-HCV reagent while 66.2% of them showed a S/Co ratio≥3.8.The consistency rate between positive results determined by the domestic reagent and RIBA reagent respectively was 53.8%.For the samples showing S/Co ratio≥3.8 by ortho anti-HCV reagent,94.2% had a S/Co ratio≥8.0 when using the domestic ELISA reagent,while the percentage of samples showing S/Co ratio

Objective:To investigate the clinical characteristics and prognosis of patients with RUNX1-RUNX1T1 fusion gene-positive acute myeloid leukemia (AML) with ASXL2 gene mutation.Methods:The clinical data of 145 newly diagnosed RUNX1-RUNX1T1 fusion gene-positive AML patients treated at the Second Hospital Center of Shanxi Medical University from October 2010 to March 2021 were retrospectively analyzed. Sanger sequencing was used to detect the gene mutation. According to the presence or absence of ASXL2 gene mutation, the patients were divided into mutation group and non-mutation group. The clinical characteristics, gene mutations and prognosis were compared among the two groups.Results:Among 145 AML patients with positive RUNX1-RUNX1T1 fusion gene, we identified recurrent mutations of c-kit, ASXL2, N/KRAS, FLT3, ASXL1, TET2, NPM1 and DNMT3A genes, with mutation rates of 40.7% (59/145), 20.7% (30/145), 15.9% (23/145), 12.4% (18/145), 11.7% (17/145), 11.0% (16/145), 5.5% (8/145), and 2.1% (3/145), respectively. A total of 18 mutation sites were detected in 30 patients with ASXL2 gene mutations including 5 point mutations and 13 frameshift mutations, which mainly occured in the exons 12 and 13. Lactate dehydrogenase (LDH) at initial diagnosis of 30 AML patients with ASXL2 mutation was lower than that of those with ASXL2 non-mutation ( Z = 2.34, P = 0.020), while prothrombin time (PT) of AML patients with ASXL2 mutation was longer than that of those with ASXL2 non-mutation ( Z = 1.99, P = 0.047). A total of 21 (21/30, 70%) patients simultaneously had other gene mutations. The incidence of RAS mutations in patients with ASXL2 mutation was higher than that those with ASXL2 non-mutation, and the difference was statistically significant [30.0% (9/30) vs. 12.1% (14/115), χ2 = 4.41, P = 0.036]. There were no statistically significant differences in complete remission rate [86.7% (26/30) vs. 74.8% (86/115)] and recurrence rate [43.3% (13/30) vs.31.3% (36/115)] of patients with ASXL2 mutation and ASXL2 non-mutation ( χ2 = 0.39, P = 0.534; χ2 = 0.54, P = 0.432). The median overall survival (OS) time was 26 months (1-135 months) and 30 months (1-120 months), respectively in patients with ASXL2 mutation and ASXL2 non-mutation; the median disease-free survival (DFS) time was 14 months (0-60 months) and 13 months (0-94 months), respectively in patients with ASXL2 mutation and ASXL2 non-mutation; and the differences in OS and DFS were not statistically significant of both groups ( χ2 = 0.05, P = 0.822; χ2 = 0.34, P = 0.562). Compared with ASXL1 mutant patients, cases with ASXL2 mutation had higher OS and DFS rates, and the differences were statistically significant ( P = 0.003, P = 0.007). The differences in OS and DFS between patients with ASXL2 mutations and those with positive mutations of c-kit, RAS, FLT3, TET2, NPM1, DNMT3A were not statistically significant (all P > 0.05). Conclusions:RUNX1-RUNX1T1 positive AML patients with ASXL2 mutation tend to have low LDH and high PT, and often coexist with RAS mutations, and their prognosis is better than that in patients with ASXL1 positive mutation.