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 screen plasma exosomal protein molecular markers in patients with spinal cord injury (SCI) by applying Label-Free quantification and bioinformatics analysis.Methods:Fifty plasma specimens from the First Affiliated Hospital of Nanjing Medical University (from January 2021 to June 2022) were collected from SCI patients and healthy people, respectively. Plasma exosomes were isolated using ultracentrifugation and identified by transmission electron microscopy, nanoparticle tracking analysis and western blot. Plasma exosomal differentially expressed proteins (DEPs) were analyzed using Label-Free quantitative proteomics, and DEPs were characterized, annotated, and enriched based on Gene Ontology (GO) and kyoto encyclopedia of genes and genomes (KEGG) databases. The screened DEPs were validated by western blot and enzyme linked immunosorbent assay (ELISA) using plasma exosomal specimens.Results:According to the spinal cord injury classification of the American Spinal Injury Association, 14 cases were grade A, 19 cases were grade B, 12 cases were grade C, and 5 cases were grade D. Plasma exosomes of SCI patients and control groups showed typical cup-like morphology, with diameters mainly ranging from 30-200 nm. A total of 493 exosomal proteins were identified by Label-Free quantification, and 126 proteins were screened for differential expression, of which 38 were up-regulated and 88 were down-regulated. GO annotation revealed that DEPs were mainly involved in functions such as protein activation cascade, complement activation and immune response. KEGG pathway analysis revealed that DEPs were involved in biological pathways such as complement and coagulation cascade reactions, proteasome and neurodegenerative disease pathways. Two candidate proteins, APOB and S100A9, were initially screened based on quantitative results from proteomics and bioinformatics analyses. Western blot results showed that the relative expression of S100A9 protein in plasma exosomes of 30 SCI patients (1.62±0.19) was elevated compared with that of 30 control groups (0.86±0.24), and the difference was statistically significant ( t=8.55, P<0.001), while the relative expression of APOB protein (1.06±0.13 and 1.02±0.23) were not statistically significant ( t=0.46, P=0.653). The results of ELISA analysis showed that the expression of S100A9 in plasma exosomes of patients with different degrees of SCI (grade A 197.7±11.7 pg/ml, grade B 151.7±15.2 pg/ml, grade C 136.3±14.7 pg/ml) had statistical significance ( F=69.94, P<0.001), the higher the severity of SCI, the higher the expression of S100A9 in plasma exosomes (A vs. B, q=13.11, P<0.001; A vs. C, q=15.66, P<0.001; B vs. C, q=4.19, P=0.005). Conclusion:S100A9 is a potentially valid plasma exosomal molecular marker for assessing the severity of SCI.

Objective To investigate the effect of anluohuaxianwan(ALHXW)using rat model of carbon tetrachloride(CC14)induced liver fibrosis on the expression of matrix metalloproteinases(MMPs)and tissue inhibitors of metalloproteinases(TIMPs).Methods Thirty-six male Wistar rats were randomly assigned into control,model and treatment groups.Rats in the model and treatment groups were injected intraperitoneally with 40% CC14(2 ml/kg),and the control group were given isotonic saline twice a week for six weeks.Meanwhile,the treatment group were gavaged with ALPIXW solution daily(concentration 0.15 g/ml,9.9 ml/kg)for 6 weeks,while the control and model groups were given isotonic saline once a day for 6 weeks.Serum levels of alanine aminotransferase(ALT)and aspartate aminotransferase(AST)were measured at the end of third and sixth week.At the end of six weeks,liver tissues were harvested for histopathological evaluation and the detection of mRNA and protein expression levels of MMP-2/13 and TIMP-1/2.According to different data,LSD method,parametric(oneway ANOVA)and non-parametric tests(Kruskal-Wallis H-test and Mann-Whitney U test)were used for statistical analysis.Results Compared with the model group,ALHXW markedly alleviated liver injury in the treatment group,and thereby improved the general state of rats,liver and spleen morphological characteristics,and ALT and AST levels.Histopathological examination demonstrated that the extent of liver fibrosis was improved(2.75±0.75 vs.3.55±0.69,P=0.015)in the treatment group as compared with the model group.The mRNA and protein expression levels of MMP-13 in the treatment group were significantly higher than that of the model group(mRNA:10.50±7.64 vs.4.40±2.97,P=0.029.Protein:1.15±0.09 vs.0.78±0.21,P=0.016),whereas the mRNA and protein expression levels of MMP-2,TIMP-1/2 in the treatment group were significantly lower than that of the model group(mRNA:4.55±3.29 vs.7.83±4.19,P=0.048;1.66±0.73 vs.3.69±2.78,P=0.023;2.25±1.16 vs.3.41±1.51,P=0.049;respectively.Protein:0.44±0.11 vs.0.65±0.05,P=0.03;0.69±0.06 vs.1.07±0.21,P=0.016;0,46±0.09 vs.0.81±0.13,P=0.003;respectively).Conclusion ALHXW exerts anti-liver fibrosis effects mainly by improving liver function,inhibiting the activation of hepatic stellate cells,enhancing the expression of MMP-13,and inhibiting the expression of MMP-2 and TIMP-1/2.

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.