Objective To investigate the changes in serum levels of nitric oxide ( NO) and endothelin ( ET) in type 2 diabetes patients with vascular complications, and to analyze the relationship between these levels and risk factors.Method We selected 98 cases of type 2 diabetes patients.Based on the grouping criteria, the patients were divided into diabetic patients with vascular complications ( group A,49 cases) and those without ( group B,49 cases) .In addition, 44 age-and body mass index-matched healthy cases were selected for control(group C).Height, weight, blood pressure, duration of diabetes, fasting blood glucose, hemoglobin A1c ( HbA1c), blood lipids, and serum levels of NO and ET-1 of all the patients were recorded.Results The NO levels of the two groups with diabetes mellitus were significantly lower than in group C[(43.87 ±12.05)and (53.29 ±11.75)μmol/L versus (66.08 ±16.48)μmol/L, P<0.01], while the ET-1 levels of the two groups with diabetes mellitus were significantly higher [(100.25 ±20.34) and (77.55 ±14.84) versus (53.62 ±8.40)ng/L, P<0.01] than those of the group C.The NO levels of group A were significantly lower than in group B [(43.87 ±12.05) versus (53.29 ±11.75)μmol/L, P<0.01].Moreover, the ET-1 levels of the group A were significantly higher than in group B [(100.25 ±20.34) versus (77.55 ±14.84)ng/L, P<0.01].Between the two diabetic groups, group A showed significantly higher systolic blood pressure(SBP), diastolic blood pressure(DBP), HbA1c, and course than group B (P<0.01).Correlation analysis showed a negative correlation between SBP, DBP, fasting blood glucose, HbA1c, and NO a positive correlation between high-density lipoprotein cholesterol ( HDL-C ) and NO, a negative correlation between HDL-C and ET-1, and a positive correlation between SBP,LDL-C, uric acid, fasting blood glucose, HbA1c, and ET-1.Conclusion The serum levels of NO and ET-1 in diabetic patients are evidently abnormal.Vascular endothelium injury will become more serious in patients with complications.Therefore, the serum levels of NO and ET-1 in diabetic patients are correlated with control of blood glucose, blood pressure, and blood lipid levels.

Objective To investigate the feasibility of VTQ value of spleen in noninvasive assessment of staging of liver fibrosis in patients with hepatitis B.Methods VTQ values of spleen were measured in 56 patients with hepatitis B by using ARFI technique and liver biopsy was performed.The patients were then grouped according to the stages of liver fibrosis stage.The results were analyzed by the intergroup comparison,Pearson Correlation analysis,and receiver operating characteristic curve (ROC curve).Results There was positive association of the VTQ value with the stages of liver fibrosis,whose correlation coefficient was 0.83 (P ＜ 0.05);There was no significant difference between the spleen VTQ value and the liver fibrosis S1 and SO (P ＞ 0.05),whereas there were significant differences among other groups (P ＜ 0.05).The area under the ROC curve was 0.95,the cut-off value was 2.79m/s,and the specificity and sensitivity were 81.8％ and 91.7％ respectively.Conclusions The VTQ value measured by ARFI technique has a better value in noninvasive diagnosis of stages of hepatitis B liver fibrosis.

Since Hosobuchi first found that spinal cord stimulation had the effect of significantly increasing cerebral blood flow (CBF) more than two decades ago, spinal cord stimulation had attracted wide attention in the field of treating cerebral ischemia. A large number of animal and clinical studies have been performed in this field, which make it another research focus following thrombolysis and interventional therapy. This article reviews the research history, mechanisms, and current status of clinical applications of spinal cord stimulation in cerebral ischemia protection.

Aim To investigate the effects of Rehmannia glutinosa oligosaccharides(ROS)on the damage induced by glutamate in hippocampal neurons.Methods The neurons isolated from hippocampus in new born SD rats were cultured for 7~9 days,which were specifically stained with NSE and then randomly divided into four groups:(Ⅰ)Normal cultures(control);(Ⅱ)ROS control cultures;(Ⅲ)Glutamate-exposed control cultures;(Ⅳ)Glutamate-exposed cultures pretreated with ROS.The neurons morphology was observed under inverted microscope;cell viability was assayed by MTT staining;LDH release was detected with chromatometry and flow cytometric analysis for identification and quantification of cell apoptosis.Results Compared with normal group,after exposure of glutamate for 24 h,the viability of neurons was decreased,LDH release and cell apoptosis were increased(P

Objective:To present evidence for the pathogenetic role of allergic factor,histamine,in type I allergy for induction of liver damage.Methods:Three groups of rabbits were fed normally and injected (iv) daily with 0, 0.04 or 0.08 ?g/kg phosphohistamine, respectively, for days. The serum level of ALT and AST in each group rabbits was assayed dynamically during the treatment. After treatment for days, the tested rabbits were sacrificed for pathological examination of the liver tissues.Results:The serum level of both ALT and AST in rabbits treated with phosphohistamine increased significantly during the tested periods, compared to that of the control group. However, both ALT and AST levels showed no significant difference between 0.04 ?g/kg and 0.08 ?g/kg groups. Liver microscopic examination, pathological damage could be observed in the tested groups in a time-and dose-dependent manner under microscopic examination. No evident pathological change appeared in the control group.Conclusion:Liver damage could be induced by histamine dosage-and time-dependently. This pathological action of histamine, a type I allergic factor, presents further evidence for a direct role of type I allergy in the pathogenesis hepatic injury.

ObjectiveTo investigate the correlation of quality of life (QOL) with aspartate aminotransferase-to-platelet ratio index (APRI), liver stiffness measurement (LSM), and histopathology after entecavir antiviral therapy for patients with chronic hepatitis B liver fibrosis. MethodsA total of 95 patients who were diagnosed with chronic hepatitis B and liver fibrosis in The Affiliated Hospital of Yanbian University from October 2013 to March 2015 were enrolled, and all patients underwent entecavir antiviral therapy. Before treatment and at weeks 26, 52, and 78 of treatment, SF-36 scale was used to assess QOL, transient elastography was used to measure LSM, and serum APRI was measured. Among these patients, 31 underwent liver biopsy before treatment and at week 78 of treatment to observe the degree of inflammation and fibrosis, and QOL, APRI, LSM, and histopathology were analyzed before and after antiviral therapy. The Kruskal-Wallis H test was used for comparison of non-normally distributed continuous data at different time points, and a Spearman correlation analysis was performed. ResultsThere was a tendency of increase in QOL after antiviral treatment, and there were significant differences in general health, role-physical, role-motional, bodily pain, social functioning, and vitality at different time points (H=25.084, 8.699, 12.293, 22.874, 12.079, and 10.403, all P＜0.05). There was a tendency of reduction in APRI, with a significant change after treatment (H=60.030, P＜0.01), and there was also a significant reduction in LSM after treatment (H=35.744, P＜0.01). APRI and LSM were negatively correlated with QOL (all P＜0.05). Among the patients who underwent liver biopsy, 22 achieved the improvement in histological inflammation after antiviral therapy, 15 achieved the improvement in fibrosis, 14 achieved the improvement in both inflammation and QOL, and 8 achieved the improvement in both fibrosis and QOL. ConclusionEntecavir antiviral therapy can improve the QOL of patients with chronic hepatitis B liver fibrosis, and reductions in APRI and LSM can predict the improvement in QOL in patients with chronic hepatitis B liver fibrosis. Improvement in histological inflammation and fibrosis have a certain effect on the improvement in QOL in patients with chronic hepatitis B liver fibrosis.

This study is to investigate the treatment of Jin Chai antiviral capsule for influenza virus FM1/47 (H1N1) infection. The model of pneumonia was established by dropping influenza virus into the nose of normal mice, real-time PCR and Western blot technique were used to detect the virus load and the interferoninducible transmembrane protein3 (IFITM3) in lung of mice at the 1st day, 3rd day, 5th day and 7th day after affected. The results showed that Jin Chai antiviral capsule in large, middle, small dose groups can decrease virus load significantly at each time point, after being affected (P<0.05, P<0.01), Jin Chai antiviral capsule can increase the interferoninducible transmembrane protein3 in lung of mice, large dose groups are significantly higher in expression of IFITM3 compared with model group at each time point (P<0.05, P<0.01). Middle dose groups are significantly higher in expression of IFITM3 compared with model group at the 3th day and the 5th day (P<0.05), small dose groups are significantly higher in expression of IFITM3 compared with model group at the 3th day (P<0.05). It can be concluded that Jin Chai antiviral capsule exerts antiviral effects against influenzavirus by raised expression of IFITM3.

Objective:To investigate cutaneous sequelae of neonatal lupus erythematosus (NLE), and to analyze possible related factors.Methods:A total of 13 NLE patients with long-term follow-up were collected from Department of Dermatology, Children′s Hospital Affiliated to Capital Institute of Pediatrics from 2016 to 2020, and clinical manifestations and cutaneous sequelae of these patients, as well as clinical manifestations of their mothers, were retrospectively analyzed.Results:Skin lesions occurred in the 13 patients within 120 days after birth, with an average onset time of 15 days, and the follow-up duration ranged from 15 to 43 months. Skin lesions mainly manifested as annular erythema, maculopapules and scales, and subsided within 2 - 18 months (average, 7.4 months). Pigmentation abnormalities occurred in 6 cases after subsidence of skin lesions, including 3 with both hypopigmentation and hyperpigmentation, 2 with hypopigmentation alone, and 1 with hyperpigmentation alone. One patient with hypopigmentation achieved repigmentation after 18 months of follow-up, and no telangiectasia, atrophy or scars were observed. No abnormalities were observed in the mothers of 8 patients before pregnancy, and the mothers of 4 patients were positive for antinuclear antibody, anti-SSA/Ro antibody and anti-SSB/La antibody.Conclusions:Cutaneous sequelae can occur after skin involvement of NLE, and mainly includes pigmentation abnormalities, most of which can not subside after a long time. Attention should be paid to potential immune system abnormalities in the mothers of patients with NLE.

Objective The potential mechanism of hepatotoxicity induced by rhubarb was preliminarily explored by network pharmacology and verified by cell experiments.Methods Based on network pharmacology,component collection and target prediction are carried out through multiple databases.PPI network construction,GO enrichment analysis and KEGG pathway analysis were combined with software to systematically predict the mechanism of hepatotoxicity induced by rhubarb.The pathway information predicted by network pharmacology was verified by primary hepatocyte experiments and Western blot experiments.Results The results of network pharmacology showed that RH was the main component of hepatotoxicity induced by rhubarb.Seventeen core targets of hepatotoxicity induced by rhubarb were obtained.KEGG results suggested that DNA damage and apoptosis were one of the key mechanisms of hepatotoxicity induced by rhubarb.The results of primary hepatocytes and Western blot showed that RH could inhibit the viability of primary hepatocytes in a time-dose dependent manner.ABT and SFP can significantly reduce the toxicity of RH on primary liver cells in mice,and RFP can increase the toxicity of RH to mouse primary liver cells.Upregulation of γ-H2AX and PARP-1 protein in primary liver cells of mice after treatment with different concentrations of RH.Conclusion RH in rhubarb can significantly inhibit the viability of mouse primary hepatocytes,and its toxicity to mouse primary hepatocytes is mainly caused by the metabolic activation of RH by CYP 2C9.RH can activate PARP-1 protein,phosphorylate H2AX,induce DNA damage and apoptosis in mouse primary hepatocytes.

Objective To investigate the effect of carrimycin on the biological function of pancreatic cancer cells. Methods Pancreatic cancer cell lines MIA PaCa-2, BxPC-3, Panc-1, and PATU 8988 were treated with carrimycin at concentrations of 0 (control group), 2, 4, 8, and 16 μmol/L for 24, 48, and 72 hours. MTT assay was used to measure cell viability; EdU cell proliferation assay was used to observe the effect of carrimycin on DNA replication of pancreatic cancer cells; colony formation assay was used to observe the effect of carrimycin on the proliferation of pancreatic cancer cells; flow cytometry was used to analyze the effect of carrimycin on the cell cycle of pancreatic cancer cells; wound healing assay was used to analyze the effect of carrimycin on the migration of pancreatic cancer cells; Western blot was used to measure the expression levels of the markers such as epithelial-mesenchymal transition (EMT) and cell cycle-dependent protein kinase inhibitor 1A (P21); immunofluorescence assay were used to measure the expression levels of EMT-related markers. An analysis of variance was used for comparison between multiple groups, and the least significant difference t -test was used for further comparison between two groups. Results Compared with the control group, carrimycin significantly inhibited the proliferative activity of MIA PaCa-2, BxPC-3, Panc-1, and PATU 8988 cells in a concentration- and time-dependent manner (all P < 0.01); carrimycin at concentrations of 4, 8, and 16 μmol/L significantly reduced DNA replication in MIA PaCa-2 cells ( t =2.378, 4.984, and 18.970, all P < 0.05) and BxPC-3 cells ( t =4.879, 6.089, and 9.521, all P < 0.01); after treatment with carrimycin at concentrations of 4, 8, and 16 μmol/L, colony formation ability significantly decreased with the increase in drug concentration in MIA PaCa-2 cells ( t =5.889, 11.240, and 15.840, all P < 0.001) and BxPC-3 cells ( t =6.717, 15.800, and 18.850, all P < 0.001). After treatment with carrimycin at concentrations of 4, 8, and 16 μmol/L, there was a significant increase in the proportion of cells in G1 phase in MIA PaCa-2 cells ( t =9.071, 12.280, and 19.360, all P < 0.0001) and BxPC-3 cells ( t =3.061, 4.962, and 8.868, all P < 0.05), and there was a significant reduction in the proportion of cells in S phase in MIA PaCa-2 cells ( t =2.316, 4.165, and 5.562, all P < 0.05) and BxPC-3 cells ( t =2.424, 3.264, and 5.744, all P < 0.05). Western blot further demonstrated that compared with the control group, the expression level of the cell cycle-related protein P21 gradually increased with the increase in the concentration of carrimycin in MIA PaCa-2 cells ( t =5.437, 6.453, and 8.799, all P < 0.001) and BxPC-3 cells ( t =25.130, 44.750, and 52.960, all P < 0.000 1). Wound healing assay showed that after treatment for 12, 24, and 48 hours, carrimycin at concentrations of 0, 4, 8, and 16 μmol/L significantly reduced the lateral migration of MIA PaCa-2 cells (all P < 0.05) and BxPC-3 cells (all P < 0.05). Western blot showed that compared with the control group, carrimycin treatment at concentrations of 4, 8, and 16 μmol/L significantly upregulated the expression of the epithelial marker E-cadherin in MIA PaCa-2 cells ( t =2.388, 4.899, and 5.819, all P < 0.05) and BxPC-3 cells ( t =2.533, 5.836, and 6.774, all P < 0.05) and significantly downregulated the expression of the interstitial marker Snail in MIA PaCa-2 cells ( t =12.440, 14.830, and 16.800, all P < 0.000 1) and BxPC-3 cells ( t=5.039, 5.893, and 7.725, all P < 0.01), and it also significantly downregulated the expression of the interstitial marker Vimentin in MIA PaCa-2 cells ( t =3.105, 7.752, and 11.200, all P < 0.05) and BxPC-3 cells ( t =2.555, 4.883, and 9.153, all P < 0.05). Conclusion Carrimycin can effectively inhibit the proliferation, migration, and EMT process of pancreatic cancer cells, thereby exerting an antitumor biological activity.