The antibody against AT1-EC2 plays a role in some kinds of inflammatory vascular diseases including malignant hypertension, preeclampsia, and renal-allograft rejection, but the detailed mechanisms remain unclear. In order to investigate the changes of NADPH oxidase and reactive oxygen species in the aorta in a mouse model which can produce AT1-EC2 antibody by active immunization with AT1-EC2 peptide, 15 mice were divided into three groups: control group, AT1-EC2-immunized group, and AT1-EC2-immunized and valsartan-treated group. In AT1-EC2-immunized group and AT1-EC2-immunized and valsartan-treated group, the mice were immunized by 50 μg peptide subcutaneously at multiple points for 4 times: 0, 5, 10, and 15 days after the experiment. In AT1-EC2-immunized and valsartan-treated group, valsartan was given at a dose of 100 mg/kg every day for 20 days. After the experiment, the mice were sacrificed under anesthesia and the aortas were obtained and frozen in liquid nitrogen for the preparation of frozen section slides and other experiments. The titer of AT1-EC2 was assayed by using ELISA. The level of NOX1 mRNA in the aorta was determined by using RT-PCR. The expression of NOX1 was detected by using Western blotting. Confocal scanning microscopy was used to assay the α-actin and NOX1 expression in the aortic tissue. The O(2)∸ production was detected in situ after DHE staining. The mice produced high level antibody against AT1-EC2 in AT1-EC2-immunized group and AT1-EC2-immunized and valsartan-treated group, and the level of NOX1 mRNA in the aortic tissues was 1.6±0.4 times higher and the NOX1 protein expression was higher in AT1-EC2-immunized group than in control group. There were no significant differences in the level of NOX1 mRNA and protein expression between control group and AT1-EC2-immunized and valsartan-treated group. The expression and co-localization of α-actin and NOX1 in AT1-EC2-immunized group increased significantly as compared with those in control group, and the O(2)∸ production increased about 2.7 times as compared with control group. There were no significant differences between control group and AT1-EC2-immunized and valsartan-treated group. It is concluded that active immunization with AT1-EC2 can activate NOX1-ROS, and increase vascular inflammation, which can be inhibited by AT1 receptor blocker valsartan. This may partially explain the mechanism of the pathogenesis of inflammatory vascular diseases related to antibody against AT1-EC2.

Objective To explore the roles of autoantibodies against ?1 adrenoceptor(?1-receptor)and M2 cholinergic receptor(M2-receptor)in patients with chronic renal insufficiency.Methods The epitopes of the second extracellular loop of ?1 receptor and M2 receptor were synthesized and used respectively to detect the sera autoantibodies against ?1 receptor and M2 receptor by enzyme linked immunosorbent assay(ELISA) in 76 patients with chronic renal insufficiency,60 cases with hypertension and 40 healthy controls.Results In patients with chronic renal insufficiency,the positive rates of the autoantibodies against ?1-receptor and M2-receptor were 56.7% and 38.1% respectively,which were much higher than those of patients with hypertension(18.3% and 11.7%) and higher than those of healthy controls(17.5% and 15.0%)(all P

AIM: The autoantibodies against ?_1-adrenergic receptor that was found in patients with malignant hypertension, primary hypertension and refractory hypertension has the agonist activity liked the NE, and may play a role in hypertension. In this paper, the effects of this antibody on vascular smooth muscle cell (VSMC) proliferation and its mechanism were to be studied. METHODS: The cultured rat VSMC proliferation induced by the antibodies against ?_1- adrenergic receptor that was purified by the immune affinity chromatography, was measured by the BrdU cell proliferation assay and cell cycle distribution. The expression of c-jun and c-fos were determined by RT-PCR and Western blotting. RESULTS: Compared to the normal IgG, the antibodies against ?_1-adrenergic receptor promoted the VSMC proliferation and increased the mRNA and protein expression of the c-jun significantly. The role was similar to the norepinephrine, and all was blocked by prazosin, while the mRNA and protein expression of c-fos were not affected by the antibodies. CONCLUSION: The antibodies against ?_1-adrenergic receptor promote the rat VSMC proliferation, and increase the expression of c-jun, which maybe play a role in the vascular remodeling in hypertension.

Objective To explore the role of the autoantibodies against ?_1-adrenergic receptor(?_1-receptor)in the development of hypertension with renal failure.Methods The epitopes of the second extracellular loop of ?_1-receptor were synthesized and used respectively to screen sera autoantibodies from patients with hypertension with renal failure(61 cases),hypertension without renal failure(58 cases) and healthy blood donors(40 cases,control) by ELISA method.Results The positive rates of the autoantibodies ?_1-receptor(69%,42/61) in patients with hypertension with renal failure were higher than those of patients with hypertension without renal failure(19%,11/58) respectively(P

Objective To explore the role of the autoantibodies against ?_1 and ?_1-adrenergic receptor(?_1-receptor)in the development of hypertension with renal failure.Methods The epitopes of the second extracellular loop of ?_1-receptor(197-222) and ?_1-receptor(192-218) were synthesized and used respectively to screen sera autoantibodies in patients with hypertension and renal failure(n=61),hypertension without renal failure(n=60) and healthy blood donors(n=40,control) by ELISA.Results The positive rates of the autoantibodies against ?_1-receptor(62.3%)and ?_1 receptor(50.8%) in patients with hypertension with renal failure were higher than those of patients with hypertension without renal failure(13.3% and10.0%)(P

BACKGROUND: Pedicle screw fixation is a common repair method for thoracolumbar fractures. Of them, pedicle screw placement into the injured vertebra is an important method. However, the long-term effects and the related biomechanical properties deserve further analysis. OBJECTIVE: To analyze the long-term effect and biomechanical characteristics of the internal fixation of thoracolumbar fractures by pedicle screw implantation. METHODS: A retrospective analysis was performed in 126 cases of thoracolumbar fractures. The patients were treated with pedicle screw implantation and the treatment was fol owed up regularly. Ten specimens of fresh calf chest and lumbar spines were obtained. Five specimens served as an experimental group to prepare models of anterior middle column fractures, and these specimens received pedicle screw fixation into the injured vertebra. The other five specimens served as the control group, and did not receive any treatment. In the two groups, along the sagittal axis, axial compression displacement, anterior flexion displacement, posterior extension displacement, torsion angle and pul -out strength were measured and recorded. RESULTS AND CONCLUSION: (1) Clinical trial results: 126 patients were fol owed up for 10-36 months. Compared with pre-treatment, compression ratio of the injured vertebra, the height of intervertebral space, vertebral slip distance, visual analogue score and Cobb angle were significantly improved at 1 month after treatment and during final fol ow-up (al P < 0.05). No significant difference in above indexed was detected between 1 month and final fol ow-up (al P > 0.05). At the end of fol ow-up, Frankel spinal cord injury grade was significantly improved (Z=-4.127, P < 0.05). After operation, three patients suffered from pulmonary infection, four patients affected urinary tract infection, and one patient experienced delayed wound healing. (2) Biomechanical results: axial compression displacement, anterior flexion displacement, posterior extension displacement, torsion angle and pul -out strength were smal er in the experimental group than in the control group (al P > 0.05). (3) Above findings showed that pedicle screw fixation into the injured vertebra for thoracolumbar fractures obtained good long-term effects, and had good biomechanical properties.

Objective: To understand the association between non suicidal self injury and self control among rural junior high school students in Guizhou Province, and to provide reference for the development of prevention and control measures. Methods: Using a multistage stratified random cluster sampling method, a questionnaire survey was administered to 4 452 junior high school students in 30 rural schools in Guizhou Province from November to December 2021 to investigate non suicidal self injury and self control using the Non suicidal Self Injury Scale and the Self Control Scale. Results: A total of 986 (22.2%) students had occasional non suicidal self injurious behaviors, 593 (13.3%) students reported frequent non suicidal self injury, and the occurrence of non suicidal self injury among junior high school students varied significantly by gender, grade, only child, residence, left behind experiences, academic performance, academic pressure, parent child relationship, peer relationship, teacher student relationship, and exposure to domestic violence ( χ 2=6.97-168.68, P <0.05); the average score of self control among junior high school students in rural Guizhou Province was 48.0 (39.0, 57.0), and the differences in self control scores, impulse control, healthy habits, resist temptation, focus on work, and moderate entertainment were of statistical significance among students with varied frequency of self injurious behavior ( Z=612.08, 464.64, 193.10, 228.86, 194.04 , 542.20, P <0.05); high self control score was associated with more non suicidal self injurious behavior ( OR=1.06, 95%CI=1.05-1.07, P <0.05). Conclusion The prevalence of non suicidal self injury is high among rural junior high school students in Guizhou province, and self control shows a predictive effect on non suicidal self injurious behavior.Schools, families and relevant government departments should pay full attention to it and formulate targeted prevention and control measures.

The antibody against AT1-EC2 plays a role in some kinds of inflammatory vascular diseases including malignant hypertension, preeclampsia, and renal-allograft rejection, but the detailed mechanisms remain unclear. In order to investigate the changes of NADPH oxidase and reactive oxygen species in the aorta in a mouse model which can produce AT1-EC2 antibody by active immunization with AT1-EC2 peptide, 15 mice were divided into three groups: control group, AT1-EC2-immunized group, and AT1-EC2-immunized and valsartan-treated group. In AT1-EC2-immunized group and AT1-EC2-immunized and valsartan-treated group, the mice were immunized by 50 μg peptide subcutaneously at multiple points for 4 times: 0, 5, 10, and 15 days after the experiment. In AT1-EC2-immunized and valsartan-treated group, valsartan was given at a dose of 100 mg/kg every day for 20 days. After the experiment, the mice were sacrificed under anesthesia and the aortas were obtained and frozen in liquid nitrogen for the preparation of frozen section slides and other experiments. The titer of AT1-EC2 was assayed by using ELISA. The level of NOX1 mRNA in the aorta was determined by using RT-PCR. The expression of NOX1 was detected by using Western blotting. Confocal scanning microscopy was used to assay the α-actin and NOX1 expression in the aortic tissue. The O(2)∸ production was detected in situ after DHE staining. The mice produced high level antibody against AT1-EC2 in AT1-EC2-immunized group and AT1-EC2-immunized and valsartan-treated group, and the level of NOX1 mRNA in the aortic tissues was 1.6±0.4 times higher and the NOX1 protein expression was higher in AT1-EC2-immunized group than in control group. There were no significant differences in the level of NOX1 mRNA and protein expression between control group and AT1-EC2-immunized and valsartan-treated group. The expression and co-localization of α-actin and NOX1 in AT1-EC2-immunized group increased significantly as compared with those in control group, and the O(2)∸ production increased about 2.7 times as compared with control group. There were no significant differences between control group and AT1-EC2-immunized and valsartan-treated group. It is concluded that active immunization with AT1-EC2 can activate NOX1-ROS, and increase vascular inflammation, which can be inhibited by AT1 receptor blocker valsartan. This may partially explain the mechanism of the pathogenesis of inflammatory vascular diseases related to antibody against AT1-EC2.
Animals ; Aorta ; metabolism ; Disease Models, Animal ; Mice ; Mice, Inbred C57BL ; NADPH Oxidases ; genetics ; Reactive Oxygen Species ; metabolism ; Vaccination ; methods

The thioredoxin system is composed of thioredoxin (Trx), thioredoxin reductase (TR) and reduced nicotinamide adenine dinucleotide phosphate. Trx is an important antioxidant molecule that can resist cell death caused by various stresses and plays a prominent role in redox reactions. TR is a protein containing selenium (selenocysteine), mainly in three forms, i.e. TR1, TR2 and TR3. TR1 mainly distributed in the cytoplasm, TR2 mainly distributed in the mitochondria, and TR3 mainly distributed in the testes. TR can regulate cell growth and apoptosis. After the cell becomes cancerous, the expression of TR increases to promote cell growth and metastasis. Trx system is closely related to neurodegenerative diseases, parasitic infections, acquired immunodeficiency syndrome, rheumatoid arthritis, hypertension, myocarditis and so on. The Trx system can remove the reactive oxygen species (ROS) in the body, keep the inside and outside of the cell in a balanced state, and it interacts with the thioredoxin interacting protein (TXNIP), which plays an important role in the regulation of glucose metabolism and tumor treatment. The Trx system is an important target for drug treatment of many diseases. In this paper, the research progress of the thioredoxin system was reviewed.

Objective: To establish comprehensive laboratory reference intervals for Chinese children. Methods: This was a cross-sectional multicenter study. From June 2013 to December 2014, eligible healthy children aged from 6-month to 17-year were enrolled from 20 medical centers with informed consent. They were assessed by physical examination, questionnaire survey and abdominal ultrasound for eligibility. Fasting blood samples were collected and delivered to central laboratory. Measurements of 15 clinical laboratory parameters were performed, including estradiol (E2), testosterone(T), luteinizing hormone(LH), follicle-stimulating hormone(FSH), alanine transaminase(ALT), serum creatinine(Scr), cystatin C, immunoglobulin A(IgA), immunoglobulin G(IgG), immunoglobulin M(IgM), complement (C3, C4), alkaline phosphatase(ALP), uric acid(UA) and creatine kinase(CK). Reference intervals were established according to central 95% confidence intervals for reference population, stratified by age and sex. Results: In total, 2 259 children were enrolled. Finally, 1 648 children were eligible for this study, including 830 boys and 818 girls, at a mean age of 7.4 years. Age- and sex- specific reference intervals have been established for the parameters. Reference intervals of sex hormones increased gradually with age. Concentrations of ALT, cystatin C, ALP and CK were higher in children under 2 years old. Serum levels of sex hormones, creatinine, immunoglobin, CK, ALP and urea increased rapidly in adolescence, with significant sex difference. In addition, reference intervals were variable depending on assay methods. Concentrations of ALT detected by reagents with pyridoxal 5'-phosphate(PLP) were higher than those detected by reagents without PLP. Compared with enzymatic method, Jaffe assay always got higher results of serum creatinine, especially in children younger than 9 years old. Conclusion This study established age- and sex- specific reference intervals, for 15 clinical laboratory parameters based on defined healthy children.