摘要:目的:动态观察大鼠脑出血后血肿周围组织补体激活与细胞凋亡的规律。方法:用胶原酶注入到大鼠尾状核的方法制作脑出血模型。将大鼠分为脑出血、假手术组、正常组3组。采用苏木素伊红(HE) 染色、免疫组织化学染色及原位末端脱氧核苷酸转移酶介导的dUTP 缺口末端标记法(TUNEL)分别观察各组在脑出血后第6 h、12 h、24 h、48 h、72 h、5 d、7 d时血肿周围补体C3、促凋亡基因(Bax)、抑凋亡基因(Bclxl)及TUNEL的表达。结果补体C3的表达峰值在24~48 h;TUNEL、Bax蛋白表达术后12h增加,48~72 h达高峰,而Bclxl蛋白表达高峰在48h。结论:大鼠脑出血后血肿周围组织补体C3的表达增加与细胞凋亡的演变趋势一致,C3与凋亡有相关。Abstract: Objective: To study the complement activation and apoptosis regular genes changes in the tissues of the perihematoma of intracerebral hemorrhage (ICH) in rats. Methods: Intracerebral hemorrhage was induced in rats by injection of bacterial collagenase into the caudate nucleus. Histopathological changes were studied in 6 h,12 h, 24 h, 2 d, 3 d, 5 d, 7 d after the injection. The immunohistochemistry and TUNEL analysis were performed. The expression of complement factor C3, the TUNELpositive cells, the proapoptotic gene expression (Bax) and the antiapoptotic gene (Bclxl) were examined. Results: The expression of C3 increased to its maximum between 2448 h. The TUNELpositive cells and Bax protein expression increased gradually and reached the peak level between 4872 h. The Bclxl protein reached the peak level at 48 h. The correlation analysis showed that the quantity of C3 was positively related to that of the TUNELpositive cells, but the bax protein was not related to Bclxl protein. Conclusion: The expression of complement factor C3 may contributes to the nerve injury after cerebral hemorrhage and relate to the apotosis in the tissues surrounding the hametoma in rats.
Thirty patients with obstructive jaundice were investigated for serum complement-3 (C3) and plasma fibronectin (FN).The levels of C3 and FN of the juandiced patients were higher than that of thirty patients without obstructive jaundice (Ｐ＜0.01). As compared to pre-operation, the level of C3 of the jaundiced patients decreased obviously within two weeks after operation(Ｐ＜0.01), and recovered in the third week after operation. The level of FN of the juandice patients decreased evidently within one week(Ｐ＜0.01), and recovered in the second week after operation. However, the levels of C3 and FN of the patients without obstructive jaundice changed slightly after operation (Ｐ＜0.05). The high levels of C3 and FN of jaundiced patients may be relative to the latent infection. Consumption and immune imparing may be the reasons of C3 and FN to decrease.
ObjectiveTo investigate the correlation of X-ray repair cross-complementing gene 1 (XRCC1-Arg399Gln, Arg280His, and Arg194Trp) polymorphisms and susceptibility to gastric cancer. MethodsOne hundred and twenty patients with gastric cancer were included in study group, 120 healthy volunteers were included in control group. The DNA was extracted from peripheral blood. Arg399Gln, Arg280His, and Arg194Trp gene polymorphisms were detected and analyzed using polymerase chain reaction-restriction fragment length polymorphism technique, and the susceptibility between different genotypes and gastric cancer was compared in two groups. ResultsThe age, gender, smoking, drinking, diet, and other common characteristics of exposure factors had no significant differences in two groups (P > 0.05). The mutation locus genotype frequencies of Arg399Gln and Arg280His had no significant differences between two groups (P > 0.05). However, the mutation locus genotype frequencies of Arg/Trp, Trp/Trp, and Arg/Trp+Trp/Trp were higher and the mutation locus genotype frequency of Arg/Arg was lower in the study group as compared with the control group (P < 0.05). ConclusionThe preliminary results from this study shows that XRCC1 Arg399Gln and Arg280His polymorphisms are not correlated with susceptibility to gastric cancer; However, Arg194Trp polymorphism is correlated with susceptibility to gastric cancer.
ObjectiveTo observe the effect of complement receptor 1 (CR1) on barrier of cultured human retinal epithelial cells (hRPE) under complement-activated oxidative stress. MethodsThe third to fifth passage of hRPE cultured on Transwell insert were used to establish a stable hRPE monolayer barrier. The hRPE monolayer barrier was exposed to 500 μmol/L ten-butyl hydroperoxide and 10% normal human serum to establish the hRPE monolayer barrier model of complement-activated oxidative stress in vitro. hRPE monolayer barriers under complement-activated oxidative stress were divided into two groups including model group and CR1 treatment (1 μg/ml) group. Model group and CR1 treatment group were treated with 1 μl phosphate buffer solution (PBS) or CR1 for 4 hours. Normal hRPE monolayer barrier were used as control in transepithelial resistance (TER) measurement experiment. TER was measured to evaluate the barrier function of hRPE. The hRPE-secreted vascular endothelial growth factor (VEGF) and chemokine (C-C Motif) Ligand 2 (CCL2), together with complement bioactive fragments (C3a, C5a) and membrane-attack complex (MAC) in the supernatant were detected by enzyme-linked immune sorbent assay. ResultsStable hRPE monolayer barrier was established 3 weeks after hRPE seeded on Transwell insert. Complement-activated oxidative stress resulted in a sharp decrease of TER to 54.51% compared with normal hRPE barrier. CR1 treatment could significantly improve TER of barrier under complement-activated oxidative stress to 63.48% compared with normal hRPE barrier(t=21.60, P < 0.05). Compared with model group, CR1 treatment could significantly decrease the concentration of VEGF and CCL2 by 11.48% and 23.47% secreted by hRPE under complement-activated oxidative stress (t=3.26, 2.43; P < 0.05). Compared with model group, CR1 treatment could also decreased the concentration of C3a, C5a and MAC by 24.00%, 27.87%, 22.44%.The difference were statistically significant (t=9.86, 2.63, 6.94; P < 0.05). ConclusionsCR1 could protect the barrier function of hRPE cells against complement-activated oxidative stress. The underlying mechanism may involve inhibiting complement activation and down-regulating the expression of VEGF and CCL2.
ObjectiveTo explore the association between single nucleotide polymorphism (SNP) in the X-ray cross complementary repair gene-1 (XRCC1) rs1799782 locus and thyroid cancer.MethodsStudies investigating the association between SNP in the XRCC1 gene and thyroid cancer susceptibility were retrieved from the PubMed, Embase, Web of Science, CNKI (Chinese National Knowledge Infrastructure), Wanfang, and CBM (China Biology Medicine) databases (published date up to February 15, 2021). Eligible studies were screened according to inclusion/exclusion criteria and principles of quality evaluation. Meta-analysis was performed using Stata 14.0 software. Odds ratios with their corresponding 95% confidence intervals (95%CI) were pooled to assess the association between SNP in the XRCC1 gene rs1799782 locus and thyroid cancer susceptibility.ResultsTwelve articles were eligible for this meta-analysis. Meta-analysis results were shown as follows: No significant association was found between XRCC1 rs1799782 polymorphism and thyroid cancer in overall population [Dominant model: CT+TT vs CC, OR=1.07, 95%CI (0.84, 1.36). Recessive model: TT vs CT+CC, OR=1.48, 95%CI (0.95, 2.31). Allelic model: T vs C, OR=1.15, 95%CI (0.93, 1.43). Codominant model: TT vs CC: OR=1.44, 95%CI (0.83, 2.53); CT vs CC, OR=1.02, 95%CI (0.82, 1.28); TT vs CT, OR=1.40, 95%CI (0.98, 1.99)]. rs1799782 polymorphism was significantly associated with the risk of thyroid cancer in Chinese population [Dominant model: CT+TT vs CC, OR=1.38, 95%CI (1.11, 1.71). Recessive model : TT vs CT+CC, OR=1.97, 95%CI (1.55, 2.50); Allelic model: T vs C, OR=1.40, 95%CI (1.16, 1.68). Codominant model: TT vs CC, OR=2.12, 95%CI (1.66, 2.71); CT vs CC, OR=1.26, 95%CI (1.09, 1.47); TT vs CT, OR=1.70, 95%CI (1.31, 2.21)]. rs1799782 polymorphism was significantly associated with the risk of thyroid cancer in Asian population [Dominant model: CT+TT vs CC, OR=0.64, 95%CI (0.49, 0.83). Codominant model: TT vs CC: OR=0.50, 95%CI (0.33, 0.74); CT vs CC, OR=0.65, 95%CI (0.49, 0.86)].ConclusionsThere is no significant correlation between XRCC1 rs1799782 polymorphism and the risk of thyroid cancer in general population. The XRCC1 rs1799782 polymorphism may be associated with an increased thyroid cancer risk among Chinese, and a tendency for decreased thyroid cancer risk among Asians (Chinese excluded). The XRCC1 rs1799782 polymorphism is not associated with thyroid cancer susceptibility among Caucasians under all genetic models.
The causes of mental disorders are complex, and early recognition and early intervention are recognized as effective way to avoid irreversible brain damage over time. The existing computer-aided recognition methods mostly focus on multimodal data fusion, ignoring the asynchronous acquisition problem of multimodal data. For this reason, this paper proposes a framework of mental disorder recognition based on visibility graph (VG) to solve the problem of asynchronous data acquisition. First, time series electroencephalograms (EEG) data are mapped to spatial visibility graph. Then, an improved auto regressive model is used to accurately calculate the temporal EEG data features, and reasonably select the spatial metric features by analyzing the spatiotemporal mapping relationship. Finally, on the basis of spatiotemporal information complementarity, different contribution coefficients are assigned to each spatiotemporal feature and to explore the maximum potential of feature so as to make decisions. The results of controlled experiments show that the method in this paper can effectively improve the recognition accuracy of mental disorders. Taking Alzheimer's disease and depression as examples, the highest recognition rates are 93.73% and 90.35%, respectively. In summary, the results of this paper provide an effective computer-aided tool for rapid clinical diagnosis of mental disorders.
Myasthenia gravis (MG) is a common antibody mediated, cell-mediated, and complement dependent neuromuscular junction immune disease. The treatment mainly includes drug therapy (symptomatic therapy, non-specific immunosuppressive therapy, targeted immunotherapy), immune regulation (intravenous injection of human immunoglobulin and plasma exchange), and thymectomy. With the continuous deepening of research on MG treatment, targeted immune regulation of B cells, complement system, and neonatal Fc receptors has become a current research hotspot in the treatment of MG. Compared with traditional immunosuppressants, MG patients have better tolerance to new biological agents. This article elaborates on the research of MG targeted therapy related drugs and summarizes their efficacy and safety in MG treatment, aiming to find more treatment options.
ObjectiveTo understand the role of complement system in the immune mechanism of hepatocellular carcinoma (HCC) and its potential therapeutic value, and to provide reference for related research in the field of HCC immunotherapy. MethodsRead and review the national and international literature on hepatocellular carcinoma and complement-related studies. ResultsA total of eight complement components closely related to HCC were summarized, which play an important role in the immune regulation of HCC, and their activation can be involved in the occurrence and development of HCC through a variety of mechanisms, and their use as complement inhibitors can regulate the activity of complement-related activation pathways and enhance anti-tumor ability, potentially providing a new strategy for the treatment of HCC. ConclusionA variety of complement components in the complement system play an important role in regulating the immune mechanism of HCC, and the activation of the complement system is closely related to the occurrence and development of HCC, which is expected to be a potential immunotherapeutic target for HCC. However, the combination of complement-related inhibitor therapy with other antitumor immunotherapies carries certain risks and benefits, which need to be thoroughly investigated.