OBJECTIVETo investigate the effect of aluminum exposure on neuronal apoptosis of rats hippocampus and the correlation of and synaptic plasticity.

METHODSThere were 40 SPF grade SD rats which were randomly divided into four groups: the control group, the low dose group, the medium dose group and the high dose group, 10 rats in each group. The rats were daily gavaged with aluminum lactate for 30 days. The hippocampal fEPSPs in rat was measured by electrophysiological grapher and the neuronal apoptosis in hippocampus was detected by Flow cytometer. In addition, the relative expression of gene which includes caspase-3, 8, 9 was measured by Real-time PCR.

RESULTSCompared to the control group, the average of fEPSPs which after HFS 10, 20, 30, 40, 50, 60 min was decreased at different time point in the low dose group, the medium dose group and the high dose group (P < 0.05). Compared with the control group, the rate of apoptosis was significantly increased in the medium dose group and the high dose group (P < 0.05). Compared to the control group, the relative expression of caspase-3 in the medium dose group and the high dose group was significantly increased in Real-time PCR (P < 0.05), and the relative expression of caspase-8 in the high dose group was significantly increased (P < 0.05).

CONCLUSIONAluminum exposure may induced neuronal apoptosis in rats, and then affect hippocampal synaptic plasticity.

Aluminum ; toxicity ; Aluminum Compounds ; toxicity ; Animals ; Apoptosis ; Caspase 3 ; metabolism ; Caspase 8 ; metabolism ; Hippocampus ; cytology ; drug effects ; Lactates ; toxicity ; Neuronal Plasticity ; drug effects ; Neurons ; cytology ; drug effects ; Rats ; Rats, Sprague-Dawley

OBJECTIVEIn this research, we have observed changes of PHF8、H3K9me2、BDNF, and their regulatory roles in changing the amplitude value of LTP in hippocampus due to aluminum exposure so that we can discuss the impact on the learning and memory that caused by chronic aluminum exposure.

METHODSForty healthy SPF grade SD male rats were randomly divided into four groups by weight, including control group and low, medium, high dose aluminum exposed group, each group had 10 rats. The exposed rats drank water containing different doses of aluminum chloride (AlCl3) (2、12、72 mg/kg Al(3+)) for 90 d. We measured LTP in hippocampus by electrophysiological grapier and detected the expression of PHF8、H3K9me2、BDNF by western-blot.

RESULTSElectrophysiological measurements shows that compared with that of control group, the average of fEPSPs was decreased at different time points in all exposed groups (P<0.01) . The results of western-bolt test demonstrated that the expression of PHF8 in the exposed groups were significantly lower than those of control group (P<0.01) . And the expression the of H3K9me2 of medium and high dose groups were significantly higher than control group (P<0.05) . While the expression of BDNF of medium and high dose groups were decreased compared with the control group (P<0.05) .

CONCLUSIONChronic aluminum exposure can reduce the LTP via the route of PHF8-H3K9me2-BDNF in the hippocampus of rats, which then may impair the ability of learning and memory.

Aluminum ; toxicity ; Aluminum Compounds ; toxicity ; Animals ; Brain-Derived Neurotrophic Factor ; metabolism ; Chlorides ; toxicity ; Hippocampus ; drug effects ; metabolism ; Histone Demethylases ; metabolism ; Learning ; drug effects ; Long-Term Potentiation ; drug effects ; Male ; Memory ; drug effects ; Pilot Projects ; Rats ; Rats, Sprague-Dawley ; Transcription Factors ; metabolism

The abnormal lipid levels caused by disorders of lipid metabolism are important factors leading to various diseases such as cardiovascular and cerebrovascular damage .Studies found that monitoring blood lipid levels can provide evidences for the early diagnosis of cardiovascular and cerebrovascular diseases, assessing the risks of cardiovascular and cerebrovascular diseases , and evaluation of the therapeutic effects. The commonly used lipid markers for the diagnosis of clinical cardiovascular and cerebrovascular diseases are the four routine blood lipids , such as total cholesterol ( TC) , total triglyceride (TG), high-density lipoprotein (HDL), and low-density lipoprotein (LDL).The application of other blood lipid markers including apolipoprotein A (ApoA), apolipoprotein B (ApoB), non high density lipoprotein cholesterol (non-HDL-C), and lipoprotein a[Lp (a)]in the diagnosis and treatment of cardiovascular and cerebrovascular diseases have also been reported .

Objective:To screen genetic and epigenetic expression differences associated with pulmonary embolism through integrated bioinformatics analysis.Methods:Four patients with pulmonary embolism and healthy physical examination in the Third Affiliated Hospital of Xinjiang Medical University in 2019 were selected as the research objects, using high-throughput sequencing technologies and methylation chip technology to detect, screening and integrated peripheral blood difference genomes and the epigenome data to identify the pathogenesis of pulmonary embolism caused by methylation of drive and differentially expressed genes, GO and KEGG enrichment analysis were performed.Results:Coexpression analysis of DNA methylation and gene expression data between the pulmonary embolism group and the healthy control group showed that differential methylation in the upstream region of genes was negatively correlated with gene expression. Among them, 8 significantly methylated genes in the upstream region of genes were screened out, and independent sample t-test and Pearson correlation analysis were done. In the pulmonary embolism group, there were 6 significant methylated genes of TSS1500, namely TSPO2, C1QA, AQP1, TNFSF9, MIA and STAB1, and the differential expression multiple log2FC of corresponding genes was 1.298, 1.629, 1.024, 2.746, 2.539, 1.060, respectively. The correlation between gene expression and gene methylation were -0.908, -0.900, -0.824, -0.784, -0.783, -0.779, respectively, and the methylation differences between the two groups were -0.049, -0.053, -0.048, -0.057, -0.050, respectively. -0.053 ( P < 0.05). There were three significantly methylated genes in the TSS200 region, namely TSPO2, SLC9A, and SIGLEC1. The gene expression differential multiple log2FC was 1.298, -2.252, and 1.866, respectively. The correlation between gene expression and gene methylation was -0.860, -0.774, and -0.739, respectively. The methylation difference between the two groups was -0.051, 0.027, -0.048 ( P < 0.05). In the pulmonary embolism group, 7 genes, including TSPO2, C1QA, AQP1, TNFSF9, MIA, STAB1 and SIGLEC1, showed hypomethylation and high expression in the TSS region. SLC9A3 gene showed high methylation and low expression. In the analysis of GO function, significant enrichment was obtained in complement activation, immune response and activation protein cascade. In the KEGG signaling pathway, the immune system, bacterial infection, and signaling molecules and interactions are significantly enriched, thereby regulating the occurrence of pulmonary embolism. Conclusions:Based on the combined analysis of DNA methylation and gene expression, a new idea of the occurrence and development of pulmonary embolism has been found, which can be further studied in the future.

Objective: To explore the relationship between serum complement 1q (C1q) and C1q/tumor necrosis factor-related protein 1 (CTRP1) levels in patients with coronary atherosclerotic heart disease (CHD) and their clinical value. Methods: Case-control study.115 patients with CHD who were hospitalized in the Department of Cardiology of Ningxia Medical University General Hospital from January 2018 to November 2018 were selected as the case group, including 72 males and 43 females, aged 35-82 years, average (59.96±9.49) years old. There were three subgroups: stable angina group (SAP, n=12), unstable angina group (UA, n=69), and acute myocardial infarction group (AMI, n=34). The control group was selected from 43 healthy subjects in the same period, including 21 males and 22 females, aged 23-71 years, with an average of (45.00±10.66) years old. Serum C1q and CTRP1 levels were tested by immunoturbidimetry and ELISA, and other biochemical indicators such as triglyceride (TG) and total cholesterol (CHOL) were detected.Multiple linear regression was used to analyze the influence of various factors on C1q level. ROC curve and area under the curve (AUC) to explore the diagnostic value of C1q and CTRP1. Results: The C1q level in the CHD group (184.06±31.05) mg/L was higher than that in the control group (122.22±28.18) mg/L (t=-11.405, P<0.001). The AMI group (192.80±34.08) mg/L was significantly higher than the SAP group (169.17±27.13) mg/L (t=-2.328, P=0.021).The CTRP1 level in the CHD group [241.85(79.38)] ng/ml was lower than that in healthy control group [292.7(67.64)] ng/ml (Z=-3.64, P<0.001). Group B with higher Gensini score (t=3.672, P<0.001) and group C (t=2.529, P=0.013) had higher C1q levels than group A.After adjusting for the effects of age, sex and other indicators, C1q levels were correlated with HDL-C (β=-0.582, P<0.001),CHOL (β=0.384,P<0.001) and systolic blood pressure (β=0.142,P=0.038). The ROC curve shows that when the CHD is diagnosed, the sensitivity of C1q level >150.82 mg/L is 87%,the specificity is 88.4%, and the AUC is 0.942. The corresponding sensitivity and specificity of CTRP1 <281.80 ng/ml are 76.5% and 60.5% respectively, and the AUC is 0.688. The AUC obtained by combined predictors was 0.944, and the sensitivity and specificity were 89.6% and 86.0% respectively. When AMI is diagnosed, C1q level >178.3 mg/L, corresponding sensitivity and specificity are 70.6% and 66.1%, the AUC is 0.726, CTRP1 has no diagnostic value. Conclusions Serum C1q levels in patients with CHD are elevated, and AMI patients are higher than SAP patients; C1q may be a potential marker reflecting the severity of coronary artery disease; there is no significant correlation between serum C1q and CTRP1 in CHD patients.