Subject(s)
Diabetes Mellitus , Hypertension , Hypertriglyceridemia , Obesity , Receptors, Calcitriol , Humans , Comorbidity , Diabetes Mellitus/epidemiology , Diabetes Mellitus/genetics , East Asian People , Hypertension/epidemiology , Hypertension/genetics , Hypertriglyceridemia/epidemiology , Hypertriglyceridemia/genetics , Obesity/epidemiology , Obesity/genetics , Receptors, Calcitriol/geneticsSubject(s)
Calcifediol/blood , Metabolic Syndrome/blood , Vitamins/blood , Adult , Aged , China/epidemiology , Female , Humans , Male , Metabolic Syndrome/epidemiology , Middle Aged , Odds Ratio , Prevalence , Risk Factors , Rural Population , Vitamin D Deficiency/blood , Vitamin D Deficiency/epidemiology , Young AdultABSTRACT
Objective: Recent studies have found that selenium (Se) levels were associated with the risk of Parkinson's disease (PD), but the results were contradictory. Therefore, this meta-analysis was conducted to investigate the correlation between Se levels and PD.Methods: PubMed, Embase and Web of Science were searched published up to 28 October 2019. The differences between groups were analyzed by forest plots and results were pooled and assessed using a random-effect model. Standardized mean difference (SMD) and 95% confidence interval (CI) were used to assess the association between Se levels and the risk of PD. Subgroup analysis, meta-regression, and sensitivity analysis were also conducted. Publication bias was estimated using Begg's regression asymmetry test.Results: Finally, 12 articles involving 601 PD patients and 749 controls were included in this meta-analysis. The meta-analysis revealed a significantly higher cerebrospinal fluid (CSF) Se level in PD patients than those in controls (SMD = 1.22; 95%CI [0.05, 2.39]; p = 0.000). No publication bias was found.Conclusion: The meta-analysis indicated that CSF Se levels in PD patients were significantly higher than those in controls.
Subject(s)
Parkinson Disease/blood , Parkinson Disease/cerebrospinal fluid , Selenium/blood , Selenium/cerebrospinal fluid , Trace Elements/blood , Trace Elements/cerebrospinal fluid , Antioxidants/metabolism , Biomarkers/blood , Biomarkers/cerebrospinal fluid , Humans , Parkinson Disease/diagnosisSubject(s)
Diabetes Mellitus, Experimental/drug therapy , Fibrosis/immunology , Hyperglycemia/prevention & control , Hypoglycemic Agents/pharmacology , Inflammation/immunology , Stilbenes/pharmacology , Animals , Fibrosis/prevention & control , Hyperglycemia/immunology , Inflammation/prevention & control , Male , Rats , Rats, Sprague-DawleySubject(s)
Chemical and Drug Induced Liver Injury/drug therapy , Diabetes Mellitus, Experimental/drug therapy , Diabetes Mellitus, Type 2/drug therapy , Dyslipidemias/drug therapy , Glycemic Load/drug effects , Protective Agents/pharmacology , Stilbenes/pharmacology , Animals , Male , Rats , Rats, Sprague-Dawley , Specific Pathogen-Free OrganismsABSTRACT
Lead exposure is a known potential risk factor for neurodegenerative diseases such as Alzheimer's disease (AD). Exposure to lead during the critical phase of brain development has been linked with mental retardation and hypophrenia in later life. This study was aimed to investigate the effects of lead exposure of pregnant mice on the expressions of insulin-degrading enzyme (IDE) and nerve growth factor (NGF) in the hippocampus of their offspring. Blood samples were collected from the tail vein, and after anesthetizing the pups, the brain was excised on postnatal day 21. Lead concentrations were determined by graphite furnace atomic absorption spectrophotometry, and the expressions of IDE and NGF were determined by immunohistochemistry and Western blotting. Results showed that the reduction in IDE and NGF expression in the hippocampus of pups might be associated with impairment of learning and memory and dementia induced by maternal lead exposure during pregnancy and lactation.
