Changes of Acylating Stimulating Protein (ASP) and Blood Lipid in Patients with Acute Myocardial Infarction

Objective: To study the changes of acylating stimulating protein (ASP) and blood lipid in patients with acute myocardial infarction. Method: There were three groups,25 cases of acute myocardial infarction patients (acute myocardial infarction group), 32 cases of coronary heart disease patients without myocardial infarction (CHD group) and 30 cases of healthy people (control group). They respectively detected the ASP, low density lipoprotein cholesterol (LDL-C), triglyceride (TG), total cholesterol (TC) and high-density lipoprotein cholesterol (HDL-C), and analyzed the correlation between them. Results: (1) ASP, TG, TC and LDL-C of acute myocardial infarction group and coronary heart disease group were significantly higher than those of control group, while HDL-C was lower than control group, the difference was statistically significant (P < 0.05). (2) TG in coronary heart disease group was higher than that in acute myocardial infarction group, while ASP, TC, LDL-C and HDL-C had no significant difference. Conclusion: ASP and blood lipid are risk factors of CHD, ASP can be used as risk index of CHD. There was no significant difference in plasma ASP between patients with acute myocardial infarction and patients with coronary heart disease without myocardial infarction. ASP cannot be used as a surrogate marker of acute myocardial infarction

RNF216 Regulates the Migration of Immortalized GnRH Neurons by Suppressing Beclin1-Mediated Autophagy

RNF216, encoding an E3 ubiquitin ligase, has been identified as a causative gene for Gordon Holmes syndrome, characterized by ataxia, dementia, and hypogonadotropic hypogonadism. However, it is still elusive how deficiency in RNF216 leads to hypogonadotropic hypogonadism. In this study, by using GN11 immature GnRH neuronal cell line, we demonstrated an important role of RNF216 in the GnRH neuron migration. RNA interference of RNF216 inhibited GN11 cell migration, but had no effect on the proliferation of GN11 cells or GnRH expression. Knockdown of RNF216 increased the protein levels of its targets, Arc and Beclin1. RNAi of Beclin1, but not Arc, normalized the suppressive effect caused by RNF216 knockdown. As Beclin1 plays a critical role in the autophagy regulation, we further demonstrated that RNAi of RNF216 led to increase in autophagy, and autophagy inhibitor CQ and 3-MA rescued the GN11 cell migration deficit caused by RNF216 knockdown. We further demonstrated that pharmacological increase autophagy by rapamycin could suppress the GN11 cell migration. We thus have identified that RNF216 regulates the migration of GnRH neuron by suppressing Beclin1 mediated autophagy, and indicated a potential contribution of autophagy to the hypogonadotropic hypogonadism

Risk factors of amyotrophic lateral sclerosis: a global meta-summary

BackgroundThe etiology of amyotrophic lateral sclerosis (ALS) remains largely unknown. This study aimed to summarize the relationship between ALS and its genetic and non-genetic risk factors.MethodA search of relevant literature from PubMed, Embase, and Cochrane Database from inception to December 2022 was performed. Random-effects or fixed-effects models were performed by Stata MP 15.0 to pool multivariate or adjusted ratios (OR). PROSPERO registration number: CRD42022301549.Results230 eligible studies were included, of which 67 involved 22 non-genetic factors, and 163 involved genetic factors. Four aspects of non-genetic factors, including lifestyle, environmental and occupational exposures, pre-existing diseases/comorbidity and medical exposures, and others, were analyzed. Exposure to heavy metals (OR = 1.79), pesticides (OR = 1.46), solvents (OR = 1.37), previous head trauma (OR = 1.37), military service (OR = 1.29), stroke (OR = 1.26), magnetic field (OR = 1.22) and hypertension (OR = 1.04) are significant risk factors, but use of antidiabetics (OR = 0.52), high BMI (OR = 0.60 for obese and overweight vs. normal and underweight), living in urban (OR = 0.70), diabetes mellitus (OR = 0.83), and kidney disease (OR = 0.84) decrease the risk for ALS. In addition, eight common ALS-related genes were evaluated, the mutation frequencies of these genes were ranked from highest to lowest as SOD1 (2.2%), C9orf72 (2.1%), ATXN2 (1.7%), FUS (1.7%), TARDBP (0.8%), VCP (0.6%), UBQLN2(0.6%) and SQSTM1 (0.6%) in all the ALS patients.ConclusionsOur findings suggested that effective intervention for risk exposure and timely modification of lifestyle might prevent the occurrence of ALS. Genetic mutations are important risk factors for ALS and it is essential to detect genetic mutations correctly and scientifically.Systematic review registrationhttps://www.crd.york.ac.uk/PROSPERO/display_record.php?RecordID=301549, identifier: CRD42022301549