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The complement system has been shown to have a critical pathogenetic role in amyotrophic lateral sclerosis (ALS). Recently a C7 variant in rs3792646 was linked to neurodegenerative diseases in a Chinese population. [https://www.selleckchem.com/products/escin.html see more] We used whole exome sequencing to evaluate the role of C7 (rs3792646) in ALS in a Chinese cohort with 1970 individuals. The minor allele frequency in cases was 0.032 while 0.016 in controls, suggesting this variant was associated with ALS. Further analyses showed the prevalence of the variant was significantly higher in Chinese than Caucasian, suggesting its importance in Han individuals. rs3792646-C was significantly associated with a lower onset age in both genders, and a survival analysis revealed a significant relationship between the variant and decreased survival. There was no significant association between the variant and other common ALS-related variants. Our study further elucidated the relationship between the complement system and ALS from a genetic perspective. In addition, the results suggested C7 (rs3792646) could be a potential predictive factor for poor prognosis in ALS.Synapse loss is an early event in late-onset Alzheimer's disease (LOAD). In this study, we have assessed the capacity of a polygenic risk score (PRS) restricted to synapse-encoding loci to predict LOAD. We used summary statistics from the International Genetics of Alzheimer's Project genome-wide association meta-analysis of 74,046 patients for model construction and tested the "synaptic PRS" in 2 independent data sets of controls and pathologically confirmed LOAD. The mean synaptic PRS was 2.3-fold higher in LOAD than that in controls (p less then 0.0001) with a predictive accuracy of 72% in the target data set (n = 439) and 73% in the validation data set (n = 136), a 5%-6% improvement compared with the APOE locus (p less then 0.00001). The model comprises 8 variants from 4 previously identified (BIN1, PTK2B, PICALM, APOE) and 2 novel (DLG2, MINK1) LOAD loci involved in glutamate signaling (p = 0.01) or APP catabolism or tau binding (p = 0.005). As the simplest PRS model with good predictive accuracy to predict LOAD, we conclude that synapse-encoding genes are enriched for LOAD risk-modifying loci. The synaptic PRS could be used to identify individuals at risk of LOAD before symptom onset.Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the causal agent of coronavirus disease 2019 (COVID-19). Diabetes is one of the most frequent comorbidities in people with COVID-19 with a prevalence that varies between 7 and 30%. Diabetics infected with SARS-CoV-2 have a higher rate of hospital admission, severe pneumonia, and higher mortality compared to non-diabetic subjects. Chronic hyperglycemia can compromise innate and humoral immunity. Furthermore, diabetes is associated with a low-grade chronic inflammatory state that favors the development of an exaggerated inflammatory response and therefore the appearance of acute respiratory distress syndrome. Recent evidence has shown that SARS-CoV-2 is also capable of causing direct damage to the pancreas that could worsen hyperglycemia and even induce the onset of diabetes in previously non-diabetic subjects. Therapeutic strategies should be aimed at facilitating patient access to the healthcare system. Control of blood glucose and comorbidities must be individualized in order to reduce the incidence of complications and decrease the burden on health systems. In this article we will review the pathophysiological mechanisms that explain the bidirectional relationship between COVID-19 and diabetes mellitus, its implication in the prognosis and management of hyperglycemia in this group of patients.Apolipoprotein C-III (apoC-III) is a small protein that is predominantly synthesized in the liver and mainly resides at the surface of triglyceride-rich lipoproteins. Its expression is upregulated by glucose and reduced by insulin, with enhanced apoC-III promoting hypertriglyceridemia and inflammation in vascular cells. The protein is also elevated in patients with diabetes, suggesting that enhanced apoC-III levels might contribute to the development of type 2 diabetes mellitus. The present review focuses on the key mechanisms by which apoC-III could promote type 2 diabetes mellitus, including exacerbation of insulin resistance in skeletal muscle, activation of β-cell apoptosis, promotion of weight gain through its effects on white adipose tissue and hypothalamus, and attenuation of the beneficial effects of high-density lipoproteins on glucose metabolism. Therapeutic strategies aimed at reducing apoC-III levels may not only reduce hypertriglyceridemia but also might improve insulin resistance, thus delaying the development of type 2 diabetes mellitus.HCV eradication by antiviral treatment reduces but does not eliminate HCC risk. Patients with established cirrhosis require HCC surveillance "indefinitely" after sustained virologic response (SVR) because they appear to have a high risk of HCC even many years after SVR. Patients without established or known cirrhosis may still require surveillance after SVR if they have a sufficiently high HCC risk. In all patients who achieve SVR, the key question is how we can reliably estimate HCC risk, and the change in HCC risk over time, to determine whether the patient might benefit from HCC surveillance. HCC risk is one of the most important factors that should inform decisions of whether and how to screen for HCC. Promising strategies for estimating HCC risk include simplified scoring systems (such as fibrosis-4), liver elastography and multivariable HCC risk calculators. Such tools may enable risk stratification and individualised, risk-based surveillance strategies ("precision HCC screening") in the future.Immune dysfunction contributes to the higher risk of communicable and non-communicable diseases among diabetics. HLA-DR expression is a robust marker of immune competence in mononuclear cells, including antigen presentation to CD4 lymphocytes. Given the high prevalence of obesity among diabetics, we evaluated the independent association between hyperglycemia and dyslipidemias with respect to HLA-DR expression in blood monocytes from type 2 diabetes patients. The monocytes from individuals with (n = 16) or without diabetes (n = 25) were phenotyped by flow cytometry to assess the differential expression of HLA-DR on their three subpopulations (classical, intermediate and non-classical monocytes). Diabetes was independently associated with lower HLA-DR expression across all monocyte subpopulations (p less then 0.05). Blood triglycerides were associated with further HLA-DR depression (interaction p less then 0.002). Cholesterols counterbalanced the reductive effect, with CD36, a receptor for oxidized cholesterol, correlating with HLA-DR (rho = 0.