Combination of machine learning-based bulk and single-cell genomics reveals necroptosis-related molecular subtypes and immunological features in autism spectrum disorder.

Background: Necroptosis is a novel form of controlled cell death that contributes to the progression of various illnesses. Nonetheless, the function and significance of necroptosis in autism spectrum disorders (ASD) remain unknown and require further investigation.

Methods: We utilized single-nucleus RNA sequencing (snRNA-seq) data to assess the expression patterns of necroptosis in children with autism spectrum disorder (ASD) based on 159 necroptosis-related genes.

Altered Caffeine Metabolism Is Associated With Recurrent Hypoglycemia in Type 2 Diabetes Mellitus: A UPLC-MS-Based Untargeted Metabolomics Study.

Background: Recurrent hypoglycemia (RH) is well known to impair awareness of hypoglycemia and increase the risk of severe hypoglycemia; the underlying mechanism requires further understanding. We aimed to investigate the metabolic characteristic profile for RH in type 2 diabetes mellitus (T2DM) patients and explore the potential metabolic mechanism and prevention strategies.

Methods: We screened 553 community-based T2DM patients.

CXXC4 mediates glucose-induced β-cell proliferation.

Aims: CXXC finger protein 4 (CXXC4) is an identified negative regulator of the Wnt/β-catenin pathway, and it is involved in cancer cell proliferation. In this study, we sought to clarify whether CXXC4 is involved in glucose-stimulated β-cell proliferation.

Materials And Methods: We investigated the biological function of CXXC4 in glucose-induced β-cell proliferation, and we investigated the underlying mechanism of this activity.

Severe hypoglycemia exacerbates myocardial dysfunction and metabolic remodeling in diabetic mice.

Although several studies have revealed that adverse cardiovascular events in diabetic patients are closely associated with severe hypoglycemia (SH), the causal relationship and related mechanisms remain unclear. This study aims to investigate whether SH promotes myocardial injury and further explores the potential mechanisms with focus on disturbances in lipid metabolism. SH promoted myocardial dysfunction and structural disorders in the diabetic mice but not in the controls.

Recurrent nonsevere hypoglycemia exacerbates imbalance of mitochondrial homeostasis leading to synapse injury and cognitive deficit in diabetes.

Recurrent nonsevere hypoglycemia (RH) can lead to cognitive dysfunction in patients with diabetes, although the involved mechanisms remain unclear. Here, we aimed to investigate the mechanism underlying RH-induced cognitive deficits with a focus on mitochondrial homeostasis. To establish a model that mimicked RH in patients with type 1 diabetes (T1DM) receiving insulin therapy, streptozotocin-induced mice with T1DM were subjected to recurrent, twice-weekly insulin injections over 4 wk.