Ultrasound-guided percutaneous microwave ablation of primary hyperthyroidism: security and efficacy analysis.

Objectives: This study aimed to analyze the safety, efficacy, and application prospects of ultrasound-guided microwave ablation (MWA) in the treatment of primary hyperthyroidism.

Methods: Eight patients with primary hyperthyroidism who underwent ultrasound-guided glandular volume reduction between January 2021 and December 2022 were included in this study. Pre- and postablative examinations, including grayscale ultrasound, contrast-enhanced ultrasound (CEUS), laboratory examination, antithyroid drug (ATD) dosage, and quality of life (QoL) assessment via Thyroid-Specific Patient-Reported Outcome Short-Form (ThyPRO-39), were analyzed retrospectively.

Origins of the short circuit current of a current mismatched multijunction photovoltaic cell considering subcell reverse breakdown.

In the photovoltaic community, short circuit current (I) of a current mismatched multijunction photovoltaic (MJPV) cell was usually thought to be limited by the lowest subcell photocurrent (I). However, under certain conditions for multijunction solar cells, I≠I was observed by researchers, while this effect has not been studied in multijunction laser power converters (MJLPCs). In this work, we provide an in-depth analysis of the formation mechanisms for the I of the MJPV cell by measuring I-V curves of the GaAs and InGaAs LPCs with different number of subcells and simulating the I-V curves with the reverse breakdown of each subcell considered.

Endoplasmic reticulum stress induced by lipopolysaccharide is involved in the association between inflammation and autophagy in INS‑1 cells.

Type 2 diabetes is a chronic inflammatory disease. Autophagy, the dynamic process of lysosomal degradation of damaged organelles and proteins, may protect β‑cells from destruction by inflammation in type 2 diabetes. The present study investigated the role of autophagy, inflammation and endoplasmic reticulum (ER) stress in type 2 diabetes.

Inhibiting autophagy promotes endoplasmic reticulum stress and the ROS‑induced nod‑like receptor 3‑dependent proinflammatory response in HepG2 cells.

Inflammation and endoplasmic reticulum (ER) stress are key contributors to insulin resistance and metabolic disease, and interleukin (IL)‑1β is involved in insulin resistance. The present study aimed to investigated the role of autophagy in LPS‑induced ER stress and inflammation, which may provide evidence for controlling metabolic disease associated with inflammation. Lipopolysaccharide (LPS) induced the activation of ER stress and the nod‑like receptor 3‑dependent expression of IL‑1β and caspase‑1, as shown by western blotting, which contributed to HepG2 cell death.

Liraglutide Improves the Survival of INS-1 Cells by Promoting Macroautophagy.

Background: Type 2 diabetes mellitus (T2D) is a metabolic disease characterized by dysfunction of pancreatic beta cell and insulin resistance. Liraglutide, which has many special anti-diabetes biological effects, is found to inhibit beta cell death and ameliorate endoplasmic reticulum stress (ERs) induced by free fatty acid (FFA). Macroautophagy (hereafter referred to as autophagy) altered by FFA is also associated with the dysfunction or death of pancreatic beta cells.

Liraglutide prevents high glucose level induced insulinoma cells apoptosis by targeting autophagy.

Background: The pathophysiology of type 2 diabetes is progressive pancreatic beta cell failure with consequential reduced insulin secretion. Glucotoxicity results in the reduction of beta cell mass in type 2 diabetes by inducing apoptosis. Autophagy is essential for the maintenance of normal islet architecture and plays a crucial role in maintaining the intracellular insulin content by accelerating the insulin degradation rate in beta cells.

Autophagy regulates inflammation following oxidative injury in diabetes.

T1D (type 1 diabetes) is an autoimmune disease characterized by lymphocytic infiltration, or inflammation in pancreatic islets called 'insulitis.' Comparatively speaking, T2D (type 2 diabetes) is traditionally characterized by insulin resistance and islet β cell dysfunction; however, a number of studies have clearly demonstrated that chronic tissue inflammation is a key contributing factor to T2D. The NLR (Nod-like receptor) family of innate immune cell sensors such as the NLRP3 inflammasome are implicated in leading to CASP1 activation and subsequent IL1B (interleukin 1, β) and IL18 secretion in T2D.

Guidelines for the use and interpretation of assays for monitoring autophagy.

In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding.

The role of autophagy in endoplasmic reticulum stress-induced pancreatic β cell death.

In pancreatic β-cells, the endoplasmic reticulum (ER) is the crucial site for insulin biosynthesis, as this is where the protein-folding machinery for secretory proteins is localized. Perturbations to ER function of the β-cell, such as those caused by high levels of free fatty acid and insulin resistance, can lead to an imbalance in protein homeostasis and ER stress, which has been recognized as an important mechanism for type 2 diabetes. Macroautophagy (hereafter referred to as autophagy) is activated as a novel signaling pathway in response to ER stress.

Effect of simvastatin on expression of transforming growth factor-β and collagen type IV in rat mesangial cells.

Objective: Diabetic nephropathy is characterized by the accumulation of extracellular matrix in the glomerular mesangium as a result of an imbalance between matrix synthesis and degradation. Since simvastatin has been proposed to decrease renal interstitial fibrosis, we hypothesized that the protective effect of statins was related to the expression of transforming growth factor-β (TGF-β) and type IV collagen (Col IV).

Methods: Cultured rat mesangial cells (RMC) were exposed to high glucose (HG), advanced glycosylation end products (AGE) or H(2)O(2) in the absence and presence of simvastatin.

The double-edged effect of autophagy in pancreatic beta cells and diabetes.

Autophagy is an intracellular catabolic system, which enables cells to capture cytoplasmic components for degradation within lysosomes. Autophagy is involved in development, differentiation and tissue remodeling in various organisms, and is also implicated in certain diseases. Recent studies demonstrate that autophagy is necessary to maintain architecture and function of pancreatic beta cells.