Pancreatic islet cells in microfluidic-spun hydrogel microfibers for the treatment of diabetes.

Islet transplantation has been developed as an effective cell therapy strategy to treat the progressive life-threatening disease Type 1 diabetes (T1DM). To mimic the natural islets and achieve immune isolation, hydrogel encapsulation of multiple islet cell types is the current endeavor. Here, we present a microfiber loading with pancreatic α and β cells by microfluidic spinning for diabetes treatment.

Hydrogel-Encapsulated Pancreatic Islet Cells as a Promising Strategy for Diabetic Cell Therapy.

Islet transplantation has now become a promising treatment for insulin-deficient diabetes mellitus. Compared to traditional diabetes treatments, cell therapy can restore endogenous insulin supplementation, but its large-scale clinical application is impeded by donor shortages, immune rejection, and unsuitable transplantation sites. To overcome these challenges, an increasing number of studies have attempted to transplant hydrogel-encapsulated islet cells to treat diabetes.

Follicle-stimulating hormone worsens osteoarthritis by causing inflammation and chondrocyte dedifferentiation.

Previous studies have found follicle-stimulating hormone (FSH) receptors on chondrocytes (cartilage cells), but the mechanism of FSH action on chondrocytes is not clear. The purpose of this experiment is to study whether FSH affects chondrocytes and how it causes changes in these cells. Our results show that osteoarthritis became worse after FSH injection in the knee joint of mice.

FSH modulated cartilage ECM metabolism by targeting the PKA/CREB/SOX9 pathway.

Introduction: Osteoarthritis (OA) is a common joint disease characterized by articular cartilage degeneration. The prevalence of OA is higher among women than men, and this prevalence is closely related to menopause. The classic view assumes that the underlying mechanism of postmenopausal OA is attributed to declining estrogen levels.

Thyroid-stimulating hormone decreases the risk of osteoporosis by regulating osteoblast proliferation and differentiation.

Background: As the incidence of secretory osteoporosis has increased, bone loss, osteoporosis and their relationships with thyroid-stimulating hormone (TSH) have received increased attention. In this study, the role of TSH in bone metabolism and its possible underlying mechanisms were investigated.

Methods: We analyzed the serum levels of free triiodothyronine (FT3), free thyroxine (FT4), and TSH and the bone mineral density (BMD) levels of 114 men with normal thyroid function.

Metformin protects chondrocytes against IL-1β induced injury by regulation of the AMPK/NF-κ B signaling pathway.

Osteoarthritis (OA) is a common joint disorder characterized by degeneration and inflammation of the articular cartilage. The etiology of OA is complex, and there is no effective drug for the treatment currently. Metformin, the first-line drug for type 2 diabetes mellitus, has been reported to play an essential role in a variety of diseases; however, whether it could be used in OA therapy remains unclear.

FSH directly regulates chondrocyte dedifferentiation and cartilage development.

Previous studies suggest that postmenopausal osteoarthritis is linked to a decrease in estrogen levels. However, whether follicle-stimulating hormone (FSH), the upstream hormone of estrogen, affects cartilage destruction and thus contributes to the onset of osteoarthritis has never been explored. To evaluate the potential involvement of FSH in joint degeneration and to identify the molecular mechanisms through which FSH influences chondrocytes, mouse cartilage chondrocytes and the ATDC5 chondrocyte cell line were treated with FSH and inhibitors of intracellular signaling pathways.

Flaxseed oil ameliorated high-fat-diet-induced bone loss in rats by promoting osteoblastic function in rat primary osteoblasts.

Background: α-Linolenic acid (ALA) is a plant-derived omega-3 unsaturated fatty acid that is rich in flaxseed oil (FO). The effect of FO on bone health is controversial. This study aims to evaluate the effect of FO on bone damage induced by a high-fat diet (HFD) and to explore the possible mechanism.