A feasibility study of DNA ploidy analysis, HPV, and TCT for screening of cervical cancer: A retrospective study.

The present study aimed to evaluate the application of DNA ploidy analysis, human papillomavirus (HPV-DNA) test, and thin-prep cytologic test (TCT) for mass screening of cervical cancer (CC). A total of 13,830 patients who underwent both TCT and HPV-DNA tests from June 2021 to June 2022 were selected as study participants (10,107 patients from Shandong Provincial Hospital, 2447 patients from First People's Hospital of Tancheng County, and 1276 patients from Liaocheng People's Hospital). We also conducted a DNA ploidy analysis and compared the results.

Estrogen Regulates Mitochondrial Activity Through Inducing Brain-Derived Neurotrophic Factor Expression in Skeletal Muscle.

Estrogen is an essential hormone for the development and functional activities of reproductive organs. Recent studies showed that estrogen signaling is also an important regulator of lipid and glucose metabolism in a number of tissues, but the molecular mechanism is not fully understood. We report here that estrogen is a stimulator of brain-derived neurotrophic factor (BDNF) synthesis in the skeletal muscle.

Elucidating the role of Brain-Derived Neurotrophic Factor (BDNF) and its receptor Tyrosine Receptor Kinase B (TrkB) in the development and symptoms of endometriosis.

Endometriosis (EMs) is a common disease among women of reproductive age, and as of now, the clinical understanding of the etiology of this disease remains unclear. The occurrence of EMs has a profound impact on the reproductive health of women, making early diagnosis and treatment of this disease a pressing challenge in clinical practice. Recent studies have found that Brain-Derived Neurotrophic Factor (BDNF), in combination with its high-affinity receptor Tyrosine Receptor Kinase B (TrkB), participates in the development of EMs and the appearance of clinically relevant symptoms by activating the Mitogen-Activated Protein Kinase (MAPK) pathway, the Phosphatidylinositol 3-Kinase/Protein Kinase B (PI3K/AKT) pathway, and the Phospholipase C-gamma (PLCγ) signaling pathway, or by interacting with other factors.

Differential regulation of hepatic SH3 domain binding kinase 1 (SBK1) expression in mouse and goldfish.

SH3 domain binding kinase 1 (SBK1) is a serine/threonine kinase that belongs to the new kinase family (NFK) with limited information on its function. Previous studies reported that SBK1 plays a role in memory formation, lipid metabolism, and cancer cell progression. Nevertheless, the regulatory mechanism of Sbk1 expression in various tissues remains unknown.

Nerve-independent formation of membrane infoldings at topologically complex postsynaptic apparatus by caveolin-3.

Junctional folds are unique membrane specializations developed progressively during the postnatal maturation of vertebrate neuromuscular junctions (NMJs), but how they are formed remains elusive. Previous studies suggested that topologically complex acetylcholine receptor (AChR) clusters in muscle cultures undergo a series of transformations, resembling the postnatal maturation of NMJs in vivo. We first demonstrated the presence of membrane infoldings at AChR clusters in cultured muscles.

Src homology 3 domain binding kinase 1 protects against hepatic steatosis and insulin resistance through the Nur77-FGF21 pathway.

Background And Aims: Metabolism in the liver is dysregulated in obesity, contributing to various health problems including steatosis and insulin resistance. While the pathogenesis of lipid accumulation has been extensively studied, the protective mechanism against lipid challenge in the liver remains unclear. Here, we report that Src homology 3 domain binding kinase 1 (SBK1) is a regulator of hepatic lipid metabolism and systemic insulin sensitivity in response to obesity.

Muscle-generated BDNF (brain derived neurotrophic factor) maintains mitochondrial quality control in female mice.

Mitochondrial remodeling is dysregulated in metabolic diseases but the underlying mechanism is not fully understood. We report here that BDNF (brain derived neurotrophic factor) provokes mitochondrial fission and clearance in skeletal muscle via the PRKAA/AMPK-PINK1-PRKN/Parkin and PRKAA-DNM1L/DRP1-MFF pathways. Depleting expression in myotubes reduced fatty acid-induced mitofission and mitophagy, which was associated with mitochondrial elongation and impaired lipid handling.