[Clinical and genetic analysis of a patient with FSIP2 compound heterozygous variants causing multiple morphological abnormalities of sperm flagella].

Objective: The aim of this study is to analyze the clinical features and genetic etiology of a patient with multiple morphological abnormalities of the sperm flagella (MMAF) retrospectively.

Methods: A severely oligospermic patient from the Reproductive Center of the First Affiliated Hospital of Ningbo University was selected as the study subject. Clinical data and examination results were collected.

Lysyl oxidase promotes seminal vesicle atrophy and fibrosis in type-2 diabetes mellitus through TGF-β1 signaling.

Type-2 diabetes mellitus (T2DM) is a complex metabolic disorder that adversely affects various physiological systems, particularly male reproductive health. Research indicates that T2DM increases the risk of retrograde ejaculation, impairing sexual function and fertility. Dysregulation of lysyl oxidase (LOX) has been linked to diabetes-related complications in the male reproductive system.

Deep generative model for protein subcellular localization prediction.

Protein sequence not only determines its structure but also provides important clues of its subcellular localization. Although a series of artificial intelligence models have been reported to predict protein subcellular localization, most of them provide only textual outputs. Here, we present deepGPS, a deep generative model for protein subcellular localization prediction.

Dominant-negative E-cadherin alters adhesion and reverses contact inhibition of growth in breast carcinoma cells.

Cadherins play a crucial role in epithelial morphogenesis and mediate intercellular adhesion. These receptors bind catenins and are involved in signal transduction pathways that regulate cell growth and apoptosis, and are frequently down-regulated in invasive and metastatic carcinomas. In order to assess the role of E-cadherin in cell adhesion and growth, we transfected MCF-7 cells, a human breast cancer cell line, with a dominant-negative construct of E-cadherin (H-2kd-E-cad).

Vasa vasorum hypoperfusion is responsible for medial hypoxia and anatomic remodeling in the newborn lamb ductus arteriosus.

Postnatal constriction of the full-term ductus arteriosus produces hypoxia of the muscle media. This is associated with anatomic remodeling (including smooth muscle death) that prevents subsequent reopening. We used late-gestation fetal and neonatal lambs to determine which factors are responsible for the postnatal hypoxia.

VEGF regulates remodeling during permanent anatomic closure of the ductus arteriosus.

Anatomic remodeling and permanent closure of the newborn ductus arteriosus appears to require the development of intense hypoxia within the constricted vessel wall. Hypoxic ductus smooth muscle cells express vascular endothelial cell growth factor (VEGF). We studied premature baboons and sheep to determine the effects of VEGF inhibition (in baboons) and VEGF stimulation (in sheep) on ductus remodeling in vivo.

In utero indomethacin alters O2 delivery to the fetal ductus arteriosus: implications for postnatal patency.

Indomethacin produces constriction and hypoxia of the fetal ductus arteriosus. This is associated with death of smooth muscle cells in the ductus wall and an increased incidence of patent ductus arteriosus in the newborn period. We used fetal sheep to determine which factors are responsible for indomethacin-induced hypoxic cell death.