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The role of estrogen receptor β in maintaining basal cells and modulating the immune environment in the prostate
Estrogen receptor β (ERβ) plays an important role in both the mouse and human prostate. The endogenous ligand for ERβ is the dihydrotestosterone metabolite, 5β-androstane-3β, 17β-diol (3β-Adiol). Thus, treatment with 5-α reductase inhibitor (5-ARI) should produce a phenotype similar to that seen in ERβ −/− mice. By comparing RNA-Seq of the ventral prostates (VP) of ERβ knockout mice (ERβ crispr−/− ) and wild-type (WT) mice, we confirmed that ERβ modulates androgen receptor (AR) signaling indirectly by suppressing AR coactivators. Compared to WT mice, basal cell genes from ERβ crispr−/− mouse VP were significantly upregulated. A population of abnormal basal cells coexpressing P63 and AR was identified in the ERβ crispr−/− mouse VP by immunohistochemistry. In men treated with 5-ARI for treatment of benign prostatic hyperplasia (BPH), there was induction of a P63-positive intermediate cell population characterized by down regulation of Krt14 without significant change in the expression of Krt15, upregulation of AR and NKX3.1, and increased proliferation. In both VP of aging ERβ crispr−/− mice and in human prostates after 5-ARI treatment, there was substantial immune infiltration. Testosterone treatment inhibited immune infiltration in the VP of ERβ crispr−/− mice. We conclude that ERβ is a gene critical in maintaining normal basal cells and modulating immune environment in the prostate. Its loss leads to histological changes suggesting prostatitis and increases the number of intermediate cells, which are considered to be the cells of origin of prostate cancers. We suggest that an ERβ agonist could protect against 5-ARI-induced inflammatory cell infiltration and defects in the basal cell layer in BPH.
Spatiotemporal distribution of sustained dengue hotspots associated with climate and urbanisation in Singapore
A renewable double plasma mirror for Petawatt-class lasers
The two-stage prediction method for traffic spillover dissipation at short-distance intersections based on Bi-LSTM
The association between physical activity and the prevalence of comorbidity: a cross-sectional survey
Identification of Protocatechuic acid as an anti-acne component in extracts of black rice bran
Nonlocality in quantum cloning states
High performance double perovskites of Cs2InAgBr6 and Cs2InAgCl6 structural electronic optical and thermoelectric properties for next generation photovoltaics
Associations of pain phenotypes and pain relief medications with stroke and its subtypes: a prospective cohort study
Bone morphogenetic protein-9 controls pulmonary vascular growth and remodeling
Pulmonary arterial hypertension (PAH) and hereditary hemorrhagic telangiectasia (HHT) are two distinct vascular diseases linked to impaired signaling through bone morphogenetic protein (BMP) receptor complexes in endothelial cells. Although BMP-9 plays a central role in activating this pathway by binding to ALK1 and BMPR-II, its precise function in the pulmonary microvasculature has remained unclear. In this study, we demonstrate a role for BMP-9 in regulating pulmonary vascular architecture and homeostasis. Our findings reveal that BMP-9 signaling intersects with VEGF pathways and contributes to the delicate balance between vascular growth and remodeling in the lungs. We also show that disruption of this pathway can shift vascular responses toward an HHT-like state, potentially altering disease susceptibility. These insights offer a unique perspective on how BMP-9 and ALK1 shape pulmonary vascular biology and suggest that targeting this axis could inform future strategies for treating complex vascular diseases such as PAH.
Ring of capillary actuators as trap, tweezers and ratchet for floating particles
Machine learning evaluation model of pilot workload in a low-visibility environment
Genome-wide association study of the taste and hedonic ratings of the low-calorie sweetener acesulfame potassium
Survival analysis of PLWH on antiretroviral therapy in Henan Province from 2004 to 2024
Comprehensive datasets for RNA design, machine learning, and beyond
Abstract RNA molecules are essential in regulating biological processes such as gene expression, cellular differentiation, and development. Accurately predicting RNA secondary structures and designing sequences that fold into specific configurations remain significant challenges in computational biology, with far-reaching implications for medicine, synthetic biology, and biotechnology. While machine learning methodologies have been proposed to enhance prediction capabilities, they require high-quality training data. The lack of standardized benchmark datasets further hinders the development and evaluation of these tools. To address this, we created a comprehensive dataset of over 320 thousand instances from experimentally validated sources to establish a new community-wide benchmark for RNA design and modeling algorithms. Our dataset comprises numerous challenging structures for which state-of-the-art RNA inverse folders provide results of varying accuracy. We demonstrated the potential of the dataset by testing it with several popular open-source RNA design algorithms. Furthermore, we illustrated how our dataset can be used to train machine learning models that consider both RNA sequence and structure, potentially advancing RNA design and prediction capabilities.
Exploring the prognostic role and expression patterns of FAM3A family genes in kidney renal clear cell carcinoma
Mass and fate estimates of plastic waste dispersed globally to marine and terrestrial environments by three major corporations
Simulated division of flood processes in the composite terrain region based on the multi-layer hydrological process combination model
Molecular contacts in self-assembling clusters of membrane proteins
Motivated by recent data pointing to the existence of homo-oligomeric assemblies of membrane proteins called higher-order transient structures, and their apparent role in connecting components of membrane signal pathways, we examine here by cryoelectron microscopy some of the protein–protein interactions that occur in cluster formation. Metabotropic glutamate receptors and HCN ion channels inside clusters contact their neighbors through structured extracellular and intracellular domains, respectively. Other ion channels, including Kv2.1 and Slo1, appear to form clusters through prominent intrinsically disordered sequences in the cytoplasm. These distinct modes of interaction are associated with clusters exhibiting varying degrees of compactness and order. We conclude that nature utilizes a variety of ways to form connections between membrane proteins in self-assembled clusters.