Influence of dynamic load and water on energy accumulation and dissipation in sandstone.

In various engineering projects such as mineral extraction, hydropower resource utilization, railway construction, and geological hazard mitigation, rock engineering is often encountered. Furthermore, dynamic loads and moisture content exert notable influence on the energy transformation processes within rocks. Yet, the specific interplay of dynamic loading and water's impact on the energy conversion mechanism within the sandstone remains unexplored.

Based on network pharmacology and experiments to explore the underlying mechanism of Mahonia bealei (Fortune) Carrière for treating alcoholic hepatocellular carcinoma.

Ethnopharmacological Relevance: Mahonia bealei (Fortune) Carrière (M. bealei) is a traditional medicine widely used by the Hmong community in Guizhou. It possesses diverse biological activities and shows promise in cancer treatment; however, contemporary pharmacological research in this area is lacking.

Material basis and action mechanism of Euryale Ferox Salisb in preventing and treating diabetic kidney disease.

The aim of this study was to determine the chemical structure and mechanism of action of Euryale ferox Salisb (ES) in the prevention and treatment of diabetic kidney disease (DKD). The TCMSP, SymMap V2, CTD, DisGeNET, and GeneCards databases were searched for ES components, targets, and DKD targets using the network pharmacology method to identify common drug-disease targets. PPI analysis was used to identify hub genes, which were then followed by DKD clinical relevance, GO, KEGG analysis, and transcription factor prediction.

Stable structures and superconducting properties of Ca-La-H compounds under pressure.

The calcium hydrides and lanthanum hydrides under high pressures have been reported to have good superconducting properties with high-. In this work, the structures and superconductivities of Ca-La-H ternary hydrides have been studied by genetic algorithm and density functional theory calculations. Our results show that at the pressure range of 100-300 GPa, the most stable structure of CaLaHhas asymmetry, in which there is a Hhydrogen cage.

Fertility factors affect the vaginal microbiome in women of reproductive age.

Problem: For women of reproductive age, achieving a successful pregnancy requires both the normal functioning of reproductive endocrine and the health of the reproductive tract environment. We aimed to study how these fertility factors, such as female age, baseline sexual hormone levels, tubal patency, and vaginal pH, affect the composition of vaginal microbiome.

Method Of Study: The 16S rRNA sequencing was carried on vaginal microbiome samples from 85 women of reproductive age without vaginal infections or reproductive endocrine diseases.

All-Optical Volumetric Physiology for Connectomics in Dense Neuronal Structures.

All-optical physiology (AOP) manipulates and reports neuronal activities with light, allowing for interrogation of neuronal functional connections with high spatiotemporal resolution. However, contemporary high-speed AOP platforms are limited to single-depth or discrete multi-plane recordings that are not suitable for studying functional connections among densely packed small neurons, such as neurons in Drosophila brains. Here, we constructed a 3D AOP platform by incorporating single-photon point stimulation and two-photon high-speed volumetric recordings with a tunable acoustic gradient-index (TAG) lens.

Bisphenol A stimulates steroidogenic acute regulatory protein expression via an unknown mechanism in adrenal cortical cells.

Bisphenol A (BPA) is one of the most widespread endocrine disrupting chemicals in the environment. Exposure to BPA is known to be associated with disruption of steroidogenesis in reproductive tissues, but little is known about its effects on the adrenal gland. We previously showed that prenatal BPA exposure resulted in elevated plasma corticosterone levels concomitant with increased adrenal levels of steroidogenic acute regulatory protein (StAR), the rate-limiting step in steroidogenesis, in adult female mouse offspring.

Bisphenol A stimulates adrenal cortical cell proliferation via ERβ-mediated activation of the sonic hedgehog signalling pathway.

We previously demonstrated that prenatal exposure to bisphenol A (BPA) resulted in increased adrenal gland weight independent of changes in plasma ACTH levels in adult mouse offspring. This finding suggested that BPA exposure likely had a direct effect on adrenal development. Given that (1) sonic hedgehog (Shh) signaling is essential for adrenal development; (2) deletion of the Shh gene in mice results in adrenal hypoplasia; (3) BPA is known to signal through estrogen receptor β (ERβ); and (4) ERβ is highly expressed in adrenal glands; we hypothesized that BPA stimulates adrenal cell proliferation via ERβ-mediated activation of the Shh pathway.

The Gut Microbiota of Healthy Aged Chinese Is Similar to That of the Healthy Young.

The microbiota of the aged is variously described as being more or less diverse than that of younger cohorts, but the comparison groups used and the definitions of the aged population differ between experiments. The differences are often described by null hypothesis statistical tests, which are notoriously irreproducible when dealing with large multivariate samples. We collected and examined the gut microbiota of a cross-sectional cohort of more than 1,000 very healthy Chinese individuals who spanned ages from 3 to over 100 years.

Bisphenol A suppresses glucocorticoid target gene (ENaCγ) expression via a novel ERβ/NF-κB/GR signalling pathway in lung epithelial cells.

We previously demonstrated that prenatal exposure to Bisphenol A (BPA) disrupts fetal lung maturation likely through the glucocorticoid signalling pathway, but the precise molecular mechanisms remain obscure. Given that BPA diminished the expression of epithelial sodium channel-γ (ENaCγ), a well-known glucocorticoid receptor (GR) target gene, in fetal lungs, we used this GR target gene to delineate the molecular pathway through which BPA exerts its effects on lung cells. The A549 lung epithelial cell line was used as an in vitro model system.

Prenatal exposure to bisphenol A disrupts adrenal steroidogenesis in adult mouse offspring.

The present study sought to determine if prenatal exposure to bisphenol A (BPA) alters adrenal steroidogenesis in adult offspring. Pregnant mice were exposed to BPA (25mg BPA/kg food pellet) via diet from day 7 to the end of pregnancy. At eight weeks of age, offsprings were sacrificed, blood samples and adrenal glands were collected for hormone assays and western blot analysis, respectively.

Prenatal exposure to bisphenol A alters mouse fetal pancreatic morphology and islet composition.

Background: Exposure to bisphenol A (BPA), an endocrine disrupting chemical, during gestation is associated with a variety of metabolic dysfunctions in adulthood, including hyperinsulinemia, glucose intolerance and insulin resistance. These modifications in glucose homeostasis largely stem from alterations in pancreatic function. However, the effects of BPA on the fetal pancreas have never been explored.

Wisp1 mediates Bmp3-stimulated mesenchymal stem cell proliferation.

Adipose tissue expansion, resulting from adipocyte hyperplasia and/or hypertrophy, is a hallmark of obesity. Adipocytes are derived from mesenchymal stem cells (MSCs) through adipogenesis, a process involving three key steps: proliferation, commitment and differentiation. Although studies have elaborated on the mechanisms regulating adipocyte commitment and differentiation, the factors that control MSC proliferation remain largely unknown.

Prenatal exposure to bisphenol A disrupts mouse fetal lung development.

Developmental exposure to bisphenol A (BPA) is associated with lung dysfunction and diseases. However, it is unknown if this association has a fetal origin. The present study addressed this important question by examining the effects of BPA on fetal lung development.

Prenatal Exposure to Bisphenol A Disrupts Mouse Fetal Liver Maturation in a Sex-Specific Manner.

Bisphenol A (BPA) is one of the most prevalent endocrine disrupting chemicals in the environment. Developmental exposure to BPA is known to be associated with liver dysfunction and diseases, such as hepatic steatosis, liver tumors, metabolic syndrome, and altered hepatic gene expression, and DNA methylation profiles. However, the effects of BPA on rodent liver development are unknown.

Bisphenol A disrupts gene expression in human placental trophoblast cells.

This study examined the effect of bisphenol A (BPA) on human placental gene expression using primary trophoblast cells as an in vitro model system. Trophoblast cells were isolated from human placentas at term, cultured and then exposed to environmentally relevant concentrations of BPA (0.1-2 μg/ml) for up to 24h, after which levels of 11β-HSD2 mRNA, protein and activity were determined by standard radiometric conversion assay, western blotting, and qRT-PCR, respectively.

The ERK1/2 signaling pathway regulates 11beta-hydroxysteroid dehydrogenase type 2 expression in human trophoblast cells through a transcriptional mechanism.

The placental 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD2; encoded by the HSD11B2 gene) plays a key role in fetal development, but its regulation is incompletely understood. We previously demonstrated that p38 MAPK was a positive regulator of placental 11beta-HSD2. However, it remains unknown if the other two MAPKs, ERK1/2 and JNK, were also involved.

Metallothionein-I- and -II-deficient mice display increased susceptibility to cadmium-induced fetal growth restriction.

Maternal cadmium exposure induces fetal growth restriction (FGR), but the underlying mechanisms remain largely unknown. The placenta is the main organ known to protect the fetus from environmental toxins such as cadmium. In this study, we examine the role of the two key placental factors in cadmium-induced FGR.

In utero programming of later adiposity: the role of fetal growth restriction.

Intrauterine growth restriction (IUGR) is strongly associated with obesity in adult life. The mechanisms contributing to the onset of IUGR-associated adult obesity have been studied in animal models and humans, where changes in fetal adipose tissue development, hormone levels and epigenome have been identified as principal areas of alteration leading to later life obesity. Following an adverse in utero development, IUGR fetuses display increased lipogenic and adipogenic capacity in adipocytes, hypoleptinemia, altered glucocorticoid signalling, and chromatin remodelling, which subsequently all contribute to an increased later life obesity risk.

Neuropeptide Y potentiates beta-adrenergic stimulation of lipolysis in 3T3-L1 adipocytes.

Recently, we have shown that neuropeptide Y (NPY) is produced and upregulated in visceral adipose tissue of an early-life programmed rat model of central obesity. Moreover, we have demonstrated that NPY promotes proliferation of adipocyte precursor cells and contributes to the pathogenesis of obesity. However, the role of NPY in regulating adipocyte metabolism is poorly understood.

Caffeine reduces 11β-hydroxysteroid dehydrogenase type 2 expression in human trophoblast cells through the adenosine A(2B) receptor.

Maternal caffeine consumption is associated with reduced fetal growth, but the underlying molecular mechanisms are unknown. Since there is evidence that decreased placental 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2) is linked to fetal growth restriction, we hypothesized that caffeine may inhibit fetal growth partly through down regulating placental 11β-HSD2. As a first step in examining this hypothesis, we studied the effects of caffeine on placental 11β-HSD2 activity and expression using our established primary human trophoblast cells as an in vitro model system.

Cortisol induces aromatase expression in human placental syncytiotrophoblasts through the cAMP/Sp1 pathway.

One of the dominant effects of glucocorticoids in triggering parturition in certain animal species is to drive the placental conversion of progesterone to estrogen. However, in the human placenta, estrogen is formed using dehydroepiandrosterone from the fetal adrenal glands rather than progesterone as precursor. Although aromatization of dehydroepiandrosterone is crucial in estrogen synthesis in human placenta, it is not known whether glucocorticoids affect aromatase expression.

BMP-3 promotes mesenchymal stem cell proliferation through the TGF-beta/activin signaling pathway.

Adipogenesis plays a key role in the pathogenesis of obesity. It begins with the commitment of mesenchymal stem cells (MSCs) to the adipocyte lineage, followed by terminal differentiation of preadipocytes to mature adipocytes. A critical, but poorly understood, component of adipogenesis involves proliferation of MSCs and preadipocytes.

Keratinocyte growth factor promotes preadipocyte proliferation via an autocrine mechanism.

Keratinocyte growth factor (KGF; also known as FGF-7) is a well-characterized paracrine growth factor for tissue growth and regeneration. However, its role in adipose tissue, which is known to undergo tremendous expansion in obesity, is virtually unknown. Given that we previously identified KGF as one of the up-regulated growth factors in adipose tissue of an early-life programmed rat model of visceral obesity, the present study was undertaken to examine the hypothesis that KGF promotes adipogenesis.