Dose-, stage- and sex- difference of prenatal prednisone exposure on placental morphological and functional development.

Prednisone, a synthetic glucocorticoid, is commonly used to treat autoimmune diseases in pregnant women. However, some studies suggest that the use of prednisone during pregnancy may lead to adverse pregnancy outcomes. In this study, we established PPE mouse models at different doses (0.

Impacts of prenatal environmental exposures on fetal-placental-maternal bile acid homeostasis and long-term health in offspring.

During pregnancy, the maternal body undergoes a series of adaptative physiological changes, leading to a slight increase in serum bile acid (BA) levels. Although the fetal liver can synthesize BAs since the first trimester through the alternative pathway, the BA metabolic system is immature in the fetus. Compared to adults, the fetus has a distinct composition of BA pool and limited expression of BA synthesis enzymes and transporters.

α7-nAChR/P300/NLRP3-regulated pyroptosis mediated poor articular cartilage quality induced by prenatal nicotine exposure in female offspring rats.

Nicotine is developmentally toxic. Prenatal nicotine exposure (PNE) affects the development of multiple fetal organs and causes susceptibility to a variety of diseases in offspring. In this study, we aimed to investigate the effect of PNE on cartilage development and osteoarthritis susceptibility in female offspring rats.

The "toxic window" of amoxicillin exposure during pregnancy on long bone development in fetal mice.

Aims: Amoxicillin is a broad-spectrum beta-lactam antibiotic used to treat infectious diseases in pregnant women. Studies have shown that prenatal amoxicillin exposure (PAmE) has developmental toxicity on fetal development. However, the effect of PAmE on long bone development has not been reported.

Autophagy activated by GR/miR-421-3p/mTOR pathway as a compensatory mechanism participates in chondrodysplasia induced by prenatal caffeine exposure in male fetal rats.

Autophagy has been implicated in the developmental toxicity of multiple organs in offspring caused by adverse environmental conditions during pregnancy. We have previously found that prenatal caffeine exposure (PCE) can cause fetal overexposure to maternal glucocorticoids, leading to chondrodysplasia. However, whether autophagy is involved and what role it plays has not been reported.

The effects of prenatal azithromycin exposure on offspring ovarian development at different stages, doses, and courses.

Azithromycin, a commonly used macrolide antibiotic for treating chlamydial infections during pregnancy, has sparked investigations into its potential effects on offspring development. Despite these inquiries, there remains uncertainty about the specific impact of prenatal azithromycin exposure (PAzE) on offspring ovarian development and the precise "effect window". Pregnant mice, following clinical guidelines for azithromycin dosing, were orally administered azithromycin at different gestational stages [(gestational day, GD) 10-12 or GD 15-17], doses (50, 100, or 200 mg/kg·d), and courses (single or multiple).

Dose- and stage-dependent toxic effects of prenatal prednisone exposure on fetal articular cartilage development.

Prednisone is frequently used to treat rheumatoid diseases in pregnant women because of its high degree of safety. Whether prenatal prednisone exposure (PPE) negatively impacts fetal articular cartilage development is unclear. In this study, we simulated a clinical prednisone treatment regimen to examine the effects of different timings and doses of PPE on cartilage development in female and male fetal mice.

Microplastics cause hepatotoxicity in diabetic mice by disrupting glucolipid metabolism via PP2A/AMPK/HNF4A and promoting fibrosis via the Wnt/β-catenin pathway.

In recent years, microplastics (MPs) have gained significant attention as a persistent environmental pollutant resulting from the decomposition of plastics, leading to their accumulation in the human body. The liver, particularly of individuals with type 2 diabetes mellitus (T2DM), is known to be more susceptible to the adverse effects of environmental pollutants. Therefore, to investigate the potential impact of MPs on the liver of diabetic mice and elucidate the underlying toxicological mechanisms, we exposed db/db mice to 0.

A physiologically based toxicokinetic model of P-glycoprotein transporter-mediated placenta perfusion of dexamethasone in the pregnant rat.

The present dosage of Dexamethasone (DEX) administered to pregnant women may pose a risk of toxicity to their unborn offspring. We aimed to develop a maternal-fetal physiologically based toxicokinetic (PBTK) model for DEX in pregnant rats, with a specific focus on the role of the P-glycoprotein (P-gp) transporter in placenta perfusion, and finally facilitate the optimization of clinical DEX dosage. We conducted animal experiments to determine DEX concentrations in various rat tissues, and constructed the PBTK model using MATLAB software.

Degree of transverse colon ptosis: an alternative surrogate for evaluation of slow transit constipation.

Background: Although transverse colon ptosis (TCP) is commonly diagnosed in patients with constipation, it has not attracted significant attention in the evaluation of constipation. Herein, we assessed the correlation between TCP-related radiological parameters and the severity of slow transit constipation (STC).

Methods: This study was a single-center retrospective cohort study, with participants enrolled between 2012 and 2020 in Zhongnan Hospital of Wuhan University, China.

[Corrigendum] Downregulation of Notch1 induces apoptosis and inhibits cell proliferation and metastasis in laryngeal squamous cell carcinoma.

Following the publication of this article, a concerned reader drew to the authors' attention that a pair of the 24 h scratch‑wound assay data panels in Fig. 4A, and three of the migration and invasion assay data panels in Fig. 4B, exhibited overlapping sections, suggesting that data which were intended to have shown the results from differently performed experiments had originated from the same sources.

The microplastics exposure induce the kidney injury in mice revealed by RNA-seq.

Microplastics (MPs) may pollute drinking water, accumulate in the food chain, and release toxic chemicals that may cause a variety of diseases. The detrimental effects of MPs on kidney injury and fibrosis under long-term accumulation have not been fully documented. In this study, mice were exposed to MPs with three different diameters (80 nm, 0.

Simvastatin promotes rat Achilles tendon-bone interface healing by promoting osteogenesis and chondrogenic differentiation of stem cells.

To investigate the effect and mechanism of simvastatin on cell components of tendon-bone healing interface. The tendon-bone healing model was established by inserting the end of the Achilles tendon into the tibial tunnel on 24 rats, and simvastatin was used locally at the tendon-bone interface. Healing was evaluated at 8 weeks by mechanical testing, micro-CT, and qualitative histology including H&E, Toluidine blue, and immunohistochemical staining.

Prenatal smoke (Nicotine) exposure and offspring's metabolic disease susceptibility in adulthood.

Exposure to smoking (nicotine) during pregnancy not only directly affects fetal development, but also increases susceptibility to metabolic diseases in adulthood, but the mechanism of action remains unclear. Here, we review epidemiological and laboratory studies linking these relationships. In addition to the direct effect of nicotine on the fetus, intrauterine neuroendocrine-metabolic programming mediated by maternal glucocorticoid overexposure also plays an important role, involving glucocorticoid-insulin-like growth factor 1 (GC-IGF1) axis, hypothalamic-pituitary-adrenal (HPA) axis, renin-angiotensin system (RAS) and other endocrine systems.

Trans-Anastomotic Drainage Tube Placement After Hand-Sewn Anastomosis in Patients Undergoing Intersphincteric Resection for Low Rectal Cancer: An Alternative Drainage Method.

Anastomotic leakage (AL) is a common complication after intersphincteric resection (ISR). It significantly reduces quality of life and causes great distress to patients. Although traditional drainage (e.

Prenatal caffeine exposure induced renal developmental toxicity and transgenerational effect in rat offspring.

Epidemiological studies revealed that prenatal caffeine exposure (PCE) is associated with adverse gestational outcomes and susceptibility to chronic diseases in offspring, yet the effects of PCE on glomerulosclerosis susceptibility in adult female offspring and its intergenerational transmission remain to be further investigated. Here, we found that PCE caused fetal kidney dysplasia and glomerulosclerosis of the female offspring. Besides, the kidney of F1 offspring in PCE group exhibited the "low expressional programming of AT2R" and "GC-IGF1 programming" alteration.

Differential expression of placental 11β-HSD2 induced by high maternal glucocorticoid exposure mediates sex differences in placental and fetal development.

A variety of adverse environmental factors during pregnancy cause maternal chronic stress. Caffeine is a common stressor, and its consumption during pregnancy is widespread. Our previous study showed that prenatal caffeine exposure (PCE) increased maternal blood glucocorticoid levels and caused abnormal development of offspring.

Alteration of imprinted genes and offspring organ development caused by environmental factors.

Imprinted genes are a special subset of about 100 genes, which are mainly expressed in the form of parental monoallelic genes, and play important roles in the growth and development of embryos. In recent years, it has been found that epigenetic modification of imprinted genes induced by environmental factors can cause fetal multi-organ dysplasia and even susceptibility to multiple diseases in adulthood, which also exhibit multi-generational inheritance. In this review, we summarize the effects of expression changes of imprinted genes on ontogenetic development and organ functions in late stage of life, and propose that abnormal epigenetic modification and expression of imprinted genes caused by environmental deleterious factors are important mechanisms for explaining the multi-organ dysplasia in offspring.

Inducible factors and interaction of pulmonary fibrosis induced by prenatal dexamethasone exposure in offspring rats.

This study aimed to investigate the correlation between prenatal dexamethasone exposure (PDE) and susceptibility to pulmonary fibrosis in offspring. Healthy female Wistar rats were given dexamethasone (0.2 mg/kg.