Impact of the intensive psychological intervention care on post-traumatic stress disorder and negative emotions of teenage female patients seeking an induced abortion.

Aim: This study aimed to investigate the effects of intensive psychological intervention care on adverse emotions and post-traumatic stress disorder (PTSD) symptoms in female teenage patients after induced abortion.

Methods: This prospective cohort study included 100 teenage female patients seeking induced abortion who were randomly divided into two groups: the intervention group ( = 50) and the control group ( = 50). The intervention group received intensive psychological intervention care, while the control group received standard routine nursing.

Organocatalytic Asymmetric Construction of Tetrasubstituted Carbon Stereocenters Bearing Three Heteroatoms via Intramolecular Cyclization of Vinylidene -Quinone Methide with Imidates.

We report herein an organocatalytic asymmetric protocol for the construction of tetrasubstituted carbon stereocenters bearing three heteroatoms. The reaction proceeded via the enantioselective intramolecular cyclization reaction of vinylidene -quinone methide (VQM) with imidates to form pentacyclic heterocycles. The formed tetrasubstituted carbon center was stable under a high temperature and the conditions for further transformations.

Manganese exposure caused reproductive toxicity of male mice involving activation of GnRH secretion in the hypothalamus by prostaglandin E2 receptors EP1 and EP2.

Exposure to manganese (Mn) can cause male reproductive damage and lead to abnormal secretion of sex hormones. Gonadotropin-releasing hormone (GnRH) plays an important role in the neuromodulation of vertebrate reproduction. Astrocytes can indirectly regulate the secretion of GnRH by binding paracrine prostaglandin E (PGE) specifically to the EP1 and EP2 receptors on GnRH neurons.

Prepubertal overexposure to manganese induce precocious puberty through GABA receptor/nitric oxide pathway in immature female rats.

Gamma-aminobutyric acid (GABA) plays a critical role in regulation of gonadotropin-releasing hormone (GnRH) through GABA receptor (GABAR). Nitric oxide (NO) production has correlation with GABA and regulates GnRH secretion. This study was performed to examine the mechanisms by which manganese (Mn) accelerate puberty onset involves GABAR/NO pathway in the preoptic area-anterior hypothalamus (POA-AH) in immature female rats.

The effect of manganese exposure on GnRH secretion via Nrf2/mGluR5/COX-2/PGE2/signaling pathway.

There are limited studies focused on the precise mechanism of gonadotropin-releasing hormone (GnRH) secretion dysfunction after overexposure to manganese (Mn). The objective of the present study was to explore the mechanism of Mn disruption of GnRH synthesis via nuclear factor erythroid-2-related factor-2 (Nrf2)/metabotropic glutamate receptor-5 (mGluR5)/cyclooxygenase-2 (COX-2)/prostaglandin E2 (PGE) signaling pathway in vitro and in vivo. Primary astrocytes were cultured and treated with different doses of Mn, tert-butylhydroquinonet (tBHQ; Nrf2 agonists), 3-[(2-methyl-4-thaizolyl) ethynyl] pyridine (MTEP; mGluR5 inhibitor), and celecoxib (COX-2 inhibitor) to measure the levels of COX-2, mGluR5, Nrf2, and Nrf2 target genes.

Occupational manganese exposure, reproductive hormones, and semen quality in male workers: A cross-sectional study.

It has been found that exposure to manganese (Mn) could induce reproductive dysfunction, but its occupational risk in male workers is unclear. This study aims to assess the association of occupational Mn exposure with reproductive hormones and semen quality in a cross-sectional study. Urinary Mn, semen quality, and reproductive hormones were explored in 84 male workers occupationally exposed to Mn and 92 referents.

Mn Inhibits GSH Synthesis via Downregulation of Neuronal EAAC1 and Astrocytic xCT to Cause Oxidative Damage in the Striatum of Mice.

Excessive manganese (Mn) can accumulate in the striatum of the brain following overexposure. Oxidative stress is a well-recognized mechanism in Mn-induced neurotoxicity. It has been proven that glutathione (GSH) depletion is a key factor in oxidative damage during Mn exposure.