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Graphic industry flaws after vigabatrin therapy through childhood: retrospective population-based review.
Additionally, advanced strategies of platelet generation were reviewed and the progress made in this field was discussed.Studies on extracellular vesicles have increased in recent years. The multi‑dimensional nature of their roles in cellular homeostasis, cell‑to‑cell and tissue‑to‑tissue communication at the level of the organism, as well as their actions on the holobiome (intra‑/interspecies interaction), have garnered the interest of a large number of researchers. Exosomes are one of the most researched classes of extracellular vesicles because they are carriers of targeted protein and DNA/RNA loads. Their multi‑functional cargo have been indicated to regulate a vast number of biological pathways in target cells. However, the mechanisms governing these interactions have not yet been fully determined. Endocrinology, by definition, focuses on homeostatic, and cell‑to‑cell and tissue‑to‑tissue communication mechanisms. Therefore exosomes should be included in this research topic. Exosomes have previously been associated with a number of endocrine disorders, including obesity, type 2 diabetes mellitus, disorders of the reproductive system and cancer. Furthermore, their biogenesis, composition and function have been associated with viruses, an entirely different domain of life. The profound roles of exosomes in homeostasis, stress and several pathological conditions, in conjunction with their selective and cell‑specific composition/function, allude to their use as promising circulating clinical biomarkers of systemic stress and specific pathologic states, and as biocompatible vehicles of therapeutic cargo. The current review provides information on exosomes and discusses their endocrine implications.The aim of the present study was to investigate the effects of the ginsenoside Rg1 on D‑galactose (D‑gal)‑induced mouse models of premature ovarian insufficiency (POI) and the related mechanisms. C57BL/6 female mice were randomly grouped into the following i) D‑gal [subcutaneously (s.c.) 200 mg/kg/d D‑gal for 42 days]; ii) Rg1 [intraperitoneally (i.p.) 20 mg/kg/d Rg1 for 28 days]; iii) D‑gal + Rg1 (s.c. 200 mg/kg/d D‑gal for 42 days followed by i.p. 20 mg/kg/d Rg1 for 28 days); and iv) saline groups (equivalent volume of saline s.c. and i.p.). Hematoxylin and eosin staining and electron microscopy were used to analyze uterine and ovarian morphology. Expression levels of senescence factors (p21, p53 and serine/threonine kinase), secretion of pro‑inflammatory cytokines [interleukin (IL)‑6, tumor necrosis factor (TNF)‑α and IL‑1β] and the activities of oxidation biomarkers [superoxide dismutase (T‑SOD), malondialdehyde (MDA) and glutathione peroxidase (GSH‑px)] were analyzed. The results showed that mice in the Rg1 + D‑gal group had significantly higher uterine and ovarian weight compared with those in the D‑gal group. Uterus morphology was also improved, based on the comparison between the D‑gal group and the Rg1 + D‑gal group. In addition, the Rg1 treatment after D‑gal administration significantly decreased the expression of senescence‑associated factors, enhanced the activities of anti‑oxidant enzymes total T‑SOD and GSH‑px in addition to reducing TNF‑α, IL‑1β, MDA and IL‑6 (based on the comparison between the D‑gal group and the Rg1 + D‑gal group). In conclusion, the present study suggested that the ginsenoside Rg1 improved pathological damages in the ovary and uterus by increasing anti‑oxidant and anti‑inflammatory abilities whilst reducing the expression of senescence signaling pathways in POI mouse models.Uterine leiomyoma presents the highest incidence among benign tumors of the female reproductive tract. The present study compared the proteome of leiomyoma treated with ulipristal acetate with that of untreated leiomyoma to investigate protein expression patterns in relation to oxidative stress. Paired tissue samples from seven treated and untreated leiomyomas were collected and the proteome was analyzed by two‑dimensional gel electrophoresis (2‑DE). Western blotting was used to validate the results of 2‑DE, and mass spectrometry was used to identify proteins. The tissue expression of 30 proteins was markedly affected by treatment with ulipristal acetate. Bioinformatics analysis revealed that several of the differentially expressed proteins were involved in the degradation of hydrogen peroxide and the synthesis of reactive oxygen species. The present study suggested the involvement of oxidative stress as a novel mechanism of action of ulipristal acetate. These findings require further investigations to understand the role of ulipristal acetate in the treatment of the leiomyoma.Treatment with mesenchymal stem cells (MSCs) has been revealed to suppress CD4 T cells from patients with pSS may provide insight regarding autoimmune diseases and offer a novel target for prospective treatment. Therefore, these results may be crucial in providing MSC treatment for pSS.Apelin‑36 is able to mediate a range of effects on various diseases, and is upregulated in lipopolysaccharide (LPS)‑induced acute lung injury (ALI). However, to the best of our knowledge, whether apelin‑36 is able to regulate LPS‑induced ALI has yet to be investigated. The present study aimed to investigate the role of apelin‑36 in LPS‑induced ALI, and the putative underlying mechanisms. Rats were assigned to one of four treatment groups The Control group, apelin‑36 group, LPS group and LPS + apelin‑36 group. BAY 2402234 At 4 h after intratracheal instillation of LPS (5 mg/kg), rats were intraperitoneally treated with 10 nmol/kg apelin‑36. Subsequently, pathological manifestations and the extent of inflammation and apoptosis of the lung tissues were assessed. Untransfected and apoptosis signal‑regulating kinase 1 (ASK1)‑overexpressing Beas‑2B cells were treated with LPS in the absence or presence of apelin‑36, and subsequently the levels of inflammation and apoptosis were assessed. The results obtained showed that the level of apelin‑36 was increased in the bronchoalveolar lavage fluid (BALF) of LPS‑treated rats. Co‑treatment with apelin‑36 alleviated LPS‑induced lung injury and pulmonary edema, reduced the levels of pro‑inflammatory cytokines, including interleukin‑6, monocyte chemoattractant protein‑1 and tumor necrosis factor‑α, in BALF, and inhibited apoptosis in the lung tissues. The presence of apelin‑36 also blocked the activation of LPS‑induced ASK1, p38, c‑Jun N‑terminal kinase and extracellular signal‑regulated kinase in lung tissues. , and these actions may be dependent on inhibition of the ASK1/mitogen‑activated protein kinase signaling pathway.In recent years, obesity has become a major public health concern. Obesity has been previously associated with low‑grade inflammation and TNF‑α induction in adipose tissue, which subsequently disrupts adipocyte metabolism. MicroRNAs (miRNAs/miRs) are important metabolic factors and their dysregulation has been associated with obesity‑related metabolic syndromes. In fact, it has been directly suggested that miR‑424 may be functionally associated with adipogenesis, although its exact role in this process remains unclear. The present study aimed to identify the function of miR‑424 in adipogenesis. In the present study, miR‑424 expression levels were analyzed during adipogenesis and the differential expression of this miRNA in the adipose tissue of obese and non‑obese children was also assessed. Furthermore, the interaction between miR‑424 and the adipocytokine TNF‑α was determined. Finally, miR‑424 target genes and downstream signaling pathways were predicted via bioinformatics and analyzed by performing a luciferase reporter assay to elucidate the functional mechanisms of miR‑424 in adipogenesis of visceral adipocytes. The results revealed that the expression levels of miR‑424 upregulated in the adipose tissue biopsies from obese children compared with the biopsies of non‑obese children. However, in cultured adipocytes, the expression levels of miR‑424 were discovered to be gradually downregulated during the adipogenesis process. TNF‑α treatment significantly downregulated the expression levels of miR‑424 via binding to its promoter region and reducing its transcriptional activity. Through bioinformatic prediction analysis, miR‑424 target genes were analyzed, of which several were identified to be involved in signaling pathways that are known to regulate adipogenesis, such as the Wnt signaling pathway. In conclusion, the present study indicated that miR‑424 was regulated by TNF‑α and served an important role in adipogenesis.Oxidative stress has been suggested to induce granulosa cell apoptosis, which contributes to follicular atresia. However, the mechanism via which oxidative stress mediates granulosa cell apoptosis remains elusive. Therefore, the aim of this study was to elucidate the molecular mechanisms regulating oxidative stress‑induced granulosa cell apoptosis. The present study demonstrated that reactive oxygen species induced by H2O2 resulted in human granulosa COV434 cell apoptosis via the regulation of sirtuin 1 (SIRT1)‑mediated p53 activity. Endogenous SIRT1 expression was alleviated by H2O2 treatment of COV434 cells in a time‑dependent manner. In addition, knockdown or inhibition of SIRT1 promoted H2O2‑induced poly(ADP‑ribose) polymerase (PARP) cleavage and p53 acetylation, which led to an increase in COV434 cell apoptosis. Treatment with H2O2 enhanced the expression levels of the p53‑dependent proteins, p53‑upregulated modulator of apoptosis (PUMA) and phorbol‑12‑myristate‑13‑acetate‑induced protein 1 (PMAIP1), as well as those of p53; however, knockdown of p53 decreased cleaved PARP, PUMA and PMAIP1 expression levels induced by H2O2 treatment. Moreover, knockdown of PUMA or PMAIP1 attenuated the H2O2 induction of PARP cleavage and COV434 cell apoptosis. In conclusion, the present findings suggested that H2O2‑induced oxidative stress causes granulosa COV434 cell apoptosis via the upregulation of p53 activity by SIRT1 suppression, indicating a mechanistic role of the SIRT1/p53 axis in H2O2‑induced granulosa cell apoptosis.The H19 long non‑coding RNA is involved in the development of tamoxifen resistance in breast cancer. However, the relationship between H19 and the metastatic potential and treatment options for tamoxifen‑resistant (TAMR) breast cancer is not completely understood. Curcumin inhibits cellular proliferation, migration and invasiveness in several cancer types, including pancreatic cancer, breast cancer and chronic myeloid leukemia. The present study aimed to investigate the role of H19 in MCF‑7/TAMR cell epithelial‑mesenchymal transition (EMT), migration and invasiveness, and to assess the ability of curcumin to inhibit H19‑mediated effects. Reverse transcription‑quantitative PCR and western blot analysis were conducted to detect the gene or protein expression. Cell Counting Kit‑8, wound healing and Transwell invasion assays were performed to estimate the capabilities of cell viability, invasion and migration. H19 overexpression enhanced MCF‑7/TAMR cell EMT, invasion and migration by upregulating Snail. Furthermore, curcumin notably decreased the expression levels of epithelial marker E‑cadherin and markedly increased the expression levels of mesenchymal marker N‑cadherin in MCF‑7/TAMR cells compared with the control group.
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