In the employed women, we only observed higher levels of Internet and Facebook addiction. The level of dependence on the Internet and Facebook was higher among younger women. Loneliness correlated with Internet and Facebook addiction, and more severe depressive symptoms entailed higher levels of Internet and Facebook addiction. Depressive symptoms and dependence on the Internet and Facebook were more common among single women. In the employed women, we only observed higher levels of Internet and Facebook addiction. The level of dependence on the Internet and Facebook was higher among younger women. Loneliness correlated with Internet and Facebook addiction, and more severe depressive symptoms entailed higher levels of Internet and Facebook addiction. The pathogenesis of acute lung injury (ALI) is complicated, the condition is developing rapidly, and the mortality rate is high. It is a common acute and critical illness in clinic. Here, we aimed to demonstrate the function and molecular mechanism of microRNA-147b (miR-147b) in ALI. MiR-147b mimic or miR-147b inhibitor was transfected into A549 cells to upregulate or downregulate miR-147b. https://www.selleckchem.com/products/ro-20-1724.html The inflammatory response of A549 cells was observed by measuring the levels of inflammatory cytokines (TNF-α, IL-6, IL-1β) and chemokines (CCL2, CCL4) by enzyme-linked immunosorbent assay (ELISA) assay. The detection of apoptosis in A549 cells relies on Cell Counting Kit-8 (CCK-8) assay, caspase-3 activity assay, and flow cytometry. Quantitative Real Time-Polymerase Chain Reaction (RT-PCR) and Western blot were employed to detect the expression of miRNA and protein. MiR-147b was downregulated in lipopolysaccharide (LPS)-induced ALI rats and LPS-treated A549 cells. Upregulation of miR-147b markedly suppressed LPS-induced inflammation and apoptosis of A549 cells, which was manifested by the reduction of inflammatory cytokines (TNF-α, IL-6, IL-1β) and chemokines (CCL2, CCL4), the reduction of LDH contents, the increase of cell viability, and the decrease of caspase-3 activity and apoptosis rate of A549 cells. The downregulation of miR-147b further induced inflammation and apoptosis of A549 cells caused by LPS, which was alleviated by inhibition of p38 MAPK pathway. Taken together, miR-147b was downregulated in ALI, and the overexpression of miR-147b inhibited LPS-induced inflammation and apoptosis in A549 cells via inhibition of p38 MAPK signaling pathway. Taken together, miR-147b was downregulated in ALI, and the overexpression of miR-147b inhibited LPS-induced inflammation and apoptosis in A549 cells via inhibition of p38 MAPK signaling pathway. To evaluate the relationship between functional abdominal pain and biopsychosocial factors the current diagnostic criteria show limits. This is a retrospective cohort study conducted in paediatric emergency department (ED) of a tertiary hospital in Rome. Children (0-18 years) evaluated for abdominal pain in the paediatric ED between January 2018 and December 2018 were enrolled. Patients were divided in 2 groups organic and functional groups. The main outcome was the prevalence of different subtypes of functional disorders (according to Rome IV criteria) and the role of possible biopsychosocial disorders related to patients with functional symptoms. In this study, 1130 patients were included. In the functional group, 37.6% of patients were classified as affected by functional dyspepsia, 26.7% by functional abdominal pain-non otherwise specified (FAP-nos), 20.8% by inflammatory bowel syndrome (IBS), and 15.9% by abdominal migraine. Children of our functional sample reported at least one of the items present in the inventory CSSI-24 (24-item Children's Somatic Symptoms Inventory), but more than 50% reported at least 4 of the items investigated. At 6 and 12 months follow up and, new prospective studies on these disorders could improve the inclusion criteria for FGIDs, thinning the dubious rate of patients expected from the literature on the Rome IV criteria. At 6 and 12 months follow up and, new prospective studies on these disorders could improve the inclusion criteria for FGIDs, thinning the dubious rate of patients expected from the literature on the Rome IV criteria. To elucidate the role of TUG1 in the onset of type 2 diabetes mellitus (T2DM) and the potential mechanism. Relative levels of TUG1 and SP1 in high-fat diet animal model and high-glucose cell model were detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR), and their correlation was analyzed. Potential binding sites in the promoter sequences of TUG1 and SP1 were predicted using the JASPAR. Their interaction was further confirmed by chromatin immunoprecipitation (ChIP) and Dual-Luciferase reporter assay. The influences of TUG1 on proliferative and apoptotic potentials in Min6 cells were examined by Cell Counting Kit-8 (CCK-8), 5-Ethynyl-2'-deoxyuridine (EdU) assay and flow cytometry, respectively. Subsequently, the interaction in the TUG1/miR-188-3p /FGF5 axis was similarly explored by Dual-Luciferase reporter assay. SP1 and TUG1 were downregulated in high-fat and high-glucose models, and they displayed a positive correlation. TUG1 bound E2 region in SP1 promoters. Knockdown of TUG1 inhibited proliferative rate and induced apoptosis in high-glucose-treated Min6 cells. Furthermore, the TUG1 / miR-188-3p /FGF5 axis was identified to be responsible for regulating Min6 cell functions. SP1 induces TUG1 downregulation in T2DM cell models, which further regulates proliferative and apoptotic potentials in islet cells by activating the miR-188-3p/FGF5 axis. SP1 induces TUG1 downregulation in T2DM cell models, which further regulates proliferative and apoptotic potentials in islet cells by activating the miR-188-3p/FGF5 axis. The aim of this study is to examine the maternal serum and cord blood irisin and preptin levels in gestational diabetes mellitus (GDM) and correlate their levels with demographic and biochemical parameters. A total of 21 pregnant women with GDM and 21 BMI and age-matched pregnant women without GDM were included in the study. They underwent 50 g glucose challenge test (GCT) between 24-28th gestational weeks. Women with a GCT result higher than 140 mg/dl received 100 g oral glucose tolerance test (OGTT). Detection of one of the following criteria after OGTT was accepted as GDM fasting plasma glucose level 92 mg/dL; 1-h plasma glucose level 180 mg/dL; and 2-h plasma glucose 153 mg/dL. Correlation between metabolic parameters and cord blood and maternal serum preptin and irisin levels in GDM and non-GDM subjects were analyzed. Maternal serum preptin values of GDM subjects were similar to the serum preptin values of non-GDM control subjects (123.12±34.3 pg/mL vs. 112.02±12.0 pg/mL, p<0.23). Cord blood preptin levels of GDM (64.