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To investigate longitudinal relationships between parenting practices in childhood and adolescent suicidality, and assess the mediating role of emotional and behavioral symptoms.
Data were drawn from the National Longitudinal Survey of Children and Youth, a Canadian population-based longitudinal cohort study. The sample included 9,490 children aged 10-11 who were followed up biennially to ages 14-15. Parents reported their positive and punitive parenting practices when children were 10-11. Adolescents self-reported symptoms of depression/anxiety, hyperactivity, conduct disorder, and social aggression at 12-13, and past-year suicidal ideation and suicide attempts at 14-15.
The inverse associations between positive parenting at 10-11 and suicidal behaviors at 14-15 were significantly mediated by symptoms of hyperactivity, conduct disorder, and social aggression at 12-13. Direct relationships between punitive parenting and suicidal behaviors were observed. These associations were significantly mediated by hyperactivity and, among boys only, by conduct disorder and social aggression. The association between punitive parenting and suicide attempt was additionally mediated by depression/anxiety.
Parenting in childhood may be associated with adolescent suicidality both directly and indirectly through emotional and behavioral symptoms. Interventions aimed at reducing the use of harsh disciplinary strategies and promoting positive parent-child interactions may reduce the burden of adolescent suicidality.
Parenting in childhood may be associated with adolescent suicidality both directly and indirectly through emotional and behavioral symptoms. Interventions aimed at reducing the use of harsh disciplinary strategies and promoting positive parent-child interactions may reduce the burden of adolescent suicidality.We present a strategy to achieve highly cooperative photoswitching, where the initial switching event greatly facilitates subsequent switching of the neighboring unit. By linking donor/acceptor substituted dihydropyrenes via suitable π-conjugated bridges, the quantum yield of the second photochemical ring-opening process could be enhanced by more than two orders of magnitude as compared to the first ring-opening. As a result, the intermediate mixed switching state is not detected during photoisomerization although it is formed during the thermal back reaction. Comparing the switching behavior of various dimers, both experimentally and computationally, helped to unravel the crucial role of the bridging moiety connecting both photochromic units. The presented dihydropyrene dimer serves as model system for longer cooperative switching chains, which, in principle, should enable efficient and directional transfer of information along a molecularly defined path. Moreover, our concept allows to enhance the photosensitivity in oligomeric and polymeric systems and materials thereof.Genomic instability is one of the hallmarks of aging, and both DNA damage and mutations have been found to accumulate with age in different species. Certain gene families, such as sirtuins and the FoxO family of transcription factors, have been shown to play a role in lifespan extension. However, the mechanism(s) underlying the increased longevity associated with these genes remains largely unknown and may involve the regulation of responses to cellular stressors, such as DNA damage. Phospho(enol)pyruvicacidmonopotassium Here, we report that FOXO3a reduces genomic instability in cultured mouse embryonic fibroblasts (MEFs) treated with agents that induce DNA double-strand breaks (DSBs), that is, clastogens. We show that DSB treatment of both primary human and mouse fibroblasts upregulates FOXO3a expression. FOXO3a ablation in MEFs harboring the mutational reporter gene lacZ resulted in an increase in genome rearrangements after bleomycin treatment; conversely, overexpression of human FOXO3a was found to suppress mutation accumulation in response to bleomycin. We also show that overexpression of FOXO3a in human primary fibroblasts decreases DSB-induced γH2AX foci. Knocking out FOXO3a in mES cells increased the frequency of homologous recombination and non-homologous end-joining events. These results provide the first direct evidence that FOXO3a plays a role in suppressing genome instability, possibly by suppressing genome rearrangements.Atmospheric pressure chemical ionizations (APCIs) of morphine, codeine, and thebaine were studied in a corona discharge ion source using ion mobility spectrometry (IMS) at temperature range of 100°C-200°C. Density functional theory (DFT) at the B3LYP/6-311++G(d,p) and M062X/6-311++G(d,p) levels of theory were used to interpret the experimental data. It was found that in the presence of H3 O+ as reactant ion (RI), ionization of morphine and codeine proceeds via both the protonation and carbocation formation, whereas thebaine participates only in protonation. Carbocation formation (fragmentation) was diminished with decrease in the temperature. At lower temperatures, proton-bound dimers of the compounds were also formed. Ammonia was used as a dopant to produce NH4+ as an alternative RI. In the presence of NH4+ , proton transfer from ammonium ion to morphine, codeine, and thebaine was the dominant mechanism of ionization. However, small amount of ammonium attachment was also observed. The theoretical calculations showed that nitrogen atom of the molecules is the most favorable proton acceptor site while the oxygen atoms participate in ammonium attachment. Furthermore, formation of the carbocations is because of the water elimination from the protonated forms of morphine and codeine.This article presents selective transformations of some readily available cyclodienes through simple chemical procedures into novel functionalized small-molecular entities. The syntheses hereby described involved selective cycloadditions, followed by ring-opening metathesis of the resulting β-lactam or isoxazoline derivatives and selective cross-metathesis by differentiation of the olefin bonds on the alkenylated heterocycles. The cross-metathesis transformations have been detailed, which were performed under various experimental conditions with the aim of exploring chemodiscrimination of the olefin bonds and delivering the corresponding functionalized β-lactam or isoxazoline derivatives.Emotion regulation may affect the levels of psychological distress of cancer survivors, but inconsistencies exist among studies regarding the direction of this effect. The systematic review and meta-analysis sought to estimate the associations between emotion regulation patterns (repression, suppression, experiential avoidance and cognitive reappraisal) and psychological distress among cancer survivors. Fifteen studies met inclusion criteria for systematic review, and seven studies focussing on suppression were included in the meta-analysis. The systematic review pointed to a marked variability in associations among the emotion regulation patterns and psychological distress. The three meta-regressions of the relationships between suppression and psychological distress found significant fixed- and random-effect sizes (except marginal significance of a random-effect model for partial correlation). Subgroup analysis showed no moderation effect of time since diagnosis or study quality, but a significant difference (fixed-effect model only, p = 0.005) was found between correlative studies and those controlling for confounders. The current study suggests that suppression is related to elevated levels of psychological distress among cancer survivors, although large inconsistencies exist among studies and publication bias could not be ruled out. Further studies with large samples and a consistent approach are thus required to evaluate the associations of emotion regulation patterns and psychological distress.
Hypoxia is a hallmark of cancer and is associated with poor prognosis. However, the molecular mechanism by which hypoxia promotes tumor progression remains unclear. MicroRNAs dysregulation has been shown to play a critical role in the tumor and tumor microenvironment. Here, we investigated the roles of miR-495 and miR-5688 in human non-small cell lung cancer (NSCLC) and their underlying mechanism.
The expression levels of miR-495 and miR-5688 in human NSCLC tissue specimens were measured by quantitative real-time polymerase chain reaction (qRT-PCR). Deferoxamine (DFO) was used to determine whether the regulation of miR-495 and miR-5688 under hypoxia was dependent on hypoxia-inducible factor 1-alpha (HIF-1α). Furthermore, the functions of miR-495 and miR-5688 in tumor progression were evaluated using colony formation, 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium (MTS), wound healing, transwell assays, and xenograft model. Two algorithms, PicTAR and Targetscan, weumor suppressive role by repressing IL-11 expression.
We found that hypoxia down-regulated the expression levels of miR-495 and miR-5688 in NSCLC to enhance IL-11 expression and tumor progression, indicating that the miR-495/miR-5688/IL-11 axis may serve as a therapeutic target and potential biomarker for NSCLC.
We found that hypoxia down-regulated the expression levels of miR-495 and miR-5688 in NSCLC to enhance IL-11 expression and tumor progression, indicating that the miR-495/miR-5688/IL-11 axis may serve as a therapeutic target and potential biomarker for NSCLC.The rs619586 polymorphism has been shown to alter the expression of MALAT1, which act as a competing endogenous RNA (ceRNA) against miR-145. And miR-145 was found to target COL5A1, the interaction between which was shown to be involved in the pathogenesis of invasive meningioma. In this study, we aimed to explore the effect of rs619586 polymorphism and its underlying molecular mechanism in invasive meningioma. Real-time PCR and Western Blot analysis were used to study the differentiated expression of miR-145, MALAT1 (metastasis-associated lung adenocarcinoma transcript 1) and COL5A1 (collagen alpha-1(V) chain) in tumour/serum samples genotyped as rs619586 AA, AG and GG. Computational analysis and luciferase reporter assay were also conducted to identify the regulatory relationship between miR-145 and MALAT1/COL5A1. Meanwhile, expression of miR-145 and COL5A1 in different cell treatment groups was measured to validate the results obtained from earlier experiments. As shown by the results and in tumour/serum samples genotyped as AA, AG and GG, the expression of both MALAT1 and COL5A1 was down-regulated in a stepwise fashion, while the expression of miR-145 was increased, suggesting a potential negative relationship between MALAT1/COL5A1 and miR-145. Meanwhile, miR-145 was shown to bind to MALAT1, while COL5A1 was identified as a virtual target gene of miR-145. As a consequence, a MALAT1/miR-145/COL5A1 molecular pathway was established based on the above results. In particular, with the presence of rs619586 A>G polymorphism, the expression of MALAT1 and COL5A1 was both reduced, leading to reduced invasiveness of meningioma.
The aim of the study was to evaluate the transurethral resection of the prostate (TURP) outcomes of unobstructed patients with detrusor underactivity (DUA), comparing the surgical results between obstructed and unobstructed males with concomitant DUA, at midterm follow-up.
This was an observational, prospective, comparative, nonrandomized study. Candidates to TURP underwent preoperative urodynamics (UD), with a diagnosis of DUA, were divided in two cohorts Group A unobstructed men, group B males with bladder outlet obstruction (BOO). Males were evaluated yearly with uroflowmetry (UF), post-void residual (PVR), and bladder voiding efficiency (BVE), International Prostate Symptom Score (IPSS) questionnaire, visual analogic scale (VAS) for subjective assessment of the quality of life. The degree of the variation of maximum flow rate (Qmax), PVR, BVE, IPSS, VAS between baseline and follow-up (Δ) was evaluated.
Patients in group A were 28 and in group B 23. Overall patient's mean ± SD age was 63.37 ± 12.41 years.
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