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Genetic expression and also mutational user profile analysis in various pathologic phases of hepatocellular carcinoma individuals.
Impulsivity and emotion dysregulation have been known to be risk factors for Internet gaming disorder (IGD), but their underlying neural mechanisms are not yet fully understood. Phlorizin ic50 Given that the prefrontal cortex has a key role in higher order cognition and addiction, the present study aimed to investigate emotional influences on response inhibition in situations with different cognitive demands. A total of 41 young male adults (20 with and 21 without IGD) were scanned while performing two versions of an emotional go/no-go task with demands on low and high working memory load. Patients with IGD showed a failure in response inhibition and increased activation of widespread brain regions, including prefrontal, motor-sensory, parietal, occipital, insula, and striatal regions across tasks. Among these regions, involvement of the dorsolateral prefrontal cortex and ventral striatum was observed only during the task with high demands on working memory. Moreover, it was also only during the high-load task that interaction between response inhibition and emotional states was observed in the dorsomedial prefrontal cortex, with observations revealing that its alteration in patients with IGD was associated with number of hours spent on Internet gaming. Our findings highlight a failure of response inhibition and dysfunction within the inhibitory control network. The special significance of our study is that dysfunctional dorsomedial prefrontal cortex may mediate abnormal emotional influences on response inhibition in patients with IGD. © 2020 Society for the Study of Addiction.BACKGROUND The several meta-analyses of the effect of vitamin D on depression have produced inconsistent results and studies dealing with anxiety were not incorporated. There has been no comprehensive analysis of how results are affected by the nature of the sample or the dosage and duration of supplementation. The study is aimed to investigate whether vitamin D supplementation reduces negative emotions and to analyze the possible influence of sample and regimen. METHOD We conducted a systematic review and meta-analysis of randomized controlled trials comparing the effect of vitamin D and placebo on negative emotion. Databases were searched for relevant articles published before February 2019. RESULTS The analysis covered 25 trials with a total of 7,534 participants and revealed an effect of vitamin D on negative emotion (Hedges' g = -0.4990, 95% CI [-0.8453, -0.1528], p = .0047, I2  = 97.7%). Subgroup analysis showed that vitamin D had an effect on patients with major depressive disorder and on subjects with serum 25(OH)D levels ≤50 nmol/L. The pooled data from trials of vitamin D supplementation lasting ≥8 weeks and dosage ≤4,000 IU/day indicated that vitamin D had an effect. CONCLUSIONS Our results support the hypothesis that vitamin D supplementation can reduce negative emotions. Patients with major depressive disorder and individuals with vitamin D deficiency are most likely to benefit from supplementation. But to interpret the results with high heterogeneity should still be cautious. © 2020 Wiley Periodicals, Inc.Acute clinical deterioration of a patient with chronic liver disease remains a decisive time point both in terms of medical management and prognosis. This condition, also known as acute decompensation, is an important event determining a crossroad in the trajectory of patients. A significant number of patients with acute decompensation may develop hepatic or extrahepatic organ failure, or both, which defines the syndrome named acute-on-chronic liver failure (ACLF), which is associated with a high morbidity and short-term mortality. ACLF may occur at any phase during chronic liver disease and is pathogenetically defined by systemic inflammation and immune metabolic dysfunction. When organ failures develop in the presence of cirrhosis, especially extrahepatic organ failures, liver transplantation (LT) may be the only curative treatment. This review outlines the evidence supporting LT in ACLF patients, highlighting the role of timing, bridging to liver transplantation, and possible indicators of futility. Importantly, prospective studies on ACLF and transplantation are urgently needed. This article is protected by copyright. All rights reserved.School health promotion in Southeast Asia has developed rapidly in recent years, and Japan has been one of the significant contributors to the reinforcement of school health promotion in the region. Starting from the Hashimoto Initiative on global parasite control, Japan advocated for international partnerships with several agencies for the development of school health programs in Southeast Asia. Through a strengthened collaboration with international organizations, countries such as the Lao PDR, Cambodia, the Philippines, and Thailand have created and implemented school health programs on nutrition, sanitation, and deworming, among others. In addition to school health program formulation and implementation, the expanded network in Southeast Asia led to a more capacitated school health personnel, with many workers in the education and health sectors benefitting from the training programs jointly held by collaborating organizations. This article is protected by copyright. All rights reserved.BACKGROUND Distal motor neuropathies with a genetic origin have a heterogeneous clinical presentation with overlapping features affecting distal nerves and including spinal muscular atrophies and amyotrophic lateral sclerosis. This indicates that their genetic background is heterogeneous. PATIENT AND METHODS In this work, we have identified and characterized the genetic and molecular base of a patient with a distal sensorimotor neuropathy of unknown origin. For this study, we performed whole-exome sequencing, molecular modelling, cloning and expression of mutant gene, and biochemical and cell biology analysis of the mutant protein. RESULTS A novel homozygous recessive mutation in the human VRK1 gene, coding for a chromatin kinase, causing a substitution (c.637T > C; p.Tyr213His) in exon 8, was detected in a patient presenting since childhood a progressive distal sensorimotor neuropathy and spinal muscular atrophy syndrome, with normal intellectual development. Molecular modelling predicted this mutant VRK1 has altered the kinase activation loop by disrupting its interaction with the C-terminal regulatory region.
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