The Prevalence and Severity of School Bullying among Left-Behind Children: A Meta-Analysis.

The involvement of left-behind children (LBC) in school bullying has raised concern in China. However, the susceptibility of LBC to engage in bullying is controversial, and comprehensive, representative studies covering the entire country are lacking. The purpose of this study was to evaluate the prevalence and severity of school bullying among LBC. The Chinese National Knowledge Network, WanFang, VIP, PubMed, Web of Science, EMBASE, and EBSCO databases were searched for literature on being left-behind and bullying before April 2022. The effect size was measured by odds ratio (ORs), standard mean difference (SMD), and 95% confidence interval (CI). Random-effects or fixed-effects models were selected for meta-analysis, and subgroup analysis was used to explore the sources of heterogeneity. The meta-analysis included 25 studies of school bullying among LBC and non-LBC (NLBC). The prevalence of bullying perpetration and victimization among LBC were 18.58% (95% CI [3.72%, 33.44%], p < .05) and 40.62% (95% CI [25.47%, 55.78%], p < .05), respectively. Compared with NLBC, the risk of bullying perpetration and victimization among LBC increased 1.97 times (OR = 1.97, 95% CI [1.77, 2.20], p < .05) and 2.17 times (OR = 2.17, 95% CI [1.43, 3.29], p < .05), respectively. The severity of bullying experienced by LBC was higher than that of NLBC (SMD = 0.49, 95% CI [0.20, 0.79], p < .05). The prevalence and severity of school bullying were higher in LBC than in NLBC, and left-behindness was positively associated with school bullying. LBC are a crucial population to protect when developing bullying interventions.

A Novel Mutation in the Myosin Binding Protein C Gene in a Prader-Willi Syndrome Pedigree.

Prader-Willi syndrome (PWS) is a neurogenetic disorder caused by deficiency expression of paternally imprinted genes of the chromosomal region 15. In this study, we report a novel mutation in the myosin binding protein C (MYBPC3) gene in a Prader-Willi syndrome pedigree. Next-generation sequencing (NGS) and Sanger sequencing were performed to define and confirm the MYBPC3 gene mutation. Bioinformatics analysis was also performed for the mutated MYBPC3 protein using available software tools. The proband was diagnosed as PWS with about 4.727Mb copy number missed in the long arm of chromosome 15 and treated with growth hormone on 0.3 IU/day. Sanger sequencing identified a novel heterozygous mutation in the MYBPC3 gene, c.2002C>G (p.R668G). Bioinformatics analysis suggested the variant disease-causing; the Pro residue at 668 in the MYBPC3 protein was highly conserved. Moreover, interactions among MYBPC3 and other proteins suggested the potential effects on the development of cardiomyopathies. This is the first report of PWS with MYBPC3 gene mutation. Besides general examinations, it is vital for physicians to amply molecular genetics to get an accurate diagnosis in the clinic especially for rare diseases.

Mitochondrial A3243G mutation causes mitochondrial encephalomyopathy in a Chinese patient: Case report.

RATIONALE: Mitochondrial mutations are associated with a wide spectrum of clinical abnormalities. More than half of these mutations are distributed in the 22 mitochondrial tRNA genes, including tRNA. In particular, the A3243G mutation in the tRNA gene causes mitochondrial encephalomyopathy. PATIENT CONCERNS: A 12-year-old boy was admitted to Shaoxing People's Hospital because there is a reduction in the volume of speech, dysphonia, unable to write, recognize words, and unable to wear clothes, accompanied by unstable walking after treatment of unexplained fever and somnolence. DIAGNOSES: The proband underwent a thorough examination in our hospital and was diagnosed as mitochondrial encephalomyopathy. The proband carried the pathogenic heteroplasmic mutation A3243G mutation in mitochondrial 12S rRNA gene. Although his parents did not carry the mutation. INTERVENTIONS: Intravenous acyclovir, ceftriaxone, and dexamethasone were used for the patient's antiviral, antimicrobial, and anti-inflammatory therapy, respectively. Intravenous mannitol was gradually tapered for reducing intracranial pressure with furosemide for inducing diuresis. Intravenous arginine could help to treat alkalosis and supple some essential amino acids. Oral oxiracetam capsules, vitamin B1, and coenzyme Q10 were used for providing nutrition and improving energy. His medications were 30 mg vitamin B1, 0.1 g vitamin C, and mecobalamin 750 µg daily after discharge from our hospital. OUTCOMES: The patient was able to walk and talk slowly with improved writing skills and no stroke-like episodes. The neurological examination was negative and muscle tension was identified as grade V. LESSONS: Mitochondrial encephalomyopathy has different phenotypes, in addition to traditional examinations, it is important for clinicians to be familiar with genetic testing methodology as well as applications of these tests in clinic to get an accurate diagnosis.

Neural substrates of the impaired effort expenditure decision making in schizophrenia.

OBJECTIVE: Unwillingness to expend more effort to pursue high value rewards has been associated with motivational anhedonia in schizophrenia (SCZ) and abnormal dopamine activity in the nucleus accumbens (NAcc). The authors hypothesized that dysfunction of the NAcc and the associated forebrain regions are involved in the impaired effort expenditure decision-making of SCZ. METHOD: A 2 (reward magnitude: low vs. high) × 3 (probability: 20% vs. 50% vs. 80%) event-related fMRI design in the effort-expenditure for reward task (EEfRT) was used to examine the neural response of 23 SCZ patients and 23 demographically matched control participants when the participants made effort expenditure decisions to pursue uncertain rewards. RESULTS: SCZ patients were significantly less likely to expend high level of effort in the medium (50%) and high (80%) probability conditions than healthy controls. The neural response in the NAcc, the posterior cingulate gyrus and the left medial frontal gyrus in SCZ patients were weaker than healthy controls and did not linearly increase with an increase in reward magnitude and probability. Moreover, NAcc activity was positively correlated with the willingness to expend high-level effort and concrete consummatory pleasure experience. CONCLUSION: NAcc and posterior cingulate dysfunctions in SCZ patients may be involved in their impaired effort expenditure decision-making. (PsycINFO Database Record

Diminished caudate and superior temporal gyrus responses to effort-based decision making in patients with first-episode major depressive disorder.

BACKGROUND: Anhedonia, the loss of interest or pleasure in reward processing, is a hallmark feature of major depressive disorder (MDD), but its underlying neurobiological mechanism is largely unknown. The present study aimed to examine the underlying neural mechanism of reward-related decision-making in patients with MDD. METHOD: We examined behavioral and neural responses to rewards in patients with first-episode MDD (N=25) and healthy controls (N=25) using the Effort-Expenditure for Rewards Task (EEfRT). The task involved choices about possible rewards of varying magnitude and probability. We tested the hypothesis that individuals with MDD would exhibit a reduced neural response in reward-related brain structures involved in cost-benefit decision-making. RESULTS: Compared with healthy controls, patients with MDD showed significantly weaker responses in the left caudate nucleus when contrasting the 'high reward'-'low reward' condition, and blunted responses in the left superior temporal gyrus and the right caudate nucleus when contrasting high and low probabilities. In addition, hard tasks chosen during high probability trials were negatively correlated with superior temporal gyrus activity in MDD patients, while the same choices were negatively correlated with caudate nucleus activity in healthy controls. CONCLUSIONS: These results indicate that reduced caudate nucleus and superior temporal gyrus activation may underpin abnormal cost-benefit decision-making in MDD.

Increased prefrontal and parietal cortical thickness does not correlate with anhedonia in patients with untreated first-episode major depressive disorders.

Cerebral morphological abnormalities in major depressive disorder (MDD) may be modulated by antidepressant treatment and course of illness in chronic medicated patients. The present study examined cortical thickness in patients with untreated first-episode MDD to elucidate the early pathophysiology of this illness. Here, we examined cortical thickness in patients with first-episode MDD (N=27) and healthy controls (N=27) using an automated surface-based method (in FreeSurfer). By assessing the correlation between caudate volume and cortical thickness at each vertex on the cortical surface, a caudate-cortical network was obtained for each group. Subsequent analysis was performed to assess the effect of anhedonia by the Temporal Experience of Pleasure Scale. We observed increased cortical thickness at the right orbital frontal cortex and the left inferior parietal gyrus in MDD patients compared with healthy controls. Furthermore, morphometric correlational analysis using cortical thickness measurement revealed increased caudate-cortical connectivity in the bilateral superior parietal gyrus in MDD patients. All changes were not related to anhedonia. These preliminary findings may reflect disorder manifestation close to illness onset and may provide insight into the early neurobiology of MDD.

Overexpression of HMGB1 A-box reduced lipopolysaccharide-induced intestinal inflammation via HMGB1/TLR4 signaling in vitro.

AIM: To investigate the inhibitory effects and mechanism of high mobility group box (HMGB)1 A-box in lipopolysaccharide (LPS)-induced intestinal inflammation. METHODS: Overexpression of HMGB1 A-box in human intestinal epithelial cell lines (SW480 cells) was achieved using the plasmid pEGFP-N1. HMGB1 A-box-overexpressing SW480 cells were stimulated with LPS and co-culturing with human monocyte-like cell lines (THP-1 cells) using a Transwell system, compared with another HMGB1 inhibitor ethyl pyruvate (EP). The mRNA and protein levels of HMGB1/toll-like receptor (TLR) 4 signaling pathways [including HMGB1, TLR4, myeloid differentiation factor88 (MYD88), Phosphorylated Nuclear Factor κB (pNF-κB) p65] in the stimulated cells were determined by real-time polymerase chain reaction and Western blotting. The levels of the proinflammatory mediators [including HMGB1, interleukin (IL)-1ß, IL-6 and tumor necrosis factor (TNF)-α] in the supernatants of the stimulated cells were determined by ELISA. RESULTS: EP downregulated the mRNA and protein levels of HMGB1, inhibited the TLR4 signaling pathways (TLR4, MYD88 and pNF-κB p65) and reduced the secretion of proinflammatory mediators (HMGB1, IL-1ß, IL-6 and TNF-α) in the SW480 and THP-1 cells activated by LPS but not in the unstimulated cells. Activated by LPS, the overexpression of HMGB1 A-box in the SW480 cells also inhibited the HMGB1/TLR4 signaling pathways and reduced the secretion of these proinflammatory mediators in the THP-1 cells but not in the transfected and unstimulated cells. CONCLUSION: HMGB1 A-box, not only EP, can reduce LPS-induced intestinal inflammation through inhibition of the HMGB1/TLR4 signaling pathways.

Standard triple therapy for Helicobacter pylori infection in China: a meta-analysis.

AIM: To assess the efficacy and safety of standard triple therapy compared with other pre-existing and new therapies in China. METHODS: Literature searches were conducted in the following databases: PubMed, EMBASE, the Cochrane Central Register of Controlled Trials, the VIP database, the China National Knowledge Infrastructure database, and the Chinese Biomedical Database. A meta-analysis of all randomized controlled trials (RCTs) comparing standard triple therapy for the eradication of Helicobacter pylori with pre-existing and new therapies in China was performed using Comprehensive Meta-Analysis 2.0. There were 49 studies that met our criteria and the qualities of these studies were assessed using the Jadad scale. The Mantel-Haenszel method was used for pooling dichotomous data. We also conducted subgroup analyses according to age, duration of treatment and drug type. Sensitivity analyses and a cumulative meta-analysis were also performed with CMA 2.0. Publication bias was evaluated using Egger's test, Begg's test or a funnel plot. RESULTS: A total of 49 RCTs including 8332 patients were assessed. This meta-analysis showed that standard triple therapy with proton pump inhibitors (PPIs), amoxicillin (AMO) and clarithromycin (CLA) was inferior to sequential therapy [relative risk (RR) = 0.863; 95% confidence interval (CI): 0.824-0.904], but was not superior to quadruple therapy (RR = 1.073; 95%CI: 0.849-1.357) or other triple therapies (RR = 1.01; 95%CI: 0.936-1.089). The meta-analysis also suggested that standard triple therapy is slightly more effective than dual therapy (RR = 1.14; 95%CI: 0.99-1.31). However, the differences were not statistically significant. We removed the only trial with a regimen lasting 14 d by sensitivity analysis and found that 7-d standard triple therapy was superior to 7-d dual therapy (RR = 1.222; 95%CI: 1.021-1.461). Moreover, a sub-analysis based on the duration of quadruple therapy indicated that the 7-d and 10-d standard triple therapies were inferior to sequential therapy (RR = 0.790; 95%CI: 0.718-0.868; RR = 0.917; 95%CI: 0.839-1.002, respectively). Additionally, there were no significant differences in cure rate or adverse events among standard triple therapy, quadruple therapy, and other triple therapies (RR = 0.940; 95%CI: 0.825-1.072; RR = 1.081; 95%CI: 0.848-1.378, respectively). Standard triple therapy had a higher occurrence of side effects than sequential therapy (RR = 1.283; 95%CI: 1.066-1.544). CONCLUSION: The eradication rates with a standard triple therapy consisting of PPI, AMO, and CLA are suboptimal in China, and new treatment agents need to be developed.

Clinical analysis of transvaginal hydrolaparoscopy in infertile patients.

OBJECTIVE: To evaluate the application of transvaginal hydrolaparoscopy for exploration of the pelvic cavity exploration in infertile women. STUDY DESIGN: A total of 510 infertile women were included in this study from May 1st, 2009 to April 30, 2012 in the clinic of the Hebei Research Institute for Family Planning. RESULTS: In 495 of 510 of the patients (97.06%), a successful operation was achieved at the first puncture. Of these 495 patients, 286 (57.78%) showed bilateral patency. Completely normal tubo-ovarian and pelvic structures were observed only in 79 patients (15.96%): 16 patients (3.23%) had bilateral tube obstruction, 18 (3.64%) had hydrosalpinx, and 8 (1.62%) had fimbrial stenosis. Pelvic abnormalities occurred in 240 patients (44.04%), including bilateral and/or unilateral tubo-ovarian adhesions in 80 patients (16.16%) and 160 (32.32%) found with adhesions in other parts of the pelvic cavity. Pelvic endometriosis was found in 82 patients (16.57%) and 19 (3.84%) had two or more lesions in the pelvic cavity. In addition, 9 cases (1.82%) of ovarian cysts, 7 (1.41%) of bilateral vesicular appendices and 43 cases (6.69%) of a unilateral vesicular appendix were observed. In addition, convoluted tubes such as bent or twisted tubes were found in 4 cases of bilateral fallopian tube occlusion patients (0.81%) and 17 cases of unilateral tubal occlusion patients (3.43%). CONCLUSIONS: Transvaginal hydrolaparoscopy is a feasible, safe, and cost-effective microinvasive technique. This technique can be considered as an alternative procedure for evaluating female infertility.

[Radiosensitizing effect of erlotinib on human lung adenocarcinoma cell line A549].

OBJECTIVE: To explore the radiosensitizing effect of erlotinib on human lung adenocarcinoma cell line A549 cells and the related mechanisms. METHODS: The inhibitory effect of erlotinib on A549 cells was assessed by MTT assay, and its IC50 concentration was calculated. The radiosensitization was evaluated by the method of clone forming assay. Flow cytometry was used to analyze the effect of erlotinib on cell cycle and apoptosis. RESULTS: The growth of A549 cells was inhibited after the cells were exposed to erlotinib for 48 hours. Moreover, the inhibitory rates increased with the increase of erlotinib concentrations, and IC50 was 19.26 µmol/L. In contrast to the irradiation alone group, the survival rates of the cells in erlotinib plus irradiation groups decreased, and erlotinib enhanced the radiosensitivity of the A549 cells. This effect was further increased as cells were exposed to erlotinib for a longer time. In the irradiation alone group and the two groups exposed to erlotinib for 24 hours and 48 hours before irradiation, D0 values were 3.01 Gy, 2.58 Gy and 2.45 Gy respectively, and Dq values were 2.16 Gy, 1.94 Gy and 1.61 Gy, respectively. In the last two groups, SERD0 values were 1.17 and 1.23, respectively. The flow cytometry analysis showed that erlotinib induced G2/M phase arrest and increased the apoptosis rate in A549 cells. With the increase of exposure time, the effects were more significant. CONCLUSIONS: Erlotinib inhibits the A549 cell growth and enhances the radiosensitivity of A549 cells in vitro. The radiosensitizing mechanisms might be related to inhibiting repair of sublethal injury and inducing G2/M phase arrest and apoptosis.