Childhood obesity is a global concern. The objectives of this meta-analytical study were to evaluate the effectiveness of school-based childhood obesity prevention programs, and to examine program components (moderators). The methods included searching databases (PubMed, Google Scholar, and the university's EBSCOhost Web service) as well as handsearching reference lists of articles published in English. Selection criteria for studies to be included in the meta-analysis were limited to studies that reported body mass index (BMI) or skinfold thickness as outcome measures and were school-based obesity prevention interventions; cross-sectional design studies were excluded. We hypothesized the meta-analysis would yield a summary effect size of magnitude which would indicate that school-based interventions have been effective in improving children's BMI or skinfold thickness values. A total of 26 114 children from 27 school-based childhood obesity prevention programs provided 54 effect sizes. A random-effects model calculated a small summary effect size of 0.039 (95% confidence interval -0.013 to 0.092). Heterogeneity among studies was observed which disappeared after pooling studies that used a randomized controlled trial design with one program moderator (physical activity or nutrition). We failed to accept our hypothesis and concluded that overall, school-based interventions have not been effective for improving body mass index or skinfold thickness to curb childhood obesity; however, randomized controlled trials that focused on physical activity or nutrition appeared to produce promising results.

Two interval estimation methods for a general linear function of binomial proportions have been proposed. One method [Zou GY, Huang W, Zhang X. A note on confidence interval estimation for a linear function of binomial proportions. Comput Statist Data Anal. 2009;53:1080–1085] combines Wilson interval estimates of individual proportions, and the other method [Price RM, Bonett DG. An improved confidence interval for a linear function of binomial proportions. Comput Statist Data Anal. 2004;45:449–456] uses an adjusted Wald interval. Both methods are appropriate in varying coefficient meta-analysis models where the risk differences are allowed to vary across studies. The two methods were compared in a simulation study under realistic meta-analysis conditions and the adjusted Wald method was found to have the best performance characteristics.

Competing predictions about the effect of social exclusion were tested by meta-analyzing findings from studies of interpersonal rejection, ostracism, and similar procedures. Rejection appears to cause a significant shift toward a more negative emotional state. Typically, however, the result was an emotionally neutral state marked by low levels of both positive and negative affect. Acceptance caused a slight increase in positive mood and a moderate increase in self-esteem. Self-esteem among rejected persons was no different from neutral controls. These findings are discussed in terms of belongingness motivation, sociometer theory, affective numbing, and self-esteem defenses.

Meta-analytic reliability generalizations (RGs) are limited by the scarcity of reliability reporting in primary articles, and currently, RG investigators lack a method to quantify the impact of such nonreporting. This article introduces a stepwise procedure to address this challenge. First, the authors introduce a formula that allows researchers to estimate the lower bound population average reliability for a desired instrument. Second, they present an equation to determine the Fail-Safe N for RG. This equation estimates the number of ''file drawer'' studies required to drop the aggregate score reliability of an instrument below a specified criterion value. Finally, the authors demonstrate the utility of these equations using published RG studies. Comments on the conclusions drawn from each RG application are provided.

Objectives: Patient-reported outcomes (PROs; self-report assessments) are increasingly important in evaluating medical care and treatment efficacy. Electronic administration of PROs via computer is becoming widespread. This article reviews the literature addressing whether computer-administered tests are equivalent to their paper-and-pencil forms. Methods: Meta-analysis was used to synthesize 65 studies that directly assessed the equivalence of computer versus paper versions of PROs used in clinical trials. A total of 46 unique studies, evaluating 278 scales, provided sufficient detail to allow quantitative analysis. Results: Among 233 direct comparisons, the average mean difference between modes averaged 0.2% of the scale range (e.g., 0.02 points on a 10-point scale), and 93% were within ±5% of the scale range. Among 207 correlation coefficients between paper and computer instruments (typically intraclass correlation coefficients), the average weighted correlation was 0.90; 94% of correlations were at least 0.75. Because the cross-mode correlation (paper vs. computer) is also a test-retest correlation, with potential variation because of retest, we compared it to the within-mode (paper vs. paper) test-retest correlation. In four comparisons that evaluated both, the average cross-mode paper-to-computer correlation was almost identical to the within-mode correlation for readministration of a paper measure (0.88 vs. 0.91). Conclusions: Extensive evidence indicates that paper- and computer-administered PROs are equivalent.

Background: Bone and mineral metabolism disorders are common among end-stage renal disease (ESRD) patients, which could lead to hip fracture. It is unclear whether the hip fracture risk is different among patients on hemodialysis (HD) versus peritoneal dialysis (PD). This meta-analysis was conducted to evaluate the hip fracture risk in ESRD patients on HD, when compared to PD. Methods: A literature review was conducted in EMBASE, MEDLINE, and Cochrane databases through January 31, 2018 to identify studies that appraised the rate or risk of hip fracture among patients on HD, when compared to PD. Effect estimates from the individual studies were derived and consolidated utilizing random-effect, generic inverse variance approach of DerSimonian and Laird. Results: Five cohort studies with 1 276 677 ESRD patients were enrolled. HD status was associated with a significantly higher risk of hip fracture with the pooled odds ratio (OR) of 1.61 (95% confidence interval [CI] 1.50-1.73, I2 = 10.0%), compared with PD. When the analysis was limited to studies with confounder-adjusted analysis, the pooled OR of hip fracture among HD patients was 1.57 (95% CI 1.43-1.72, I2 = 13.6%). Funnel plots and Egger's regression test demonstrated no significant publication bias in our meta-analysis. Conclusions: Among ESRD patients, HD status is associated with a 61% higher risk of hip fracture compared to PD.

Objective: We aimed to summarize the up-to-date epidemiology evidence on biomarkers of long-chain (LC) n-3 fatty acid (FA) intake in relation to breast cancer (BC). Methods: Epidemiology studies determining FA levels in biospecimen (circulating blood or adipose tissue (AT)) were identified from PubMed, EMBASE, and Cochrane Library databases until March 2018. Multivariate-adjusted risk ratios (RRs) with 95% confidence intervals (CIs) were pooled using a random-effect model. Difference in biospecimen proportions of LC n-3 FA between BC cases and non-cases were analyzed as a standardized mean difference (SMD). Results: Thirteen cohort and eleven case-control studies were eligible for the present meta-analysis. The estimated SMD was -0.14 (95% CI: -0.27, -0.11) for LC n-3 FA and -0.27 (95% CI: -0.42, -0.11) for LC n-3/n-6 FA ratio. When comparing the top tertiles with the bottom baseline levels, circulating LC n-3 FA was significantly associated with a lower risk of BC (RR: 0.84, 95% CI: 0.74, 0.96), but not AT (RR: 1.02, 95% CI: 0.70, 1.48). Significant inverse dose-response associations were observed for each 1% increment of circulating 20:5n-3 and 22:6n-3. Conclusion: This meta-analysis highlights that circulating LC n-3 FA as a biomarker of intake may be an independent predictive factor for BC, especially 20:5n-3 and 22:6n-3.

Background/objectives The relationship between nonalcoholic fatty liver disease (NAFLD) and albuminuria has been shown in many epidemiologic studies, although the results were inconsistent. This meta-analysis was conducted to summarize all available data and to estimate the risk of albuminuria among patients with NAFLD. Methods Comprehensive literature review was conducted utilizing Medline and Embase database through January 2018 to identify studies that compared the risk of albuminuria among patients with NAFLD versus those without NAFLD. Effect estimates from each study were extracted and combined using the random-effect, generic inverse variance method of DerSimonian and Laird. Results Nineteen studies (17 cross-sectional studies and two cohort studies) with 24 804 participants fulfilled the eligibility criteria and were included in this meta-analysis. The risk of albuminuria among patients with NAFLD was significantly higher than those without NAFLD with the pooled odds ratio (OR) of 1.67 [95% confidence interval (CI): 1.32-2.11]. Subgroup analysis demonstrated the significantly increased risk of albuminuria among patients with NAFLD without diabetes with pooled OR of 2.25 (95% CI: 1.65-3.06). However, we found no significant association between albuminuria and NAFLD among diabetic patients [pooled OR 1.28 (95% CI: 0.94-1.75)]. Conclusion A significantly increased risk of albuminuria among patients with NAFLD was observed in this meta-analysis. Physicians should pay more attention to the early detection and subsequent treatment of individuals with microalbuminuria especially in patients with NAFLD.

Objective: The aims of this project were to (a) perform a systematic review and meta-analysis of the associations between multiple neurological disorders (or neurological diseases) and potential influencing factors, including the association between fine particulate matter (PM 2.5) and intestinal dysfunction, and (b) investigate the mechanisms and toxicological effects of PM 2.5 exposure in the brain and intestines using a mouse model of Alzheimer's disease (AD). Design: A systematic review and meta-analysis was conducted to assess the risks of PM 2.5 exposure, as manifested by the incidence of exposure-associate neurological disorders or intestinal dysfunction. An APP/PS1 transgenic mouse model for AD was used to study the brain damage resulting from PM 2.5 exposure, and the miRNA/mRNA regulatory mechanisms contributing to this damage. The inflammatory injuries and bacterial community changes in the intestines of AD mice exposed to PM 2.5 were also investigated. Data sources: Articles for systematic review and meta-analysis were obtained by searching PubMed and China National Knowledge Infrastructure (CNKI), which were published for more than ten years. Animal experiments were conducted at Shanxi University of Taiyuan in China, and toxicological tests were performed according to the stipulated methods and protocols. Review and experimental methods: Data on the risks of incidence of neurological disorders associated with the environmental factor (PM 2.5) and biological factors (intestinal disorders and bacteria) were obtained, and random- or fixed-effects models (depending on the I 2 value) were used to pool the odds ratios (OR) with the 95% confidence intervals (CI) from individual studies. In the animal experiments, mice were divided into four groups of five animals per group, as follows: normal control mice in filtered air, AD mice in filtered air, normal control mice in PM 2.5 air, and AD mice in PM 2.5 air. PM 2.5 mice were exposed to ambient PM 2.5 in a whole-body inhalation exposure device for 8 weeks in Taiyuan, China. Well-established methods were used to explore the toxicological mechanisms by which PM 2.5 exacerbated brain damage in AD mice, namely open-field testing, enzyme-linked immunosorbent assay (ELISA), real-time quantitative RT-PCR, hematoxylin-eosin (HE) staining, and transmission electron microscopy (TEM). Brain damage and related biomarkers in the brains were measured, and miRNA and mRNA profiles were detected using high-throughput sequencing methods. The signaling pathways of miRNAs or mRNAs were predicted and summarized, and specific miRNAs and mRNAs were screened to explore the possible regulatory mechanisms of PM 2.5 -induced brain damage in AD mice. Intestinal and fecal samples from these mice were also subjected to 16S rRNA gene sequencing. HE staining, ELISA, and metagenome bacterial diversity analyses were performed to investigate the effects of PM 2.5 inhalation on intestinal tissue damage, inflammatory responses, and changes of bacterial diversity and communities in AD mice. Results: Long-term PM 2.5 exposure has been associated with increased risks of stroke, dementia, AD, autism spectrum disorder (ASD), and Parkinson's disease (PD) in humans, with the risks of ischemic and hemorrhagic stroke being higher than that of stroke in general. Furthermore, a relatively higher risk of stroke has been observed in heavily polluted countries compared to less polluted countries. It is known that some intestinal disorders and related problems such as constipation, inflammatory bowel disease, irritable bowel syndrome, small intestinal bacterial overgrowth, and diarrhea significantly increase the risks of developing AD or PD. For example, the risk estimates of Helicobacter pylori infection were significantly associated with AD and PD. From another angle, preliminary animal experimental results showed that PM 2.5 promoted brain morphological damage and decreased spatial exploration ability in AD mice, and was concomitant with increases in the concentrations of amyloid-β-42, acetylcholinesterase, tumor necrosis factor-α, and interleukin-6 and decreases in the concentrations of choline acetyltransferase. High-throughput sequencing and bioinformatics analyses revealed that miRNAs and mRNA had differential expression profiles subsequent to PM 2.5 exposure, which suggested that these species are involved in the molecular regulatory mechanisms and possible signal pathways of PM 2.5 -aggravated brain injury in AD mice. These PM 2.5 -aggravated brain injuries were correlated with pathological intestinal injury, inflammatory responses, and changes in bacterial diversity in the intestines and feces of PM 2.5 -exposed AD mice, and decreases in predominant bacteria were identified. These data will assist in delineating the ability of PM 2.5 exposure to induce pathological changes in the brain and gut tissue via the brain-gut axis and thereby aggravate AD. Conclusions: A systematic review and meta-analysis showed that there is a significant association between PM 2.5 exposure and the occurrence of stroke, dementia, AD, ASD, and PD, and a strong association between intestinal disorders and the presence of certain bacteria and the development of AD and PD. PM 2.5 (environmental factors) and intestinal disorders accompanied by changes in bacterial diversity (internal biological factors) appeared to be the two most important factors that increase the risk of developing neurological disorders. Experimental animal data showed that PM 2.5 potently damaged the brain and intestines of AD mice, and that the toxicological mechanisms of this PM 2.5 -mediated brain injury led to morphological changes, inflammation, and perturbation of miRNA/mRNA regulation in the brain. These data suggest that PM 2.5 inhalation also have modulatory effects on the abundance and diversity of intestinal bacteria in AD mice. The findings of this study have clarified positive relationships between environmental and biological factors and neurological disorders and have elucidated the potential mechanisms by which PM 2.5 may mediate the initiation or exacerbation of AD

Objective A systematic review and meta-analysis was conducted to assess the efficacy of low-sodium salt substitutes (LSSS) as a potential intervention to reduce cardiovascular (CV) diseases. Methods Five engines and ClinicalTrials.gov were searched from inception to May 2018. Randomised controlled trials (RCTs) enrolling adult hypertensive or general populations that compared detected hypertension, systolic blood pressure (SBP), diastolic blood pressure (DBP), overall mortality, stroke and other CV risk factors in those receiving LSSS versus regular salt were included. Effects were expressed as risk ratios or mean differences (MD) and their 95% CIs. Quality of evidence assessment followed GRADE (Grading of Recommendations Assessment, Development and Evaluation) methodology. Results 21 RCTs (15 in hypertensive (n=2016), 2 in normotensive (n=163) and 4 in mixed populations (n=5224)) were evaluated. LSSS formulations were heterogeneous. Effects were similar across hypertensive, normotensive and mixed populations. LSSS decreased SBP (MD-7.81 mm Hg, 95% CI-9.47 to-6.15, p<0.00001) and DBP (MD-3.96 mm Hg, 95% CI-5.17 to-2.74, p<0.00001) compared with control. Significant increases in urinary potassium (MD 11.46 mmol/day, 95% CI 8.36 to 14.55, p<0.00001) and calcium excretion (MD 2.39 mmol/day, 95% CI 0.52 to 4.26, p=0.01) and decreases in urinary sodium excretion (MD-35.82 mmol/day, 95% CI-57.35 to-14.29, p=0.001) were observed. Differences in detected hypertension, overall mortality, total cholesterol, triglycerides, glucose or BMI were not significant. Quality of evidence was low to very low for most of outcomes. Conclusions LSSS significantly decreased SBP and DBP. There was no effect for detected hypertension, overall mortality and intermediate outcomes. Large, long-term RCTs are necessary to clarify salt substitute effects on clinical outcomes. / Wellcome Trust / Revisión por pares