ObjectiveThe purpose of the present meta-analysis was to evaluate the association between the inflammatory potential of diet, determined by the dietary inflammatory index (DII®) score, and depression.DesignSystematic review and meta-analysis.SettingA comprehensive literature search was conducted in PubMed, Web of Science and EMBASE databases up to August 2018. All observational studies that examined the association of the DII score with depression/depressive symptoms were included.SubjectsFour prospective cohorts and two cross-sectional studies enrolling a total of 49 584 subjects.ResultsOverall, individuals in the highest DII v. the lowest DII category had a 23 % higher risk of depression (risk ratio (RR)=1·23; 95 % CI 1·12, 1·35). When stratified by study design, the pooled RR was 1·25 (95 % CI 1·12, 1·40) for the prospective cohort studies and 1·16 (95 % CI 0·96, 1·41) for the cross-sectional studies. Gender-specific analysis showed that this association was observed in women (RR=1·25; 95 % CI 1·09, 1·42) but was not statistically significant in men (RR=1·15; 95 % CI 0·83, 1·59).ConclusionsThe meta-analysis suggests that pro-inflammatory diet estimated by a higher DII score is independently associated with an increased risk of depression, particularly in women. However, more well-designed studies are needed to evaluate whether an anti-inflammatory diet can reduce the risk of depression.
The prognostic value of the ankle–brachial index (ABI) in patients with coronary artery disease (CAD) remains undefined. This meta-analysis sought to investigate the association of abnormal ABI and adverse outcomes in patients with CAD. PubMed, Embase, China National Knowledge Infrastructure, VIP, and Wanfang databases were comprehensively searched for studies published from inception to September 10, 2019. All observational studies investigating the association of abnormal baseline ABI and risk of major adverse cardiovascular events (MACE) or all-cause mortality were selected. Normal ABI is usually defined as between 0.9 and 1.4. The prognostic values were summarized by pooling risk ratio (RR) with 95% confidence intervals (CIs) for abnormal versus normal ABI category. Nine (9384 patients with CAD) studies were included. Abnormal ABI was independently associated with MACE (RR: 2.46; 95% CI: 2.02-2.99) and all-cause mortality (RR: 1.74; 95% CI: 1.32-2.30). Subgroup analysis showed that the pooled RR for MACE was 2.34 (95% CI: 1.73-3.16) for an abnormal low ABI. Abnormal ABI predicts MACE and all-cause mortality in patients with CAD, even after adjusting conventional confounding factors. However, the prognostic value of abnormal ABI is mainly dominated by a low ABI rather than a high ABI.
BackgroundPulmonary arterial hypertension (PAH) caused by congenital heart disease (CHD) is very common in clinics. Some studies have shown that PAH is related to the number of endothelial progenitor cells (EPCs), but there is no report on the relationship between PAH and the number of EPCs in children with CHD.MethodsIn this study, a total of 173 cases with CHD (from 0 to 6 years old) were collected. According to the mean pulmonary arterial pressure (mPAP) measured by right heart catheterization, these cases were divided into PAH groups (including high PAH group, mPAP> 25 mmHg, n = 32, and the middle PAH group, 20 mmHg ≤ mPAP≤25 mmHg, n = 30) and non-PAH group (mPAP< 20 mmHg, n = 111). Peripheral blood was taken for flow cytometry, and the number of EPCs (CD133+/KDR+ cells) was counted. The number of EPCs /μL of peripheral blood was calculated using the following formula: EPCs /μL = WBC /L × lymphocytes % × EPCs % × 10− 6.ResultsThe median EPCs of the non-PAH group, middle PAH group and high PAH group is 1.86/μL, 1.30 /μL and 0.98/μL, respectively. The mPAP decreases steadily as the level of EPCs increases (P < 0.05). After adjustment of gender, age and BMI, the number of EPCs was significantly associated with a decreased risk of high PAH (OR = 0.37, 95% CI: 0.16–0.87, P < 0.05). However, EPCs was not significantly associated with middle PAH (P > 0.05).ConclusionThe findings revealed that the EPCs and high PAH in patients with CHD correlate significantly and EPCs may become an effective treatment for PAH in patients with CHD. EPCs may be a protective factor of high PAH for children with CHD.
Background Using random forest to predict arrhythmia after intervention in children with atrial septal defect. Methods We constructed a prediction model of complications after interventional closure for children with atrial septal defect. The model was based on random forest, and it solved the need for postoperative arrhythmia risk prediction and assisted clinicians and patients’ families to make preoperative decisions. Results Available risk prediction models provided patients with specific risk factor assessments, we used Synthetic Minority Oversampling Technique algorithm and random forest machine learning to propose a prediction model, and got a prediction accuracy of 94.65 % and an Area Under Curve value of 0.8956. Conclusions Our study was based on the model constructed by random forest, which can effectively predict the complications of arrhythmia after interventional closure in children with atrial septal defect.
Background: To assess the relationship between endothelial progenitor cells (EPCs) in peripheral blood and pulmonary hypertension (PH) in children with congenital heart disease (CHD) and explore the possibility of applying EPCs to treatment of PH in children with CHD. Methods: In this study, a total of 173 cases with CHD (from 0 to 6 years old) were collected. According to the right heart catheterization of mean pulmonary arterial pressure (mPAP) results, these cases were divided into PH groups (including high PH group, n=32, and the middle PH group, n=30) and non-PH group (n=111). We took their peripheral blood for flow cytometry, and counted the number of EPCs(CD133+/KDR+ cells). The number of EPCs /μL of peripheral blood was calculated using the following formula: EPCs /μL =WBC /L × lymphocytes % × EPCs % × 10-6. Results: The median EPCs of the non-PH group, middle PH group and high PH group are 1.86/μL, 1.30 /μL and 0.98/μL, respectively. The mPAP decreases steadily as the level of EPCs increases (P<0.05). After adjustment of gender, age and BMI, the EPCs was significantly associated with a decreased risk of high PH (OR=0.37, 95%CI: 0.16-0.87, P<0.05). However, EPCs was not significantly associated with middle PH (P>0.05). Conclusion: The findings revealed that the EPCs and high PH in CHD patients correlate significantly and EPCs may become an effective treatment for PH in CHD patients.EPCs may be a protective factor of high PH for children with CHD.
Background: Pulmonary arterial hypertension (PAH) caused by congenital heart disease (CHD) is very common in clinics. Some studies have shown that PAH is related to the number of endothelial progenitor cells (EPCs), but there is no report on the relationship between PAH and the number of EPCs in children with CHD. Methods: In this study, a total of 173 cases with CHD (from 0 to 6 years old) were collected. According to the mean pulmonary arterial pressure (mPAP) measured by right heart catheterization, these cases were divided into PAH groups (including high PAH group, mPAP>25mmHg, n=32, and the middle PAH group, 20mmHg≤mPAP≤25mmHg, n=30) and non-PAH group (mPAP<20mmHg, n=111). Peripheral blood was taken for flow cytometry, and the number of EPCs (CD133+/KDR+ cells) was counted. The number of EPCs /μL of peripheral blood was calculated using the following formula: EPCs /μL =WBC /L × lymphocytes % × EPCs % × 10-6. Results: The median EPCs of the non-PAH group, middle PAH group and high PAH group is 1.86/μL, 1.30 /μL and 0.98/μL, respectively. The mPAP decreases steadily as the level of EPCs increases (P<0.05). After adjustment of gender, age and BMI, the number of EPCs was significantly associated with a decreased risk of high PAH (OR=0.37, 95% CI: 0.16-0.87, P<0.05). However, EPCs was not significantly associated with middle PAH (P>0.05). Conclusion: The findings revealed that the EPCs and high PAH in patients with CHD correlate significantly and EPCs may become an effective treatment for PAH in patients with CHD. EPCs may be a protective factor of high PAH for children with CHD.
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