Numerical Simulation of Full-Scale Three-Dimensional Fluid Flow in an Oscillating Reactor

Marine reactors are subjected to additional motions due to ocean conditions. These additional motions will cause large fluctuation of flow rate and change the coolant flow field, making the system unstable. Therefore, in order to understand the effect of oscillating motion on the flow characteristics, a numerical simulation of fluid flow is carried out based on a full-scale three-dimensional oscillating marine reactor. In this study, the resistance coefficients of the lattice, rod buddle and steam generator are fitted, and the distribution of flow rate, velocity as well as pressure in different regions is investigated through the standard model. After additional oscillation is introduced, the flow field in an oscillating reactor is presented and the effect of oscillating angle and elevation on the flow rate is investigated. Results show that the oscillating motion can greatly change the flow field in the reactor; most of the coolant circulates in the downcommer and lower head with only a small amount of coolant entering the core; the flow fluctuation period is consistent with the oscillating period, and the flow variation patterns under different oscillating conditions are basically the same; since the flow amplitude is related to oscillating speed, the amplitude of flow rate rises when decreasing the maximum oscillating angle; the oscillating elevation has little effect on the flow rate

The value of IGF-1 and IGFBP-1 in patients with heart failure with reduced, mid-range, and preserved ejection fraction

Background: Previous studies have reported inconsistent results regarding the implications of deranged insulin-like growth factor 1 (IGF-1)/insulin-like growth factor-binding protein 1 (IGFBP-1) axis in patients with heart failure (HF). This study evaluates the roles of IGF1/IGFBP-1 axis in patients with HF with reduced ejection fraction (HFrEF), mid-range ejection fraction (HFmrEF), or preserved ejection fraction (HFpEF). Methods: Consecutive patients with HFrEF, HFmrEF, and HFpEF who underwent comprehensive cardiac assessment were included. The primary endpoint was the composite endpoint of all-cause death and HF rehospitalization at one year. Results: A total of 151 patients with HF (HFrEF: n = 51; HFmrEF: n = 30; HFpEF: n = 70) and 50 control subjects were included. The concentrations of IGFBP-1 (p < 0.001) and IGFBP-1/IGF-1 ratio (p < 0.001) were significantly lower in patients with HF compared to controls and can readily distinguish patients with and without HF (IGFBP-1: areas under the curve (AUC): 0.725, p < 0.001; IGFBP-1/IGF-1 ratio: AUC:0.755, p < 0.001; respectively). The concentrations of IGF-1, IGFBP-1, and IGFBP-1/IGF-1 ratio were similar among HFpEF, HFmrEF, and HFrEF patients. IGFBP-1 and IGFBP-1/IGF-1 ratio positively correlated with N-terminal probrain natriuretic peptide (NT-proBNP) levels (r = 0.255, p = 0.002; r = 0.224, p = 0.007, respectively). IGF-1, IGFBP-1, and IGFBP-1/IGF-1 ratio did not predict the primary endpoint at 1 year for the whole patients with HF and HF subtypes on both univariable and multivariable Cox regression. Conclusion: The concentrations of plasma IGFBP-1 and IGFBP-1/IGF-1 ratio can distinguish patients with and without HF. In HF, IGFBP-1 and IGFBP-1/IGF-1 ratio positively correlated with NT-proBNP levels

The impact of FDI on ecological unequal exchange in China’s manufacturing industry

This paper uses the panel data of manufacturing subdivision industry from 2000 to 2014 to calculate the exchange of ecological inequality through MRIO model. On this basis, the systematic GMM model is used to investigate the direct and indirect effects of Foreign Direct Investment on the unequal exchange of manufacturing ecology. In addition, the ecological unequal exchange in China’s manufacturing industry is decomposed into ecological unequal exchange on the production side, on the consumption side, with developed regions and with lessdeveloped regions. The study finds that: 1) Industry-wide research indicates that FDI inflows have a significant positive impact on reducing the unequal exchange in the manufacturing sector. This finding contributes to the existing literature on the effects of FDI on ecological inequality. 2) Path-specific studies reveal that FDI primarily reduces ecological inequality in the manufacturing sector through technological effects. However, the scale and structural effects of FDI exacerbate ecological inequality, confirming the findings of some scholars. This nuanced understanding of the effects of FDI on ecological inequality adds to the existing body of research. 3) From the perspective of FDI sources, FDI from Asian countries and regions is more beneficial for improving China’s ecological unequal exchange. This finding provides guidance for China’s FDI attraction policies. 4) Assessing pollution emissions inventories based on the principle of production responsibility is unfair to China from both the production and consumption perspectives. 5) From a regional perspective, FDI effectively reduces the impact of ecological unequal exchange in the manufacturing sector between China and developed economies. These findings confirm that China bears an unequal exchange in the trade process and enrich the understanding of the impact of FDI on ecological unequal exchange

Cardiac abnormalities after induction of endoplasmic reticulum stress are associated with mitochondrial dysfunction and connexin43 expression

The endoplasmic reticulum (ER) is responsible for protein synthesis and calcium storage. ER stress, reflected by protein unfolding and calcium handling abnormalities, has been studied as a pathogenic factor in cardiovascular diseases. The aim of this study is to examine the effects of ER stress on mechanical and electrophysiological functions in the heart and explore the underlying molecular mechanisms. A total of 30 rats were randomly divided into control, ER stress inducer (tunicamycin[TN]) and ER stress inhibitor (tunicamycin+4-phenylbutyric acid [4-PBA]) groups. ER stress induction led to significantly systolic and diastolic dysfunction as reflected by maximal increasing/decreasing rate of left intraventricular pressure (±dp/dt), left ventricular peaksystolic pressure(LVSP) and LV end-diastolic pressure(LVEDP). Epicardial mapping performed in vivo revealed reduced conduction velocity and increased conduction heterogeneity associated with the development of spontaneous ventricular tachycardia. Masson’s trichrome staining revealed marked fibrosis in the myocardial interstitial and sub-pericardial regions, and thickened epicardium. Western blot analysis revealed increased pro-fibrotic factor transforming growth factor-β1 (TGF-β1), decreased mitochondrial biogenesis protein peroxlsome proliferator-activated receptor-γ coactlvator-1α （PGC-1a）, and decreased mitochondrial fusion protein mitofusin-2 (MFN2). These changes were associated with mitochondria dysfunction and connexin 43(CX43)translocation to mitochondria. These abnormalities can be partially prevented by the ER stress inhibitor 4-PBA. Our study shows that ER stress induction can produce cardiac electrical and mechanism dysfunction as well as structural remodelling. Mitochondrial function alterations are contributed by CX43 transposition to mitochondria. These abnormalities can be partially prevented by the ER stress inhibitor 4-PBA

A Machine Learning Aided Systematic Review and Meta-Analysis of the Relative Risk of Atrial Fibrillation in Patients With Diabetes Mellitus

Background: Meta-analysis is a widely used tool in which weighted information from multiple similar studies is aggregated to increase statistical power. However, the exponential growth of publications in key areas of medical science has rendered manual identification of relevant studies increasingly time-consuming. The aim of this work was to develop a machine learning technique capable of robust automatic study selection for meta-analysis. We have validated this approach with an up-to-date meta-analysis to investigate the association between diabetes mellitus (DM) and new-onset atrial fibrillation (AF).Methods: The PubMed online database was searched from 1960 to September 2017 where 4,177 publications that mentioned both DM and AF were identified. Relevant studies were selected as follows. First, publications were clustered based on common text features using an unsupervised K-means algorithm. Clusters that best matched the selected set of potentially relevant studies (a “training” set of 139 articles) were then identified by using maximum entropy classification. The 139 articles selected automatically on this basis were screened manually to identify potentially relevant studies. To determine the validity of the automated process, a parallel set of studies was also assembled by manually screening all initially searched publications. Finally, detailed manual selection was performed on the full texts of the studies in both sets using standard criteria. Quality assessment, meta-regression random-effects models, sensitivity analysis and publication bias assessment were then conducted.Results: Machine learning-assisted screening identified the same 29 studies for meta-analysis as those identified by using manual screening alone. Machine learning enabled more robust and efficient study selection, reducing the number of studies needed for manual screening from 4,177 to 556 articles. A pooled analysis using the most conservative estimates indicated that patients with DM had ~49% greater risk of developing AF compared with individuals without DM. After adjusting for three additional risk factors i.e., hypertension, obesity and heart disease, the relative risk was 23%. Using multivariate adjusted models, the risk for developing AF in patients with DM was similar for all DM subtypes. Women with DM were 24% more likely to develop AF than men with DM. The risk for new-onset AF in patients with DM has also increased over the years.Conclusions: We have developed a novel machine learning method to identify publications suitable for inclusion in meta-analysis.This approach has the capacity to provide for a more efficient and more objective study selection process for future such studies. We have used it to demonstrate that DM is a strong, independent risk factor for AF, particularly for women

The Value of IGF-1 and IGFBP-1 in Patients With Heart Failure With Reduced, Mid-range, and Preserved Ejection Fraction

Background: Previous studies have reported inconsistent results regarding the implications of deranged insulin-like growth factor 1 (IGF-1)/insulin-like growth factor-binding protein 1 (IGFBP-1) axis in patients with heart failure (HF). This study evaluates the roles of IGF1/IGFBP-1 axis in patients with HF with reduced ejection fraction (HFrEF), mid-range ejection fraction (HFmrEF), or preserved ejection fraction (HFpEF). Methods: Consecutive patients with HFrEF, HFmrEF, and HFpEF who underwent comprehensive cardiac assessment were included. The primary endpoint was the composite endpoint of all-cause death and HF rehospitalization at one year. Results: A total of 151 patients with HF (HFrEF: n = 51; HFmrEF: n = 30; HFpEF: n = 70) and 50 control subjects were included. The concentrations of IGFBP-1 (p < 0.001) and IGFBP-1/IGF-1 ratio (p < 0.001) were significantly lower in patients with HF compared to controls and can readily distinguish patients with and without HF (IGFBP-1: areas under the curve (AUC): 0.725, p < 0.001; IGFBP-1/IGF-1 ratio: AUC:0.755, p < 0.001; respectively). The concentrations of IGF-1, IGFBP-1, and IGFBP-1/IGF-1 ratio were similar among HFpEF, HFmrEF, and HFrEF patients. IGFBP-1 and IGFBP-1/IGF-1 ratio positively correlated with N-terminal probrain natriuretic peptide (NT-proBNP) levels (r = 0.255, p = 0.002; r = 0.224, p = 0.007, respectively). IGF-1, IGFBP-1, and IGFBP-1/IGF-1 ratio did not predict the primary endpoint at 1 year for the whole patients with HF and HF subtypes on both univariable and multivariable Cox regression. Conclusion: The concentrations of plasma IGFBP-1 and IGFBP-1/IGF-1 ratio can distinguish patients with and without HF. In HF, IGFBP-1 and IGFBP-1/IGF-1 ratio positively correlated with NT-proBNP levels

Meta-analysis of T peak –T end and T peak –T end /QT ratio for risk stratification in congenital long QT syndrome

Background and objectives: Congenital long QT syndrome (LQTS) predisposes affected individuals to ventricular tachycardia/fibrillation (VF/VF), potentially resulting in sudden cardiac death. The Tpeak–Tend interval and the Tpeak–Tend/QT ratio, electrocardiographic markers of dispersion of ventricular repolarization, were proposed for risk stratification but their predictive values in LQTS have been controversial. A systematic review and meta-analysis was conducted to examine the value of Tpeak–Tend intervals and Tpeak–Tend/QT ratios in predicting arrhythmic and mortality outcomes in congenital LQTS. Method: PubMed and Embase databases were searched until 9th May 2017, identifying 199 studies. Results: Five studies on long QT syndrome were included in the final meta-analysis. Tpeak–Tend intervals were longer (mean difference [MD]: 13 ms, standard error [SE]: 4 ms, P = 0.002; I2 = 34%) in congenital LQTS patients with adverse events [syncope, ventricular arrhythmias or sudden cardiac death] compared to LQTS patients without such events. By contrast, Tpeak–Tend/QT ratios were not significantly different between the two groups (MD: 0.02, SE: 0.02, P = 0.26; I2 = 0%). Conclusion: This meta-analysis showed that Tpeak–Tend interval is significant higher in individuals who are at elevated risk of adverse events in congenital LQTS, offering incremental value for risk stratification

Diagnostic and prognostic value of serum C-reactive protein in heart failure with preserved ejection fraction:a systematic review and meta-analysis

Heart failure (HF) is a major epidemic with rising morbidity and mortality rates that encumber global healthcare systems. While some studies have demonstrated the value of CRP in predicting (i) the development of HFpEF and (ii) long-term clinical outcomes in HFpEF patients, others have shown no such correlation. As a result, we conducted the following systematic review and meta-analysis to assess both the diagnostic and prognostic role of CRP in HFpEF. PubMed and Embase were searched for studies that assess the relationship between CRP and HFpEF using the following search terms: (((C-reactive protein) AND ((preserved ejection fraction) OR (diastolic heart failure))). The search period was from the start of database to August 6, 2019, with no language restrictions. A total of 312 and 233 studies were obtained from PubMed and Embase respectively, from which 19 studies were included. Our meta-analysis demonstrated the value of a high CRP in predicting the development of not only new onset HFpEF (HR: 1.08; 95% CI: 1.00–1.16; P = 0.04; I 2 = 22%), but also an increased risk of cardiovascular mortality when used as a categorical (HR: 2.52; 95% CI: 1.61–3.96; P < 0.0001; I 2 = 19%) or a continuous variable (HR: 1.24; 95% CI: 1.04–1.47; P = 0.01; I 2 = 28%), as well as all-cause mortality when used as a categorical (HR: 1.78; 95% CI: 1.53–2.06; P < 0.00001; I 2 = 0%) or a continuous variable: (HR: 1.06; 95% CI: 1.02–1.06; P = 0.003; I 2 = 61%) in HFpEF patients. CRP can be used as a biomarker to predict the development of HFpEF and long-term clinical outcomes in HFpEF patients, in turn justifying its use as a simple, accessible parameter to guide clinical management in this patient population. However, more prospective studies are still required to not only explore the utility and dynamicity of CRP in HFpEF but also to determine whether risk stratification algorithms incorporating CRP actually provide a material benefit in improving patient prognosis

Association between gout and atrial fibrillation: A meta-analysis of observational studies

Background: Gout is a systemic inflammatory arthritis characterized by the deposition of monosodium urate crystals due to hyperuricemia. Previous studies have explored the link between gout and atrial fibrillation (AF). Given the increasing prevalence and incidence of gout, there is a need to quantify the relationship between gout and the risk of AF. Therefore, we conducted a systematic review and meta-analysis on this topic. Methods: PubMed and Embase were searched for studies that reported the association between gout and AF using the following search term: (‘Gout’ and ‘Arrhythmia’). The search period was from the start of the database to 3rd August 2018 with no language restrictions. Results: A total of 75 and 22 articles were retrieved from PubMed and Embase, respectively. Of these, four observational studies (three cohort studies, one case-control study) including 659,094 patients were included. Our meta-analysis demonstrated that gout was significantly associated with increased risk of AF (adjusted hazard ratio: 1.31; 95% confidence interval: 1.00-1.70; P = 0.05; I2 = 99%) after adjusting for significant comorbidities and confounders. Conclusions: Our meta-analysis confirms the significant relationship between gout and AF. More data are needed to determine whether this risk can be adequately reduced by urate-lowering therapy

The Involvement of Renin-Angiotensin System in Lipopolysaccharide-Induced Behavioral Changes, Neuroinflammation, and Disturbed Insulin Signaling

Brain insulin signaling is accounted for the development of a variety of neuropsychiatric disorders, such as anxiety and depression, whereas both inflammation and the activated renin-angiotensin system (RAS) are two major contributors to insulin resistance. Intriguingly, inflammation and RAS can activate each other, forming a positive feedback loop that would result in exacerbated unwanted tissue damage. To further examine the interrelationship among insulin signaling, neuroinflammation and RAS in the brain, the effect of repeated lipopolysaccharide (LPS) exposure and co-treatment with the angiotensin II (Ang II) receptor type 1 (AT1) blocker, candesartan (Cand), on anxiety and depression-like behaviors, RAS, neuroinflammation and insulin signaling was explored. Our results demonstrated that prolonged LPS challenge successfully induced the rats into anxiety and depression-like state, accompanied with significant neural apoptosis and neuroinflammation. LPS also activated RAS as evidenced by the enhanced angiotensin converting enzyme (ACE) expression, Ang II generation and AT1 expression. However, blocking the activated RAS with Cand co-treatment conferred neurobehavioral protective properties. The AT1 blocker markedly ameliorated the microglial activation, the enhanced gene expression of the proinflammatory cytokines and the overactivated NF-κB signaling. In addition, Cand also mitigated the LPS-induced disturbance of insulin signaling with the normalized phosphorylation of serine 307 and tyrosine 896 of insulin receptor substrate-1 (IRS-1). Collectively, the present study, for the first time, provided the direct evidence indicating that the inflammatory condition may interact with RAS to impede brain insulin pathway, resulting in neurobehavioral damage, and inhibiting RAS seems to be a promising strategy to block the cross-talk and cut off the vicious cycle between RAS and immune system