An open science resource for establishing reliability and reproducibility in functional connectomics

Efforts to identify meaningful functional imaging-based biomarkers are limited by the ability to reliably characterize inter-individual differences in human brain function. Although a growing number of connectomics-based measures are reported to have moderate to high test-retest reliability, the variability in data acquisition, experimental designs, and analytic methods precludes the ability to generalize results. The Consortium for Reliability and Reproducibility (CoRR) is working to address this challenge and establish test-retest reliability as a minimum standard for methods development in functional connectomics. Specifically, CoRR has aggregated 1,629 typical individuals’ resting state fMRI (rfMRI) data (5,093 rfMRI scans) from 18 international sites, and is openly sharing them via the International Data-sharing Neuroimaging Initiative (INDI). To allow researchers to generate various estimates of reliability and reproducibility, a variety of data acquisition procedures and experimental designs are included. Similarly, to enable users to assess the impact of commonly encountered artifacts (for example, motion) on characterizations of inter-individual variation, datasets of varying quality are included

Performance of market order execution strategy: the Australian evidence

This study examines the performance of market order execution strategy in a pure limit order driven environment based on three bid-ask spread forecasting models. While a naive spread forecasting model based on previous day's spread and average 10 trading days' spread could deliver a cost saving of 3.94% and 14.87%, this benefit increases to 22.14% for a seasonal autoregressive moving average spread forecasting model. The empirical results are evident that the intraday spread forecasting benefits follow a downward-sloping pattern.

Alterations in Running Biomechanics after 12 Week Gait Retraining with Minimalist Shoes

Purpose: The intervention of 12 week gait retraining with minimalist shoes was established to examine its effect on impact forces, joint mechanics, and vertical stiffness during running. Methods: Thirty male recreational runners were randomly assigned to the gait retraining + minimalist shoe (n = 15, GR) and minimalist shoe (n = 15, MIN) groups. The ground reaction force and marker trajectories were collected before and after intervention at a speed of 3.33 ± 5% m/s. Results: A total of 17 participants (9 in the GR group and 8 in the MIN group) completed the training. After training, (1) the loading rate of both groups decreased significantly, and the loading rate of the GR group was lower than that of the MIN group. (2) The foot strike angle of the GR group decreased significantly after training, and the plantarflexion angle and hip joint angular extension velocity increased in both groups. (3) The moment of ankle joint increased in the GR group, and the stiffness of lower limbs was significantly improved in both groups. Conclusion: The 12 week gait retraining with minimalist shoes converted rearfoot strikers into forefoot strikers with a rate of 78% (7/9). More importantly, such a combined program, compared to the training with only minimalist shoes, can avoid the peak impact force and decrease the loading rate more effectively, thus providing a potential means of reducing risk of running injury caused by impact forces. Moreover, the increased vertical stiffness of lower extremity after gait retraining may improve running economy and corresponding energy utilization. However, these observations also suggest that the sole use of minimalist footwear may have limited effects on reducing running-related impacts

Characterizing ecosystem water-use efficiency of croplands with eddy covariance measurements and MODIS products

How to quantify the variability in ecosystem water use efficiency (WUE) of croplands is of vital importance. Especially in the context of changing hydrologic environment, much attention need to be paid on how to use limited water to improve crop yield. However, the biophysical performances of environmental/biological controls, crop types, and effects of diverse farming practices on WUE remain unclear. Therefore, this study aims to address these questions through tower-based measurements from eddy covariance and satellite-based estimates from MODIS GPP and ET products at the two annual soybean/corn rotation fields. The results exhibited that temperature and solar radiation are the most important meteorological factors. MODIS WUE estimates captured the broad trend of 8-day tower-based observations. However, ecosystem WUE was overpredicted at the seedling stage and after harvest, and was severely underestimated at the peak periods of maize, which was mainly ascribed to the uncertainties in MODIS GPP. Finally, we evaluated the effects of two farming practices (conventional vs alternative) on WUE and carbon sequence (NEE). On annual time scale, WUE of both soybean and maize are improved obviously under the alternative management whereas contrasting effects are observed on NEE. But the overall carbon balance for both treatments is nearly identical over 2-year rotation

HAMP as a Potential Diagnostic, PD-(L)1 Immunotherapy Sensitivity and Prognostic Biomarker in Hepatocellular Carcinoma

Hepatocellular carcinoma (HCC) remains a global medical problem. Programmed cell death protein 1 (PD-1) is a powerful weapon against many cancers, but it is not sensitive to some patients with HCC. We obtained datasets from the Gene Expression Omnibus (GEO) database on HCC patients and PD-1 immunotherapy to select seven intersecting DEGs. Through Lasso regression, two intersecting genes were acquired as predictors of HCC and PD-1 treatment prognosis, including HAMP and FOS. Logistic regression was performed to build a prediction model. HAMP had a better ability to diagnose HCC and predict PD1 treatment sensitivity. Further, we adapted the support vector machine (SVM) technique using HAMP to predict triple-classified outcomes after PD1 treatment in HCC patients, which had an excellent classification ability. We also performed external validation using TCGA data, which showed that HAMP was elevated in the early stage of HCC. HAMP was positively correlated with the infiltration of 18 major immune cells and the expression of 2 important immune checkpoints, PDCD1 and CTLA4. We discovered a biomarker that can be used for the early diagnosis, prognosis and PD1 immunotherapy efficacy prediction of HCC for the first time and developed a diagnostic model, prognostic model and prediction model of PD1 treatment sensitivity and treatment outcome for HCC patients accordingly

Role of long noncoding RNAs in diabetes-associated peripheral arterial disease

Abstract Diabetes mellitus (DM) is a metabolic disease that heightens the risks of many vascular complications, including peripheral arterial disease (PAD). Various types of cells, including but not limited to endothelial cells (ECs), vascular smooth muscle cells (VSMCs), and macrophages (MΦs), play crucial roles in the pathogenesis of DM-PAD. Long non-coding RNAs (lncRNAs) are epigenetic regulators that play important roles in cellular function, and their dysregulation in DM can contribute to PAD. This review focuses on the developing field of lncRNAs and their emerging roles in linking DM and PAD. We review the studies investigating the role of lncRNAs in crucial cellular processes contributing to DM-PAD, including those in ECs, VSMCs, and MΦ. By examining the intricate molecular landscape governed by lncRNAs in these relevant cell types, we hope to shed light on the roles of lncRNAs in EC dysfunction, inflammatory responses, and vascular remodeling contributing to DM-PAD. Additionally, we provide an overview of the research approach and methodologies, from identifying disease-relevant lncRNAs to characterizing their molecular and cellular functions in the context of DM-PAD. We also discuss the potential of leveraging lncRNAs in the diagnosis and therapeutics for DM-PAD. Collectively, this review provides a summary of lncRNA-regulated cell functions contributing to DM-PAD and highlights the translational potential of leveraging lncRNA biology to tackle this increasingly prevalent and complex disease. Graphical Abstrac

Contributions of biomass burning to global and regional SO2 emissions

Harmful SO2 largely originates from coal and oil combustions, but in some areas the biomass burning contribution could not be ignored. Here, we evaluated SO2 emissions from biomass burning (BB-SO2) with largely focusing on regional difference and temporal trends in the relative contributions of biomass burning from different sectors. Globally, the biomass burning emitted 4.26 (3.20–6.20) Tg SO2 in 2014, contributing 4.0% of the total SO2 emissions stemming from anthropogenic sources and natural open fires. But in some African and South Asian countries, biomass burning was a major source of SO2 with the contribution as high as 80–90%. Regarding sector contributions of biomass SO2, open fires contributed nearly half, followed by the residential sector (~29%) on the global scale, however, substantially different profiles were revealed across countries. Residential sector is the largest anthropogenic BB-SO2 source in the developing countries, while in the developed countries, industry and energy production were the two main anthropogenic BB-SO2sources. From 1960 to 2014, biomass SO2 emission, either the absolute amount or the relative contribution to the total, increased in the U.S. and Europe, and the contributions were over 20% in some countries. The biomass burning SO2 emission showed an increasing trend in India and a unimodal change in China, while a decreasing trend in the relative contributions were revealed in these two largest developing countries, which were 2.7% and 0.8%, respectively in 2014. With unignorable biomass burning contribution to SO2, as well as other hazardous air pollutants, in some regions, it is suggested that in assessing climate and health impacts of promoted biomass utilization when phasing out of fossil fuels, multiple components should be co-evaluated

Genetic Deletion of the <i>LINC00520</i> Homolog in Mouse Aggravates Angiotensin II-Induced Hypertension

(1) Background: Hypertension is a complex, multifactorial disease that is caused by genetic and environmental factors. Apart from genetic predisposition, the mechanisms involved in this disease have yet to be fully understood. We previously reported that LEENE (lncRNA enhancing endothelial nitric oxide expression, transcribed from LINC00520 in the human genome) regulates endothelial cell (EC) function by promoting the expression of endothelial nitric oxide synthase (eNOS) and vascular growth factor receptor 2 (VEGFR2). Mice with genetic deletion of the LEENE/LINC00520 homologous region exhibited impaired angiogenesis and tissue regeneration in a diabetic hindlimb ischemia model. However, the role of LEENE in blood pressure regulation is unknown. (2) Methods: We subjected mice with genetic ablation of leene and wild-type littermates to Angiotensin II (AngII) and monitored their blood pressure and examined their hearts and kidneys. We used RNA-sequencing to identify potential leene-regulated molecular pathways in ECs that contributed to the observed phenotype. We further performed in vitro experiments with murine and human ECs and ex vivo experiments with murine aortic rings to validate the select mechanism. (3) Results: We identified an exacerbated hypertensive phenotype of leene-KO mice in the AngII model, evidenced by higher systolic and diastolic blood pressure. At the organ level, we observed aggravated hypertrophy and fibrosis in the heart and kidney. Moreover, the overexpression of human LEENE RNA, in part, restored the signaling pathways impaired by leene deletion in murine ECs. Additionally, Axitinib, a tyrosine kinase inhibitor that selectively inhibits VEGFR suppresses LEENE in human ECs. (4) Conclusions: Our study suggests LEENE as a potential regulator in blood pressure control, possibly through its function in ECs

Regulation of nuclear transcription by mitochondrial RNA in endothelial cells

Chromatin-associated RNAs (caRNAs) form a relatively poorly recognized layer of the epigenome. The caRNAs reported to date are transcribed from the nuclear genome. Here, leveraging a recently developed assay for detection of caRNAs and their genomic association, we report that mitochondrial RNAs (mtRNAs) are attached to the nuclear genome and constitute a subset of caRNA, thus termed mt-caRNA. In four human cell types analyzed, mt-caRNAs preferentially attach to promoter regions. In human endothelial cells (ECs), the level of mt-caRNA–promoter attachment changes in response to environmental stress that mimics diabetes. Suppression of a non-coding mt-caRNA in ECs attenuates stress-induced nascent RNA transcription from the nuclear genome, including that of critical genes regulating cell adhesion, and abolishes stress-induced monocyte adhesion, a hallmark of dysfunctional ECs. Finally, we report increased nuclear localization of multiple mtRNAs in the ECs of human diabetic donors, suggesting many mtRNA translocate to the nucleus in a cell stress and disease-dependent manner. These data nominate mt-caRNAs as messenger molecules responsible for mitochondrial–nuclear communication and connect the immediate product of mitochondrial transcription with the transcriptional regulation of the nuclear genome