Six-month adherence to Statin use and subsequent risk of major adverse cardiovascular events (MACE) in patients discharged with acute coronary syndromes

Acknowledgements: The authors thank all participants who contributed to the study. Funding: CPACS-1 was funded by unrestricted educational grants from Guidant and Sanofi-Aventis, and grants from The Royal Australasian College of Physicians. AP is supported by an Australian National Heart Foundation Career Development Award. CPACS-2 was funded by an unrestricted grant from Sanofi-Aventis China. The George Institute for Global Health at Peking University Health Science Center sponsored the study and owns the data. Data analyses and reports were supported by Beijing Science and Technology Key Research Plan (D151100002215001). However, the authors are solely responsible for the design, analyses, the drafting and editing of the manuscript, and its final contents.Peer reviewedPublisher PD

Epstein-barr virus-encoded microRNA-BART18-3p promotes colorectal cancer progression by targeting de novo lipogenesis

The Epstein-Barr virus (EBV) genome encodes a cluster of 22 viral microRNAs, called miR-BamHI-A rightward transcripts (miR-BARTs), which are shown to promote the development of cancer. Here, this study reports that EBV-miR-BART18-3p is highly expressed in colorectal cancer (CRC) and is closely associated with the pathological and advanced clinical stages of CRC. Ectopic expression of EBV-miR-BART18-3p leads to increased migration and invasion capacities of CRC cells in vitro and causes tumor metastasis in vivo. Mechanistically, EBV-miR-BART18-3p activates the hypoxia inducible factor 1 subunit alpha/lactate dehydrogenase A axis by targeting Sirtuin, which promotes lactate accumulation and acetyl-CoA production in CRC cells under hypoxic condition. Increased acetyl-CoA utilization subsequently leads to histone acetylation of fatty acid synthase and fatty acid synthase-dependent fat synthesis, which in turn drives de novo lipogenesis. The oncogenic role of EBV-miR-BART18-3p is confirmed in the patient-derived tumor xenograft mouse model. Altogether, the findings define a novel mechanism of EBV-miR-BART18-3p in CRC development through the lipogenesis pathway and provide a potential clinical intervention target for CRC

Assessment, Distribution and Regional Geochemical Baseline of Heavy Metals in Soils of Densely Populated Area: A Case Study

To understand the content, pollution, distribution and source and to establish a geochemical baseline of heavy metal elements in soil under the influence of high-density population, the concentrations of heavy metal elements Cr, Mn, Co, Ni, Cu, Zn, As, Cd, Hg, Pb and Fe were determined in 23 soil samples in Suzhou University, and geo-accumulation index, enrichment factor, principal component analysis, spatial analysis and regression analysis were completed. The results showed the following: The elements Cu and As were slightly polluted, while the other heavy metal elements were not. The elements Cd, Cu, Ni and As in soils were mainly caused by agricultural activities of chemical fertilizer, whereas the elements Zn and Hg were impacted by the chemicals and batteries. The heavy metal elements in the north were lower than in the south of the campus, as a whole. The enrichment of elements Cu, As and Cd was caused by the east–west river on the campus, and the enrichment of the elements Mn, Ni and Zn was induced by the reservoir. Biochemical experiments and vehicle parking influenced the spatial enrichment of Cr, Co and Pb, while domestic waste led to the spatial differentiation of Hg concentrations. The regression curve between heavy metal elements and Fe was established, and the background values of the heavy metals Cr, Mn, Co, Ni, Cu, Zn, As, Cd, Hg and Pb are 50.90, 489.37, 11.76, 37.74, 55.70, 58.22, 20.07, 0.09, 0.08 and 24.13 mg/kg, respectively

Increase of Atmospheric Methane Observed from Space-Borne and Ground-Based Measurements

It has been found that the concentration of atmospheric methane (CH4) has rapidly increased since 2007 after a decade of nearly constant concentration in the atmosphere. As an important greenhouse gas, such an increase could enhance the threat of global warming. To better quantify this increasing trend, a novel statistic method, i.e. the Ensemble Empirical Mode Decomposition (EEMD) method, was used to analyze the CH4 trends from three different measurements: the mid–upper tropospheric CH4 (MUT) from the space-borne measurements by the Atmospheric Infrared Sounder (AIRS), the CH4 in the marine boundary layer (MBL) from NOAA ground-based in-situ measurements, and the column-averaged CH4 in the atmosphere (XCH4) from the ground-based up-looking Fourier Transform Spectrometers at Total Carbon Column Observing Network (TCCON) and the Network for the Detection of Atmospheric Composition Change (NDACC). Comparison of the CH4 trends in the mid–upper troposphere, lower troposphere, and the column average from these three data sets shows that, overall, these trends agree well in capturing the abrupt CH4 increase in 2007 (the first peak) and an even faster increase after 2013 (the second peak) over the globe. The increased rates of CH4 in the MUT, as observed by AIRS, are overall smaller than CH4 in MBL and the column-average CH4. During 2009–2011, there was a dip in the increase rate for CH4 in MBL, and the MUT-CH4 increase rate was almost negligible in the mid-high latitude regions. The increase of the column-average CH4 also reached the minimum during 2009–2011 accordingly, suggesting that the trends of CH4 are not only impacted by the surface emission, however that they also may be impacted by other processes like transport and chemical reaction loss associated with [OH]. One advantage of the EEMD analysis is to derive the monthly rate and the results show that the frequency of the variability of CH4 increase rates in the mid–high northern latitude regions is larger than those in the tropics and southern hemisphere

Factors attributed to the higher in-hospital mortality of ST elevation myocardial infarction patients admitted during off-hour in comparison with those during regular hour.

In-hospital mortality of patients with ST elevation myocardial infarction (STEMI) admitted during off-hour was reported higher than those admitted during regular hour, but which factors cause the difference remains largely unknown though the difference in medical resources was often accused.This registry-based study recruited 7456 STEMI patients prospectively from 99 level two hospitals across China. Generalized linear mixed models were applied to quantify the risk of in-hospital death attributed to admission time and the explainers of its change, accounting for the clustering of patients within hospitals. There were 45.2% patients admitted during regular hour and 54.8% during off-hour. In-hospital mortality was 7.0% for patients admitted during regular hour and 8.3% for those during off-hour (p<0.05). Generalized linear mixed models adjusting for age, gender and education showed that patients' disease severity at admission and medical treatments received after admission could explain the risk difference attributed to admission time by 55% and 20%, respectively. After all factors accounted, the residual relative risk difference left only 6% (adjusted OR = 0.94) and became no longer significant.The regular-and-off-hour mortality difference exists among STEMI patients in Chinese level two hospitals, which could be attributed primarily to disease severity at admission and secondly to the poorer medical treatments. These results call for public attention to the more severity of STEMI patients admitted during off-hour in addition to improving medical resources for STEMI at off-hour

Matairesinol nanoparticles restore chemosensitivity and suppress colorectal cancer progression in preclinical models: role of lipid metabolism reprogramming

: Oncogenic-driven lipogenic metabolism is a common hallmark of colorectal cancer (CRC) progression. Therefore, there is an urgent need to develop novel therapeutic strategies for metabolic reprogramming. Herein, the metabolic profiles in the plasma between CRC patients and paired healthy controls were compared using metabolomics assays. Matairesinol downregulation was evident in CRC patients, and matairesinol supplementation significantly represses CRC tumorigenesis in azoxymethane/dextran sulfate sodium (AOM/DSS) colitis-associated CRC mice. Matairesinol rewired lipid metabolism to improve the therapeutic efficacy in CRC by inducing mitochondrial damage and oxidative damage and blunting ATP production. Finally, matairesinol-loaded liposomes significantly promoted the enhanced antitumor activity of 5-Fu/leucovorin combined with oxaliplatin (FOLFOX) in CDX and PDX mouse models by restoring chemosensitivity to the FOLFOX regimen. Collectively our findings highlight matairesinol-mediated lipid metabolism reprogramming as a novel druggable strategy to restore CRC chemosensitivity, and this nanoenabled approach for matairesinol will improve the chemotherapeutic efficacy with good biosafety