Project description:Predatory publishing represents a major challenge to scholarly communication. This paper maps the infiltration of journals suspected of predatory practices into the citation database Scopus and examines cross-country differences in the propensity of scholars to publish in such journals. Using the names of "potential, possible, or probable" predatory journals and publishers on Beall's lists, we derived the ISSNs of 3,293 journals from Ulrichsweb and searched Scopus with them. 324 of journals that appear both in Beall's lists and Scopus with 164 thousand articles published over 2015-2017 were identified. Analysis of data for 172 countries in 4 fields of research indicates that there is a remarkable heterogeneity. In the most affected countries, including Kazakhstan and Indonesia, around 17% of articles fall into the predatory category, while some other countries have no predatory articles whatsoever. Countries with large research sectors at the medium level of economic development, especially in Asia and North Africa, tend to be most susceptible to predatory publishing. Arab, oil-rich and/or eastern countries also appear to be particularly vulnerable. Policymakers and stakeholders in these and other developing countries need to pay more attention to the quality of research evaluation.Supplementary informationThe online version contains supplementary material available at (10.1007/s11192-020-03852-4).
Project description:Acid-sensing ion channel 1a (ASIC1a), as a member of the proton-gated cation channel family, can be activated by low extracellular pH, and takes part in many acidity-associated physiopathological processes. However, whether ASIC1a is expressed in human pancreatic stellate cells (PSCs) and involved in acid-induced physiopathological events has not been reported yet. In this study, we investigated the expression of ASIC1a in PSCs and its possible role in the activation and autophagy of PSCs evoked by extracellular acid. Our results show that ASIC1a is present in PSCs, and an enhanced expression of ASIC1a occurs under acid stimuli. More importantly, the activation and autophagy of PSCs can be induced in acidic medium, and inhibition of ASIC1a by ASIC1a-specific blocker psalmotoxin-1 (PcTx1) or siRNA knockdown could suppress these two acid-associated processes. Collectively, our present study reports for the first time that ASIC1a is expressed in PSCs, and provides evidence for the involvement of ASIC1a in the acidic microenvironment-induced activation and autophagy of PSCs.
Project description:MicroRNAs (miRNAs) have recently attracted increasing attention for their involvement in atherosclerosis (AS). The purpose of this study was to further explore the function and underlying mechanism of miR-135a in AS progression. The expression levels of miR-135a and lipoprotein lipase (LPL) mRNA were detected by qRT-PCR, and LPL protein expression was measured by western blotting. The levels of blood lipids and inflammatory cytokines, and LPL activity were assessed using corresponding Assay Kits, and an HPLC assay was used to determine the levels of free cholesterol (FC), total cholesterol (TC) and cholesterol ester (CE). A Dil-oxLDL binding assay was performed to evaluate the ability of cholesterol uptake. The direct interaction between miR-135a and LPL was confirmed by a dual-luciferase reporter assay and RNA immunoprecipitation assay. Our data indicated that miR-135a was downregulated in serum samples of AS patients and mice. Upregulation of miR-135a alleviated lipid metabolic disorders and inflammation in AS mice. Moreover, miR-135a negatively regulated lipid accumulation and inflammation in ox-LDL-treated THP-1 macrophages. Mechanistically, miR-135a directly targeted LPL and repressed LPL expression. LPL mediated the regulatory effect of miR-135a on lipid accumulation and inflammation in ox-LDL-treated THP-1 macrophages. In conclusion, our study indicated that miR-135a upregulation ameliorated lipid accumulation and inflammation at least partly by targeting LPL in THP-1 macrophages, highlighting miR-135a as a potential antiatherogenic agent.