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Incentivizing academic publications in internationally-indexed journals is a current topic of national debate especially in non-anglophone countries. To boost the dissemination of Chinese research results, the central government and higher education institutions had introduced various schemes to encourage international publications. However, a significant policy change took place when the Chinese government recently announced a break with SSCI supremacy conventions in research evaluation systems. Based on semi-structured interviews with five university managers and 30 academics in humanities and social sciences in five universities in China, this study examines the responses of both institution managers and individual scholars to the latest national guidelines. A qualitative analysis shows mixed attitudes among both HSS managers and individual academics towards the policy change: supportive but with doubts about the policy practicality as well as concerns about ensuing pressures to be generated by new evaluation systems. The findings suggest the policy change will not significantly affect HSS academics' pursuit of international publishing in a short term. It will, however, lead to some adjustments in the existing institutional evaluation regulations. The findings can contribute to the understanding of HE policy influence on academics as well as its potential implications for the global trend of anglicized academic publishing.

Several studies have shown the effects of PM2.5 exposure on respiratory and cardiovascular systems. However, there is no cohort study evidence of adverse effects of PM2.5 exposure on survival in patients with hepatocellular carcinoma (HCC) in China. This study is aimed at evaluating this association. This cohort study included 1440 HCC patients treated at the Third Central Clinical College of Tianjin Medical University from September 2013 to December 2018. We collected patient information, including demographic data, medical history, lifestyle characteristics, and disease characteristics. Based on PM2.5 concentrations measured at monitoring stations, the inverse distance weighted (IDW) method was used to assess the individuals' exposure during their survival period. Survival status was analysed by the Kaplan–Meier method. Restricted cubic splines and Cox proportional hazards models were used to estimate the relationship between PM2.5 and mortality, and potential confounders were adjusted for. The mortality rate of HCC patients exposed to PM2.5 ≥ 58.56 μg/m3 was significantly higher than that of HCC patients living in environments with PM2.5 < 58.56 μg/m3 (79.0% vs 50.7%, P < 0.001). The restricted cubic spline model showed a linear relationship between the PM2.5 concentration and mortality risk (P overall-association < 0.0001 and P nonlinear-association = 0.3568). Cox regression analysis showed that after adjusting for confounding factors, for every 10-μg/m3 increase in atmospheric PM2.5, the risk of death for HCC patients increased by 44% [hazard ratio (HR) = 1.44, 95% confidence interval (CI) 1.34, 1.56; P < 0.001]. Compared with patients exposed to PM2.5 <58.56 μg/m3, those exposed to PM2.5 ≥ 58.56 μg/m3 had a 1.55-fold increased risk of death. Stratified analysis results showed that the effects of PM2.5 on HCC mortality were more significant in patients aged ≥60 years or patients living in central urban areas. We found that exposure to elevated PM2.5 after HCC diagnosis may affect survival, with a higher concentration corresponding to a greater effect. [ABSTRACT FROM AUTHOR]

Background: The emergence of promising compounds to lower lipoprotein(a) [Lp(a)] has increased the need for a precise characterisation and comparability assessment of Lp(a)‐associated cardiometabolic disease risk. This study aimed to evaluate the distribution of Lp(a) levels in a Chinese population and characterise the association with cardiometabolic diseases. Methods: We assessed data from individuals from the Cohort Study on Chronic Diseases of the General Community Population in the Beijing‐Tianjin‐Hebei Region project. All Lp(a) measurements were performed in the same hospital. The cardiometabolic diseases considered were coronary heart disease (CHD), stroke, hypertension and type 2 diabetes (T2DM). Results: A total of 25343 individuals were included in the study. The median level of Lp(a) was 11.9 mg/dl (IQR 5.9 to 23.7 mg/dl), and higher Lp(a) levels showed a significant concentration‐dependent association with CHD risk. Individuals with Lp(a) levels lower than the 25th percentile were at increased risk of hypertension (OR: 1.15, 95% CI: 1.06–1.25) and T2DM (OR: 1.15, 95% CI: 1.03–1.28); however, Lp(a) levels were not significantly associated with stroke. The addition of Lp(a) levels to the prognostic model led to a marginal but significant C‐index, integrated discrimination improvement and net reclassification improvement. Conclusions: In this large sample size study, we observed that elevated Lp(a) levels were significantly associated with CHD. Furthermore, we found that the lowest Lp(a) levels were also significantly associated with hypertension and T2DM. These results provide evidence for differential approaches to higher levels of Lp(a) in individuals with different cardiometabolic diseases. [ABSTRACT FROM AUTHOR]

Acute dietary salt intake may cause an elevation in blood pressure (BP). The study aimed to assess the acute effect of saline loading on BP in subjects with different levels of salt intake. This study is based on the baseline survey of systemic epidemiology of salt sensitivity study. The sodium excretion in the 24‐hour urine was calculated for estimating the level of salt intake. Subjects were performed an acute oral saline loading test (1 L), and data of 2019 participants were included for analyses. Multivariate linear regression and stratified analyses were performed to identify associations between 24‐hour urinary sodium (24hUNa) with BP changes. Due to saline loading, systolic BP (SBP), pulse pressure, and urinary sodium concentration were significantly increased, while diastolic BP, heart rate, and urinary potassium concentration were significantly decreased. The SBP increments were more significant in subjects with lower salt intake, normotensives, elders, males, smokers, and drinkers. There was a significant linear negative dose‐response association between SBP increment with 24hUNa (β = −0.901, 95% CI: −1.253, −0.548), especially in lower salt intake individuals (β = −1.297, 95% CI: −2.338, −0.205) and hypertensive patients (β = −1.502, 95% CI: −2.037, −0.967). After excluding patients who received antidiabetic or antihypertensive medicines, the effects of negative associations weakened but remained significantly. In conclusion, acute salt loading leads to an increment in SBP, and the increased SBP was negatively related with 24hUNa. This study indicated avoiding acute salt loading was important for escaping acute BP changes, especially in lower salt intake populations. [ABSTRACT FROM AUTHOR]

Objectives: To identify long noncoding RNAs (lncRNAs) and construct a competing endogenous RNA (ceRNA) network for essential hypertension., Methods: An RNA microarray and two-step quantitative real-time PCR were applied to identify differentially expressed RNAs (DE-RNAs), and a luciferase assay was performed to explore the binding relationship between RNAs. A generalized linear model and logistic regression model were used to analyze the associations between different RNAs and of RNAs with hypertension. Receiver operating characteristic curve analysis was executed to evaluate the diagnostic performance. Bioinformatics analysis was applied for network construction., Results: In total, 439 DE-RNAs (387 lncRNAs and 52 mRNAs) were identified in the microarray, and 71 'lncRNA-miRNA-mRNA' loops formed the ceRNA network. The first validation confirmed that five RNAs (NR&#95;104160, lnc-GPR63-8:1, lnc-HPRT1-9:1, ID1 and RSL24D1 ) were significantly upregulated in hypertensives ( P < 0.05). NR&#95;104160 was significantly associated with hypertension (OR = 2.863, 95% CI: 1.143-7.172; P = 0.025) after adjusting for confounding factors. NR&#95;104160 was included in the hypertension diagnostic model, with an area under the curve of 0.852 (95% CI: 0.761-0.944). In the second validation, NR&#95;104160 showed a constant significant difference ( P = 0.001). An elevated expression level of NR&#95;104160 was associated with the expression of ID1 ( β = 0.2235, P = 0.005). Luciferase assays showed hsa-miR-101-3p stimulation significantly inhibited the reporter gene activation ability of the NR&#95;104160 wild-type plasmid ( P < 0.001)., Conclusions: Our study constructed a ceRNA network to provide hypotheses regarding the mechanism of hypertension development. lncRNA-NR&#95;104160 was identified as a hub element that participates in hypertension transcriptional regulation and as a potential biomarker., Competing Interests: None., (AJTR Copyright © 2020.)