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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: Although the genetic susceptibility to diabetes and ischemic heart disease (IHD) has been well demonstrated, studies aimed at exploring gene variations associated with diabetic IHD are still limited; Methods: Our study included 204 IHD cases who had been diagnosed with diabetes before the diagnosis of IHD and 882 healthy controls. Logistic regression was used to find the association of candidate SNPs and polygenic risk score (PRS) with diabetic IHD. The diagnostic accuracy was represented with AUC. Generalized multifactor dimensionality reduction (GMDR) was used to illustrate gene-gene interactions; Results: For IL6R rs4845625, the CT and TT genotypes were associated with a lower risk of diabetic IHD than the CC genotype (OR = 0.619, p = 0.033; OR = 0.542, p = 0.025, respectively). Haplotypes in the AGER gene (rs184003-rs1035798-rs2070600-rs1800624) and IL6R gene (rs7529229-rs4845625-rs4129267-rs7514452-rs4072391) were both significantly associated with diabetic IHD. PRS was associated with the disease (OR = 1.100, p = 0.005) after adjusting for covariates, and the AUC were 0.763 (p < 0.001). The GMDR analysis suggested that rs184003 and rs4845625 were the best interaction model after permutation testing (p = 0.001) with a cross-validation consistency of 10/10; Conclusions: SNPs and haplotypes in the AGER and IL6R genes and the interaction of rs184003 and rs4845625 were significantly associated with diabetic IHD. [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]

IQ67-domain (IQD) proteins, first identified in Arabidopsis and rice, are plant-specific calmodulin-binding proteins containing highly conserved motifs. They play a critical role in plant defenses, organ development and shape, and drought tolerance. Driven by comprehensive genome identification and analysis efforts, IQDs have now been characterized in several species and have been shown to act as microtubule-associated proteins, participating in microtubule-related signaling pathways. However, the precise molecular mechanisms underpinning their biological functions remain incompletely understood. Here we review current knowledge on how IQD family members are thought to regulate plant growth and development by affecting microtubule dynamics or participating in microtubule-related signaling pathways in different plant species and propose some new insights. [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]

Background: Evidence regarding the effects of lipoprotein (a) [lp(a)] and renal function remains unclear. The present study aimed to explore the causal association of serum lp(a) with renal function damage in Chinese general adults., Methods: A total of 25343 individuals with available lp(a) data were selected from the baseline survey of the Cohort Study on Chronic Disease of Communities Natural Population in Beijing, Tianjin, and Hebei (CHCN-BTH). Five renal function indexes [estimated glomerular filtration rate (eGFR), serum creatinine (Scr), blood urea nitrogen (BUN), uric acid (UA), high-sensitivity C-reactive protein(CRPHS)] were analyzed. The restricted cubic spline (RCS) method, logistic regression, and linear regression were used to test the dose-response association between lp(a) and renal function. Stratified analyses related to demographic characteristics and disease status were performed. Two-sample Mendelian randomization (MR) analysis was used to obtain the causal association of lp(a) and renal function indexes. Genotyping was accomplished by MassARRAY System., Results: Lp(a) levels were independently associated with four renal function indexes (eGFR, Scr, BUN, CRPHS). Individuals with a higher lp(a) level had a lower eGFR level, and the association with Scr estimated GFR was stronger in individuals with a lower lp(a) level (under 14 mg/dL). . The association was similar in individuals regardless of diabetes or hypertension. MR analysis confirmed the causal association of two renal function indexes (Scr and BUN). For MR analysis, each one unit higher lp(a) was associated with 7.4% higher Scr (P=0.031) in the inverse-variance weighted method. But a causal effect of genetically increased lp(a) level with increased eGFR level which contrasted with our observational results was observed., Conclusion: The observational and causal effect of lp(a) on Scr and BUN were founded, suggesting the role of lp(a) on the risk of renal function damage in general Chinese adults., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Xie, Qi, Li, Wen, Zhang, Guo and Zhang.)

Introduction: Personal lifestyle and air pollution are potential risk factors for major non-communicable diseases (NCDs). However, these risk factors have experienced dramatic changes in the Beijing-Tianjin-Hebei (BTH) region in recent years, and few cohorts have focused on identifying risk factors for major NCDs in this specific region. The current study is a large, prospective, long-term, population-based cohort study that investigated environmental and genetic determinants of NCDs in BTH areas. The results of this study may provide scientific support for efforts to develop health recommendations for personalized prevention. Methods: About 36,000 participants 18 years or older would be obtained by multistage, stratified cluster sampling from five cities for the baseline assessment. Participants underwent seven examinations primarily targeting respiratory and circulatory system function and filled out questionnaires regarding lifestyle behavior, pollutant exposure, medical and family history, medication history, and psychological factors. Biochemistry indicators and inflammation markers were tested, and a biobank was established. Participants will be followed up every 2 years. Genetic determinants of NCDs will be demonstrated by using multiomics, and risk prediction models will be constructed using machine learning methods based on a multitude of environmental exposure, examination data, biomarkers, and psychosocial and behavioral assessments. Significant spatial and temporal differentiation is well-suited to demonstrating the health determinants of NCDs in the BTH region, which may facilitate public health strategies with respect to disease prevention and survivorship-related aspects., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2021 Liu, Cao, Guo, Pan, Cui, Sun, Zhao, Han, Zhang, Wang, Niu, Tang, Shan and Zhang.)

Background: To evaluate the contributions of elevated lipoprotein(a) [Lp(a)] to the risk of coronary heart disease (CHD) in the general Chinese community population according to different lipid profiles., Methods: We recruited individuals aged over 18 years from the baseline survey of the Cohort Study on Chronic Disease of Communities Natural Population in Beijing, Tianjin and Hebei (CHCN-BTH) using a stratified, multistage cluster sampling method. Data were collected through questionnaire surveys, anthropometric measures and laboratory tests. Restricted cubic spline (RCS) functions, multivariate logistic regression, sensitivity analyses and stratified analyses were used to evaluate the association between Lp(a) and CHD., Results: A total of 25,343 participants were included, with 1,364 (5.38%) identified as having CHD. Elevated Lp(a) levels were linearly related to an increased risk of CHD (P overall-association <0.0001 and P nonlinear-association =0.8468). Multivariate logistic regression analysis indicated that subjects with Lp(a) ≥300 mg/L had a higher risk of CHD [OR (95% CI): 1.36 (1.17, 1.57)] than did individuals with Lp(a) <300 mg/L. Compared with individuals with Lp(a) <119.0 mg/L (<50th percentile), the ORs (95% CI) for CHD in the 51st-80th, 81st-95th and >95th percentiles were 1.07 (0.93, 1.23), 1.26 (1.07, 1.50) and 1.68 (1.30, 2.17), respectively (P for trend <0.0001). This association was also found among the subgroup of subjects without dyslipidemia, including those with normal total cholesterol (TC) (<6.2 mmol/L), triglycerides (TG) (<2.3 mmol/L), high-density lipoprotein cholesterol (HDL-C) (≥1.0 mmol/L) and low-density lipoprotein cholesterol (LDL-C) (<4.1 mmol/L). Elevated Lp(a) and dyslipidemia significantly contributed to a higher risk of CHD with synergistic effects. Stratified analyses showed that elevated Lp(a) concentrations were significantly associated with an increased risk of CHD in the subgroups of individuals who were noncurrent drinkers, overweight individuals, individuals with hypertension, individuals who engaged in moderate physical activity, those without diabetes mellitus and individuals in Beijing and Tianjin., Conclusions: Elevated Lp(a) concentrations were linearly associated with a higher risk of CHD in the general Chinese community population, especially in normolipidemic subjects. Both dyslipidemia and elevated Lp(a) independently or synergistically contributed to the risk of CHD. Our results suggest that more attention should be paid to the levels of Lp(a) in normolipidemic subjects, which may be an early predictor of CHD., Competing Interests: Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at http://dx.doi.org/10.21037/atm-20-3899). The authors have no conflicts of interest to declare., (2021 Annals of Translational Medicine. All rights reserved.)

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.)

Purpose: The systemic epidemiology of salt sensitivity (EpiSS) study aims to combine molecular biology, epidemiology and bioinformatics methods to discover the potential causes of salt sensitivity of blood pressure (SSBP) using single-nucleotide polymorphisms in the genome and non-coding RNAs in the transcriptome to uncover both the genetic and environmental factors of SSBP., Participants: Between July 2014 and July 2016, we enrolled adults from 11 study centres in Beijing and Liaoning Province; participants were of the Han population and were 35-70 years of age. We collected blood samples, spot urine samples and 24-hour urine samples, in addition to baseline data on demographics, health-related lifestyle factors, chronic diseases, family history of illness and anthropometric information through face-to-face interviews using a standardised questionnaire. EpiSS uses the modified Sullivan's acute oral saline load and diuresis shrinkage test (MSAOSL-DST) to evaluate the effects of salt on blood pressure., Findings to Date: In total, 2163 participants were included in the EpiSS, of which 2144 participants completed the questionnaire, 2120 (98.0%) completed the MSAOSL-DST and 2083 (96.3%) provided a 24-hour urine sample. A total of 2057 participants (1501 women and 556 men) completed all the steps of the investigation and were included in the analysis. Among them, 583 (28.3%) subjects were classified as having salt sensitivity of blood pressure, and 1061 (51.6%) had hypertension., Future Plans: The next step of our study is to evaluate the incidence of cardiovascular disease in the participants. Biennial follow-up, including face-to-face questionnaire surveys, laboratory measurements of blood, urinary creatinine, glomerular filtration rate and anthropometric measurements, will occur two additional times. DNA and RNA will be collected for subsequent genetic biomarker studies. We plan on screening the salt-sensitive-related gene loci and non-coding RNAs based on relative environmental risk factors., Trial Registration Number: ChiCTR-EOC-16009980; Pre-results., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2018. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.)