bluuebunny/crossref_metadata_2025_split huggingface dataset:
Trends in unhealthy lifestyle factors in US NHANES respondents with cardiovascular disease for the period between 1999 and 2018
Authors: Liang Yanting , Liu Fengyao , Yin Han , Shi Xiaohe , Chen Yilin , Wang Haochen , Wang Yu , Bai Bingqing , Liu Yuting , Liu Quanjun , Wu Chao , Yu Xueju , Ma Huan , Geng Qingshan 
Published: May 2023

ObjectivesTo examine national trends in unhealthy lifestyle factors among adults with cardiovascular disease (CVD) in the United States (US) between 1999 and 2018.MethodsWe analyzed data from National Health and Nutrition Examination Survey (NHANES), a nationally representative survey of participants with CVD who were aged ≥20 years, which was conducted between 1999 and 2000 and 2017–2018. CVD was defined as a self-report of congestive heart failure, coronary heart disease, angina, heart attack, or stroke. The prevalence rate of each unhealthy lifestyle factor was calculated among adults with CVD for each of the 2-year cycle surveys. Regression analyses were used to assess the impact of sociodemographic characteristics (age, sex, race/ethnicity, family income, education level, marital status, and employment status).ResultsThe final sample included 5610 NHANES respondents with CVD. The prevalence rate of their current smoking status remained stable among respondents with CVD between 1999 and 2000 and 2017–2018. During the same period, there was a decreasing trend in the age-adjusted prevalence rate of poor diet [primary American Heart Association (AHA) score &lt;20; 47.5% (37.9%–57.0%) to 37.5% (25.7%–49.3%), p &lt; 0.01]. Physical inactivity marginally increased before decreasing, with no statistical significance. The prevalence rate of sedentary behavior increased from 2007 to 2014 but subsequently returned to its original level in 2018 with no statistical significance. The age-adjusted prevalence rate of obesity increased from 32% (27.2%–36.8%) in 1999–2000 to 47.9% (39.9%–55.8%) in 2017–2018 (p &lt; 0.001). The age-adjusted prevalence rate of depression increased from 7% (4.2%–9.9%) in 1999–2000 to 13.9% (10.2%–17.6%) in 2017–2018 (p = 0.056). Trends in mean for each unhealthy lifestyle factor were similar after adjustment for age. We found that respondents who had low education and income levels were at a higher risk of being exposed to unhealthy lifestyle factors (i.e., smoking, poor diet, and physical inactivity) than those who had high education and income levels.ConclusionsThere is a significant reduction in the prevalence rate of poor diet among US adults with CVD between 1999 and 2018, while the prevalence rate of obesity showed increasing trends over this period. The prevalence rate of current smoking status, sedentary behavior, and depression was either stable or showed an insignificant increase. These findings suggest that there is an urgent need for health policy interventions targeting unhealthy lifestyles among adults with CVD.
Distribution of harmful gas and ventilation length design of high altitude long gas tunnel construction: a case study
Authors: Zhang Xueqiang , Hu Juyi , Zhang Danfeng , Cai Shuang , Yang Feng 
Published: May 2023

The air density in high altitude gas tunnel is small and the air supply is difficult. The jet tunnel ventilation is a common construction ventilation mode. In order to explore the pollutant distribution characteristics and the optimal ventilation length of tunnel ventilation in high altitude gas tunnel, Ningchan tunnel has been taken as the engineering background, the fluid dynamics software Fluent has been used to establish a three-dimensional model of jet tunnel ventilation, the distribution characteristics of methane, hydrogen sulfide and other harmful gas in the tunnel have been studied, and the optimal ventilation length of tunnel ventilation in high altitude gas tunnel degree has been explored. The results show that: the minimum ventilation length required in the existing technical specifications of gas tunnel is not reasonable, which leads to the existence of low-speed wind area in the tunnel, and harmful gas is easy to gather in the single head section, and the gas concentration can reach 0.59% at 2 m away from the working face; by reducing the ventilation length, the gas concentration in the single head section can be effectively reduced, and when the ventilation length is 1,200 m, the gas concentration at 2 m away from the working face will be reduced to 0.31%; setting local fan in front of the roadway can also significantly improve the accumulation degree of harmful gas in the single end section. The maximum gas concentration of working face reduced to 0.24%, and the average gas concentration of reduced to 0.15%. The results can provide reference for ventilation scheme of high altitude gas tunnel construction.
Processes of communication and dissemination of science: the challenges of science policy guidelines in Colombia
Authors: Niño-Sandoval Yaddy , Alvarez-Risco Aldo , Simbaqueba-Uribe John , Del-Aguila-Arcentales Shyla , Villalobos-Alvarez Diego , Yañez Jaime A. 
Published: May 2023

IntroductionThe present study aims to identify the characteristics of public policy relating to the Social Appropriation of Knowledge (SAK) in Colombia, generated between 2020 and 2021, on the communication and dissemination of science. Furthermore, the study aims to determine what incentives are offered by these policies to promote the communication and dissemination of science, and what importance is given to the use of digital scenarios.MethodThis is done through a comparative analysis of Colombia’s guidelines of public science policies using a bibliographical review.Results and discussionWith this analysis, it is concluded that the policies resulting from 22 years of reflection in Colombia aim to strengthen the SAK in the communication of science, understood in specific relation to dissemination, which is understood as activities that make scientific knowledge accessible to a much wider audience.ConclusionThe digital scenarios are proposed as communicative spaces to spread knowledge to communities and strengthen the science-society relationship.
Klotho inversely relates with carotid intima- media thickness in atherosclerotic patients with normal renal function (eGFR ≥60 mL/min/1.73m2): a proof-of-concept study
Authors: Donate-Correa Javier , Martín-Núñez Ernesto , Martin-Olivera Alberto , Mora-Fernández Carmen , Tagua Víctor G. , Ferri Carla M. , López-Castillo Ángel , Delgado-Molinos Alejandro , López-Tarruella Victoria Castro , Arévalo-Gómez Miguel A. , Pérez-Delgado Nayra , González-Luis Ainhoa , Navarro-González Juan F. 
Published: May 2023

IntroductionKlotho protein is predominantly expressed in the kidneys and has also been detected in vascular tissue and peripheral blood circulating cells to a lesser extent. Carotid artery intima-media thickness (CIMT) burden, a marker of subclinical atherosclerosis, has been associated with reductions in circulating Klotho levels in chronic kidney disease patients, who show reduced levels of this protein at all stages of the disease. However, the contribution of serum Klotho and its expression levels in peripheral blood circulating cells and in the carotid artery wall on the CIMT in the absence of kidney impairment has not yet been evaluated.MethodsWe conducted a single-center study in 35 atherosclerotic patients with preserved kidney function (eGFR≥60 mL/min/1.73m2) subjected to elective carotid surgery. Serum levels of Klotho and cytokines TNFa, IL6 and IL10 were determined by ELISA and transcripts encoding for Klotho (KL), TNF, IL6 and IL10 from vascular segments were measured by qRT-PCR. Klotho protein expression in the intima-media and adventitia areas was analyzed using immunohistochemistry.ResultsAPatients with higher values of CIMT showed reduced Klotho levels in serum (430.8 [357.7-592.9] vs. 667.8 [632.5-712.9] pg/mL; p&lt;0.001), mRNA expression in blood circulating cells and carotid artery wall (2.92 [2.06-4.8] vs. 3.69 [2.42-7.13] log.a.u., p=0.015; 0.41 [0.16-0.59] vs. 0.79 [0.37-1.4] log.a.u., p=0.013, respectively) and immunoreactivity in the intimal-medial area of the carotids (4.23 [4.15-4.27] vs. 4.49 [4.28-4.63] log µm2 p=0.008). CIMT was inversely related with Klotho levels in serum (r= -0.717, p&lt;0.001), blood mRNA expression (r=-0.426, p=0.011), and with carotid artery mRNA and immunoreactivity levels (r= -0.45, p=0.07; r= -0.455, p= 0.006, respectively). Multivariate analysis showed that serum Klotho, together with the gene expression levels of tumor necrosis factor TNFa in blood circulating cells, were independent determinants of CIMT values (adjusted R2 = 0.593, p&lt;0.001).DiscussionThe results of this study in subjects with eGFR≥60mL/min/1.73m2 show that patients with carotid artery atherosclerosis and higher values of CIMT present reduced soluble Klotho levels, as well as decreased KL mRNA expression in peripheral blood circulating cells and Klotho protein levels in the intima-media of the carotid artery wall.
Identification of ribosomal protein family as immune-cell-related biomarkers of NAFLD by bioinformatics and experimental analyses
Authors: Li Gerui , Li Hang , Chen Ze 
Published: May 2023

BackgroundImmune cells play an integral role in the development and progression of non-alcoholic fatty liver disease (NAFLD). This study was to identify immune-cell-related biomarkers for the diagnosis and treatment of NAFLD.Methods and findingsFirst, we introduced human liver transcriptome data from the GEO database (GSE48452 and GSE126848) and performed a weighted gene co-expression network analysis (WGCNA) to screen out the modules related to immune cell infiltration and to identify immune-cell-related differentially expressed genes (ICR-DEGs) associated with NAFLD progression. Further, the protein-protein interaction (PPI) network of ICR-DEGs was established to obtain hub genes and subsequently, the expression trend analysis was conducted to identify immune-cell-related biomarkers of NAFLD. Finally, the mRNA expression of biomarkers was validated in a NAFLD mouse model induced by high-fat diet (HFD) feeding. In total, we identified 66 ICR-DEGs and 13 hub genes associated with NAFLD. Among them, 9 hub genes (CD247, CD74, FCGR2B, IL2RB, INPP5D, MRPL16, RPL35, RPS3A, RPS8) were correlated with the infiltrating immune cells by the Pearson correlation analysis. Subsequently, 4 immune-cell-related biomarkers (RPL35, RPS3A, RPS8, and MRPL16) with the same expression trends in GSE48452 and GSE126848 datasets were identified. These biomarkers were enriched in immune-related pathways and had a good ability to distinguish between NASH and healthy samples. Moreover, we constructed a competing endogenous RNA (ceRNA) network of biomarkers and predicted twenty potential therapeutic drugs targeting RPS3A such as taxifolin and sitagliptin. Finally, experimental validation indicated that the hepatic mRNA expression of Rpl35, Rps3A, and Rps8 was significantly decreased in NAFLD mice.ConclusionsThis study identified four ribosomal protein genes (RPL35, RPS3A, RPS8, and MRPL16) as immune-cell-related biomarkers of NAFLD, which may actively participate in the immune processes during NAFLD progression and could serve as potential targets for the diagnosis and treatment of NAFLD.
Disentangling the spread dynamics of insect invasions using spatial networks
Authors: Estay Sergio A. , Silva Carmen P. , López Daniela N. , Labra Fabio A. 
Published: May 2023

IntroductionDescribing and understanding spatiotemporal spread patterns in invasive species remains a long-standing interdisciplinary research goal. Here we show how a network-based top-down approach allows the efficient description of the ongoing invasion byDrosophila suzukiiin Chile.MethodsTo do so, we apply theoretical graph methods to calculate the minimum cost arborescence graph (MCA) to reconstruct and understand the invasion dynamics ofD. suzukiisince the first detection in 2017. This method estimates a directed rooted weighted graph by minimizing the total length of the resulting graph. To describe the temporal pattern of spread, we estimate three metrics of spread: the median dispersal rate, the median coefficient of diffusion, and the median dispersal acceleration.ResultsThe estimated MCA shows that over four years,D. suzukiicolonized a ~1,000km long strip in the central valley of Chile, with an initial phase with long paths and connections and no clear direction pattern, followed by a clearer north–east propagation pattern. The median dispersal rate for the entire period was 8.8 (7.4–10.6, 95% CI), while the median diffusion coefficient was 19.6 meters2/day (13.6–27.9, 95% CI). The observed spread dynamics and the log-normal distribution of accelerations are consistent with long-distance dispersal events.DiscussionThe complexities of real landscapes cannot be summarized in any model, but this study shows how an alternative top-down approach based on graph theory can facilitate the ecological analysis of the spread of an invasive species in a new territory.
Deciphering the single-cell transcriptome network in keloids with intra-lesional injection of triamcinolone acetonide combined with 5-fluorouracil
Authors: Xia Yijun , Wang Youbin , Hao Yan , Shan Mengjie , Liu Hao , Liang Zhengyun , Kuang Xinwen 
Published: May 2023

ObjectivesKeloid is a highly aggressive fibrotic disease resulting from excessive extracellular matrix deposition after dermal injury. Intra-lesional injection of triamcinolone acetonide (TAC) in combination with 5-fluorouracil (5-FU) is a commonly used pharmacological regimen and long-term repeated injections can achieve sustained inhibition of keloid proliferation. However, the molecular mechanisms underlying the inhibitory effect on keloids remain insufficiently investigated.Methods and materialsThis study performed single-cell RNA sequencing analysis of keloids treated with TAC+5-FU injections, keloids, and skins to explore patterns of gene expression regulation and cellular reprogramming. ResultsThe results revealed that TAC+5-FU interrupted the differentiation trajectory of fibroblasts toward pro-fibrotic subtypes and induced keloid atrophy possibly by inhibiting the FGF signaling pathway in intercellular communication. It also stimulated partial fibroblasts to develop the potential for self-replication and multidirectional differentiation, which may be a possible cellular source of keloid recurrence. T cell dynamics demonstrated elevated expression of secretory globulin family members, which may be possible immunotherapeutic targets. Schwann cell populations achieved functional changes by increasing the proportion of apoptotic or senescence-associated cell populations and reducing cell clusters that promote epidermal development and fibroblast proliferation. ConclusionsOur findings elucidated the molecular and cellular reprogramming of keloids by intra-lesional injection of TAC+5-FU, which will provide new insights to understand the mechanism of action and therapeutic targets.
The circadian rhythm key gene ARNTL2: a novel prognostic biomarker for immunosuppressive tumor microenvironment identification and immunotherapy outcome prediction in human cancers
Authors: Wu Gujie , Ren Hefei , Hu Qin , Ma Huiyun , Chen Hongyu , Zhou Lin , Xu Kun , Ding Liang 
Published: May 2023

BackgroundAryl hydrocarbon receptor nuclear translocator-like 2 (ARNTL2) belongs to the b HLH- PAS domain transcription factor family and is one of the key clock genes that control the circadian rhythm. ARNTL2 plays an important role in human biological functions. However, its role in various tumors, especially in the tumor immune microenvironment (TIME) and immunotherapy, remains unclear.MethodsWe integrated data from cancer patients from multiple databases, including the Cancer Genome Atlas, Cancer Cell Lineage Encyclopedia, Genotype Tissue Expression, Human Protein Atlas, cBioPortal, TIMER, and ImmuCellAI, with data from a large clinical study, three immunotherapy cohorts, and in vitro experiments to investigate the involvement of ARNTL2 expression in cancer prognosis and immune response.ResultsARNTL2 displayed abnormal expression within most malignant tumors, and is significantly associated with poorer survival and pathologic staging. Through gene-set enrichment analysis (GSEA) and gene-set variation analysis (GSVA), we found that ARNTL2 not only regulates cell cycle-related functions to promote cell proliferation but also regulates autoimmunity-related functions of the innate and adaptive immune systems, and other immune-related signaling pathways. In addition, ARNTL2 overexpression contributes to an immunosuppressive tumor microenvironment that plays a key role in immunosuppression-related features, such as the expression of immunosuppression-related genes and pathways and the number of immunosuppressive-infiltrating cells, including regulatory T cells (Tregs), tumor-associated macrophages (TAMs), and cancer-associated fibroblasts (CAFs). The group of patients with low ARNTL2 expression who received immune checkpoint inhibitors (ICI) therapy had better response rates and longer survival when compared to those with high ARNTL2 expression.ConclusionThe findings of this study suggest that ARNTL2 is a potential human oncogene that plays an important role in tumorigenesis and cancer immunity. Elevated ARNTL2 expression indicates an immunosuppressive tumor microenvironment. Targeting ARNTL2 in combination with ICI therapy could bring more significant therapeutic benefits to patients with cancer. Our study sheds light on the remarkable potential of ARNTL2 in tumor immunity and provides a novel perspective for anti-tumor strategies.
Transcriptome-wide identification of altered RNA m6A profiles in cardiac tissue of rats with LPS-induced myocardial injury
Authors: Wang Wei , Zhang Tie-Ning , Yang Ni , Wen Ri , Wang Yu-Jing , Zhang Bing-Lun , Yang Yu-Hang , Liu Chun-Feng 
Published: May 2023

PurposeMyocardial injury is a common complication in patients with endotoxaemia/sepsis, especially in children. Moreover, it develops through an unclear pathophysiological mechanism, and effective therapies are lacking. Recently, RNA modification, particularly N6-methyladenosine (m6A) modification, has been found to be involved in various physiological processes and to play important roles in many diseases. However, the role of m6A modification in endotoxaemia/sepsis-induced myocardial injury is still in its infancy. Therefore, we attempted to construct the m6A modification map of myocardial injury in a rat model treated by lipopolysaccharide (LPS) and explore the role of m6A modification in LPS-induced myocardial injury.MethodMyocardial injury adolescent rat model was constructed by intraperitoneal injection of LPS. m6A RNA Methylation Quantification Kit was used to detect overall level of m6A modification in rat cardiac tissue. m6A-specific methylated RNA immunoprecipitation followed by high-throughput sequencing (MeRIP-seq) and RNA sequencing (RNA-seq) were conducted to identify the altered m6A-modified genes and differentially expressed genes in cardiac tissue of rats treated by LPS and control rats (6 versus. 6). Bioinformatics was used to analyze the functions of differentially m6A modified genes, differentially expressed genes, and genes with both differential m6A modification and differential expression. qPCR was used to detect expression of m6A modification related enzymes.ResultWe found that the overall level of m6A modification in cardiac tissue of the LPS group was up-regulated compared with that of the control group. MeRIP-seq and RNA-seq results showed that genes with differential m6A modification, genes with differential expression and genes with both differential m6A modification and differential expression were closely associated with inflammatory responses and apoptosis. In addition, we found that m6A-related enzymes (Mettl16, Rbm15, Fto, Ythdc2 and Hnrnpg) were differentially expressed in the LPS group versus. the control group.Conclusionm6A modification is involved in the pathogenesis process of LPS-induced myocardial injury, possibly through the regulation of inflammatory response and apoptosis-related pathways. These results provide valuable information regarding the potential pathogenic mechanisms underlying LPS-induced myocardial injury.
Bladder cancer patients have increased NETosis and impaired DNaseI-mediated NET degradation that can be therapeutically restored in vitro
Authors: Herranz Raquel , Oto Julia , Hueso Marta , Plana Emma , Cana Fernando , Castaño María , Cordón Lourdes , Ramos-Soler David , Bonanad Santiago , Vera-Donoso César D. , Martínez-Sarmiento Manuel , Medina Pilar 
Published: May 2023

BackgroundNeutrophils, key players of the immune system, also promote tumor development through the formation of neutrophil extracellular traps (NETs) in a process called NETosis. NETs are extracellular networks of DNA, histones and cytoplasmic and granular proteins (calprotectin, myeloperoxidase, elastase, etc.) released by neutrophils upon activation. NETs regulate tumor growth while promoting angiogenesis and invasiveness, and tumor cells also stimulate NETosis. Although NETosis seems to be increased in cancer patients, an increase of NETs in plasma may also be mediated by an impaired degradation by plasma DNaseI, as evidenced in several immunological disorders like lupus nephritis. However, this has never been evidenced in bladder cancer (BC) patients. Herein, we aimed to evaluate the occurrence of increased NETosis in plasma and tumor tissue of BC patients, to ascertain whether it is mediated by a reduced DNaseI activity and degradation, and to in vitro explore novel therapeutic interventions.MethodsWe recruited 71 BC patients from whom we obtained a plasma sample before surgery and a formalin-fixed paraffin embedded tumor tissue sample, and 64 age- and sex-matched healthy controls from whom we obtained a plasma sample. We measured NETs markers (cell-free fDNA, calprotectin, nucleosomes and neutrophil elastase) and the DNaseI activity in plasma with specific assays. We also measured NETs markers in BC tissue by immunofluorescence. Finally, we evaluated the ability of BC and control plasma to degrade in vitro-generated NETs, and evaluated the performance of the approved recombinant human DNaseI (rhDNaseI, Dornase alfa, Pulmozyme®, Roche) to restore the NET-degradation ability of plasma. In vitro experiments were performed in triplicate. Statistical analysis was conducted with Graphpad (v.8.0.1).ResultsNETosis occurs in BC tissue, more profusely in the muscle-invasive subtype (P&lt;0.01), that with the worst prognosis. Compared to controls, BC patients had increased NETosis and a reduced DNaseI activity in plasma (P&lt;0.0001), which leads to an impairment to degrade NETs (P&lt;0.0001). Remarkably, this can be therapeutically restored with rhDNaseI to the level of healthy controls.ConclusionTo the best of our knowledge, this is the first report demonstrating that BC patients have an increased NETosis systemically and in the tumor microenvironment, in part caused by an impaired DNaseI-mediated NET degradation. Remarkably, this defect can be therapeutically restored in vitro with the approved Dornase alfa, thus Pulmozyme® could become a potential therapeutic tool to locally reduce BC progression.