bluuebunny/crossref_metadata_2025_split huggingface dataset:
Investigating the impact of gut microbiota on gastric cancer through the involvement of immune cells: a comprehensive Mendelian randomization study and mediation analysis
Authors: Wang Chao , Wang Jia , Guan Wenxian , Fei Bojian 
Published: May 2024

Abstract

Purpose
Recent observational studies have highlighted the role of altered gut microbiota (GM) involving the activation of the host immune system in the development of gastric cancer (GC), but the exact causal relationship and mechanisms at play are still not fully understood.
Materials and Methods
We used two-sample Mendelian randomization (MR) and Two-step mediation MR analysis with genetic data from published GWAS to examine the causal effect of 207 taxa and 205 bacterial pathways on GC. We focused on 731 immune cell traits as potential mediators. The primary methodological approach employed was inverse variance-weighted (IVW) estimation, augmented by a range of alternative estimators, notably the Bayesian weighted MR method.
Results
Our study indicated that four taxa and five bacterial pathways demonstrated a negative correlation with GC, while one taxon and two bacterial pathways showed a positive association. There was no evidence of reverse causality found in the reverse MR analysis. Additional validation was performed through sensitivity analyses. Mediation MR analyses revealed that the GM influences GC through various phenotypes of 16 immune cells acting as mediators. For example, s_Alistipes_sp_AP11 inhibited GC through NKT %T cell (total effect: -0.3234, mediation effect: 0.0212). The mediating effect further elucidates the complex relationship between GMs, immune cell traits, and their combined effects on GC.
Conclusions
Our research demonstrates a genetic connection between specific GMs and GC, emphasizing the possible role of immune cells as mediators, and the findings offer valuable perspectives on potential therapeutic strategies aimed at manipulating GM to address GC.
Metabolomic changes in mice induced by copper exposure: systematic analysis and exploration of toxicity mechanisms
Authors: Xiao Shuai , Gong Linqiang , Zhao Shiyuan , Chu Xue , Li Fengfeng , Zhang Yazhou , Song Fangqiang , Jiang Pei 
Published: May 2024

Abstract

Copper, an essential trace element, is indispensable for the growth and physiological functions of living beings, influencing several critical processes like cellular energy production, antioxidant defense, communication within cells, and functioning of enzymes. However, when copper levels exceed normal limits, it can lead to significant health issues. Recent investigations into the adverse effects of copper have shed light on its toxicological impacts, particularly focusing on metabolic alterations in certain organs. Yet, comprehensive research that examines the primary organs at risk from copper toxicity through a metabolomic lens remains scarce. In this study, an untargeted metabolomics strategy was adopted to assess how copper exposure alters organ metabolites leveraging gas chromatography-mass spectrometry (GC-MS) with the aim of identifying possible biomarkers and investigating their association with metabolic pathway disorders. Male C57BL/6J mice were randomly assigned to different experimental groups and metabolite levels in different organs were measured using GC-MS. Analyses showed very different metabolite profiles between groups, with 11, 32, 12, 18, 16, 15, 9, and 27 metabolites identified and 14 metabolites altered in serum, liver, kidney, muscle, hippocampus, cortex, lung, and pancreas, respectively, and examined the relationship between metabolites and metabolic pathways. Our findings reveal that copper is closely associated with disruption of metabolic pathways, and that copper can trigger a wide range of toxic effects through multiple pathways, such as triggering oxidative stress, interfering with mitochondrial function, altering enzyme function, weakening the body's ability to detoxify, and interfering with cell signaling. These findings reveal the complex mechanisms of copper toxicity and provide valuable information for the development of preventive and therapeutic measures for copper toxicity.
Biofilm formation and antimicrobial resistance in Enterobacterales isolated from cases of septicemia-Protocol
Authors: Devi Akoijam Nisha , Mudey Gargi 
Published: May 2024

Abstract

Introduction: This is a presentation of a study protocol in order to evaluate biofilm formation in enterobacterales causing septicemia so that clinical issues regarding increase in infections due to antimicrobial resistance can be solved.
Materials and methods: This is a study protocol of a prospective cross sectional simple random sampling method. A total of 100 patients blood samples will be included in the study. The bacteria from blood culture bottles will be isolated and identified using Bac-T Alert 3D/VITEK ID/Conventional method. Biofilm formation from cases of septicemia will be identified by tube method and tissue culture plate method.
Presence of biofilm production will be detected by tube method .and tissue culture plate
method Reference strain of positive biofilm producer Klebsiella pneumoniae 700603 will be
used as control. Isolates positive by both the methods will be labelled biofilm producers.
Their antimicrobial resistance will be studied.
Antibiotic susceptibility will be carried out by Kirby Bauer disc diffusion method as per
CLSI recommendations. The medium, Muller Hilton Agar (MHA) will be used.
Quality control strains of Escherichia coli (ATCC 25922), Staphylococcus aureus (ATCC
25923), and Pseudomonas aeruginosa (ATCC 27853) will be used to validate the results of antibiotic susceptibility test.
Results: This is an ongoing study protocol, and we are expecting the analysis of the results in July 2024.
Conclusion: The ability of Enterobacterales to form biofilms and acquire antimicrobial resistance significantly contributes to the pathogenesis of septicemia and treatment failure. Understanding the mechanism of formation and antimicrobial resistance will help design effective treatment and therapeutic strategies.
Categories: Microbiology, experiment
Effect of CYP2D6 and ABCB1 polymorphisms on pharmacokinetics and efficacy of aripiprazole in pediatric tic disorders
Authors: Xin Yingying , Gao Liuliu , Li Sichan , Wang Jun , Chen Chen , Tuo Yali , Nie Gang , Li Ruizhen , Sun Dan , Fu Yongli , Wang Yang , Liu Zhisheng 
Published: May 2024

Abstract

Backgrounds: Aripiprazole(ARI) is the first-line treatment for tic disorders (TD). It is metabolized by cytochrome P450(CYP)2D6(CYP2D6) and ATP‐binding cassette, sub-family B, member 1(ABCB1) genes. However, whether the clinical efficacy/pharmacokinetics of ARI will be influenced by genetic polymorphisms is not clear.
Methods: CYP2D6 and ABCB1 genotyping was performed. The pharmacokinetic parameters of ARI and DARI were obtained by the population pharmacokinetic model established previously. Drug response after ARI administration was evaluated according to reduction rate of Yale Global Tic Severity Scale score.
Results: The DARI/ARI metabolic ratios(MRs) of AUC0-t, Cmin and Cmax at the steady state were significantly associated with polymorphisms of rs1135840, rs5030865, rs1058164, rs28371702, rs1065852, rs1080989. The clearance(CL) of ARI were influenced by rs1135840, rs5030865, rs1080989. Rs16947, rs29001518, rs1080985 were correlated with CL of DARI. CYP2D6 polymorphisms(rs5030865) variant was associated with volume of distribution(V) of DARI. ABCB1(C3435T) rs1045642 influenced V or ARI. Rs1065852, rs1080989 was significantly associated with drug response of ARI in children with TD.
Conclusion: Clinical efficacy of TD was related with polymorphisms of rs1065852, rs1080989 and CYP2D6 genotyping was recommended in ARI treatment. More evidence and researches are needed to support the role of ABCB1 SNPs in ARI metabolization.
Exploring the potential immune cells related to the heredity of acute pancreatitis based on Mendelian randomization study
Authors: Mo Shaojian , Ling Ruiqi , Zhao Xuchen , Hu CongZhong , Liu Jiao , Xu Yingying , Xu Jiale , Xu Musen , Gao Fei , Fu Xifeng , Tian Yanzhang 
Published: May 2024

Abstract

Objective
Through Mendelian randomization (MR) analysis method, exploring the potential innate immune cells associated with acute pancreatitis.
Methods
This study is based on publicly available genetic data, and selects SNP related to immune cells from the immune cell data set after filtering a series of steps, and matches SNP related to immune cells as covariates for MR analysis from the AP data set.Five regression model analysis methods, including MR Egger, weighted median (WME), inverse variance weighting (IVW), simple model, and weighted model, were used to analyze the causal relationship between these immune cells and AP, and to verify the diversity of results. ity, heterogeneity and robustness.
Results
This study found that 36 types of immune cell phenotypes have potential causal relationships with AP, and further correction revealed that 4 types of immune cells have causal relationships with AP, including CD14+ CD16- OR=0.93 (95%CI=0.899-0.970, P=0.00045), CD28 OR=0.87 (95%CI=0.801-0.937,P=0.00036),CD14+ OR=0.93 (95%CI=0.897-0.971,P=0.00068),Mo MDSC OR=1.07 (95%CI=1.030-1.113, P=0.00049).The study was assessed by IVW and MR-Egger tests (P>0.05), indicating that there was no heterogeneity in the study. After the MR-Egger intercept test P>0.05, it indicated that the data did not have multiple effects and the study results were robust. The leave-one-out method removed SNPs one by one and did not find SNPs that had a large impact on the causal association estimates, indicating that the results were robust.
Conclusions
Our study found by MR that increased levels of CD14+CD16-, CD28, CD14+ may be protective factors for AP, and increased level of Mo MDSC may be a risk factor for AP. These four types of immune cells are potential immune cells genetically associated with AP.
Physical Activity Mitigates Negative Effects of Serum Cotinine Induced by Tobacco on the Risk of Metabolic Syndrome
Authors: Xu Liya , Dong Xiaosheng , Gao Zan , Sun Tingting , Zhou Cailiang , Wen Xu , Hou Xiao 
Published: May 2024

Abstract

Introduction/Objective: This study aims to assess the complex interactions between tobacco exposure, confirmed through serum cotinine (SC) levels, physical activity (PA), and the likelihood of developing metabolic syndrome (MetS). Methods This study involved 8,423 adults from the National Health and Nutrition Examination Survey (NHANES) spanning the years 2007 to 2018. The logistic regression and quantile regression analyses were conducted to estimate the associations among SC, PA and the risk of MetS with its components. We also investigated the sex differences on these outcome variables via the analysis of variance (ANOVA) and the Chi-square test. Results The covariate-adjusted logistic regression analysis results suggest that SC concentration (unit: ng/mL) was significantly and positively associated with MetS (OR: 6.41, 95%CI: 5.81–7.08), abdominal obesity (OR: 1.92, 95%CI: 1.75–2.11), hypertension (OR: 2.70, 95%CI: 2.46–2.96), hyperglycemia (OR: 12.50, 95%CI: 10.63–14.71), hypertriglyceridemia (OR: 2.10, 95%CI: 1.90–2.33), and low HDL-C (OR: 1.61, 95%CI: 1.46–1.77). PA energy consumption (unit: MET*h/wk) was significantly and negatively associated with MetS (OR: 0.56, 95%CI: 0.51–0.61), abdominal obesity (OR: 0.71, 95%CI: 0.65–0.78), hypertension (OR: 0.55, 95%CI: 0.50–0.60), hyperglycemia (OR: 0.59, 95%CI: 0.52–0.67), and hypertriglyceridemia (OR: 0.84, 95%CI: 0.76–0.93). For males, an increase of 6 MET*h/wk in PA energy consumption compensated for the risk impact of 1 ng/mL SC on MetS. Similarly, for females, an increase of 7 MET*h/wk in PA energy consumption compensated for the risk impact of 1 ng/mL SC on MetS. Conclusions This study indicates a positive correlation between SC concentration and a higher risk of MetS, while energy expenditure through PA was inversely related to the increased risk of MetS. Additionally, there appears to be a compensatory effect between PA energy expenditure and SC levels on the risk of developing MetS.
The Impact of High-Altitude Migration on Cardiac Structure and Function: A One-Year Prospective Study
Authors: Deng Ming-dan , Zhang Xin-jie , Feng Qin , Wang Rui , He Fen , Yang Feng-wu , Liu Xian-mei , Sun Fei-fei , Tao Jie , Li Shuang , Chen Zhong 
Published: May 2024

Abstract

Background
The trend of human migration to terrestrial high altitudes (HA) has been increasing over the years. However, the long-term impact of this migration on cardiac structure and function remains unclear. This prospective study aimed to investigate the changes in cardiac structure and function in healthy young male lowlanders following long-term migration to HA.
Methods
A total of 122 Chinese healthy young males were divided into two groups: those migrating to altitudes between 3600 meters and 4000 meters (low HA group, n = 65) and those migrating to altitudes between 4000 meters and 4700 meters (high HA group, n = 57). Traditional echocardiographic parameters were measured at sea level, one month, and one year after migration to HA.
Results
All four cardiac chamber dimensions, areas, and volumes decreased after both one month and one year of HA exposure. This reduction was more pronounced in the high HA group than in the low HA group. Bi-ventricular diastolic function declined after one month of HA exposure, while systolic function decreased after one year. Notably, these functional changes were not significantly influenced by altitude differences. Dilation of the pulmonary artery and a progressive increase in pulmonary artery systolic pressure were observed with both increasing exposure time and altitude. Additionally, decreased diameter of the inferior vena cava and reduced bicuspid and tricuspid blood flow velocity indicated reduced blood flow following migration to HA.
Conclusions
One year of migration to HA is associated with decreased blood volume and enhanced hypoxic pulmonary vasoconstriction. These factors contribute to reduced cardiac chamber size and slight declines in bi-ventricular function.
Link fault tolerability of 3-ary n-cube based on $g$-good-neighbor $r$-component edge-connectivity
Authors: Zhang Qifan , Zhou Shuming , Yang Lulu 
Published: May 2024

Abstract

High-performance computing relies heavily on parallel and distributed systems, which promptes us to establish both qualitative and quantitative criteria to assess the fault tolerability and vulnerability of the system’s underlying interconnection networks. Consider the scenario in which large-scale link failures disconnect the interconnection network, resulting in several components and each processor has multiple neighboring processors. In this scenario, the fault tolerability of the system can be measured by ggood- neighbor r-component edge-connectivity, denoted by λg,r(G), which is defined as the minimum number of edges whose removal results in a disconnected network with at least r connected components and each vertex has at least g neighbors. It combines the strategies of g-good-neighbor edge-connectivity and component edge-connectivity. In this paper, the g-good-neighbor (r + 1)-component edge-connectivity of 3-ary n-cube is investigated. This work is the first attempt enhancing link fault tolerability for 3-ary ncube under double constraints in the presence of the large-scale faulty links, which breaks down the inherent idea that pose one limitation on the resulting network. In addition, our results cover the work of Xu et al. ([IEEE Trans. Reliab., 71 (3) (2022)]) and Li et al. ([J. Parallel Distrib. Comput., 27 (2024)]). Finally, the compared results reveal that the g-good-neighbor (r+1)-component edge-connectivity is almost r times the size of g-goodneighbor edge-connectivity and much larger than (r + 1)-component edge-connectivity in
3-ary n-cube.
Simultaneous in situ monitoring of belowground, stem and relative stomatal hydraulic conductances of grapevine demonstrates a soil-texture specific transpiration control
Authors: Delval Louis , Jonard François , Javaux Mathieu 
Published: May 2024

Abstract

Background and aims Assessing the interrelationships between belowground, stem and stomatal hydraulics, under various edaphic conditions, is essential to enhance understanding of how grapevine (Vitis vinifera) responds to drought. This work aimed to understand the roles of belowground and stem hydraulics of the soil-grapevine system on the transpiration control of in situ grapevine during drought.Methods We simultaneously monitored soil water potential, stem water potential, leaf water potential and actual transpiration and investigated how belowground, stem and relative stomatal hydraulic conductances of in situ grapevines evolve and coordinate during a drought event on different soil types.Results Stomatal response was triggered by a decrease of belowground hydraulic conductance, but not by xylem cavitation in the stem. Stomata started to close at less negative soil water potential in sand than in loam and stomatal downregulation is sharper in coarse-textured than in fine-textured soils. Despite these contrasted responses to soil water potential, we observed, for the first time on in situ perennial plants such as grapevine, that the onset of stomatal closure was at the same belowground hydraulic conductance for each subplot, independently of the soil texture.Conclusion These findings prove that in situ grapevines coordinate short-term hydraulic mechanisms (e.g. stomatal regulation) and longer-term growth (e.g. root:shoot ratio). These belowground and aboveground adjustments should therefore be soil-texture specific.
Loop unrolling optimization for dual SIMD extension
Authors: Yao Jinyang , Liu Lili , Fu Xuanyu , Liu Wenbo , Wu Wei , Shan Zheng 
Published: May 2024

Abstract

SIMD extensions are playing an increasingly important role in high-performance computing and artificial intelligence fields. To fully utilize these components, various manufacturers and institutions have implemented many optimizations for SIMD extensions, with dual SIMD extension pipeline optimization being one of them. This method generates instructions suitable for parallel execution of the integrated dual SIMD extension on processors by unrolling vectorizable loops in programs. It is integrated into a mainstream compiler GCC as an optimization pass and can be enabled with just one compilation option. Experiments were conducted on an SW421 processor, testing standard benchmark suites such as SPEC CPU 2006 and NPB. The experiments showed that after using this optimization pass, programs generated by the compiler can fully utilize the dual SIMD extension during execution. Compared with turning on the autovectorization option, the method has an acceleration effect on multiple applications in the test set, and the execution efficiency is improved by an average of 5.6% and a maximum of 14%.
Empirical Study to Compare Theperformance of Novel Cpu Implementationof Deep Learning Algorithms Withgpu-based Implementations
Authors: Al-Sobeh Eslam , Jararweh Yaser , Jarrah Prof. Moath 
Published: May 2024

Abstract

Deep learning architectures and algorithms have shown promising results in differentapplications. However, training deep learning algorithms is a time-consuming step and researchers used graphics processing unit (GPU) accelerators in order to achieve an acceptable execution time, especially for real life applications. Sub-LInear Deep Learning Engine (SLIDE) is a relatively new work that aims at speeding up deep learning using only central processing unit (CPUs) implementation. Additionally, TorchSLIDE used PyTorch libraries to speed up SLIDE by 2.6X. This research study attempts to provide an empirical comparison for four models which are: PyTorch baseline CPU, PyTorch baseline GPU, TorchSLIDE, and SLIDE. In the experiments, we used a server with 10 cores (Intel i9-7900X) and NVIDIA Quadro P4000 (GP104GL) GPU. Five datasets were used in the evaluation which are: Amazon-670K, Delicious-200K, AmazonCat-13K, LF-AmazonTitles-131K, and Wiki10-31K. Based on the experiments, Py-Torch baseline GPU outperforms the other three implementations and achieved the highest accuracy in less time compared with the others for all datasets. Moreover, SLIDE outperformed TorchSLIDE when using the AmazonCat-13K dataset.
Alk1/Endoglin signaling restricts vein cell size increases in response to hemodynamic cues and limits ribosomal biogenesis
Authors: Diwan Zeenat , Kang Jia , Tsztoo Emma , Siekmann Arndt F. 
Published: May 2024

Abstract

Hemodynamic cues are thought to control blood vessel hierarchy through a shear stress set point, where flow increases lead to blood vessel diameter expansion, while decreases in blood flow cause blood vessel narrowing. Aberrations in blood vessel diameter control can cause congenital arteriovenous malformations (AVMs). We show in zebrafish embryos that while arteries behave according to the shear stress set point model, veins do not. This behavior is dependent on distinct arterial and venous endothelial cell (EC) shapes and sizes. We show that arterial ECs enlarge more strongly when experiencing higher flow, as compared to vein cells. Through the generation of chimeric embryos, we discover that this behavior of vein cells depends on the Bone Morphogenetic Protein (BMP) pathway components Endoglin and Alk1. Endoglin (eng) or alk1 (acvrl1) mutant vein cells enlarge when in normal hemodynamic environments, while we do not observe a phenotype in either acvrl1 or eng mutant ECs in arteries. We further show that an increase in vein diameters initiates AVMs in eng mutants, secondarily transmitting higher flow to arteries. These enlarge in response to higher flow through increasing arterial EC sizes, fueling the AVM. Finally, single cell sequencing results and immunofluorescence analysis indicate that increases in vein EC sizes in eng mutants are likely caused by increases in ribosome biogenesis and downregulation of the translational inhibitor dap1b. This study thus reveals a mechanism through which BMP signaling limits vein EC size increases in response to flow and provides a framework for our understanding of how a small number of mutant vein cells via flow-mediated secondary effects on wildtype arterial ECs can precipitate larger AVMs in disease conditions, such as hereditary hemorrhagic telangiectasia (HHT).
A single injection of ng level of malp2 are sufficient to save 50 percent of lethally irradiated mice
Authors: Zhang Jianyi , Cheng Ying , Li Jiaxun , Fang Duo , Zhai Xuanlu , Huang Daqian , Du Jicong , Liu Cong 
Published: May 2024

Abstract

Accidental radiation exposure causes the acute lethal damage of hematopoietic system and gastrointestinal tract1,2. By establishing an ionizing radiation (IR) induced injury model, we found macrophage-activating lipopeptide-2 (MALP-2) exhibited significant radioprotective effects in mice. MALP-2 improved the survival of irradiated mice, inhibited the radiation-induced gastrointestinal tract damage. Through intestinal organoid experiments, we found that MALP-2 protected the intestinal organoid against IR-induced injury. Next, we identified the differentially expressed genes (DEGs) between PBS and MALP-2 groups based on the RNA sequencing result3. And the RNA-seq results showed that MALP-2 increased the levels of interleukin 6 (IL-6), IL-12, G-CSF, GM-CSF, TNF-α, CCL-3, PGE-2 and SOD2. KEGG enrichment analysis showed that DEGs were significantly enriched in Toll-like receptor signaling pathway and NF-κB signaling pathway. In line with these observations, the expression level of IL-6 and GM-CSF were increased by using flow cytometry. Moreover, MALP-2 protected WT mice from IR induced death but had no radioprotective effects on the TLR2 KO and IL-6 KO mice, suggesting that the radioprotection of MALP-2 was mediated by activating TLR2/IL-6 axis. In conclusion, our data suggested that the MALP-2 could induce significant radioprotective effects and MALP-2 might be a potential radioprotective agent.