bluuebunny/crossref_metadata_2025_split huggingface dataset:
Knockdown of liver cancer cell‐secreted exosomal PSMA5 controls macrophage polarization to restrain cancer progression by blocking JAK2/STAT3 signaling
Authors: Xie Shujie , Li Xiang , Yan Jia , Yu Hua , Chen Shuhuai , Chen Kana 
Published: February 2024

AbstractIntroductionTumor‐associated macrophages, a major component of the tumor microenvironment, undergo polarization into M2 macrophages (M2), and thereby exert an immunosuppressive effect to induce cancer metastasis. This study strives to uncover a molecular mechanism underlying this event in hepatocellular carcinoma (HCC).MethodsProteasome subunit alpha 5 (PSMA5) expression in liver hepatocellular carcinoma (LIHC) tissues and its association with LIHC patients were predicted using StarBase. PSMA5 level in human HCC cells was manipulated via transfection. Exosomes were isolated from HCC cells, and internalized into macrophages which were cocultured with HCC cells. Exosome internalization was observed after fluorescence labeling. HCC cell migration and invasion were evaluated by wound healing and Transwell assays. Xenograft assay was performed to investigate the role of PSMA5 in in vitro tumorigenesis. M2 polarization was assessed by enzyme‐linked immunosorbent assay, quantitative reverse transcription polymerase chain reaction, and immunohistochemistry. PSMA5 expression in exosomes and Janus Kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) activation in macrophages and tumors were detected by Western blot analysis.ResultsHigh PSMA5 expression was observed in LIHC tissues and associated with compromised survival of LIHC patients. PSMA5 knockdown inhibited HCC cell migration and invasion. PSMA5 knockdown in HCC cells downregulated PSMA5 level in exosomes from these HCC cells. HCC cell‐isolated exosomes were successfully internalized into macrophages, and facilitated M2 polarization and JAK2/STAT3 pathway activation. HCC cell‐secreted exosomal PSMA5 knockdown inhibited the exosome‐induced effect on macrophages, and attenuated the promotion induced by exosome‐treated macrophages on HCC cell migration/invasion and tumorigenesis along with in vivo M2 polarization and JAK2/STAT3 pathway activation.ConclusionHCC cell‐secreted exosomal PSMA5 knockdown hinders M2 polarization to suppress cancer progression by restraining JAK2/STAT3 signaling.
Effects of myeloperoxidase on inflammatory responses with hypoxia in Citrobacter rodentium‐infectious mice
Authors: Gao Xiang , Zhang Yu , Zhu Qinfang , Han Ying , Jia Ruhan , Zhang Wei 
Published: February 2024

AbstractPurposeMyeloperoxidase (MPO) has been identified as a mediator in various inflammatory diseases. Bacterial infection of the intestine and hypoxia can both lead to inflammatory responses, but the role of MPO in these phenomena remains unclear.MethodsBy building the MPO‐/‐ mice, we evaluated relevant inflammatory factors and tissue damage in mice with intestinal Citrobacter rodentium infection and hypoxia. The body weight and excreted microorganisms were monitored. Intestinal tissues were collected 7 days after bacterial infection under hypoxia to undergo haematoxylin‐eosin staining and assess the degree of pathological damage. ELISA assays were performed to quantify the serum levels of TNF‐α, IFN‐γ, IL‐6, and IL‐1β inflammatory cytokines. PCR, WB, and IF assays were conducted to determine the expression of chemokines MCP1, MIP2, and KC in the colon and spleen.ResultsThe C. rodentium infection and hypoxia caused weight loss, intestinal colitis, and splenic inflammatory cells active proliferation in wild‐type mice. MPO deficiency alleviated this phenomenon. MPO‐/‐ mice also displayed a significant decline in bacteria clearing ability. The level of TNF‐α in the serum and spleen was both lower in MPO‐/‐ hypoxia C. rodentium‐infected mice than that in wild‐type mice. The chemokines expression levels of MIP2, KC, and MCP1 in the spleen and colon of each bacterial infected group were significantly increased (p < .05), while in hypoxia, the factors in the spleen and colon were decreased (p < .05). MPO deficiency was found to lower the levels of these chemokines compared with wild‐type mice.ConclusionMPO plays an important role of the inflammatory responses in infectious enteritis and hypoxia in mice, and the loss of MPO may greatly reduce the body's inflammatory responses to fight diseases.
Sirtuin2 suppresses the polarization of regulatory T cells toward T helper 17 cells through repressing the expression of signal transducer and activator of transcription 3 in a mouse colitis model
Authors: Ge Liuqing , Xu Min , Huang Meifang , Liu Shaoping , Zhou Zhidai , Xia Ziqin , Zhao Qiu , Zhou Feng 
Published: February 2024

AbstractIntroductionRegulatory T cells (Tregs) play an important role in inflammatory bowel diseases (IBDs) through modulating intestinal inflammation. However, the factors affecting Treg function and plasticity during IBD progression are not thoroughly disclosed. The current study aims to reveal new molecular mechanisms affecting Treg plasticity.MethodsA mouse strain, in which tdTomato and enhanced green fluorescent protein were under the control of the Foxp3 promoter and Il17a promoter, was established and subjected to colitis induction with dextran sulfate sodium. The existence of Tregs and IL‐17‐expressing Tregs (i.e., Treg/T helper 17 [Th17] cells) were observed and sorted from the spleen, mesenteric lymph nodes, and lamina propria by flow cytometry, followed by measuring Sirtuin2 (Sirt2) expression using quantitative reverse transcription polymerase chain reaction and Immunoblotting. Lentivirus‐induced Sirt2 silencing was applied to determine the impact of Sirt2 on Treg polarization to Treg/Th17 cells and even Th17 cells. The effect of Sirt2 on Stat3 was analyzed by flow cytometry and immunoblotting.ResultsSirt2 was highly expressed in lamina propria Tregs and it moderately suppressed Foxp3 expression as well as the immunosuppressive function of Tregs. Surprisingly, lentivirus‐mediated Sirt2 silencing promoted the generation of Treg/Th17 cells out of Tregs. Sirt2 silencing also enhanced the generation of Th17 cells out of Tregs under the Th17 induction condition. Furthermore, Sirt2 inhibited Th17 induction by suppressing the protein level of the signal transducer and activator of transcription 3.ConclusionSirt2 suppresses Treg function but also inhibits Treg polarization toward Treg/Th17 cells and Th17 cells. The ultimate effect of Sirt2 on colitis might depend on the balance among Tregs, Treg/Th17 cells, and Th17 cells.
Self‐monitoring and public posting improve competitive youth cyclists' training performance
Authors: Ayvazo Shiri , Naveh Mey‐Elle 
Published: January 2024

AbstractThis study investigated the effects of self‐monitoring and public posting on the cycling performance of competitive youth cyclists. We measured three primary dependent variables: performance volume, intensity precision, and performance‐duration deviation. In addition, we evaluated self‐monitoring accuracy and social validity. The participants were three males aged 14–16 years. We used an ABAB design to evaluate an intervention package that consisted primarily of self‐monitoring and public posting. Athletes self‐monitored their performance after training using an online summative Google Form. The coach publicly posted performance‐based rankings on the social media application WhatsApp. Results indicate that the intervention package positively improved all performance measures across all athletes. Social‐validity measures were also favorable.
CEO turnover after product‐harm crises
Authors: Paik Daniel Gyung , Meng Bo , Lee Brandon Byunghwan , Nguyen Nhat Q. 
Published: February 2024

AbstractProduct‐harm crises are discrete events in which product failures expose consumers to safety hazards. Firms facing such crises must legally recall their products to protect consumers from further harm. In this study, we examine the effects of product‐harm crises and their recall strategies on CEO turnover. We find that firms are more likely to replace their CEOs after issuing product recalls, especially for recalls that are proactive and that offer extensive corrective actions. We further find that firms with poor performance and with limited financial flexibility are more likely to dismiss their CEOs after product recalls. Our study contributes to the disciplines of accounting, finance, and management by documenting product‐harm crises are a strong predictor of CEO dismissal, that is, incremental to other measures of firm performance for U.S. companies.
The importance of cybersecurity disclosures in customer relationships
Authors: Nelson Aaron , Wang Shensi 
Published: February 2024

AbstractThe escalating use of digital technologies has spotlighted the crucial role of cybersecurity in safeguarding sensitive information within companies. This study explores the relationship between a firm's major customers and its cybersecurity awareness. Drawing on SEC‐mandated disclosures, we employ four proxies to measure changes in customer‐supplier relationships. Our findings reveal that customers increase their purchases from suppliers whose cybersecurity awareness scores improve. Additionally, we examine the interplay between customers and suppliers more susceptible to nonpublic adverse news, particularly during cyber events. The study emphasizes the importance of cybersecurity disclosure for regulators, supply chain partners, and corporate management. It also contributes to the literature on factors influencing the duration of customer‐supplier relationships and underscores the significance of supplier characteristics. “Understanding and disclosing cybersecurity risks are” paramount in an increasingly digital business landscape.
RACK1 promotes the occurrence and progression of cervical carcinoma
Authors: Yang Dandan , Lu Xiaojuan , Zhang Xuegang , Zhang Xiaojuan , Zhu Lixia , Liu Qin 
Published: February 2024

AbstractBackgroundRACK1 has been identified as a multifunctional cytosolic protein, and plays a pivotal role in multiple biological responses involved in several kinds of tumors, while its effect in cervical cancer has not been well elucidated yet. The study aimed to investigate the role of RACK1 in cervical cancer occurrence and progression.MethodsThe expression of RACK1 in cervical specimens was measured by immunohistochemical staining and Western blot assay. Transgenic mice were used to detect the role of RACK1 in modulating tumorigenesis in vivo. Cervical carcinoma cell lines were used to explore the underlying mechanisms of RACK1 on the behaviors of tumor cells in vitro.ResultsWe found that RACK1 expression was upregulated in cancer tissues compared with adjacent tissues, and its expression was gradually increased from cervictis, and cervical intraepithelial neoplasis (CIN) to carcinoma. Genetic overexpression of RACK1 facilitated tumor formation and growth in nude mice. Mechanism studies disclosed that RACK1 over‐expression prolonged the G0/G1 phase by up‐regulating the expression of cyclinD1, down‐regulating p21 and p27 probably by modulating the phosphorylation of AKT.ConclusionsTaken together, we concluded that RACK1 stimulates tumorigenesis and progression of cervical cancer via modulating the proliferation of tumor cells, implying that targeting RACK1 may serve as a promising method for cervical cancer therapy.
The role of the complement system in disc degeneration and Modic changes
Authors: Heggli Irina , Teixeira Graciosa Q. , Iatridis James C. , Neidlinger‐Wilke Cornelia , Dudli Stefan 
Published: February 2024

AbstractDisc degeneration and vertebral endplate bone marrow lesions called Modic changes are prevalent spinal pathologies found in chronic low back pain patients. Their pathomechanisms are complex and not fully understood. Recent studies have revealed that complement system proteins and interactors are dysregulated in disc degeneration and Modic changes. The complement system is part of the innate immune system and plays a critical role in tissue homeostasis. However, its dysregulation has also been associated with various pathological conditions such as rheumatoid arthritis and osteoarthritis. Here, we review the evidence for the involvement of the complement system in intervertebral disc degeneration and Modic changes. We found that only a handful of studies reported on complement factors in Modic changes and disc degeneration. Therefore, the level of evidence for the involvement of the complement system is currently low. Nevertheless, the complement system is tightly intertwined with processes known to occur during disc degeneration and Modic changes, such as increased cell death, autoantibody production, bacterial defense processes, neutrophil activation, and osteoclast formation, indicating a contribution of the complement system to these spinal pathologies. Based on these mechanisms, we propose a model how the complement system could contribute to the vicious cycle of tissue damage and chronic inflammation in disc degeneration and Modic changes. With this review, we aim to highlight a currently understudied but potentially important inflammatory pathomechanism of disc degeneration and Modic changes that may be a novel therapeutic target.
Development of physiologically‐informed computational coronary artery plaques for use in virtual imaging trials
Authors: Sauer Thomas J. , Buckler Andrew J. , Abadi Ehsan , Daubert Melissa , Douglas Pamela S. , Samei Ehsan , Segars William P. 
Published: February 2024

AbstractBackgroundAs a leading cause of death, worldwide, cardiovascular disease is of great clinical importance. Among cardiovascular diseases, coronary artery disease (CAD) is a key contributor, and it is the attributed cause of death for 10% of all deaths annually. The prevalence of CAD is commensurate with the rise in new medical imaging technologies intended to aid in its diagnosis and treatment. The necessary clinical trials required to validate and optimize these technologies require a large cohort of carefully controlled patients, considerable time to complete, and can be prohibitively expensive. A safer, faster, less expensive alternative is using virtual imaging trials (VITs), utilizing virtual patients or phantoms combined with accurate computer models of imaging devices.PurposeIn this work, we develop realistic, physiologically‐informed models for coronary plaques for application in cardiac imaging VITs.MethodsHistology images of plaques at micron‐level resolution were used to train a deep convolutional generative adversarial network (DC‐GAN) to create a library of anatomically variable plaque models with clinical anatomical realism. The stability of each plaque was evaluated by finite element analysis (FEA) in which plaque components and vessels were meshed as volumes, modeled as specialized tissues, and subjected to the range of normal coronary blood pressures. To demonstrate the utility of the plaque models, we combined them with the whole‐body XCAT computational phantom to perform initial simulations comparing standard energy‐integrating detector (EID) CT with photon‐counting detector (PCD) CT.ResultsOur results show the network is capable of generating realistic, anatomically variable plaques. Our simulation results provide an initial demonstration of the utility of the generated plaque models as targets to compare different imaging devices.ConclusionsVast, realistic, and variable CAD pathologies can be generated to incorporate into computational phantoms for VITs. There they can serve as a known truth from which to optimize and evaluate cardiac imaging technologies quantitatively.
Nachruf: Egon Fanghänel (1935 – 2023)
Authors: Hartmann Horst , Hennig Horst , Kießling Renate , Taube Rudolf 
Published: January 2024

AbstractAuf vielen Feldern aktiv: GDCh‐Ehrenmitglied Egon Fanghänel war Wissenschaftler, Hochschullehrer, Lehrbuchautor und Wissenschaftsorganisator.
Thermal conductive nylon 6 composites using hybrid fillers to construct a three‐dimensional thermal conductive network
Authors: Li Qian , Rao Ranyi , Hong Xiansheng , Hu Hanwen , Li Yu , Gong Ziyu , Zheng Yuying 
Published: February 2024

AbstractThe rapid progress in miniaturization and integration of semiconductor power devices has made heat dissipation a critical concern in the development of high‐performance semiconductor devices, thereby increasing the demands for the heat transfer efficiency of polymer composites. To address this issue, an efficient three‐dimensional (3D) heat conduction network structure is constructed in the polymer matrix by leveraging the mutual reaction of amino and epoxy groups on the surface of the filler treated by coupling during the melt mixing process, this approach leads to an enhancement in the thermal conductivity of the composites. First, the inert surfaces of graphene nanosheets (EX‐G) and carbon fibers (CF) are coated with polydopamine (PDA) to form active sites. Subsequently, the graphene (EX‐G), alumina (Al2O3), and carbon fiber (CF) are treated with an amine coupling agent (KH550) and epoxy coupling agent (KH560), respectively. Notably, at a filler content of 25 wt%, the thermal conductivity (TC) of the composites increases by approximately 282% compared to pure nylon 6. This research contributes novel insights into the field of thermally conductive polymer composites.Highlights
The surface of the EX‐G and CF covered by PDA generates active sites.
Fillers reduce the interface thermal resistance through chemical bonds.
Fillers surface reaction builds a 3D thermal conductive network.
3D network structure can significantly improve the TC of composites.
Only 25 wt% of hybrid fillers in a 282% increased TC of composites.
In‐situ experimental study on the hydrolysis and pyrolysis processes of polylactic acid
Authors: Zhao Xia , Zheng Zhi , Chen Jiangzhi , Sun Jianhui , Xiong Mengjun , Hou Xue , Mei Shenghua 
Published: February 2024

AbstractIn order to better understand the hydrolysis and pyrolysis process of polylactic acid (PLA), we carried out in‐situ experiments by observing the decomposition process of PLA at high temperature (up to 285°C) in both aqueous and anhydrous environments through fused silica capillary reactor (FSCR) combined with Raman spectroscopy analysis. By analyzing the strength change of characteristic peaks of PLA with increasing temperature, it was found that the initial melting temperature of PLA, in both the hydrolysis and pyrolysis processes, is around 170°C. Based on infrared spectroscopy analysis, it was found that the products of PLA pyrolysis are CO2, CH3CHCO, and CH3CHO, indicating that the pyrolysis process of PLA results from a free radical reaction. By comparing the Raman peak area ratios at different peak positions at different temperatures, it was found that the hydrolysis process of PLA mainly involves breaking the COC and CCO bonds of PLA, producing lactic acid, ethanol, CO2, and H2O. The hydrolysis reaction rate of PLA increases with the increase of temperature and exhibits a slow‐fast‐slow S‐shaped trend. The kinetic process of hydrolysis of PLA was well described using the Logistic model. The activation energy for the hydrolysis (Q) of PLA is 18.1 kcal∙mol−1 in the temperature range of 250–285°C. The results of this study provide important insights and crucial parameters for the production and application of PLA.
Natural products targeting macroautophagy signaling in hepatocellular carcinoma therapy: Recent evidence and perspectives
Authors: Chen Yuan , Tan Xiyue , Zhang Wenwen , Li Yubing , Deng Xinyu , Zeng Jinhao , Huang Lihua , Ma Xiao 
Published: February 2024

AbstractHepatocellular carcinoma (HCC), presently the second leading cause of global cancer‐related mortality, continues to pose significant challenges in the realm of medical oncology, impacting both clinical drug selection and mechanistic research. Recent investigations have unveiled autophagy‐related signaling as a promising avenue for HCC treatment. A growing body of research has highlighted the pivotal role of autophagy‐modulating natural products in inhibiting HCC progression. In this context, we provide a concise overview of the fundamental autophagy mechanism and delineate the involvement of autophagic signaling pathways in HCC development. Additionally, we review pertinent studies demonstrating how natural products regulate autophagy to mitigate HCC. Our findings indicate that natural products exhibit cytotoxic effects through the induction of excessive autophagy, simultaneously impeding HCC cell proliferation by autophagy inhibition, thereby depriving HCC cells of essential energy. These effects have been associated with various signaling pathways, including PI3K/AKT, MAPK, AMPK, Wnt/β‐catenin, Beclin‐1, and ferroautophagy. These results underscore the considerable therapeutic potential of natural products in HCC treatment. However, it is important to note that the present study did not establish definitive thresholds for autophagy induction or inhibition by natural products. Further research in this domain is imperative to gain comprehensive insights into the dual role of autophagy, equipping us with a better understanding of this double‐edged sword in HCC management.
Experimental Schistosoma haematobium pulmonary hypertension
Authors: Kassa Biruk , Fonseca‐Balladares Dara C. , Kumar Rahul , Lee Michael H. , Mickael Claudia , Sanders Linda , Nolan Kevin , Graham Brian B. 
Published: February 2024

AbstractWhether all Schistosoma species cause pulmonary hypertension (PH) is unclear. Experimentally exposing mice to Schistosoma haematobium eggs caused PH, which was less severe than that induced by S. mansoni exposure. These findings align with the relatively uncommon reports of pulmonary arterial hypertension associated with S. haematobium.
Cytological diagnosis of exercise‐induced pulmonary haemorrhage: Comparison of tracheal wash and bronchoalveolar lavage in standardbred racehorses
Authors: Barbazanges Pauline , Richard Eric A. , Lemonnier Louise C. , Wouters Clovis P. , Toquet Marie‐Pierre , Couroucé Anne 
Published: January 2024

AbstractBackgroundCytology of airway samples is sensitive for diagnosis of exercise‐induced pulmonary haemorrhage (EIPH), but the association between tracheal wash (TW) and bronchoalveolar lavage fluid (BALF) is unknown. The objective of this study was to determine whether diagnosis of EIPH, using haemosiderophages/macrophages (H/M) ratio, differs when based on TW or BALF.MethodsA prospective cross‐sectional study was conducted on 102 standardbred horses in training. TW and BALF were collected concomitantly from all horses at rest (at least 24 hours after their last training or race), and their H/M ratios were calculated. Spearman's correlation, Cohen's kappa and Gwet's coefficient tests were performed to evaluate the association between TW and BALF samples.ResultsWith BALF, 21 horses met the cytological inclusion criteria for an EIPH diagnosis from individual and/or pooled samples. With TW, 20 horses had occasional (H/M < 10%) haemosiderophages, and nine, one and three horses had small (10%–25%), moderate (25%–50%) and large (>50%) proportions, respectively. Poor correlations and inconsistent concordances between TW and BALF were found for H/M ratio.LimitationsLimitations include the use of a single staining method and the absence of a total haemosiderin score.ConclusionNo association between TW and BALF was found for the cytological diagnosis of EIPH. Based on H/M ratio, BALF remains the sample type of choice for cytological diagnosis of EIPH.