Publications by authors named "Chuyi Tan"

This study aims to investigate the mechanism of relapse tendency in male drug abusers and provide empirical evidence for reducing relapse tendency of drug abusers. A survey was conducted on 310 male individuals with drug addiction using Chinese Perceived Stress Scale (CPSS), Simple Coping Style Questionnaire (SCSQ), the Regulatory Emotional Self-Efficacy Scale, and the Relapse Tendency Scale (RTS). (1) Stress is significantly positively correlated with the relapse tendency of individuals with drug addiction; (2) Stress indirectly affects relapse tendency through regulatory emotional self-efficacy; (3) Regulatory emotional self-efficacy can directly and negatively predict relapse tendency, and can also indirectly and negatively predict relapse tendency through coping style.

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Article Synopsis
  • B-1a cells help fight infections and control swelling by releasing special proteins.
  • In sepsis, these cells move to the spleen, changing their abilities, which can cause problems.
  • A protein called Siglec-G helps keep B-1a cells in place, but in sepsis, a substance from neutrophils can break it down, and scientists found a special decoy that can protect Siglec-G and help B-1a cells stay healthier.
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Extensions of objectification theory to pregnant women are few and continued research is needed to better understand the psychological consequences of significant changes to physical appearance during pregnancy. Specific interests in this area include functionality appreciation which may be particularly relevant to pregnancy. Research in this area is also lacking representation of non-Western cultural contexts.

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B-1a cells, a regulatory subset of B lymphocytes, produce natural IgM and interleukin-10. Neutrophil extracellular traps (NETs) play a crucial role in pathogen defense, but their excessive formation during sepsis can cause further inflammation and tissue damage. In sepsis, extracellular cold-inducible RNA-binding protein (eCIRP), a damage-associated molecular pattern, is released to induce NET formation.

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Article Synopsis
  • Sepsis is a serious condition caused by too much inflammation in the body, and a protein called eCIRP plays a big role in this problem.
  • Researchers discovered that another protein, MFG-E8, can help get rid of eCIRP, reducing inflammation and improving health.
  • Their study shows that using MFG-E8 or special parts of it could help treat and protect against serious conditions like sepsis.
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Objective: This study assessed picky eating in pregnant women by exploring whether picky eating is associated with pregnant women's well-being, including life satisfaction, psychological distress, and psychosocial impairment.

Method: Data collected were from 345 Chinese pregnant women ( = 29.95 years, SD = 5.

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Background: Sepsis is caused by the dysregulated immune response due to an initial infection and results in significant morbidity and mortality in humans. Extracellular cold inducible RNA binding protein (eCIRP) is a novel mediator identified in sepsis. We have previously discovered that microRNA 130b-3p inhibits eCIRP mediated inflammation.

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Background: The prevalence of inflammatory bowel disease (IBD) is rapidly increasing in China. Beyond disease management, frailty is an important predictor of adverse outcomes in IBD patients, which has not been well investigated. This study aimed to assess frailty status and explore the impact factors in IBD inpatients.

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Introduction: Extracellular cold-inducible RNA-binding protein (eCIRP) is an endogenous pro-inflammatory mediator that exacerbates injury in inflammation and sepsis. The mechanisms in which eCIRP is released have yet to be fully explored. Necroptosis is a programmed cell death that is dependent on the activation of mixed lineage kinase domain-like pseudo kinase (MLKL) which causes the release of damage-associated molecular patterns.

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Extracellular cold-inducible RNA binding protein (eCIRP) is an inflammatory mediator that causes inflammation and tissue injury in sepsis. Gasdermin D (GSDMD) is a protein that, when cleaved, forms pores in the cell membrane, releasing intracellular contents into the extracellular milieu to exacerbate inflammation. We hypothesize that eCIRP is released actively from viable macrophages via GSDMD pores.

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Extracellular cold-inducible RNA-binding protein (eCIRP) is a damage-associated molecular pattern promoting inflammation and tissue injury. During bacterial or viral infection, macrophages release DNA decorated with nuclear and cytoplasmic proteins known as macrophage extracellular traps (METs). Gasdermin D (GSDMD) is a pore-forming protein that has been involved in extracellular trap formation in neutrophils.

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Extracellular cold-inducible RNA-binding protein (eCIRP) is an important damage-associated molecular pattern (DAMP). Despite our understanding of the potentially harmful effects of eCIRP in sepsis, how eCIRP is released from cells remains elusive. Exosomes are endosome-derived extracellular vesicles, which carry proteins, lipids, and nucleic acids to facilitate intercellular communication and several extracellular functions.

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Stimulator of IFN genes (STING) activates TANK-binding kinase 1 (TBK1) and IFN regulatory factor 3 (IRF3) to produce type I IFNs. Extracellular cold-inducible RNA-binding protein (eCIRP) is released from cells during hemorrhagic shock (HS). We hypothesized that eCIRP activates STING to induce inflammation and acute lung injury (ALI) after HS.

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Background: Early and accurate diagnosis of microorganism(s) is important to optimize antimicrobial therapy. Shotgun metagenomic sequencing technology, an unbiased and comprehensive method for pathogen identification, seems to potentially assist or even replace conventional microbiological methodology in the diagnosis of infectious diseases. However, evidence in clinical application of this platform is relatively limited.

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To explore the relationship between family functioning, psychological capital, life history strategy, and relapse tendency of individuals with drug addiction, 842 individuals with drug addiction completed a questionnaire. The results showed that (1) there was a significant negative correlation between the family functioning of individuals with drug addiction and their relapse tendency; (2) psychological capital played an intermediary role between family functioning and relapse tendency; and (3) life history strategy regulated the mediating effect of psychological capital. The results of this study suggest that family members should collaborate with drug addiction treatment centers and participate in the education and treatment process to help reduce drug relapse tendency.

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Metabolism reprogramming influences the severity of organ dysfunction, progression to fibrosis, and development of disease in acute kidney injury (AKI). Previously we showed that inhibition of aerobic glycolysis improved survival rates and protected septic mice from kidney injury. However, the underlying mechanisms remain unclear.

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Heat shock factor 1 (HSF1) is a transcription factor involved in the heat shock response and other biological processes. We have unveiled here an important role of HSF1 in acute lung injury (ALI). knockout mice were used as a model of lipopolysaccharide- (LPS-) induced ALI.

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Neutrophils produce neutrophil extracellular traps (NETs) by expelling their extracellular chromatin embedded with citrullinated histone H3, myeloperoxidase, and other intracellular molecules. Since their discovery in 2004, numerous articles have demonstrated the mechanism of NET formation and their function in innate immunity and inflammation. NET components often play an antimicrobial role, but excessive NETs are deleterious and can cause inflammation and tissue damage.

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Sepsis is a life-threatening complication of infection closely associated with coagulation abnormalities. Heat shock factor 1 (HSF1) is an important transcription factor involved in many biological processes, but its regulatory role in blood coagulation remained unclear. We generated a sepsis model in HSF1-knockout mice to evaluate the role of HSF1 in microthrombosis and multiple organ dysfunction.

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Extracellular cold-inducible RNA-binding protein (eCIRP) induces acute lung injury (ALI) in sepsis. Triggering receptor expressed on myeloid cells-1 (TREM-1) serves as a receptor for eCIRP to induce inflammation in macrophages and neutrophils. The effect of eCIRP on alveolar epithelial cells (AECs) remains unknown.

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Myeloid-derived suppressor cells (MDSCs) are functionally immunosuppressive cells that are persistently increased in abundance and associated with adverse clinical outcomes in sepsis. Here, we investigated the therapeutic potential of an anaplastic lymphoma kinase inhibitor, LDK378, in cecal ligation and puncture (CLP)-induced polymicrobial sepsis and examined its effects on the recruitment of MDSCs. LDK378 significantly improved the survival of CLP-induced polymicrobial septic mice, which was paralleled by reduced organ injury, decreased release of inflammatory cytokines and decreased recruitment of MDSCs to the spleen.

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Article Synopsis
  • Endotoxemia can lead to systemic inflammatory response syndrome (SIRS), coagulation issues, and acute lung injury (ALI), driven by activation of key blood and vascular cells.
  • The study investigated the role of P-selectin glycoprotein ligand 1 (PSGL-1) using a mouse model of endotoxemia induced by lipopolysaccharide (LPS), while also administering PSGL-1 antibodies.
  • Results indicated that blocking PSGL-1 reduced platelet and leukocyte activity, lessened inflammation, improved survival rates, and mitigated lung damage in the endotoxemic mice, highlighting PSGL-1's significant contribution to these conditions.
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Sepsis is a critical, complex medical condition, and the major causative pathogens of sepsis are both () and (). Genome-wide studies identify differentially expressed genes for sepsis. However, the results for the identification of DEGs are inconsistent or discrepant among different studies because of heterogeneity of specimen sources, various data processing methods, or different backgrounds of the samples.

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Recent evidences suggest that metabolic reprogramming plays an important role in the regulation of innate inflammatory response; however, the specific mechanism is unclear. In this study, we found that glycolytic inhibitor 2-deoxyglucose (2-DG) significantly improved the survival rate in cecal ligation and puncture (CLP)-induced septic mice. 2-DG-treated mice developed increased neutrophil migration to the infectious site and more efficient bacterial clearance than untreated mice.

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