Relationship between occupational factors and sleep disorders among petrochemical workers on Hainan Island, South China: a cross-sectional study.

Objectives: The study aimed to examine the relationship between occupational factors and sleep disorders among employees in petrochemical enterprises.

Material And Methods: All participants from the employees of Hainan Petroleum Refining and Chemical Enterprises were recruited by the cluster sampling in June 1, 2022. The questionnaire used in this research was primarily composed of 3 sections: demographic characteristics, (PSQI) questionnaire and occupation-related factors affecting sleep disorders.

Upregulation of CIRP by its agonist prevents the development of heart failure in myocardial infarction rats.

Background: Downregulated expression of cold-inducible RNA binding protein (CIRP), a stress-response protein, has been demonstrated in the hearts of patients with heart failure (HF). However, whether CIRP plays a critical role in the pathogenesis of HF remains unknown. Zr17-2 is a recently identified CIRP agonist, which can enhance the expression of CIRP in hearts.

Crocin alleviates neurotoxicity induced by bupivacaine in SH-SY5Y cells with inhibition of PI3K/AKT signaling.

Background: Bupivacaine, a common local anesthetic, can cause neurotoxicity and permanent neurological disorders. Crocin has been widely reported as a potential neuroprotective agent in neural injury models.

Objective: The aim of this study was to investigate the role and regulatory mechanism of crocin underlying bupivacaine-induced neurotoxicity.

CTRP5 Attenuates Doxorubicin-Induced Cardiotoxicity Via Inhibiting TLR4/NLRP3 Signaling.

Background: C1q/tumor necrosis factor-related protein 5 (CTRP5) has been reported to be a crucial regulator in cardiac ischemia/reperfusion (I/R) injury. Nevertheless, the potential role of CTRP5 in doxorubicin (DOX)-induced cardiotoxicity and the potential mechanisms remain largely unclear.

Methods: We overexpressed CTRP5 in the hearts using an adeno-associated virus 9 (AAV9) system through tail vein injection.

Loss of MD1 Promotes Inflammatory and Apoptotic Atrial Remodelling in Diabetic Cardiomyopathy by Activating the TLR4/NF-κB Signalling Pathway.

Introduction: Myeloid differentiation protein 1 (MD1), a negative regulator of toll-like receptor 4 (TLR4), is widely expressed in the heart. Recent studies have shown that MD1 plays an important role in cardiac remodelling. However, the effects and potential mechanisms underlying MD1-mediated atrial remodelling in diabetic cardiomyopathy (DCM) remain unclear.

Mitochondrial derived peptide MOTS-c prevents the development of heart failure under pressure overload conditions in mice.

MOTS-c, a mitochondrial-derived peptide (MDP), has been shown to have multiple biological activities such as antioxidation, anti-inflammation, and anti-apoptosis properties. In the present study, we aimed at evaluating the therapeutic effect of MOTS-c peptide in an animal model of heart failure. The heart failure mouse model was made by transverse aortic constriction (TAC) operations.

The role of Cold-Inducible RNA-binding protein in respiratory diseases.

Cold-inducible RNA-binding protein (CIRP) is a stress-response protein that is expressed in various types of cells and acts as an RNA chaperone, modifying the stability of its targeted mRNA. Intracellular CIRP could also be released into extracellular space and once released, extracellular CIRP (eCIRP) acts as a damage-associated molecular pattern (DAMP) to induce and amplify inflammation. Recent studies have found that eCIRP could promote acute lung injury (ALI) via activation of macrophages, neutrophils, pneumocytes and lung vascular endothelial cells in context of sepsis, haemorrhagic shock, intestinal ischemia/reperfusion injury and severe acute pancreatitis.

The Mitochondrial-Derived Peptide MOTS-c Attenuates Oxidative Stress Injury and the Inflammatory Response of H9c2 Cells Through the Nrf2/ARE and NF-κB Pathways.

Aim: Oxidative stress and the inflammatory response contribute to the progression of cardiovascular disease. The present study aimed to investigate whether the mitochondrial-derived peptide MOTS-c could alleviate HO-induced oxidative stress and inflammatory status in H9c2 cells through activation of nuclear factor erythroid 2-related Factor 2 (Nrf2)/antioxidative response element (ARE) and inhibition of the NF-κB pathway.

Methods: Rat H9c2 cardiomyocytes were obtained, and 10, 20 or 50 μM MOTS-c was pretreated for 24 h before treatment with HO Then, the cell was treated with 100 μM HO for 1 h to induce oxidative stress.

AAV9-Mediated Cardiac CNTF Overexpression Exacerbated Adverse Cardiac Remodeling in Streptozotocin-Induced Type 1 Diabetic Models.

Ciliary neurotrophic factor (CNTF), which is a neural peptide, has been reported to confer cardioprotective effects. However, whether CNTF-based gene delivery could prevent cardiac remodeling in diabetes mellitus remains unknown. In this study, we used adeno-associated viral vector serotype 9 (AAV9)-based cardiac gene delivery to test the effects of CNTF overexpression on adverse ventricular remodeling in streptozotocin-induced type 1 diabetic mice models.

The Akt pathway mediates the protective effects of myeloid differentiation protein 1 in pathological cardiac remodelling.

Aims: Myeloid differentiation protein 1 (MD1) was shown to ameliorate pressure overload-induced cardiac hypertrophy and fibrosis by negatively regulating the MEK-ERK1/2 and NF-κB pathways. However, whether MD1 modulates cardiac function and whether the Akt pathway mediates the benefits of MD1 in pressure overload-induced cardiac remodelling remain unclear.

Methods And Results: Male cardiac-specific transgenic MD1 (MD1-TG) mice, MD1-knockout (KO) mice and wild-type (WT) littermates aged 8-10 weeks were subjected to sham operation and aortic banding (AB) for 4 weeks.

The Role of Cold Inducible RNA-Binding Protein in Cardiac Physiology and Diseases.

Cold-inducible RNA-binding protein (CIRP) is an intracellular stress-response protein that can respond to various stress conditions by changing its expression and regulating mRNA stability. As an RNA-binding protein, CIRP modulates gene expression at the post-transcriptional level, including those genes involved in DNA repair, cellular redox metabolism, circadian rhythms, telomere maintenance, and cell survival. CIRP is expressed in a large variety of tissues, including testis, brain, lung, kidney, liver, stomach, bone marrow, and heart.

Ciliary neurotrophic factor overexpression protects the heart against pathological remodelling in angiotensin II-infused mice.

Background: Ciliary neurotrophic factor (CNTF), which is a neural peptide, has been reported to confer cardioprotective effects. However, whether CNTF-based gene therapy could prevent cardiac remodelling remains incompletely clear. In this study, we used adeno-associated viral vector serotype 9 (AAV9)-based cardiac gene therapy to test the effects of CNTF overexpression on adverse ventricular remodelling in angiotensin II (Ang II)-infused mice.

Cold-inducible RNA-binding protein (CIRP) in inflammatory diseases: Molecular insights of its associated signalling pathways.

Cold-inducible RNA-binding protein (CIRP) was previously identified as an intracellular stress-response protein, which can respond to a variety of stress conditions by changing its expression and regulating mRNA stability through its binding site on the 3'-UTR of its targeted mRNAs. Recently, extracellular CIRP (eCIRP) was discovered to be present in various inflammatory conditions and could act as a pro-inflammatory factor. Genetic studies have demonstrated a key role for eCIRP in inflammatory conditions that led to the importance of targeting eCIRP in these diseases.

Loss of MD1 exacerbates pressure overload-induced left ventricular structural and electrical remodelling.

Myeloid differentiation protein 1 (MD1) has been implicated in numerous pathophysiological processes, including immune regulation, obesity, insulin resistance, and inflammation. However, the role of MD1 in cardiac remodelling remains incompletely understood. We used MD1-knockout (KO) mice and their wild-type littermates to determine the functional significance of MD1 in the regulation of aortic banding (AB)-induced left ventricular (LV) structural and electrical remodelling and its underlying mechanisms.

Role of CaMKII in free fatty acid/hyperlipidemia-induced cardiac remodeling both in vitro and in vivo.

Rationale: The cellular mechanisms of obesity/hyperlipidemia-induced cardiac remodeling are many and not completely elucidated. Ca/calmodulin-dependent protein kinase II (CaMKII), a multifunctional serine/threonine kinase, has been reported to be involved in a variety of cardiovascular diseases. However, its role in obesity/hyperlipidemia-induced cardiac remodeling is still unknown.

Novel Protective Role of Myeloid Differentiation 1 in Pathological Cardiac Remodelling.

Myeloid differentiation 1 (MD-1), a secreted protein interacting with radioprotective 105 (RP105), plays an important role in Toll-like receptor 4 (TLR4) signalling pathway. Previous studies showed that MD-1 may be restricted in the immune system. In this study, we demonstrated for the first time that MD-1 was highly expressed in both human and animal hearts.

Regulator of G-protein signaling 5 protects cardiomyocytes against apoptosis during in vitro cardiac ischemia-reperfusion in mice by inhibiting both JNK1/2 and P38 signaling pathways.

Ischemic heart disease is one of the most common diseases in modern society. Ischemic myocardium can be salvaged by vascular recanalization therapy, but its benefit is attenuated by injury that can occur during reperfusion. And apoptotic cell death plays an important part in myocardial ischemia-reperfusion (IR) injury.