This study evaluated the diagnostic value of plasma Neutrophil extracellular traps (NETs) levels and the index of cardiac electrophysiological balance (iCEB) in identifying silent myocardial ischemia (SMI) in maintenance hemodialysis (MHD) patients.

Chronic liver disease ranks as the 11th leading cause of death worldwide, while hepatocellular carcinoma (HCC) is the fourth leading cause of cancer-related mortality, representing a substantial risk to public health. Over the past few decades, the global landscape of chronic liver diseases, including hepatitis, metabolic dysfunction-associated steatotic liver disease (MASLD), liver fibrosis, and HCC, has undergone substantial changes. Copper, a vital trace element for human health, is predominantly regulated by the liver. Both copper deficiency and excess can lead to cellular damage and liver dysfunction. Copper deposition is a genetic process of copper-dependent cell death associated with mitochondrial respiration, which is associated with cardiovascular disease and IBD. However, the roles of copper overload and cuproptosis in liver disease remain largely underexplored. This article examines recent studies on copper metabolism and cuproptosis in chronic liver disease, investigating the potential of targeting copper ions as a therapeutic approach. The objective is to offer insights and guidance for future investigations in this developing field of study.

Ovarian cancer (OC) remains one of the most lethal gynecological malignancies, largely due to its late-stage diagnosis and high recurrence rates. Chronic inflammation is a critical driver of OC progression, contributing to immune evasion, tumor growth, and metastasis. Inflammatory cytokines, including IL-6, TNF-α, and IL-8, as well as key signaling pathways such as nuclear factor kappa B (NF-kB) and signal transducer and activator of transcription 3 (STAT3), are upregulated in OC, promoting a tumor-promoting environment. The tumor microenvironment (TME) is characterized by immune cells like tumor-associated macrophages (TAMs) and regulatory T cells (Tregs), which suppress anti-tumor immune responses, facilitating immune evasion. Furthermore, OC cells utilize immune checkpoint pathways, including PD-1/PD-L1, to inhibit cytotoxic T cell activity. Targeting these inflammatory and immune evasion mechanisms offers promising therapeutic strategies. COX-2 inhibitors, Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway blockers, and NF-kB inhibitors have shown potential in preclinical studies, while immune checkpoint inhibitors targeting PD-1/PD-L1 and CTLA-4 have been explored with mixed results in OC. Additionally, emerging research on the microbiome and inflammation-related biomarkers, such as microRNAs (miRNAs) and exosomes, points to new opportunities for early detection and precision medicine. Future approaches to OC treatment must focus on personalized strategies that target the inflammatory TME, integrating anti-inflammatory therapies with immunotherapy to enhance patient outcomes. Continued research into the interplay between inflammation and immune evasion in OC is essential for developing effective, long-lasting treatments.

Ankylosing spondylitis (AS) is a chronic autoimmune disease characterized by inflammation of the sacroiliac joints and spine. Cuproptosis is a newly recognized copper-induced cell death mechanism. Our study explored the novel role of cuproptosis-related genes (CRGs) in AS, focusing on immune cell infiltration and molecular clustering.

Adenoid hypertrophy is a common disorder of childhood, and has an unclear pathogenesis. At the beginning of the COVID-19 pandemic, there was a significant reduction in the incidence of adenoid hypertrophy in children under long-term home quarantine, providing a rare research model to explore the pathogenesis and treatment targets of adenoidal hypertrophy in children.

Allergic diseases have escalated to epidemic levels worldwide, impacting nearly 30% of the global population. Fungi are a significant source of allergens responsible for up to 6% of respiratory diseases in the general population. However, the specific cause of respiratory allergies often remains unidentified. This study aimed to investigate the potential of two common rust fungi, and , to trigger a proinflammatory response in vitro models representing the upper and lower respiratory tract.

Renal failure related death caused by diabetic kidney disease (DKD) is an inevitable outcome for most patients. This study aimed to identify the critical genes involved in the onset and progression of DKD and to explore potential therapeutic targets of DKD.

Chronic kidney disease (CKD) is a progressive condition that arises from diverse etiological factors, resulting in structural alterations and functional impairment of the kidneys. We aimed to establish the Anoikis-related gene signature in CKD by bioinformatics analysis.

Oral lichen planus (OLP) is a chronic, immune-mediated inflammatory disease involving T cells. Mitochondrial fission plays a crucial role in T cell fate through structural remodeling. Nicotinamide adenine dinucleotide (NAD) regulates mitochondrial remodeling and function. This study explored the role of NAD in modulating mitochondrial fission and apoptosis in T cells under the OLP immune-inflammatory environment.

To evaluate the effects of Fu Tu Sheng Jin Rehabilitation Formula (FTSJRF) on airway inflammation, mucus secretion, and immunoreaction in a severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) spike protein-induced mouse model.

Myocardial ischemia/reperfusion (I/R) injury significantly impacts the recovery of ischemic heart disease patients. Non-coding RNAs, including miRNAs, have been increasingly recognized for their roles in regulating cardiomyocyte responses to hypoxia/reoxygenation (H/R) injury. miR-181c-5p, in particular, has been implicated in inflammatory and apoptotic processes, suggesting its potential involvement in exacerbating cellular damage.

Crohn's disease (CD) is a chronic inflammatory condition of the intestines with a rising global incidence. Traditional diagnostic and therapeutic methods have limitations, necessitating the exploration of more effective strategies.

Neuroinflammatory reactions are crucial factors in secondary brain damage following intracerebral hemorrhage (ICH). Although previous studies have shown that IRAK3 is involved in immune responses, the potential effects of IRAK3 on ICH remain unclear.

Necrotizing fasciitis (NF) is a scarce but potentially life-threatening infection. However, no research has reported the cellular heterogeneity in patients with NF. We aim to investigate the change of cells from deep fascia in response to NF by single-cell RNA-seq.

Inflammatory bowel disease (IBD) is a non-specific inflammatory disease of digestive tract, primarily manifesting as ulcerative colitis (UC) and Crohn's disease (CD). The precise etiology of IBD remains elusive. The interplay of genetic factors, environmental influences, and intestinal microbiota contributes to the establishment of an uncontrolled immune environment within the intestine, which can progressively lead to atypical hyperplasia and ultimately to malignancy over a long period. This colorectal malignant tumor that arises from chronic IBD is referred to as colitis-associated colorectal cancer (CAC). Dysregulation in the quantity and functionality of neutrophils plays a significant role in the onset, progression, and recurrence of IBD, as well as in the transition from IBD to CAC. Neutrophils affect the pathophysiology of IBD through various mechanisms, including the production of reactive oxygen species (ROS), degranulation, the release of inflammatory mediators and chemokines, and the formation of neutrophil extracellular traps (NETs). These processes can induce DNA mutations, thereby facilitating the development of colon cancer. Given the incomplete understanding of the disease mechanisms underlying IBD and CAC, effective treatment and prevention strategies remain challenging. Consequently, a comprehensive review of the functional roles of neutrophils in IBD and CAC is essential for advancing our understanding of IBD pathogenesis and identifying potential therapeutic targets.

Sepsis is a severe complication in leukemia patients, contributing to high mortality rates. Identifying early predictors of sepsis is crucial for timely intervention. This study aimed to develop and validate a predictive model for sepsis risk in leukemia patients using machine learning techniques.

Prolonged psychological stress is closely associated with cancer due to its role in promoting the release of stress hormones through the sustained activation of the sympathetic-adrenal-medullary system. These hormones interact with receptors on inflammatory cells, leading to the activation of key signaling pathways, including the transcription factors signal transducer and activator of transcription 3 (STAT-3) and kappa-light-chain-enhancer of activated B cells (NF-κB). These factors drive the production of pro-inflammatory substances, such as interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α), which can influence the initiation and progression of cancer.

The phenomenon of "kidney-brain crosstalk" has stimulated scholarly inquiry into the correlations between kidney injury (KI) and Alzheimer's disease (AD). Nonetheless, the precise interactions and shared mechanisms between KI and AD have yet to be fully investigated. The primary goal of this study was to investigate the link between KI and AD, with a specific focus on identifying diagnostic biomarkers for KI-related AD.

Immunoglobulin G4-related disease (IgG4-RD) share clinical features with primary Sjögren's syndrome (pSS). This study aimed to identify altered serological parameters and potential biomarkers of IgG4-RD and pSS.

Gastric cancer (GC) is a common malignant tumor of the digestive tract. Accumulating studies suggest that inflammation is linked with the pathogenesis of GC. The study delves into novel hematological inflammatory markers, such as systemic immune-inflammation index (SII), systemic inflammation response index (SIRI), and prognostic nutritional index (PNI), to explore their potential applications in early diagnosis of GC.

Sepsis is regarded as a dysregulated immune response to infections. Recent study showed partially reversal of immunosuppression by trained immunity, which fosters an enhanced immune response towards a secondary challenge. However, the role of trained immunity in sepsis has not been fully understood.