Analysis of the effects of postoperative cluster nursing care on the incidence rate of postoperative complications and nutritional indicators in patients with primary laryngeal cancer.

OBJECTIVE: In this study, we investigated the effects of cluster nursing care on postoperative infection risk and nutritional indicators in patients with primary laryngeal cancer. METHODS: This study comprised 50 patients with primary laryngeal cancer diagnosed between March 2020 and December 2022. They were randomly divided into the test and control groups, with each group comprising 25 patients. The test group received cluster nursing care, while the control group received standard nursing care. Indicators for quantitative scoring, such as Patient Generated Subjective Global Assessment (PG-SGA), Zubrod Performance Status (ZPS), Karnofsky score, and Nutrition Risk Screening 2002 (NRS-2002), measurement indicators such as body mass index (BMI), body mass, hip circumference, calf circumference, grip strength, weight loss, and laboratory indicators, such as hemoglobin, albumin, and transaminase levels, were used to analyze change. RESULTS: Improvements were observed in the scores of PG-SGA, ZPS, and NRS-2002 in the test group following the implementation of nursing care for the test and control groups for 1 week, which were statistically significantly different from those at baseline (P < 0.05), and compared to the control group (P < 0.05). No statistically significant differences were observed in other indicators (P > 0.05). There was a statistically significant difference (P < 0.05) between the incidence rate of infections and complications in the test and control groups, which were 20.00% and 48.00%. CONCLUSION: The postoperative nutritional status of patients with primary laryngeal cancer improved in phases through specialized nursing care. It is also a factor closely related to postoperative complications.

Trained Immunity and Reactivity of Macrophages and Endothelial Cells.

Innate immune cells can develop exacerbated immunologic response and long-term inflammatory phenotype following brief exposure to endogenous or exogenous insults, which leads to an altered response towards a second challenge after the return to a nonactivated state. This phenomenon is known as trained immunity (TI). TI is not only important for host defense and vaccine response but also for chronic inflammations such as cardiovascular and metabolic diseases such as atherosclerosis. TI can occur in innate immune cells such as monocytes/macrophages, natural killer cells, endothelial cells (ECs), and nonimmune cells, such as fibroblast. In this brief review, we analyze the significance of TI in ECs, which are also considered as innate immune cells in addition to macrophages. TI can be induced by a variety of stimuli, including lipopolysaccharides, BCG (bacillus Calmette-Guerin), and oxLDL (oxidized low-density lipoprotein), which are defined as risk factors for cardiovascular and metabolic diseases. Furthermore, TI in ECs is functional for inflammation effectiveness and transition to chronic inflammation. Rewiring of cellular metabolism of the trained cells takes place during induction of TI, including increased glycolysis, glutaminolysis, increased accumulation of tricarboxylic acid cycle metabolites and acetyl-coenzyme A production, as well as increased mevalonate synthesis. Subsequently, this leads to epigenetic remodeling, resulting in important changes in chromatin architecture that enables increased gene transcription and enhanced proinflammatory immune response. However, TI pathways and inflammatory pathways are separated to ensure memory stays when inflammation undergoes resolution. Additionally, reactive oxygen species play context-dependent roles in TI. Therefore, TI plays significant roles in EC and macrophage pathology and chronic inflammation. However, further characterization of TI in ECs and macrophages would provide novel insights into cardiovascular disease pathogenesis and new therapeutic targets. Graphic Abstract: A graphic abstract is available for this article.

Ly6C+ Inflammatory Monocyte Differentiation Partially Mediates Hyperhomocysteinemia-Induced Vascular Dysfunction in Type 2 Diabetic db/db Mice.

OBJECTIVE: Hyperhomocysteinemia (HHcy) is a potent risk factor for diabetic cardiovascular diseases. We have previously reported that hyperhomocysteinemia potentiates type 1 diabetes mellitus-induced inflammatory monocyte differentiation, vascular dysfunction, and atherosclerosis. However, the effects of hyperhomocysteinemia on vascular inflammation in type 2 diabetes mellitus (T2DM) and the underlying mechanism are unknown. Approach and Results: Here, we demonstrate that hyperhomocysteinemia was induced by a high methionine diet in control mice (homocysteine 129 µmol/L), which was further worsened in T2DM db/db mice (homocysteine 180 µmol/L) with aggravated insulin intolerance. Hyperhomocysteinemia potentiated T2DM-induced mononuclear cell, monocyte, inflammatory monocyte (CD11b+Ly6C+), and M1 macrophage differentiation in periphery and aorta, which were rescued by folic acid-based homocysteine-lowering therapy. Moreover, hyperhomocysteinemia exacerbated T2DM-impaired endothelial-dependent aortic relaxation to acetylcholine. Finally, transfusion of bone marrow cells depleted for Ly6C by Ly6c shRNA transduction improved insulin intolerance and endothelial-dependent aortic relaxation in hyperhomocysteinemia+T2DM mice. CONCLUSIONS: Hyperhomocysteinemia potentiated systemic and vessel wall inflammation and vascular dysfunction partially via inflammatory monocyte subset induction in T2DM. Inflammatory monocyte may be a novel therapeutic target for insulin resistance, inflammation, and cardiovascular complications in hyperhomocysteinemia+T2DM.