Cardiac microvascular injury often occurs in patients with type 2 diabetes mellitus (T2DM) who develop hyperglycemia and hyperlipidemia. However, besides reported contradictory roles in cardiac diseases, the function of TRPV1 (transient receptor potential vanilloid 1) in cardiac microvessels is not well defined. This study was performed to determine the detailed role of TRPV1 in cardiac microvascular endothelial cells (CMECs) in T2DM. T2DM mice were established by multiple injections of low-dose streptozotocin and high-fat feeding. CMECs were cultured separately in mediums of normal glucose, high glucose (HG), high fatty acid (HF), and HG plus HF (HG-HF). HG-HF inhibited TRPV1 expression in CMECs, reducing cellular Ca ²⁺ content ([Ca ²⁺ ] _i ). T2DM impaired cardiac function, disturbed glucose uptake, and damaged microvascular barrier, which were further aggravated by TRPV1 ^−/− . Exposure to HG-HF, particularly in TRPV1 ^−/− CMECs, led to a higher level of apoptosis and a lower level of nitric oxide production in viable CMECs. HG-HF markedly enhanced generation of reactive oxygen species and nitrotyrosine, especially in the absence of TRPV1. H ₂ O ₂ administration reduced TRPV1 expression in CMECs. HG-HF significantly depressed expression of PGC-1α (peroxisome proliferator–activated receptor-γ coactivator-1α) and OPA1 (optic atrophy 1) by reducing [Ca ²⁺ ] _i , whereas OPA1 supplementation partly reversed those detrimental effects induced by TRPV1 ^−/− . Furthermore, capsaicin treatment not only attenuated CMECs injury induced by HG-HF but also mitigated cardiac microvascular injury induced by T2DM. Collectively, T2DM leads to cardiac microvascular injury by exacerbating the vicious circle of TRPV1 blockage and reactive oxygen species overload. Long-term capsaicin can protect cardiac microvessels against T2DM via suppressing oxidative/nitrative stress mediated by TRPV1/Ca ²⁺ /PGC-1α/OPA1 pathway in CMECs.

Sepsis is a common critical illness in intensive care unit (ICU) and an important risk factor for intensive care unit-acquired weakness (ICU-AW). The objective of the study is to analyze the risk factors of ICU-AW in septic patients. A total of 264 septic patients admitted to the General Hospital of the Western Theater Command from January 2018 to April 2022 were included in this study. The cohort was divided into 2 groups according to the presence or absence of ICU-AW. Clinical characteristics included age, sex, body mass index, length of ICU stay, multiple organ dysfunction syndrome, acute physiology and chronic health evaluation Ⅱ (APACHE Ⅱ), mechanical ventilation time, intubation, tracheotomy, protective constraint, lactic acid, fasting blood glucose, etc. The clinical characteristics of sepsis were evaluated using logistic regression analysis. A total of 114 septic patients suffered ICU-AW during their ICU stay. Multivariate binary logistic regression analysis showed that APACHE Ⅱ score, mechanical ventilation time, protective constraint, and lactic acid were independent risk factors for ICU-AW in septic patients. The areas under the receiver operating characteristic curve (AUCs) were 0.791, 0.740 and 0.812, all P < 0.05, and the optimal cut-off values were 24 points, 5 days and 2.12 mmol/L, respectively. A high APACHE Ⅱ score, long mechanical ventilation time, protective constraint and high lactate concentration are independent risk factors for ICU-AW in septic patients. An APACHE Ⅱ score greater than 24 points, mechanical ventilation time longer than 5 days and lactate concentration higher than 2.12 mmol/L are likely to cause ICU-AW.

Immune cells are pivotal in the dynamic interplay between hypoxia and inflammation. During hypoxic conditions, HIF-1α, a crucial transcription factor, facilitates the adaptation of immune cells to the hypoxic micro-environment. This adaptation includes regulating immune cell metabolism, significantly impacting inflammation development. Strategies for anti-inflammatory and hypoxic relief have been proposed, aiming to disrupt the hypoxia-inflammation nexus. Research extensively focuses on anti-inflammatory agents and materials that target immune cells. These primarily mitigate hypoxic inflammation by encouraging M2-macrophage polarization, restraining neutrophil proliferation and infiltration, and maintaining Treg/TH17 balance. Additionally, oxygen-releasing nano-materials play a significant role. By alleviating hypoxia and clearing reactive oxygen species (ROS), these nano-materials indirectly influence immune cell functions. This paper delves into the response of immune cells under hypoxic conditions and the resultant effects on inflammation. It provides a comprehensive overview of various therapies targeting specific immune cells for anti-inflammatory purposes and explores nano-materials that either carry or generate oxygen to alleviate anoxic micro-environments.

Streptomyces, the largest genus in the Streptomycetaceae family and a prolific producer of antibacterial drugs, is a saprophytic soil organism that rarely causes invasive infections. Here we report a case of necrotic pneumonia caused by Streptomyces albireticuli in a 75-year-old man who presented with progressive chest tightness and dyspnea. Streptomyces albireticuli was isolated from his bronchoalveolar lavage fluid and identified through whole-genome sequencing (WGS) and phylogenetic analysis. The patient responded satisfactorily to clarithromycin therapy. The findings of this study may enhance our vigilance in identifying visceral infections caused by Streptomyces.