Choline is an essential nutrient for human body, but dietary choline is metabolized into the hazard metabolite for the cardiovascular system. Because of the conflicting results between dietary choline intake and cardiovascular disease (CVD) risk in previous studies, we aimed to investigate this in US adults. Non-pregnant participants and those aged >20 years from National Health and Nutrition Examination Survey 2011–2016, with CVD assessment and reliable dietary recall status, were included. The dietary choline intake was assessed as a mean value of two total dietary choline intakes, including dietary choline intake and supplemental choline intake, in 24-h dietary recall interviews. The association between dietary choline intake and the presence of CVD was examined using logistic regression. We enrolled 14,323 participants. The participants without CVD had substantially higher dietary choline intakes (318.4 mg/d vs. 297.2 mg/d) compared to those with CVD (p < 0.05). After multivariable adjustments, the highest quartile of dietary choline intake was associated with a lower CVD risk, OR 0.693, 95%CI [0.520, 0.923], when compared to the lowest quartile. Consistent results were also found for stroke. Subgroup analyses also supported these, especially in participants aged ≥60 years and in those with BMI < 30 kg/m². We found that a higher dietary choline intake was associated with a lower CVD risk, especially the risk of stroke. Further clinical trials are needed in order to confirm this finding and to provide dietary suggestions for the appropriate amount of choline intake.

Fibroblast growth factor (FGF)21 is a peptide hormone that improves mitochondrial function and energy metabolism, and the deficiency of its co‑receptor β‑klotho (KLB) causes decreased FGF21 sensitivity. The present study examined whether the cardiac delivery of plasmids containing the KLB gene via ultrasound‑targeted microbubble destruction (UTMD) enhances the efficacy of FGF21 against heart failure post‑acute myocardial infarction (AMI). For this purpose, the levels of FGF21 in patients and rats with heart dysfunction post‑infarction were determined using ELISA. Sprague‑Dawley rats received the 3X UTMD‑mediated delivery of KLB@cationic microbubbles (KLB@CMBs) 1 week following the induction of AMI. Echocardiography, histopathology and biochemical analysis were performed at 4 weeks following the induction of AMI. The results revealed that patients with heart failure post‑infarction had higher serum FGF21 levels than the healthy controls. However, the downstream signal, KLB, but not α‑klotho, was reduced in the heart tissues of rats with AMI. As was expected, treatment with FGF21 did not substantially attenuate heart remodeling post‑infarction. It was found that decreased receptors KLB in the heart may result in the insensitivity to FGF21 treatment. In vivo, the UTMD technology‑mediated delivery of KLB@CMBs to the heart significantly enhanced the effects of FGF21 administration on cardiac remodeling and mitochondrial dysfunction in the rats following infarction. The delivery of KLB to the heart by UTMD and the administration of FGF21 attenuated mitochondrial impairment and oxidative stress by activating nuclear factor erythroid 2‑related factor 2 signals. On the whole, the present study demonstrates that the cardiac delivery of KLB significantly optimizes the cardioprotective effects of FGF21 therapy on adverse heart remodeling. UTMD appears a promising interdisciplinary approach with which to improve heart failure post‑myocardial infarction.

Background: Prone positioning has emerged as a crucial intervention in managing acute respiratory failure, especially in acute respiratory distress syndrome and patients with COVID-19. Given the increasing interest in this field, it is important to characterize global research trends and key contributors to identify future research directions. Objective: This study aimed to analyze global research trends, collaboration networks, and research hotspots related to prone positioning in respiratory failure through a comprehensive bibliometric analysis. Methods: Bibliometric analyses were conducted using CiteSpace and Biblioshiny software on publications up to December 31, 2023, from the Web of Science Core Collection, focusing on prone positioning in respiratory failure. Results: A total of 1263 research articles were identified, published in 50 countries by numerous institutions. The United States, France, and Germany contributed the most publications, with the United States producing 21.9% (275/1263) of the total. Key authors such as Claude Guerin and Luciano Gattinoni were identified as major contributors to the field. Keyword co-occurrence analysis revealed the dynamic nature of prone positioning research in respiratory failure. It highlighted protective ventilation and COVID-19-related acute respiratory distress syndrome as emerging hotspots, indicating a shift in focus during the pandemic. Conclusions: This study revealed a rapidly growing body of literature on prone positioning in respiratory failure, especially in the context of COVID-19. The findings underscore the importance of further multicenter clinical trials to validate current practices and refine treatment protocols. In addition, the application of prone positioning in non-intubated patients represents a potential future research direction.

Abdominal organs are important organs that sense and respond to ischemia and hypoxia, but there are few evaluation methods.We use ultrasonography to evaluate abdominal organ function and blood flow in patients with mechanical ventilation (MV) after cardiopulmonary bypass and to obtain a semiquantitative score for abdominal organ function and blood flow. Patients with cardiopulmonary bypass in the Critical Care Department of Peking Union Medical College Hospital in China from March to July 2021 were enrolled in this prospective observational study. The correlation of the abdominal-visceral-blood-flow-and-function score (AVBFS) with the duration of MV, number of days spent in the intensive care unit (ICU), acute physiology and chronic health evaluation II (APACHE-II), sequential organ failure assessment (SOFA), lactate, epinephrine, and norepinephrine use was analyzed, and the results were used to assess the predictive value of the receiver operating characteristic curve (ROC) regression analysis score for the duration of MV. Of the 92 patients who underwent cardiopulmonary bypass, 41 were finally included. The AVBFS were significantly correlated with the duration of MV, number of days spent in the ICU, APACHE-II score, SOFA score, and norepinephrine use time. The AVBFS in a group of patients using ventilators ≥36 h were significantly higher than those obtained for a group of patients using ventilators <36 h (P <0.05). The evaluation results for the AVBFS at 0-12 h after ICU admission were as follows: area under the ROC curve (AUC)=0.876 (95% confidence interval [CI]: 0.767 to 0.984), cut-off value=2.5, specificity=0.842, and sensitivity=0.773. Abdominal visceral organ function and blood perfusion can be used to evaluate gastrointestinal function. It is related to early and late extubation after cardiac surgery.

Lipopolysaccharide (LPS) induces endotoxemia‐associated inflammatory cardiac injury rather than classical viral or autoimmune myocarditis. Sphingosine‐1‐phosphate (S1P) regulates cardiovascular and immune responses, predominantly through S1P receptors, but whether it also modulates macrophage‐associated inflammatory signaling during LPS‐induced cardiac injury remains incompletely understood. This study investigated the role of the RASGRP1–S100A9–NLRP3 signaling axis in the cardioprotective effects of S1P. Transcriptomic and single‐cell RNA‐sequencing analyses were used to identify inflammation‐associated candidate genes and their cellular distribution. Male Sprague‐Dawley rats received a single intraperitoneal injection of LPS (8 mg/kg) followed by S1P treatment for 6 weeks. Histopathology, echocardiography, serum cardiac‐injury markers, oxidative‐stress indices, inflammatory cytokines, Western blotting, and cellular metabolic‐flux assays were evaluated. RAW264.7 macrophages were used for mechanistic cellular studies. RASGRP1 or NLRP3 overexpression and S100A9‐R101Q mutation were used to assess functional contributions. Molecular docking and molecular‐dynamics simulations were complemented by SPR, MST, CETSA, DARTS, and Co‐IP assays to evaluate S1P–RASGRP1 target engagement and pathway‐associated protein interactions. Bioinformatic analyses identified RASGRP1 as a macrophage‐enriched, inflammation‐associated hub gene. In LPS‐treated rats, S1P reduced myocardial inflammatory injury and collagen deposition, improved ejection fraction and fractional shortening, and decreased cardiac‐injury, oxidative‐stress, and inflammatory markers. In RAW264.7 macrophages, S1P attenuated inflammatory and oxidative‐stress responses, restored oxidative phosphorylation and glycolytic capacity, and reduced the abundance of RASGRP1, S100A9, NLRP3, and ASC. SPR and MST supported a concentration‐dependent biophysical interaction between S1P and RASGRP1; CETSA and DARTS provided complementary target‐stability evidence. The molecular‐dynamics trajectory showed substantial rearrangement of S1P from the starting pose before reaching a plateau and therefore supports conformational sampling rather than preservation of the original docked pose. Co‐IP supported protein associations within the proposed inflammatory network. RASGRP1 or NLRP3 overexpression attenuated several S1P‐associated protective effects. The S100A9‐R101Q mutation also weakened several S1P‐associated protective responses. SPR indicated a lower apparent dissociation constant for R101Q than for WT S100A9 after model‐specific fitting, which is consistent with stronger or more persistent NLRP3 binding rather than loss of the S100A9–NLRP3 interaction. S1P mitigates LPS‐induced inflammatory cardiac injury in association with altered macrophage RASGRP1–S100A9–NLRP3 signaling. Biophysical and target‐stability assays support direct engagement of RASGRP1 by S1P. However, these findings do not establish RASGRP1 as the sole mediator of S1P activity, exclude contributions from canonical S1P receptor signaling, or demonstrate a strictly linear RASGRP1–S100A9–NLRP3 signaling cascade. Because the LPS model primarily represents endotoxemia‐associated inflammatory cardiac injury, extrapolation of these findings to classical viral or autoimmune myocarditis should be made with caution.