Nutritional risk factors for all-cause mortality of critically ill patients: a retrospective cohort study.

OBJECTIVES: This study aimed to explore the predictive value of single and multiple risk factors for the clinical outcomes of critically ill patients receiving enteral nutrition and to establish an effective evaluation model. DESIGN: Retrospective cohort study. SETTING: Data from the 2020-2021 period were collected from the electronic records of the First Affiliated Hospital, Nanjing Medical University. PARTICIPANTS: 459 critically ill patients with enteral nutrition in the geriatric intensive care unit were included in the study. PRIMARY AND SECONDARY OUTCOME MEASURES: The primary outcome was 28-day mortality. The secondary outcomes were 28-day invasive mechanical ventilation time, intensive care unit stay, Nutrition Risk Screening 2002 (NRS2002) score and Acute Physiology and Chronic Health Evaluation II (APACHE II) score. RESULTS: Independent prognostic factors, including prealbumin/procalcitonin (PCT) ratio and APACHE II score, were identified using a logistic regression model and used in the nomogram. The area under the receiver operating characteristic curve and concordance index indicated that the predictive capacity of the model was 0.753. Moreover, both the prealbumin/PCT ratio and the combination model of PCT, prealbumin and NRS2002 had a higher predictive value for clinical outcomes. Subgroup analysis also identified that a higher inflammatory state (PCT >0.5 ng/mL) and major nutritional risk (NRS2002 >3) led to worse clinical outcomes. In addition, patients on whole protein formulae bore less nutritional risk than those on short peptide formulae. CONCLUSIONS: This nomogram had a good predictive value for 28-day mortality in critically ill patients receiving enteral nutrition. Both the prealbumin/PCT ratio and the combination model (PCT, prealbumin and NRS2002), as composite models of inflammation and nutrition, could better predict the prognosis of critically ill patients.

Case report: Multiple gastrointestinal perforations in a rare musculocontractural Ehlers-Danlos syndrome with multiple organ dysfunction.

A 36-year-old male with congenital equinovarus deformity was admitted to the hospital due to worsen deformity. He was known to have ear perforation in childhood. After hospitalization, he received equinovarus correction surgery, fourth toe osteotomy, and external fixation for right foot during the procedure. During his hospital stay, the patient has been treated with multiple gastrointestinal perorations, accompanied with multiple organ dysfunction and fragile soft tissues. During his in-hospital stay, multiple organ dysfunctions were observed, including the heart, kidney, liver, and intestines. In order to identify the mutation site, whole-exome sequencing (WES) was performed, and further verified with Sanger sequencing analysis in this patient. One-site mutation located at CHST14 [c.883_884del, p (Phe295Cysfs*5)] was identified in this patient, whereas this mutation was not observed in other 100 healthy controls. Also, this variant has not been reported in public databases (ExAC and gnomAD). Our report showed that unanticipated multiple tissue deformation observed the musculocontractural EDS patient was caused by mutation located at CHST14 [c.883_884del, p (Phe295Cysfs*5)] induced truncated CHST14 protein.

GYY4137 ameliorates sepsis-induced cardiomyopathy via NLRP3 pathway.

Sepsis-induced cardiomyopathy (SICM) has a poor prognosis, with no effective therapeutic strategy currently. This study aimed to explore the mechanism underlying SICM and investigate the protective role of the hydrogen sulfide (H2S) donor GYY4137. This study included patients with SICM and animal models of SICM with wild-type and Nlrp3-/- mice, which were treated with or without GYY4137. Echocardiography, ELISA, TUNEL staining, and immunofluorescence were used to investigate phenotypic alterations. Serum levels of H2S and cytokines were measured. Inflammatory cell infiltration in the myocardial tissue was identified using immunohistochemistry and immunofluorescence. RNA expression profiles were identified using RNA sequencing. The protective mechanism of GYY4137 was further validated in the crosstalk between macrophages and cardiomyocytes using immunoblotting, real-time polymerase chain reaction (RT-PCR), and immunofluorescence when conditional medium of macrophages boosted by LPS were co-cultured with cardiomyocytes. Patients and animal models of SICM presented with lower serum H2S levels and heart dysfunction. GYY4137 reduced macrophage infiltration in septic heart tissue. GO analysis suggested that GYY4137 was involved in the inflammatory process. GYY4137 inhibited NLRP3 inflammasome activity in macrophages, reduced the secretion of inflammatory factors, and decreased the production of reactive oxygen species (ROS) in cardiomyocytes, thus exerting protective effects against SICM. We further found that the protective effects of GYY4137 were absent in Nlrp3-knockout models. GYY4137 ameliorates myocardial injury in SICM via the NLRP3 pathway by inhibiting the inflammatory response and reducing the production of myocardial ROS.

Dioscin Attenuates Myocardial Ischemic/Reperfusion-Induced Cardiac Dysfunction through Suppression of Reactive Oxygen Species.

Myocardial ischemic/reperfusion (MI/R) is a leading cause of cardiovascular disease with high morbidity and mortality. However, the mechanisms underlying pathological reperfusion remain obscure. In this study, we found that dioscin, a natural product, could be a potential candidate for treating MI/R through modulating cardiac dysfunction. Mechanistically, our work revealed that dioscin could suppress the production of reactive oxygen species (ROS) via repressing the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 2 (Nox2) and enhancing the expression of antioxidant enzymes, including superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), and glutathione peroxidase (GPx). These findings indicate that dioscin may be a potential candidate for therapeutic interventions in MI/R injury.