As a major challenge in the global field of critical care medicine, sepsis is associated with high morbidity and mortality, driving intensive research into the development of precise risk prediction models. Among these, machine learning and deep learning-based predictive models have garnered particular attention. This article systematically reviews the evolution of sepsis risk prediction models and the challenges associated with their clinical translation, with a focus on their clinical applicability in common septic complications, including acute kidney injury, encephalopathy, and coagulation disorders. Current evidence indicates that machine learning models, by integrating multidimensional dynamic data from electronic health records, significantly enhance early warning capabilities and individualized predictive performance. However, major bottlenecks limiting clinical translation include insufficient data standardization, lack of model interpretability, and inadequate external validation. Future research should prioritize multicenter collaboration, time-series modeling strategies, and explainable artificial intelligence frameworks to optimize clinical translation pathways and facilitate the paradigm shift from traditional empirical approaches to data-driven precision strategies in sepsis risk stratification.

Pneumonia is a major disease threatening the health of children, and its diagnosis mainly depends on medical history, physical examination, chest X-ray and CT examination. The reliability of the physical examination was low, while the chest X-ray and CT examination had certain radiation damage to children. Therefore, in recent years, the application of lung ul-trasound is popular in diagnosis of pneumonia in pediatric patients. This article reviewed the application of lung ultrasonography in diagnosis and follow-up of pneumonia in pediatric patients..

Objective To investigate the effects of swimming exercise training on left ventricular (LV)remodeling and its possible mechanism in spontaneous hypertensive rats (SHR).Methods Twenty eightweek-old male SHRs were divided into SHR control (SC) group and SHR exercise training (ST) group,with 10 rats in each group.Ten eight-week-old male Wistar rats were used as normal control (WC) group.The ST group was subject to 60-min moderate swimming exercise without loading once daily,6 times a week,for a total of 12 weeks; while the SC and WC group had no special intervention.The blood pressure was examined once weekly.After 12 weeks,the norepinephrine (NE)and serum angiotonin Ⅱ (ANG Ⅱ) levels were determined by ELISA.The LV hypertrophy was assessed by analysing the ratio of LV weights to body weights (LVW/BW) and cardiomyocyte diameter.The collagen deposited in LV was detected by sirius red staining.The expressions of tumor necrosis factor-α (TNF-α),interleukin-6 (IL-6),interleukin-1β (IL-1β) and transforming growth factor-β1 (TGF-β1) in LV were determined by semi-quantitative real time-polymerase chain reaction (RT-PCR) and Western blotting.Results After 12 weeks,the blood pressure,serum NE and ANG Ⅱ levels,LVW/BW ratio,cardiomyocyte diameter and collagen volume fraction (CVF) increased significantly in SC group compared with WC group; while those in ST group decreased significantly.In addition,in ST group the mRNA and protein expressions of TNF-α,IL-6,IL-1 βand TGF-β1 also decreased significantly.Conclusions The swimming exercise could reduce the blood pressure of SHR and improve LV remodeling.This effect was mediated not only by improving the hemodynamics,but also by decreasing sympathetic nerve and renin-angiotensin system (RAS) activities,decreasing the gene expressions of cytokines.The swimming exercise may be an effective strategy for improving LV remodeling in hypertension.

BACKGROUNDHepatocyte growth factor (HGF) inhibits the development of pulmonary artery hypertension (PAH) by reducing pulmonary artery pressure and right ventricle (RV) hypertrophy. However, whether HGF can prevent RV remodeling via inhibiting apoptosis in RV cardiomyocytes and decreasing neurohormonal activation remains unknown.

METHODSThe PAH and subsequent RV remodeling in rats were induced by subcutaneous injection of monocrotaline (MCT). The PAH rats were transfected with adenovirus carrying HGF (Ad-HGF) via intratracheal instillation. Three weeks after transfection, the hemodynamics indexes were measured, serum levels for angiotonin II (ANG II) and brain natriuretic peptide (BNP) were determined by ELISA. Histological analysis was used to assess the RV hypertrophy and fibrosis. The cardiomyocyte apoptosis in RV was assayed by TUNEL staining. The mRNA expression of BNP, angiotensin-converting enzyme (ACE), Bax and Bcl-2 in RV was determined by reverse transcriptase polymerase chain reaction (RT-PCR), the protein expression of transforming growth factor (TGF)-β1 and tumor necrosis factor (TNF)-α in RV was determined by Western blotting.

RESULTSHGF treatment significantly decreased the mean PAH, RV systolic pressure, serum ANG II and BNP levels. HGF treatment also significantly decreased the RV hypertrophy, collagen deposition, and the number of apoptotic cardiomyocytes. Moreover, HGF treatmemt significantly decreased the expression of BNP, ACE, Bax, TGF-β1, and TNF-α, while it significantly increased the expression of Bcl-2.

CONCLUSIONSGene transfer of HGF decreases MCT-induced PAH and improves RV remodeling. This effect is mediated not only by improving the hemodynamics but also by decreasing neurohormonal activation and inhibiting cardiomyocytes apoptosis. HGF gene treatment may be an effective strategy for improving RV remodeling in MCT-induced PAH.

Animals ; Apoptosis ; genetics ; physiology ; Hepatocyte Growth Factor ; genetics ; physiology ; therapeutic use ; Humans ; Hypertension, Pulmonary ; metabolism ; therapy ; Male ; Rats ; Rats, Sprague-Dawley ; Ventricular Remodeling ; genetics ; physiology