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ObjectiveThe purpose of this study is to develop a multimodal model based on artificial intelligence to assist clinical doctors in the early diagnosis of necrotizing enterocolitis in newborns.MethodsThis study is a retrospective study that collected the initial laboratory test results and abdominal x-ray image data of newborns (non-NEC, NEC) admitted to our hospital from January 2022 to January 2024.A multimodal model was developed to differentiate multimodal data, trained on the training dataset, and evaluated on the validation dataset. The interpretability was enhanced by incorporating the Gradient-weighted Class Activation Mapping (GradCAM) analysis to analyze the attention mechanism of the multimodal model, and finally compared and evaluated with clinical doctors on external datasets.ResultsThe dataset constructed in this study included 11,016 laboratory examination data from 408 children and 408 image data. When applied to the validation dataset, the area under the curve was 0.91, and the accuracy was 0.94. The GradCAM analysis shows that the model's attention is focused on the fixed dilatation of the intestinal folds, intestinal wall edema, interintestinal gas, and portal venous gas. External validation demonstrated that the multimodal model had comparable accuracy to pediatric doctors with ten years of clinical experience in identification.ConclusionThe multimodal model we developed can assist doctors in early and accurate diagnosis of NEC, providing a new approach for assisting diagnosis in underdeveloped medical areas.

In order to cope with the impact of the COVID-19 epidemic on student learning, the Chinese government has launched a "School's Out, But Class's On" strategy. With the further control of the epidemic, schools in some provinces have begun to resume classes, but the epidemic prevention and control work should not be lax after the class is resumed. Guizhou is one of the provinces where the middle schools and senior high schools resumed classes earlier. The epidemic prevention and control is still very critical even the school was resumed. I herein used the Experimental High School in Wangmo County, Guizhou Province as an example to introduce the epidemic prevention and control strategies after the school resumes classes.

This paper presents the stability and bifurcation of the Hindmarsh–Rose neuronal model with time delay. First, we discuss the existence and stability of the equilibria, revealing that the system can have a maximum of three equilibria which exhibit always stable, always unstable, and stability switching dynamics, depending on the stability of the equilibria when there is no time delay. Furthermore, an explicit formula for the time delay at which Hopf bifurcation occurs is derived, and the direction and stability of the Hopf bifurcation are also given. Finally, numerical simulations are carried out to support our theoretical results. We find that due to the existence of time delay, our system can exhibit many interesting dynamical behaviors depending on the number of equilibria and the increase in time delay. For instance, with increasing time delay, bistability transitions to the coexistence of a periodic solution and a stable equilibrium, followed by the emergence of quasi-periodic motion alongside stable equilibria, and eventually leading to chaotic motion coexisting with a stable equilibrium. [ABSTRACT FROM AUTHOR]

In this paper, we investigate a general time-periodic stoichiometric ODE model, which describes the algal growth. The model system has singularities induced by the zero nitrogen concentration. We first observe that there exists a threshold value $ \lambda_0 $, which is exactly the principal eigenvalue of a nonlinear eigenvalue problem associated with a homogeneous of degree one system, and further show the global dynamics of the model system in terms of $ \lambda_0 $. In particular, we obtain the uniqueness of the positive periodic solution when $ \lambda_0>0 $. Finally, we carry out simulations to illustrate the analytic results. [ABSTRACT FROM AUTHOR]

Genomic full‐length sequence of HLA‐B*37:46 was identified by a group‐specific sequencing approach in a Chinese individual. [ABSTRACT FROM AUTHOR]

Aims  Endothelial cell (EC) homoeostasis plays an important role in normal physiological cardiac functions, and its dysfunction significantly influences pathological cardiac remodelling after myocardial infarction (MI). It has been shown that the sphingosine 1-phosphate receptor 1 (S1pr1) was highly expressed in ECs and played an important role in maintaining endothelial functions. We thus hypothesized that the endothelial S1pr1 might be involved in post-MI cardiac remodelling. Methods and results  Our study showed that the specific loss of endothelial S1pr1 exacerbated post-MI cardiac remodelling and worsened cardiac dysfunction. We found that the loss of endothelial S1pr1 significantly reduced Ly6clow macrophage accumulation, which is critical for the resolution of inflammation and cardiac healing following MI. The reduced reparative macrophages in post-MI myocardium contributed to the detrimental effects of endothelial S1pr1 deficiency on post-MI cardiac remodelling. Further investigations showed that the loss of endothelial S1pr1 -reduced Ly6clow macrophage proliferation, while the pharmacological activation of S1pr1-enhanced Ly6clow macrophage proliferation, thereby ameliorated cardiac remodelling after MI. A mechanism study showed that S1P/S1pr1 activated the ERK signalling pathway and enhanced colony-stimulating factor 1 (CSF1) expression, which promoted Ly6clow macrophage proliferation in a cell-contact manner. The blockade of CSF1 signalling reversed the enhancing effect of S1pr1 activation on Ly6clow macrophage proliferation and worsened post-MI cardiac remodelling. Conclusion  This study reveals that cardiac microvascular endothelium promotes reparative macrophage proliferation in injured hearts via the S1P/S1PR1/ERK/CSF1 pathway and thus ameliorates post-MI adverse cardiac remodelling. [ABSTRACT FROM AUTHOR]

Cardiac vascular microenvironment is crucial for cardiac remodelling during the process of heart failure. Sphingosine 1‐phosphate (S1P) tightly regulates vascular homeostasis via its receptor, S1pr1. We therefore hypothesize that endothelial S1pr1 might be involved in pathological cardiac remodelling. In this study, heart failure was induced by transverse aortic constriction (TAC) operation. S1pr1 expression is significantly increased in microvascular endothelial cells (ECs) of post‐TAC hearts. Endothelial‐specific deletion of S1pr1 significantly aggravated cardiac dysfunction and deteriorated cardiac hypertrophy and fibrosis in myocardium. In vitro experiments demonstrated that S1P/S1pr1 praxis activated AKT/eNOS signalling pathway, leading to more production of nitric oxide (NO), which is an essential cardiac protective factor. Inhibition of AKT/eNOS pathway reversed the inhibitory effect of EC‐S1pr1‐overexpression on angiotensin II (AngII)‐induced cardiomyocyte (CM) hypertrophy, as well as on TGF‐β‐mediated cardiac fibroblast proliferation and transformation towards myofibroblasts. Finally, pharmacological activation of S1pr1 ameliorated TAC‐induced cardiac hypertrophy and fibrosis, leading to an improvement in cardiac function. Together, our results suggest that EC‐S1pr1 might prevent the development of pressure overload‐induced heart failure via AKT/eNOS pathway, and thus pharmacological activation of S1pr1 or EC‐targeting S1pr1‐AKT‐eNOS pathway could provide a future novel therapy to improve cardiac function during heart failure development. [ABSTRACT FROM AUTHOR]