The two core causes of obesity in modern lifestyle are high-fat diet (HFD) and insufficient physical activity. HFD can lead to disruption of gut microbiota and abnormal lipid metabolism, further exacerbating the process of obesity. The small intestine, as the “first checkpoint” for the digestion and absorption of dietary lipids into the body, plays a pivotal role in lipid metabolism. The small intestine is involved in the digestion, absorption, transport, and synthesis of dietary lipids. The absorption of lipids in the small intestine is a crucial step, as overactive absorption leads to a large amount of lipids entering the bloodstream, which affects the occurrence of obesity. HFD can lead to insulin resistance, disruption of gut microbiota, and inflammatory response in the body, which can further induce lipid absorption and metabolism disorders in the small intestine, thereby promoting the occurrence of chronic metabolic diseases such as obesity. Long term HFD can accelerate pathological structural remodeling and lipid absorption dysfunction of the small intestine: after high-fat diet, the small intestine becomes longer and heavier, with excessive villi elongation and microvilli elongation, thereby increasing the surface area of lipid absorption and causing lipid overload in the small intestine. In addition, overexpression of small intestine uptake transporters, intestinal mucosal damage induced “intestinal leakage”, dysbiosis of intestinal microbiota, ultimately leading to abnormal lipid absorption and chronic inflammation, accelerating lipid accumulation and obesity. Exercise, as one of the important means of simple, economical, and effective proactive health interventions, has always been highly regarded for its role in improving lipid metabolism homeostasis. The effect of exercise on small intestine lipid absorption shows a dose-dependent effect. Moderate to low-intensity aerobic exercise can improve the intestinal microenvironment, regulate the structure and lipid absorption function of the small intestine, promote lipid metabolism and health, while vigorous exercise, excessive exercise, and long-term high-intensity training can cause intestinal discomfort, leading to the destruction of intestinal structure and related symptoms, affecting lipid absorption. Long term regular exercise can regulate the diversity of intestinal microbiota, inhibit inflammatory signal transduction such as NF-κB, enhance intestinal mucosal barrier function, and improve intestinal lipid metabolism disorders, further enhancing the process of small intestinal lipid absorption. Exercise also participates in the remodeling process of small intestinal epithelial cells, regulating epithelial structural homeostasis by activating cell proliferation related pathways such as Wnt/β-catenin. Exercise can regulate the expression of lipid transport proteins CD36, FATP, and NPC1L1, and regulate the function of small intestine lipid absorption. However, the research on the effects of long-term exercise on small intestine structure, villus structure, absorption surface area, and lipid absorption related proteins is not systematic enough, the results are inconsistent, and the relevant mechanisms are not clear. In the future, experimental research can be conducted on the dose-response relationship of different intensities and forms of exercise, exploring the mechanisms of exercise improving small intestine lipid absorption and providing theoretical reference for scientific weight loss. It should be noted that the intestine is an organ that is sensitive to exercise response. How to determine the appropriate range, threshold, and form of exercise intensity to ensure beneficial regulation of intestinal lipid metabolism induced by exercise should become an important research direction in the future.

Metaflammation is a crucial mechanism in the onset and advancement of metabolic disorders, primarily defined by the activation of immune cells and increased concentrations of pro-inflammatory substances. The function of brain-derived neurotrophic factor (BDNF) in modulating immune and metabolic processes has garnered heightened interest, as BDNF suppresses glial cell activation and orchestrates inflammatory responses in the central nervous system via its receptor tyrosine kinase receptor B (TrkB), while also diminishing local inflammation in peripheral tissues by influencing macrophage polarization. Exercise, as a non-pharmacological intervention, is extensively employed to enhance metabolic disorders. A crucial mechanism underlying its efficacy is the significant induction of BDNF expression in central (hypothalamus, hippocampus, prefrontal cortex, and brainstem) and peripheral (liver, adipose tissue, intestines, and skeletal muscle) tissues and organs. This induction subsequently regulates inflammatory responses, ameliorates metabolic conditions, and decelerates disease progression. Consequently, BDNF is considered a pivotal molecule in the motor-metabolic regulation axis. Despite prior suggestions that BDNF may have a role in the regulation of exercise-induced inflammation, systematic data remains inadequate. Since that time, the field continues to lack structured descriptions and conversations pertinent to it. As exercise physiology research has advanced, the academic community has increasingly recognized that exercise is a multifaceted activity regulated by various systems, with its effects contingent upon the interplay of elements such as type, intensity, and frequency of exercise. Consequently, it is imperative to transcend the prior study paradigm that concentrated solely on localized effects and singular mechanisms and transition towards a comprehensive understanding of the systemic advantages of exercise. A multitude of investigations has validated that exercise confers health advantages for individuals with metabolic disorders, encompassing youngsters, adolescents, middle-aged individuals, and older persons, and typically enhances health via BDNF secretion. However, exercise is a double-edged sword; the relationship between exercise and health is not linearly positive. Insufficient exercise is ineffective, while excessive exercise can be detrimental to health. Consequently, it is crucial to scientifically develop exercise prescriptions, define appropriate exercise loads, and optimize health benefits to regulate bodily metabolism. BDNF mitigates metaflammation via many pathways during exercise. Initially, BDNF suppresses pro-inflammatory factors and facilitates the production of anti-inflammatory factors by modulating bidirectional transmission between neural and immune cells, therefore diminishing the inflammatory response. Secondly, exercise stimulates the PI3K/Akt, AMPK, and other signaling pathways via BDNF, enhancing insulin sensitivity, reducing lipotoxicity, and fostering mitochondrial production, so further optimizing the body’s metabolic condition. Moreover, exercise-induced BDNF contributes to the attenuation of systemic inflammation by collaborating with several organs, enhancing hepatic antioxidant capacity, regulating immunological response, and optimizing “gut-brain” axis functionality. These processes underscore the efficacy of exercise as a non-pharmacological intervention for enhancing anti-inflammatory and metabolic health. Despite substantial experimental evidence demonstrating the efficacy of exercise in mitigating inflammation and enhancing BDNF levels, numerous limitations persist in the existing studies. Primarily, the majority of studies have concentrated on molecular biology and lack causal experimental evidence that explicitly confirms BDNF as a crucial mediator in the exercise regulation of metaflammation. Furthermore, the outcomes of current molecular investigations are inadequately applicable to clinical practice, and a definitive pathway of “exercise-BDNF-metaflammation” remains unestablished. Moreover, the existing research methodology, reliant on animal models or limited human subject samples, constrains the broad dissemination of the findings. Future research should progressively transition from investigating isolated and localized pathways to a comprehensive multilevel and multidimensional framework that incorporates systems biology and exercise physiology. Practically, there is an immediate necessity to undertake extensive, double-blind, randomized controlled longitudinal human studies utilizing multi-omics technologies (e.g., transcriptomics, proteomics, and metabolomics) to investigate the principal signaling pathways of BDNF-mediated metaflammation and to elucidate the causal relationships and molecular mechanisms involved. Establishing a more comprehensive scientific evidence system aims to furnish a robust theoretical framework and practical guidance for the mechanistic interpretation, clinical application, and pharmaceutical development of exercise in the prevention and treatment of metabolic diseases.

The intelligent oxygen management system is a software designed with various algorithms to automatically titrate inhaled oxygen concentration according to specific patterns. This system can be integrated into various ventilator devices and used during assisted ventilation processes, aiming to maintain the patient's blood oxygen saturation within a target range. This paper employs a scoping review methodology, focusing on research related to intelligent oxygen management systems in neonatal intensive care units. It reviews the fundamental principles, application platforms, and clinical outcomes of these systems, providing a theoretical basis for clinical implementation.
Humans ; Intensive Care Units, Neonatal ; Infant, Newborn ; Oxygen/administration & dosage* ; Oxygen Inhalation Therapy/methods* ; Respiration, Artificial

Objective:To explore the mechanism of Xuanfei Dahe Decoction in treating asthmatic mice through network pharmacology and animal experiments.Methods:The active components and their targets of Xuanfei Dahe Decoction were retrieved from TCMSP, and the asthma targets were obtained by searching the GeneCards, DisGeNet, OMIM, TTD and DrugBank databases. PPI network of intersection targets was constructed using string database and Cytoscape 3.9.0 software. Go function and KEGG pathway enrichment were analyzed by metascape database. The mice were divided into a blank group of 6 mice and a model group of 30 mice according to the random number table method. The asthma model was prepared in the model group. Totally 30 successfully modeled mice were divided into the model group, the dexamethasone group, and Xuanfei Dahe Decoction low-, medium- and high-dosage groups according to the random number table method, with 6 mice in each group. On the 5th day, gavage was initiated. Xuanfei Dahe Decoction low-, medium- and high-dosage groups were respectively gavaged with Xuanfei Dahe Decoction liquid at concentrations of 6.84, 13.68 and 27.36 g/kg. The dexamethasone group was gavaged with dexamethasone acetate tablets at concentrations of 2.73 mg/kg. The blank group and the model group were gavaged with the same volume of sterile normal saline once a day for 14 consecutive days. The pathological changes of lung tissue were observed by HE staining, the level of serum IL-17 was detected by ELISA, and the expression of IL-17 in lung tissue was detected by immunohistochemistry.Results:120 asthma targets and 13 key targets were obtained from Xuanfei Dahe Decoction. Pathway enrichment analysis suggested that IL-17 signaling pathway was one of the key pathways. Compared with the model group, the levels of IL-17 in the serum of the low-dose, medium-dose and high-dose Xuanfei Dahe Decoction groups and the expression of IL-17A in the lung tissue of the medium-dose Xuanfei Dahe Decoction group decreased ( P<0.05). Conclusion:Xuanfei Dahe Decoction may treat asthma by restrain airway inflammation mediated by Th17/IL-17.

Objective To investigating the microbial communities and physicochemical properties of soil and distribution of Oncomelania hupensis snails in marshlands along the Yangtze River basin at different types of land use, and to examine the effects of soil microorganisms and physicochemical properties on snail distribution, so as to provide insights into snail control and schistosomiasis prevention in marshland along the Yangtze River basin. Methods Marshlands with four types of land use were selected along the Yangtze River basin on April 2021, including poplar forest-crops integrated planting, reed areas, agricultural cultivation lands and ditches. The distribution of snails and physicochemical properties of soil were investigated in marshlands with different types of land use, and the V3 to V4 regions of the bacterial 16S ribosomal RNA (16S rRNA) gene, fungal internal transcribed spacer-1 (ITS1) gene and algal ribulose-bisphosphate carboxylase (rbcL) gene in soils were subjected to high-throughput sequencing. The occurrence of frames with living snails and density of living snails were compared in marshland with different types of land use. The associations of soil microorganisms and physicochemical properties with the density of living snails were examined using Pearson correlation analysis, and the contributions of soil microorganisms and physicochemical properties to the density of living snails were evaluated using variance partitioning analysis. Results In marshlands with four types of land use, the greatest occurrence of frames with living snails [(4.94 ± 2.14)%] and density of living snails [(0.070 ± 0.026) snails/0.1 m²] were seen in ditches, and the lowest were found in [(1.23 ± 1.23)%] agricultural cultivation lands [(0.016 ± 0.019) snails/0.1 m²]. A total of 2 phyla, 5 classes, 8 orders, 9 families and 11 genera of algae were detected in soils at four types of land use, with Chlorophyta as the dominant phylum and Pseudoneochloris as the dominant genus. A total of 44 phyla, 134 classes, 281 orders, 338 families and 516 genera of bacteria were detected in soils at four types of land use, with Proteobacteria and Acidobacteriota as the dominant phyla and uncultured Acidobacterium, MND1, Mitrospira, Haliangium and Sphingomonas as dominant genera. A total of 11 phyla, 41 classes, 108 orders, 223 families and 408 genera of fungi were detected in soils at four types of land use, with phyla Ascomycota, Basidiomycota and Mortierellomycota presenting high relative abundances and genera Cladorrhinum, Mortierella and Humicola presenting high relative abundances. Pearson correlation analysis revealed that the density of living snails correlated negatively with the relative abundance of Proteobacteria (r = −0.965, P < 0.05) and soil electronic conductivity (r = −0.962, P < 0.05) and positively with soil moisture (r = 0.951, P < 0.05). Variance partitioning analysis demonstrated that the physicochemical properties and microorganisms of soil contributed 69% and 10% to the density of living snails, respectively. Conclusion The diversity of microbial communities varies in soils at different types of land use in marshland along the Yangtze River basin, and the physicochemical properties and microorganisms of soils may affect the distribution of O. hupensis snails.

Objective To explore the application effect of family integrated care (FIC) based on family ward (FW) on premature infants with bronchopulmonary dysplasia.Methods A total of 171 premature in-fants with bronchopulmonary dysplasia and their parents in the neonatology department of a hospital from March 2022 to March 2023 were selected as the research subjects.According to the wishes of parents,they were divided into three groups:NICU-FIC group,FW-FIC group and no accompanying group.In the NICU-FIC group,the parents entered the centrally managed neonatal intensive care unit to take care of premature in-fants at the bedside.The parents in the FW-FIC group shared a single ward with the premature infants,and participated in the care throughout the day.The parents in the unaccompanied group did not participate in the care of premature infants during hospitalization.The conditions of the three groups of premature infants at discharge and on 30 d after discharge were compared among 3 groups.Results A total of 167 premature in-fants completed the trial.At discharge,the breastfeeding rate,total oxygen days,and total hospitalization days of the NICU-FIC group and FW-FIC group were significantly different from those of the unaccompanied group (P<0.05).However,there was no statistically significant difference between the NICU-FIC group and FW-FIC group(P>0.05).After 30 d of discharge,the breastfeeding rate,weight gain,proportion of home oxygen therapy,and readmission rate of the NICU-FIC group and FW-FIC group were significantly different from those of the unaccompanied group (P<0.05).The breastfeeding rate,weight gain and readmission rate in the FW-FIC group were significantly different from those in the NICU-FIC group (P<0.05).Conclusion The FIC method based on the family ward is consistent with the FIC method based on the open neonatal intensive care unit in promoting the clinical prognosis of premature infants with bronchopulmonary dysplasia,moreover the FIC method based on the family ward has better strengthening effect and out-of-hospital continuity.

Ferroptosis and disulfidpthosis are associated with various diseases.Ferroptosis is distinguished by abnormal accumulation of iron ions and lipid reactive oxygen species,while disulfidptosis is marked by abnormal accumu-lation of disulfides.Solute carrier family 3 member 2(SLC3A2),a component of the solute carrier family,is implicated not only involved in the regulation of tumor cell proliferation,migration,invasion and apoptosis,but also in the processes of ferroptosis and disulfidptosis,playing a pivotal role in tumor growth and progression.This article provides an overview of the latest advancements in understanding the relationship between SLC3A2 and ferroptosis,disulfidptosis and tumors,aiming to establish a theoretical basis for targeted cancer therapies.

Objective To explore the correlation between coronary fat attenuation index of perivascular adipose tissue(FAIPVAT),as well as volumetric perivascular characterization index(VPCI),and coronary heart disease(CHD).Methods A total of 112 patients who underwent coronary computed tomography angiography(CCTA)and coronary angiography(CAG)examinations within 2 weeks were selected.The patients were divided into CHD group and control group according to the degree of coronary artery stenosis,and were divided into calcified plaque group,non-calcified plaque group and mixed plaque group according to the nature of plaque.The correlation between FAIPVAT,VPCI and CHD were evaluated.Results Of the 112 patients,71 patients in the CHD group and 41 patients in the control group.There were significant differences in gender,age,FAIPVAT and VPCI between the two groups.FAIPVAT and VPCI were positively correlated with CHD(r=0.445,P＜0.01;r=0.669,P＜0.01).FAIPVAT and VPCI were analyzed by receiver operating characteristic(ROC)curve,the area under the curve(AUC)of FAIPVAT was 0.770,the cut-off value was-81.659 HU,the sensitiv-ity was 0.592,and the specificity was 0.878,while the AUC of VPCI was 0.892,the cut-off value was 8.056,the sensitivity was 0.887,and the specificity was 0.805.There were significant differences in FAIPVAT and VPCI between non-calcified plaque group and calci-fied plaque group.FAIPVAT and VPCI of mixed plaque group and calcified plaque group were significantly different.Conclusion FAIPVAT and VPCI have some certain correlation with CHD.FAIPVAT and VPCI can accurately evaluate the risk level of CHD and coronary artery inflammation,and the value of individualized VPCI is higher.

Objective To investigate the impact of matrine(Mat)on renal injury in rats with chronic glomerulonephritis by regulating the monocyte chemotactic protein-1(MCP-1)/chemokine C-C-motif receptor 2(CCR2)signaling pathway.Methods The rat model of chronic glomerulonephritis was established by subcutaneous injection of bovine serum albumin,the rats were randomly grouped into control group,model group,low and high dose matrine groups(Mat-L group,Mat-H group),and matrine+CCR2 group(Mat+CCR2 group),with 10 rats in each group.After continuous gavage for 4 weeks,24-hour urine protein excretion was measured;spleen and thymus were removed and organ index was calculated;The levels of blood urea nitrogen(BUN)and serum creatinine(Scr)in the serum of each group were detected,the pathological changes of renal tissue were observed by HE staining;the levels of tumor necrosis factor α(TNF-α)and interleukin(IL)-6 in renal tissue were detected by ELISA;Flow cytometry was applied to detect the proportion of T lymphocyte subsets in peripheral blood of rats in each group;Western blotting was applied to determine the expression of MCP-1 and CCR2 proteins.Results The spleen index and thymus index of rats in the model group rats were obviously reduced,and there were a large number of inflammatory cell infiltration in the renal tissue,the 24-hour urine protein,BUN,Scr,TNF-α,IL-6,and the expression of MCP-1 and CCR2 obviously increased,the peripheral blood T cell subpopulations CD3+,CD4+,and CD4+/CD8+ratio obviously reduced,the proportion of CD8+obviously increased(P＜0.05);The spleen index and thymus index of rats in the Mat-L and Mat-H groups of rats increased,and the phenomenon of renal tissue inflammation and infiltration improved,the 24-hour urine protein,BUN,Scr,TNF-α,IL-6,and the expression of MCP-1 and CCR2 obviously decreased,the peripheral blood T cell subpopulations CD3+,CD4+,and CD4+/CD8+ratio obviously increased,the proportion of CD8+obviously decreased(P＜0.05);CCR2 attenuated the effect of Mat-H on immune function in rats with chronic glomerulonephritis.Conclusion Matrine can alleviate the inflammatory damage and improve the peripheral immune function of rats with chronic glomerulonephritis,and its mechanism may be related to the inhibition of MCP-1/CCR2 signaling pathway.

In this study,the immunological characteristics of the PhoP protein were explored with a two-component system of Mycobacterium tuberculosis(Mtb).Bioinformatics was used to predict the B and T cell epitopes of the PhoP protein.A re-combinant expression plasmid was constructed by PCR analysis of the phoP sequence and cloning into the prokaryotic expres-sion vector pET-28a(+).Competent Escherichia coli BL21 cells were transformed with the recombinant plasmid and expres-sion was induced with IPTG.The recombinant PhoP protein was purified by affinity chromatography.Serum levels of PhoP-specific antibodies in Mtb-infected mice and tuberculosis(TB)patients were analyzed with an ELISA.BALB/c mice were im-munized with the PhoP recombinant protein by intramuscular injection.Sera of mice were collected and antibody titers were detected with an ELISA and specificity was assessed by West-ern blot analysis.Mouse splenocytes were isolated and the pro-portions of IFN-y-positive cells and cytokine levels were detec-ted with an ELISpot and ELISA,respectively.Bioinformatics i-dentified 24 B cell and 11 T cell epitopes of the PhoP protein.A prokaryotic recombinant vector of PhoP was successfully con-structed and the recombinant PhoP protein was obtained by purification.Specific antibody levels to PhoP in sera of Mtb in-fected mice and TB patients increased significantly,with preci-sion of 99.9％and 82.5％,and specificity of 100％,respectively.PhoP protein immunization successfully induced production of specific antibodies in mice.Stimulated by antigens in vitro,IL-2 and IFN-γ levels were significantly increased in the splenocytes of immunized mice.Immunization with the PhoP protein induce a humoral immune response and Thl-dominated cellular immu-nity,indicating that the PhoP protein was immunogenic with diagnostic efficacy for TB.These results lay a foundation to clari-fy the role of PhoP in Mtb infection and application for diagnosis and prevention of TB.