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

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.

Objective:To investigate the factors in fluencing thyroid function abnormality(TFA)and its relationship with the clinical efficacy of sindilizumab treatment in patients with advanced gastric cancer.Methods:The clinical data of 180 patients with advanced gastric cancer treated with sintilimab at Jinan People's Hospital from January 2021 to June 2024 were retrospectively reviewed.Patients were assigned in-to the TFA group and the normal control group according to thyroid function.Factors influencing the occurrence of TFA were investigated using the χ2 test and multifactorial Logistic regression.Kaplan-Meier analysis and the Log-rank test were used for comparison between groups.Univariate and multivariate Cox regression were used to assess the correlation between TFA and therapeutic efficacy.Results:A total of 52 patients developed TFA.Univariate analysis showed that history of thyroid nodule,treatment regimen,liver metastasis,and car-cinoembryonic antigen(CEA)were associated with the development of TFA.Multifactorial Logistic regression analysis showed that history of thyroid nodule,treatment regimen,and CEA were independent risk factors for the development of TFA(P<0.05).The objective response rate(ORR;34.6%vs.14.1%,P=0.002),disease control rate(DCR;69.2%vs.59.8%,P=0.024),and 1-year survival rate(59.6%vs.28.9%,P=0.012)were all better in the normal control group than those in the TFA group.Cox regression analysis showed that occurrence of TFA,liver meta-stasis,and≥6 treatment cycles were all independently associated with progression-free survival and overall survival in patients with ad-vanced gastric cancer(P<0.05).Conclusions:History of thyroid nodule,treatment regimen,and CEA may influence the occurrence of TFA.TFA may be a potential predictor of the efficacy of sindilizumab therapy for advanced gastric cancer,with patients who develop TFA poten-tially having better treatment outcomes.

Objective:To explore the effect of kidney-strengthening and blood stasis-eliminating formula on nutritional status and quality of life in patients with osteoporosis combined with hemodialysis.Methods:From January 2024 to January 2025,60 patients with liver and kidney yin deficiency and blood stasis obstruction were selected from the Pizhou City Traditional Chinese Medicine Hospital's Hemodialysis Center.60 patients were randomly divided into two groups,30 in each group.The matched group received general treatment plus paricalcitol,while the treatment group received the same treatment plus Yishen Zhuyu Fang(a traditional Chinese medicine formula for kidney and blood stasis).The treatment course lasted 12 weeks.Changes in TCM syndrome scores,the Modified Subjective Global Assessment(MQSGA),the Kidney and Life Quality(KDQOLTM-36)scale,lipid levels,and nutritional indicators were compared before and after treatment.Results:After treatment,the TCM syndrome scores in both groups decreased(P＜0.05),with a more pronounced decrease in the treatment group(P＜0.05).The KDQOLTM-36 score in the treatment group increased(P＜0.05),while the increase was not significant in the matched group(P＞0.05),indicating that the treatment group performed better than the matched group(P＜0.05).Both groups experienced a decrease in the MQSGA score(P＜0.05),although the difference was not statistically significant(P＞0.05),the treatment group showed a more noticeable decline.The TC,TG,LDL,and TG/HDL levels in the treatment group all decreased significantly,while HDL levels increased(P＜0.05).In contrast,the TC and HDL levels in the matched group did not change(P＞0.05),while the TG,LDL,and TG/HDL levels increased(P＜0.05).The treatment group performed significantly better than the matched group(P＜0.05).The TRF,Hb,and ALB levels in the treatment group increased(P＜0.05),while the increase was not significant in the matched group(P＞0.05).The total effective rate of the treatment group was 90％,higher than the matched group(23.3％)(P＜0.05).Conclusion:The formula of tonifying the kidney and removing stasis can improve the nutritional status and quality of life of patients with liver and kidney yin deficiency and blood stasis obstruction in hemodialysis combined with osteoporosis.

A recombinant adenovirus(rAd)for expression of Mycobacterium tuberculosis(M.tb)c-di-AMP phosphodiesterase CnpB was constructed,and its induced humoral immune response was detected.The codon-optimized gene of M.tb CnpB was cloned into the adenoviral plasmid pcADV.The recombinant plasmid pcADV-CnpB was transfected into HEK293T cells,and expression was detected with Western blot.The recombinant plasmid pcADV-CnpB and the backbone plasmid were co-transfected into HEK293T cells to obtain the recombinant adenovirus rAd-CnpB.rAd-CnpB was amplified in HEK293T cells,and the target protein expression of rAd-CnpB was detected with Western blot and immunofluorescence.Mice were immunized with rAd-CnpB intranasally,and their sera and bronchoalveolar lavage fluid(BALF)were collected.ELISA was used to detect levels of antigen-specific antibodies.Restriction enzyme digestion and sequencing indicated that the recombinant plasmid pcADV-CnpB was successfully constructed and led to protein expression in eukaryotic cells.rAd-CnpB was packaged and produced in HEK293T cells.After amplification and purification,rAd-CnpB with a titer of 5.53×1010 PFU/mL was obtained.rAd-CnpB led to CnpB expression in HEK293T cells.Intranasal immunization with rAd-CnpB increased levels of IgG and secretory IgA in BALF and led to high levels of IgG in sera.rAd-CnpB,the recombinant adenovirus for expression of c-di-AMP phosphodiesterase CnpB was successfully constructed,and was found to induce antigen-specific humoral and mucosal immune responses through mucosal immunization.Thus,rAd-CnpB may be used in further research on new TB vaccine strategies.

This study assessed the role and mechanism of the recombinant Bacillus Calmette-Gue?rin vaccine(rBCG)with c-di-AMP adjuvant in regulating metabolism and immunity in epididymal white adipose(eWAT)in mice.Male C57BL/6 mice were intravenously immunized with BCG and rBCG,and their body weights were monitored.eWAT was isolated from the mice,and the stromal vascular fractions(SVFs)cell number was counted with a hemocytometer.Sections of mouse adipose tissue were prepared,and the size,number,and morphology of eWAT adipocytes and crown-like structure(CLS)formation were compared under a microscope after HE staining.The transcription levels of lipid metabolism-associated factors,cytokines and aging-associated genes in each group were determined with qRT-PCR.The body weights of mice gradually increased after immunization with BCG and rBCG.The proportions of eWAT increased,and the SVFs cell number decreased,in rBCG immunized mice.HE staining indicated that BCG immunization promoted hyperplasia,whereas rBCG immunization promoted hypertrophy of eWAT adipocytes;moreover,both BCG and rBCG immunization induced CLS formation in eWAT.The qRT-PCR results indicated that rBCG immunization inhibited the expression of genes associated with lipolysis and energy expenditure in eWAT.BCG immunization had little effect on cytokine transcription,whereas rBCG significantly induced the transcription of IFN-γ and IL-1Ra,and inhibited that of IL-15 and IL-2,but did not induce the expression of aging-associated genes.Thus,rBCG immunization induced eWAT adipocyte hypertrophy,which was associated with the inhibition of eWAT lipolysis and the regulation of cytokine expression.

Based on the theory of circulation of qi,a theoretical model of the circulation of phase fire in the human body was con-structed.It is proposed that cancer toxicity is the key factor that triggers the disorder of phase fire and hinders the circulation of phase fire.The disorder of phase fire and poor circulation are important pathogenesis of the occurrence and development of cancer toxicity.With the principle of strengthening healthy qi and eliminating evil qi,the Wenzi Jiedu method is used to treat tumors,which plays an important role in warming and nourishing,regulating yin and yang,and eliminating cancer toxicity.The combination of war-ming,nourishing and detoxification can promote the return of the phase fire and make the human body's generation and transformation active,providing a new treatment idea for TCM diagnosis and treatment of tumors with mainly cold poison or mixed cold and heat.

Objective:To investigate the effects of psychological state on the setup errors of radiotherapy for breast cancer patients.Methods:A prospective cohort study was conducted. A total of 193 breast cancer patients in Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College from October 2022 to May 2023 were selected. Radiotherapy was performed after fixation with an integrated multi-functional device for the head, chest and abdomen. Psychological status of patients was assessed by using 9-item health questionnaire (PHQ-9) and generalized anxiety disorder 7 self-rating scale (GAD-7) before first radiotherapy, the 10th radiotherapy and the last radiotherapy. Based on the results of the questionnaires, patients were divided into psychological problem (anxiety or depression) group and non-psychological problem group. The general data and setup errors of radiotherapy in both groups were compared.Results:All the 193 patients were female, with a median age of 47 years. There were 53 patients in psychological problem group and they underwent a total of 507 image-guided procedures, with setup errors [ M ( Q1, Q3)] of 0.18 (0.07, 0.33), 0.20 (0.10, 0.33) and 0.19 (0.09, 0.30) in the left-right (X), superior-inferior (Y), and anterior-posterior (Z) directions, respectively; the remaining 140 patients in non-psychological problem group underwent 1 240 image-guided procedures, with setup errors [ M ( Q1, Q3)]of 0.17 (0.08, 0.30), 0.20 (0.10, 0.30) and 0.18 (0.09, 0.28) in the X, Y, and Z directions, respectively, and the differences were statistically significant ( Z values were -3.78, -2.00; P < 0.001, P = 0.046). Conclusions:Anxiety and depression have an influence on the setup errors of radiotherapy in patients with breast cancer. In the processs of radiotherapy for breast cancer, it is important to pay attention to the psychological status of patients.

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.