In recent years, the rising prevalence of obesity and its associated metabolic syndromes has emerged as a critical global public health concern. Sustained weight loss exceeding 10% of total body weight has been shown to ameliorate obesity-related comorbidities, including type 2 diabetes mellitus, hypertension, and hepatic steatosis. Recently, the potential of brown adipose tissue (BAT) to improve metabolism has garnered significant attention. However, evidence regarding weight loss therapies that promote BAT activation remains limited in preclinical models and is even scarcer in clinical studies, partly due to the paucity of appropriate BAT assessment techniques. This review aims to explore the potential impact of various weight loss therapies on BAT, with the goal of providing novel insights and strategies for the treatment of obesity.

ObjectiveTo evaluate the effectiveness of exhalation-inhalation exercise on early pulmonary rehabi-litation for patients with acute exacerbation of chronic obstructive pulmonary disease （AECOPD）. MethodsA total of 120 participants with AECOPD were randomly divided into a treatment group and a control group， with 60 participants in each group. The control group treated with conventional western medicine， while the treatment group received exhalation-inhalation exercise training on the basis of conventional western medicine treatment， with 30 minutes per session and 5 sessions per week. The course of treatment for both groups was 12 weeks. The primary outcome was the 6-minute walking distance （6MWD）. The secondary outcomes included pulmonary function indexes including forced expiratory volume in one second/forced vital capacity （FEV1/FVC）， percentage of predicted forced expiratory volume in one second （FEV1%） and percentage of predicted forced vital capacity （FVC%）， St.George's Respiratory Questionnaire （SGRQ） score， modified Medical Research Council （mMRC） dyspnea scale score， COPD assessment test （CAT） score， hospital anxiety and depression scale-anxiety subscale ［HADS（A）］ score， and hospital anxiety and depression scale-depression subscale ［HADS（D）］ score. Meanwhile， safety of all participants was recorded and assessed. ResultsDuring the treatment， 12 participants dropped out from both the treatment group and the control group， with 48 participants in each group finally included in the analysis. The 6MWD of both groups after treatment was higher than that before treatment， and the 6MWD of the treatment group was higher than that of the control group （P＜0.05 or P＜0.01）. After treatment， the SGRQ score， mMRC score and CAT score of the treatment group were lower than those before treatment， while FEV1%， FVC% and FEV1/FVC were higher than those before treatment （P＜0.05）. Moreover， after treatment， the FEV1/FVC of the treatment group was higher than that of the control group， while the SGRQ score， mMRC score and CAT score were lower than those of the control group （P＜0.05 or P＜0.01）. There was no statistically significant difference in pulmonary function indexes， SGRQ score， mMRC score and CAT score after treatment in the control group （P＞0.05）. No statistically significant difference was observed in HADS（A） score and HADS（D） score after treatment within and between groups （P＞0.05）. The incidence of adverse reactions in the treatment group was 6.25% （3/48）， and 0 in the control group， with no statistically significant difference between groups （P＞0.05）. ConclusionExhalation-inhalation exercise for patients with AECOPD in early pulmonary rehabilitation can improve patients' exercise tole-rance， quality of life， clinical symptoms and pulmonary function， with good safety.

BackgroundIndividuals with schizophrenia are prone to higher rates of hospital readmission， presenting significant clinical challenges and imposing considerable social burdens within the mental health domain. In recent years， various risk prediction models have been developed to forecast readmission in patients with schizophrenia and support clinical decision-making， but their predictive performance and clinical applicability require comprehensive evaluation. ObjectiveTo systematically evaluate the risk prediction models for readmission in patients with schizophrenia， so as to provide insights for the development of high-performance and highly applicable readmission risk prediction models for patients with schizophrenia. MethodsOn July 5， 2025， a systematic literature search was conducted across multiple electronic databases， including PubMed， Embase， Cochrane Library， Web of Science， CINAHL， CNKI， China Biomedical Literature Database， Wanfang Database， and VIP Database， to identify risk prediction models for readmission in patients with schizophrenia. The search period was from the establishment of the databases to July 1， 2025. Two researchers independently performed literature screening， data extraction， risk of bias assessment， and applicability assessment. ResultsA total of 9 studies were included in this review， encompassing 18 risk prediction models for readmission in patients with schizophrenia. Among them， 4 models reported the area under the receiver operating characteristic （ROC） curve （AUC）， ranging from 0.734 to 0.820， 16 models provided AUC values of 0.642–0.879 for internal validation， and 1 model demonstrated an AUC of 0.841 for external validation. Key predictors included disease duration and the concomitant therapy of antipsychotic medications. The risk of bias was assessed as "high" in all included studies. ConclusionThe development of risk prediction models for readmission in patients with schizophrenia remains in an exploratory stage. Although the model exhibits favorable predictive performance， it is associated with a high risk of bias and insufficient performance evaluation.

Objective: To compare the in vitro quality differences of leukoreduced pooled concentrated platelets prepared from whole blood preserved at different temperatures and for various durations, determine the safe time window for refrigerated whole blood in platelet preparation, and provide experimental evidence for optimizing blood component preparation procedures and improving the comprehensive utilization rate of blood resources. Methods: A total of 324 units of 400 mL ACD-B anticoagulated whole blood were randomly divided into two groups and stored at 4℃ and 22℃, respectively. The buffy coat was separated at three time intervals: <6 h, 6-12 h, and >12 h (≤18 h) post-collection, and allowed to rest overnight at 22℃. On the following day, the buffy coats from each group were pooled to prepare leukoreduced pooled platelet concentrates (LPPCs). Cell counts were performed, and metabolic parameters including pH, glucose, and lactate levels were measured to evaluate metabolic status. Platelet in vitro function and activation were assessed by thromboelastography (TEG), platelet aggregation rate, and the expression of PAC-1 and CD62P. The differences between the two groups were compared. Results: For pooled concentrated platelets prepared from whole blood stored at 4℃ and 22℃ for <6 h and 6-12 h, there were no significant differences in platelet count, pH, glucose levels, lactic acid levels, thromboelastography (TEG), platelet aggregation rate, or platelet activation rate (P>0.05). With prolonged refrigeration time of whole blood, compared with pooled concentrated platelets prepared from whole blood stored at 22℃ for >12 h but ≤18 h, those prepared from whole blood stored at 4℃ for >12 h but ≤18 h showed a decreased platelet count (1 152.83±180.08 vs 1 368.83±134.86, P=0.040), a significantly increased ADP-induced aggregation rate (26.82±6.59 vs 13.88±10.21, P=0.030), and significantly elevated expression rates of PAC-1 and CD62P (72.64±6.74 vs 63.28±5.97, P=0.030). However, there were no significant differences in pH, glucose content, lactate content, or thromboelastography (P>0.05). Conclusion: There was no significant difference in the in vitro count, function, or activation of pooled concentrated platelets prepared from whole blood stored at 4℃ and 22℃ within 12 hours. However, statistically significant differences were observed between the mixed concentrated platelets prepared from whole blood stored at 4℃ and those stored at 22℃ for more than 12 hours but not exceeding 18 hours. These findings can provide a reference for the preparation methods and clinical application of refrigerated platelets.

ObjectiveTo investigate the effect of Semaphorin 3A （Sema3A） on the progression of pathological cardiac hypertrophy. MethodsWild-type C57BL 6J mice， Sema3A global overexpressing （Sema3A/Cre-ER^TM） mice， and their littermate controls （Cre-ER^TM） were used， with 6 mice per group. A pressure-overload induced cardiac hypertrophy model was established via transverse aortic constriction （TAC）， with a sham-operated group （Sham） as the control. Cardiac hypertrophy was assessed by gross morphology， heart weight/body weight ratio （HW/BW）， heart weight/tibia length ratio （HW/HL）， and heart weight/lung weight ratio （HW/PW）. Cardiac function was evaluated by measuring ejection fraction （EF） and fractional shortening （FS） via echocardiography. In heart tissues， the mRNA level of atrial natriuretic peptide （ANP） and Sema3A were detected by RT-qPCR， Sema3A protein level was detected by western blot， morphological structure was detected by hematoxylin and eosin （HE） staining， level of fibrosis was detected by Masson’s trichrome staining， and angiogenesis was detected by immunohistochemical detection of CD31. For in vitro experiments， rat H9C2 cardiomyocytes were treated with angiotensin Ⅱ （Ang Ⅱ） to induce hypertrophy， with PBS-treated cells as the control. After 48 hours， the mRNA expression of ANP， B-type natriuretic peptide （BNP） and Sema3A were measured by RT-qPCR， and Sema3A protein level was assessed by western blot. ResultsAt the animal level， compared with the sham group， mice subjected to TAC showed significantly increased mRNA levels of ANP in cardiac tissue， as well as markedly elevated mRNA and protein levels of Sema3A （all P<0.05）. Compared with the Cre-ER^TM + TAC group， the Sema3A/Cre-ER^TM + TAC group exhibited more pronounced cardiac hypertrophy， greater ventricular wall thickening， higher HW/BW， HW/HL， and HW/PW ratios， more significant reductions in EF and FS， more severe cardiac fibrosis， and a significant decrease in cardiac CD31 expression levels （all P<0.05）. At the cellular level， compared with the control group， H9C2 cells treated with Ang Ⅱ displayed significantly increased mRNA levels of ANP and BNP， along with markedly elevated mRNA and protein levels of Sema3A （all P<0.05）. ConclusionSema3A promotes the progression of pressure overload-induced cardiac hypertrophy by inhibiting angiogenesis.

Acute lung injury （ALI） is one of the most common and critical diseases in clinical practice， with extremely high morbidity and mortality， seriously threatening human life and health. The pathogenesis of ALI is complex， in which the inflammatory response is a key factor. Studies have shown that NOD-like receptor protein 3 （NLRP3） inflammasomes are involved in ALI through mechanisms such as inflammation induction， increased microvascular permeability， recruitment of neutrophils， oxidative stress， and pyroptosis， playing a key role in the occurrence and progression of ALI. Therefore， regulating NLRP3 inflammasomes and inhibiting the release of inflammatory factors can alleviate the damage in ALI. At present， ALI is mainly treated by mechanical ventilation and oxygen therapy， which have problems such as high costs and poor prognosis. In recent years， studies have shown that traditional Chinese medicine （TCM） can reduce the inflammatory response and the occurrence of oxidative stress and pyroptosis by regulating the NLRP3 inflammasome， thus alleviating the damage and decreasing the mortality of ALI. Based on the relevant literature in recent years， this article reviews the research progress in TCM treatment of ALI by regulating NLRP3 inflammasomes， discusses how NLRP3 inflammasomes participate in ALI， and summarizes the active ingredients， extracts， and compound prescriptions of TCM that regulate NLRP3 inflammasomes， aiming to provide new ideas for the clinical treatment of ALI and the development of relevant drugs.

ObjectiveTo explore the mechanism by which Buyang Huanwutang regulates the glutathione peroxidase 4 （GPX4）-acyl-CoA synthetase long-chain family member 4 （ACSL4） axis to inhibit ferroptosis and promote neurological functional recovery after spinal cord injury （SCI）. MethodsNinety rats were randomly divided into five groups： sham operation group， model group， low-dose Buyang Huanwutang group （12.5 g·kg^-1）， high-dose Buyang Huanwutang group （25 g·kg^-1）， and Buyang Huanwutang + inhibitor group （25 g·kg^-1 + 5 g·kg^-1 RSL3）. The SCI model was established by using the allen method. Tissue was collected on the 7th and 28th days after operation. Motor function was assessed by using the Basso-Beattie-Bresnahan （BBB） scale. Hematoxylin-eosin （HE）， Nissl， and Luxol fast blue （LFB） staining were performed to observe spinal cord histopathology. Transmission electron microscopy was used to examine mitochondrial ultrastructure. Immunofluorescence staining was used to detect the number of NeuN-positive cells and the fluorescence intensity of myelin basic protein （MBP）， GPX4， and ACSL4. Real-time fluorescent quantitative polymerase chain reaction （Real-time PCR） was used to analyze the mRNA expression of GPX4 and ACSL4. Enzyme linked immunosorbent assay （ELISA） was performed to measure the levels of reactive oxygen species （ROS）， malondialdehyde （MDA）， glutathione （GSH）， and superoxide dismutase （SOD）. Colorimetric assays were used to determine the iron content in spinal cord tissue. ResultsCompared to the sham operation group， the model group exhibited significantly reduced BBB scores （P<0.01）， severe pathological damage in spinal cord tissue， and marked mitochondrial ultrastructural disruption. In addition， the model group showed a decrease in the number of NeuN-positive cells （P<0.01）， reduced fluorescence intensity of MBP and GPX4 （P<0.01）， lower levels of GSH and SOD （P<0.01）， and downregulated mRNA expression of GPX4 （P<0.01）. Moreover， compared to the sham operation group， the model group had elevated levels of ROS， MDA， and tissue iron content （P<0.01）， along with increased fluorescence intensity and mRNA expression of ACSL4 （P<0.01）. Compared with the model group and Buyang Huanwutang + inhibitor group， the Buyang Huanwutang group showed significantly improved BBB scores （P<0.05， P<0.01） and exhibited less severe spinal cord tissue damage， reduced edema and inflammatory cell infiltration， increased neuronal survival， and more intact myelin structures. Additionally， mitochondrial ultrastructure was significantly improved in the Buyang Huanwutang group. Compared to the model group and Buyang Huanwutang + inhibitor group， the Buyang Huanwutang group significantly increased the number of NeuN-positive cells and the fluorescence intensity of MBP （P<0.05， P<0.01）. Furthermore， Buyang Huanwutang significantly increased the fluorescence intensity and mRNA expression of GPX4 （P<0.01） and decreased the fluorescence intensity and mRNA expression of ACSL4 （P<0.01） compared to the model group and Buyang Huanwutang + inhibitor group. Finally， the Buyang Huanwutang group significantly decreased ROS， MDA， and tissue iron content （P<0.01） and significantly increased GSH and SOD levels （P<0.01） compared to the model group and Buyang Huanwutang + inhibitor group. ConclusionBuyang Huanwutang inhibits ferroptosis through the GPX4/ACSL4 axis， reduces secondary neuronal and myelin injury and oxidative stress， and ultimately promotes the recovery of neurological function.

Objective To investigate the biomechanical effects of implant-anchored retraction and intrusion of maxillary anterior teeth under different force systems using three-dimensional finite element analysis(3D-FEA),by constructing models simulating both normal periodontium and mild alveolar bone resorption.Methods Cone-beam computed tomography(CBCT)data from a patient with skeletal protrusion and gummy smile was utilized.3D finite element models integrating micro-implants anchorage(MIA)and a straight-wire ap-pliance for en-mass retraction of maxillary anterior teeth were established using Mimics,Geomagic,SolidWorks,and Ansys software.Six experimental groups were designed based on alveolar bone height and vertical positioning of posterior MIA.Groups A1,A2,A3:Normal alveolar bone height.Groups B1,B2,B3:Mild alveolar bone resorption.Posterior MIA were placed between the first molar and second premolar at vertical heights of 4,6,and 8 mm(relative to the cementoenamel junction),respectively,each loaded with 200 g retraction force.Anterior MIA between the central and lateral incisors delivered 50 g intrusion force.Stress distribution,anterior tooth displacement patterns,and torque changes were analyzed and compared across all groups.Results Under varying force conditions,greater torque loss was observed in the anterior teeth of the mild alveolar bone resorption group compared to the periodontally healthy group.Differential displacement patterns emerged among central incisors,lateral incisors,and canines when posterior MIA were placed at different vertical heights.The center of resistance in the resorption group shifted apically,resulting in undesirable extrusion and com-promised torque control during intrusion-retraction of maxillary anterior teeth.Conclusion Anterior torque control is more challenging in the alveolar bone resorption group than in the periodontally normal group.Elevating posterior MIA height promotes bodily movement of central incisors,thereby mitigating the ＂bowing effect＂ to a clinically relevant extent.

Objective To screening and validation of key genes for programmed cell death(PCD)in gout through bioinformatics and machine learning and immunoinfiltration analysis.Methods Gout-related datasets were obtained from the Gene Expression Omnibus(GEO)database,comprising the human gout dataset GSE160170 and murine gout dataset GSE190138,which served as the training cohort.Differentiall expression genes(DEGs)were screened with difference factor>2 and P<0.05.The DEGs of two data sets were intersected to obtain the common DEGs(co-DEGs).The co-DEGs were enriched by GO function and KEGG pathway analysis.The combination of co-DEGs and PCD related gene set was used to obtain PCD related DEGs.A PPI network was built in the STRING database.The key module genes were screened in Cytoscape's MCODE,the hub genes were screened in 12 algorithms built into the Cytohubba plugin,including Degree,MCC,DMNC,MCN,EPC,BottleNeck,EcCentricity,closness,Radiality,Betweeness,Stress and Clusteringcoefficoent,the common genes of the two was as candidate genes.The regression model of least absolute shrinkage and selection operator(LASSO)was used to screen key genes in the GSE160170 and GSE190138 data sets respectively,and the intersection of the two was adopted to obtain key genes.The diagnostic value of key genes in gout was evaluated by receiver operating characteristic(ROC)curve.The expression difference of gout related immune cells was investigated by single sample gene set enrichmemt analysis(ssGSEA)immunoinfiltration analysis.Finally,blood samples from 30 gout patients admitted to the Department of Rheumatology,Xi'an Fifth Hospital from February to April 2024 were collected as the experimental group,while blood samples from 30 healthy subjects were collected as the control group.RNA was extracted from the Peripheral blood mononuclear cell(PBMC).Quantitative real time polymerase chain reaction(RT-qPCR)was used to validate the expression of key genes in clinical samples.Results 53 common DEGs of GSE160170 and GSE190138 were obtained,among which 43 genes were up-regulated and 10 were down-regulated.GO and KEGG indicated that most genes were involved in cell death,apoptosis,interlenkin(IL)-17 signaling pathway,tumor necrosis facter(TNF)signaling pathway and nucleotide-binding oligomerization domain-(NOD)-like receptor signaling pathway.12 co-DEGs of programmed cell death and gout were obtained.A total of 7 candidate genes were screened.LASSO regression model screened 5 genes and 4 genes respectively in two datasets,and 3 key genes were abtained by the intersection of the two datasets,which were IL-6,plasminogen activator urokinase receptor(PLAUR)and NOD-like receptor thermal protein domain associated protein3(NLRP3).Validation within the training set revealed that all three genes attained perfect diagnostic performance for gout,with area under the ROC(AUC-ROC)curve values of 1.00.Immunoinfiltration analysis showed that the changes of activated CD4+T cells,activated CD8+T cells and natural killer cells were closely related to the occurrence and development of gout.In the clinical samples,compared with the control group,PLAUR,NLRP3 and IL-6 were highly expressed in gout patients,and the differences were statistically significant(t=18.852,9.633,8.293,all P＜0.05).Conclusion IL-6,PLAUR and NLRP3 provide potential biomarkers and therapeutic targets for the diagnosis and treatment of gout,offering new directions in this field.

[Objective]To investigate the effects of puerarin regulation of purinergic receptor P2X ligand-gated ion channel 7(P2X7)/nucleotide-binding oligomeric domain receptor protein 3(NLRP3)pathway on mast cell activity in mice with allergic rhinitis(AR).[Methods]BALB/c mice were randomly divided into normal group,AR group,puerarin low-dose group,puerarin high-dose group,dexamethasone group,puerarin high-dose+P2X7 activator adenosine triphosphate(ATP)group,with 12 mice in each group.Except for normal group and the AR mouse models in the other groups received intraperitoneal ovalbumin-alum sensitization followed by intranasal ovalbumin challenge to induce AR.After successful modeling,the puerarin low-and high-dose groups were intragastrically administered with puerarin at 12.5 mg·kg-1 and 50 mg·kg-1 respectively;the dexamethasone group was intragastrically administered with dexamethasone at 1 mg·kg-1;the puerarin high-dose+ATP group was intragastrically administered with puerarin at 50 mg·kg-1,and simultaneously injected with ATP(7.5×10-3 mmol per mouse)via the tail vein;the normal group and the AR group were given equal amounts of 0.9%sodium chloride solution via both intragastric administration and tail vein injection.The treatment was performed once a day for 14 consecutive days.AR score,serum immunoglobulin E(IgE),leukotriene,histamine,tumor necrosis factor-α(TNF-α),interleukin-18(IL-18)and IL-1β levels were detected.Hematoxylin-eosin(HE)staining was used to detect nasal mucosa pathological Change.The number of mast cells,the number of degranulated mast cells and the degranulated rate were detected by toluidine blue staining.The mean optical density of Tryptase expression in nasal mucosa was detected by immunohistochemical staining.The expressions of P2X7,NLRP3,cleaved-Caspase-1 proteins in nasal mucosa were measured by Western blot.[Results]Compared with normal group,the nasal mucosal epithelium in AR group was significantly thickened,accompanied with a large number of inflammatory cell infiltration and significant mucosal interstitial edema.The levels of AR score,serum IgE,leukotriene,histamine and TNF-α,IL-18,IL-1β were raised(P<0.05).What's more,the number of mast cells and the number of degranulated mast cells were increased,with a corresponding rise in the degranulation rate(P<0.05).The mean optical density of Tryptase expression,as well as the expressions of P2X7,NLRP3 and cleaved-Caspase-1 in nasal mucosa were all amplified(P<0.05).Compared with AR group,the pathological injury of nasal mucosa in puerarin low-dose group,puerarin high-dose group and dexamethasone group was reduced.The levels of AR score,serum IgE,leukotriene,histamine,TNF-α,IL-18 and IL-1β were decreased.Additionally,the number of mast cells and the number of degranulated mast cells were reduced,with a corresponding decrease in the degranulation rate.The mean optical density of Tryptase expression,as well as the expressions of P2X7,NLRP3 and cleaved-Caspase-1 in nasal mucosa were also diminished(P<0.05).Compared with the puerarin high-dose group,the puerarin high-dose+ATP group showed more severe pathological damage to nasal mucosal tissues.The AR score,serum levels of IgE,leukotrienes,histamine,TNF-α,IL-18 and IL-1β were increased.Meanwhile,the number of mast cells and degranulated mast cells,the degranulation rate were significantly added,and the mean optical density of Tryptase expression,and the expressions of P2X7,NLRP3 and cleaved-Caspase-1 in nasal mucosa tissues were all amplified(P<0.05).[Conclusion]Puerarin may reduce the activity of mast cells in AR model mice by inhibiting the P2X7/NLRP3 pathway.