Childhood simple obesity has become a significant public health issue in China. Modern medicine primarily relies on lifestyle interventions and often suffers from poor long-term compliance， while pharmacological options are limited and associated with potential adverse effects. Traditional Chinese Medicine （TCM） has a long history in the prevention and management of this condition， demonstrating eight distinct advantages， including systematic theoretical foundation， diversified therapeutic approaches， definite therapeutic efficacy， high safety profile， good patient compliance， comprehensive intervention strategies， emphasis on prevention， and stepwise treatment protocols. Additionally， TCM is characterized by six distinctive features： the use of natural medicinal substances， non-invasive external therapies， integration of medicinal dietetics， simple exercise regimens， precise syndrome differentiation， and diverse dosage forms. By combining internal and external treatments， TCM facilitates individualized regimen adjustment and holistic regulation， demonstrating remarkable effects in improving obesity-related metabolic indicators， regulating constitutional imbalance， and promoting healthy behaviors. However， challenges remain， such as inconsistent operational standards， insufficient high-quality clinical evidence， and a gap between basic research and clinical application. Future efforts should focus on accelerating the standardization of TCM diagnosis and treatment， conducting multicenter randomized controlled trials， and fostering interdisciplinary integration， so as to enhance the scientific validity and international recognition of TCM in the prevention and treatment of childhood obesity.

The incidence of vascular compression in the neck caused by an elongated styloid process is relatively low.However,it is an important and non-negligible factor because this condition can lead to transient ischemic attacks,carotid artery dissection,cerebral infarction,narrowing of the jugular vein,and even increased intracranial pressure.The clinical manifestations are diverse,which can easily lead to missed or misdiagnoses.Moreover,an elongated styloid process may also affect the therapeutic outcome of carotid artery dissection.In patients with carotid artery dissection who lack common high-risk factors,or in cases where conventional examinations cannot explain the causes of impaired Venous drainage,the possibility of an elongated styloid process should be considered.When diagnosing vascular compression in the neck caused by an elongated styloid process,it is important to consider specific head positions and be vigilant to avoid false negatives.A comprehensive assessment should be made using a variety of diagnostic tools,including carotid artery ultrasound,CTA,MRI,and DSA.There is currently no unified consensus on the treatment of vascular compression in the neck caused by an elongated styloid process.In patients with carotid artery dissection that cannot be explained by other causes and where the dissection site is closely related to the styloid process,styloidectomy should be considered.Additionally,it is crucial to guide patients to avoid head positions that may exacerbate the condition during the perioperative period.

The incidence of vascular compression in the neck caused by an elongated styloid process is relatively low.However,it is an important and non-negligible factor because this condition can lead to transient ischemic attacks,carotid artery dissection,cerebral infarction,narrowing of the jugular vein,and even increased intracranial pressure.The clinical manifestations are diverse,which can easily lead to missed or misdiagnoses.Moreover,an elongated styloid process may also affect the therapeutic outcome of carotid artery dissection.In patients with carotid artery dissection who lack common high-risk factors,or in cases where conventional examinations cannot explain the causes of impaired Venous drainage,the possibility of an elongated styloid process should be considered.When diagnosing vascular compression in the neck caused by an elongated styloid process,it is important to consider specific head positions and be vigilant to avoid false negatives.A comprehensive assessment should be made using a variety of diagnostic tools,including carotid artery ultrasound,CTA,MRI,and DSA.There is currently no unified consensus on the treatment of vascular compression in the neck caused by an elongated styloid process.In patients with carotid artery dissection that cannot be explained by other causes and where the dissection site is closely related to the styloid process,styloidectomy should be considered.Additionally,it is crucial to guide patients to avoid head positions that may exacerbate the condition during the perioperative period.

This study was aimed at establishing a method of ultra-fast quantitative PCR for Brucella detection.We used an exogenous recombinant plasmid as the internal reference and targeted the T4SS secretion system,an important Brucella viru-lence factor,to design specific primers and probes.The sensitivity,specificity,and repeatability of this method were evaluated,and a standard curve was constructed.The coincidence rate of detection findings with this method versus quantitative PCR was determined.This method markedly decreased the detection time to only 10 minutes.The standard curve demonstrated a good linear relationship(Y=-3.410 7x+38.357,R2=0.998 5)with a low minimum detection limit of 10 copies/μL.The method exhibited good specificity and did not specifically amplify several common clinical bacteria other than Brucella.The de-tection of three concentrations of positive plasmids yielded coefficients of variation(CVs)of 0.20％to 0.91％,thus demonstra-ting the method's excellent repeatability.Furthermore,140 clinical samples were analyzed concurrently with the fluorescence PCR method,which yielded a 100％compliance rate and consistent results.Our findings indicated that the Brucella ultra-fast quantitative PCR was ultrafast;had high sensitivity,high specificity,and good specificity;and can be used for the clinical de-tection of Brucella and emergency investigation of epidemics.Therefore,this method is valuable for the early diagnosis of Bru-cella.

Aim To investigate the expression of al-pha-enolase 1(ENO1)in FLT3-mutated acute myeloid leukemia(AML)and its impact on prognosis,as well as to assess the influence of ENO1 on the antitumor effects of FLT3 inhibitors.Methods Data from the Cancer Genome Atlas(TCGA)and Gene Expression Omnibus(GEO)databases were analyzed to compare the expression differences of ENO1 in various tumors and normal tissues.ENO1 knockdown cells were con-structed using the AML cell line MOLM13.The impact of ENO1 on AML cell proliferation,apoptosis,and drug sensitivity was evaluated through CCK-8 assays,flow cytometry,drug synergy experiments,transcriptome se-quencing,and lipid peroxide and reactive oxygen spe-cies(ROS)levels were detected.Results The ex-pression level of ENO1 was significantly elevated in FLT3 internal tandem duplication mutation(FLT3-ITD)positive AML patients and was associated with poor prognosis.Knockdown of ENO1 significantly in-hibited AML cell proliferation and induced apoptosis.Inhibition of ENO1 significantly increased the chemo-sensitivity of AML cells to FLT3 inhibitors.Transcrip-tome sequencing analysis revealed differential expres-sion of genes in the NADPH oxidase-related pathway following ENO1 knockdown,and a positive correlation between ENO1 and glutathione peroxidase 4(GPX4)expression.Inhibition of ENO1 significantly increased the levels of lipid peroxides and ROS induced by FLT3 inhibitors.Conclusions High expression of ENO1 is significantly associated with poor prognosis in FLT3(+)AML.Inhibition of ENO1 can enhance the anti-tumor effects of FLT3 inhibitors by regulating the an-tioxidant defense capacity of AML cells,providing a new target and therapeutic strategy for the treatment of FLT3/ITD(+)AML.

Aim To investigate the expression of al-pha-enolase 1(ENO1)in FLT3-mutated acute myeloid leukemia(AML)and its impact on prognosis,as well as to assess the influence of ENO1 on the antitumor effects of FLT3 inhibitors.Methods Data from the Cancer Genome Atlas(TCGA)and Gene Expression Omnibus(GEO)databases were analyzed to compare the expression differences of ENO1 in various tumors and normal tissues.ENO1 knockdown cells were con-structed using the AML cell line MOLM13.The impact of ENO1 on AML cell proliferation,apoptosis,and drug sensitivity was evaluated through CCK-8 assays,flow cytometry,drug synergy experiments,transcriptome se-quencing,and lipid peroxide and reactive oxygen spe-cies(ROS)levels were detected.Results The ex-pression level of ENO1 was significantly elevated in FLT3 internal tandem duplication mutation(FLT3-ITD)positive AML patients and was associated with poor prognosis.Knockdown of ENO1 significantly in-hibited AML cell proliferation and induced apoptosis.Inhibition of ENO1 significantly increased the chemo-sensitivity of AML cells to FLT3 inhibitors.Transcrip-tome sequencing analysis revealed differential expres-sion of genes in the NADPH oxidase-related pathway following ENO1 knockdown,and a positive correlation between ENO1 and glutathione peroxidase 4(GPX4)expression.Inhibition of ENO1 significantly increased the levels of lipid peroxides and ROS induced by FLT3 inhibitors.Conclusions High expression of ENO1 is significantly associated with poor prognosis in FLT3(+)AML.Inhibition of ENO1 can enhance the anti-tumor effects of FLT3 inhibitors by regulating the an-tioxidant defense capacity of AML cells,providing a new target and therapeutic strategy for the treatment of FLT3/ITD(+)AML.

Numerous studies have shown that depression is main-ly associated with the abnormal expression of connexin 43(Cx43)in astrocytes(Astro)and its mediated dysfunction of gap junction(GJ).However,the molecular mechanism of post-translational modifications targeting Cx43 to regulate neuroin-flammation-associated depression is still unclear.Post-transla-tional modifications of Cx43 mainly include phosphorylation of specific amino acid sites by PKC,PKA,PKG,MAPK and PTK,and protein degradation of Cx43 through the K48/K63 polyubiq-uitylation and deubiquitination pathways,which ultimately lead to protein degradation through K48/K63 polyubiquitination and deubiquitination.These modifications are ultimately involved in the regulation of neuroinflammatory responses through the associ-ation of GJ function.In this paper,we systematically review the role of Cx43 post-translational modifications in neuroinflamma-tion,with the aim of further exploring the potential application of targeting these modifications to modulate the inflammatory re-sponse mechanism in improving depressive symptoms.

Objective:To explore the risk factors of adverse events during the perioperative period of transurethral resection of bladder tumor(TURBT)in bladder cancer patients with coronary atherosclerotic heart disease(CAD).Methods:We retrospectively analyzed the clinical data of bladder cancer patients who underwent TURBT in Beijing Anzhen Hospital from June 2022 to September 2024.All patients with bladder cancer and CAD underwent coronary computed tomography angiography(CCTA)for diagnosis and assessment of CAD before surgery.Based on the CCTA results,the patients with bladder cancer and CAD were divided into two groups:those with mild to moderate coronary stenosis and those with severe coronary stenosis.The severe coronary stenosis group was further divided into two subgroups based on whether they received low-molecular-weight heparin(LMWH)bridging therapy or continued their anti-platelet treatment before surgery.Perioperative anticoagulation and antiplatelet strategies were adjusted according to the opinions of the specialists.The incidence of adverse events within 30 days postoperative-ly was followed up and analyzed.Results:A total of 80 bladder cancer patients with CAD who underwent TURBT were included in the study.Among the 80 patients with CAD,55(68.8％)had mild to moder-ate coronary stenosis,and 25(31.2％)had severe coronary stenosis.Compared with those had mild to moderate coronary stenosis,the patients who had severe coronary stenosis had a higher incidence of post-operative bleeding and pulmonary embolism,although the differences were not statistically significant(P＞0.05).However,the incidence of postoperative myocardial infarction was significantly higher in the patients who had severe coronary stenosis(P=0.034).Among the patients with severe coronary stenosis,8(32.0％)received LMWH bridging therapy before TURBT,and 17(68.0％)continued their previous antiplatelet treatment.Compared with those who continued antiplatelet treatment,the patients who re-ceived LMWH bridging therapy had a higher incidence of postoperative bleeding and pulmonary embo-lism,although the differences were not statistically significant(P＞0.05).However,the incidence of postoperative myocardial infarction was significantly higher in the LMWH bridging group(P=0.032).Conclusion:Patients with mild-to-moderate coronary stenosis demonstrate relatively low perioperative risk during TURBT procedures and may safely undergo TURBT following antiplatelet therapy discontinuation.Conversely,those with severe coronary stenosis exhibit significantly higher perioperative risk and require intensive monitoring.In bladder cancer patients with concomitant severe coronary stenosis,perioperative LMWH bridging therapy is associated with increased myocardial infarction risk,whereas continued anti-platelet therapy does not elevate postoperative bleeding risk.Current evidence therefore supports maintai-ning antiplatelet therapy in these patients,with appropriate bleeding risk assessment.

Numerous studies have shown that depression is main-ly associated with the abnormal expression of connexin 43(Cx43)in astrocytes(Astro)and its mediated dysfunction of gap junction(GJ).However,the molecular mechanism of post-translational modifications targeting Cx43 to regulate neuroin-flammation-associated depression is still unclear.Post-transla-tional modifications of Cx43 mainly include phosphorylation of specific amino acid sites by PKC,PKA,PKG,MAPK and PTK,and protein degradation of Cx43 through the K48/K63 polyubiq-uitylation and deubiquitination pathways,which ultimately lead to protein degradation through K48/K63 polyubiquitination and deubiquitination.These modifications are ultimately involved in the regulation of neuroinflammatory responses through the associ-ation of GJ function.In this paper,we systematically review the role of Cx43 post-translational modifications in neuroinflamma-tion,with the aim of further exploring the potential application of targeting these modifications to modulate the inflammatory re-sponse mechanism in improving depressive symptoms.

With the rapid development of generative artificial intelligence(GAI)technologies,their widespread application in academic research and writing is continuously expanding the boundaries of sci-entific inquiry.However,this trend has also raised a series of ethical and regulatory challenges,inclu-ding issues related to authorship,content authenticity,citation accuracy,and accountability.In light of the growing involvement of AI in generating academic content,establishing an open,controllable,and trustworthy ethical governance framework has become a key task for safeguarding research integrity and maintaining trust within the academic community.This expert consensus outlines ethical requirements across key stages of AI-assisted academic writing-including topic selection,data management,citation practices,and authorship attribution.It aims to clarify the boundaries and ethical obligations surrounding AI use in academic writing,ensuring that technological tools enhance efficiency without compromising in-tegrity.The goal is to provide guidance and institutional support for building a responsible and sustainable research ecosystem.