Functional dyspepsia (FD), characterized by persistent or recurrent dyspeptic symptoms without identifiable organic, systemic or metabolic causes, is an increasingly recognized global health issue. The objective of this guideline is to equip clinicians and nursing professionals with evidence-based strategies for the management and treatment of adult patients with FD using traditional Chinese medicine (TCM). The Guideline Development Group consulted existing TCM consensus documents on FD and convened a panel of 35 clinicians to generate initial clinical queries. To address these queries, a systematic literature search was conducted across PubMed, EMBASE, the Cochrane Library, China National Knowledge Infrastructure (CNKI), VIP Database, China Biology Medicine (SinoMed) Database, Wanfang Database, Traditional Medicine Research Data Expanded (TMRDE), and the Traditional Chinese Medical Literature Analysis and Retrieval System (TCMLARS). The evidence from the literature was critically appraised using the Grading of Recommendations Assessment, Development, and Evaluation (GRADE) approach. The strength of the recommendations was ascertained through a consensus-building process involving TCM and allopathic medicine experts, methodologists, pharmacologists, nursing specialists, and health economists, leveraging their collective expertise and empirical knowledge. The guideline comprises a total of 43 evidence-informed recommendations that span a range of clinical aspects, including the pathogenesis according to TCM, diagnostic approaches, therapeutic interventions, efficacy assessments, and prognostic considerations. Please cite this article as: Zhang SS, Zhao LQ, Hou XH, Bian ZX, Zheng JH, Tian HH, Yang GH, Hong WS, He YY, Liu L, Shen H, Li YP, Xie S, Shu J, Zeng BF, Li JX, Liu Z, Xiao ZH, Xiao JD, Zheng PY, Huang SG, Chen SL, Fei GJ. International clinical practice guideline on the use of traditional Chinese medicine for functional dyspepsia (2025). J Integr Med. 2025; 23(5):502-518.
Dyspepsia/drug therapy* ; Humans ; Medicine, Chinese Traditional/methods* ; Practice Guidelines as Topic ; Drugs, Chinese Herbal/therapeutic use*

Microglia, the resident immune cells in the central nervous system (CNS), rapidly transition from a resting to an active state in the acute phase of ischemic brain injury. This active state mediates a pro-inflammatory response that can exacerbate the injury. Targeting the pro-inflammatory response of microglia in the semi-dark band during this acute phase may effectively reduce brain injury. Shionone (SH), an active ingredient extracted from the dried roots and rhizomes of the genus Aster (Asteraceae), has been reported to regulate the inflammatory response of macrophages in sepsis-induced acute lung injury. However, its function in post-stroke neuroinflammation, particularly microglia-mediated neuroinflammation, remains uninvestigated. This study found that SH significantly inhibited lipopolysaccharide (LPS)-induced elevation of inflammatory cytokines, including interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), and inducible nitric oxide synthase (iNOS), in microglia in vitro. Furthermore, the results demonstrated that SH alleviated infarct volume and improved behavioral performance in middle cerebral artery occlusion (MCAO) mice, which may be attributed to the inhibition of the microglial inflammatory response induced by SH treatment. Mechanistically, SH potently inhibited the phosphorylation of serine-threonine protein kinase B (AKT), mammalian target of rapamycin (mTOR), and signal transducer and activator of transcription 3 (STAT3). These findings suggest that SH may be a potential therapeutic agent for relieving ischemic stroke (IS) by alleviating microglia-associated neuroinflammation.
Animals ; Microglia/immunology* ; Mice ; Male ; Mice, Inbred C57BL ; Brain Ischemia/immunology* ; Neuroinflammatory Diseases/drug therapy* ; Neuroprotective Agents/administration & dosage* ; Interleukin-1beta/genetics* ; STAT3 Transcription Factor/genetics* ; TOR Serine-Threonine Kinases/genetics* ; Tumor Necrosis Factor-alpha/genetics* ; Proto-Oncogene Proteins c-akt/immunology* ; Nitric Oxide Synthase Type II/genetics* ; Lipopolysaccharides

OBJECTIVE: The study aim was to investigate the effects of exposure to multiple environmental organic pollutants on cardiopulmonary health with a focus on the potential mediating role of oxidative stress. METHODS: A repeated-measures randomized crossover study involving healthy college students in Beijing was conducted. Biological samples, including morning urine and venous blood, were collected to measure concentrations of 29 typical organic pollutants, including hydroxy polycyclic aromatic hydrocarbons (OH-PAHs), bisphenol A and its substitutes, phthalates and their metabolites, parabens, and five biomarkers of oxidative stress. Health assessments included blood pressure measurements and lung function indicators. RESULTS: Urinary concentrations of 2-hydroxyphenanthrene (2-OH-PHE) ( β = 4.35% [95% confidence interval ( CI): 0.85%, 7.97%]), 3-hydroxyphenanthrene ( β = 3.44% [95% CI: 0.19%, 6.79%]), and 4-hydroxyphenanthrene (4-OH-PHE) ( β = 5.78% [95% CI: 1.27%, 10.5%]) were significantly and positively associated with systolic blood pressure. Exposures to 1-hydroxypyrene (1-OH-PYR) ( β = 3.05% [95% CI: -4.66%, -1.41%]), 2-OH-PHE ( β = 2.68% [95% CI: -4%, -1.34%]), and 4-OH-PHE ( β = 3% [95% CI: -4.68%, -1.29%]) were negatively associated with the ratio of forced expiratory volume in the first second to forced vital capacity. These findings highlight the adverse effects of exposure to multiple pollutants on cardiopulmonary health. Biomarkers of oxidative stress, including 8-hydroxy-2'-deoxyguanosine and extracellular superoxide dismutase, mediated the effects of multiple OH-PAHs on blood pressure and lung function. CONCLUSION Exposure to multiple organic pollutants can adversely affect cardiopulmonary health. Oxidative stress is a key mediator of the effects of OH-PAHs on blood pressure and lung function.
Humans ; Oxidative Stress/drug effects* ; Male ; Cross-Over Studies ; Female ; Young Adult ; Environmental Pollutants/toxicity* ; Environmental Exposure/adverse effects* ; Biomarkers/blood* ; Adult ; Blood Pressure/drug effects* ; Polycyclic Aromatic Hydrocarbons/urine* ; Beijing

Spine fracture and dislocation are common traumatic spinal conditions that often require surgical intervention due to compromised spinal stability. Surgical approaches include anterior, posterior, and combined anterior-posterior spinal procedures. According to the specific surgical requirements, patients may be placed in the prone position or repositioned between prone and supine positions during surgery. Intraoperative repositioning has become an essential step in patient positioning. However, during repositioning, patients with spinal fracture and dislocation are at increased risk for complications such as hemodynamic instability, nerve injury, and pressure injuries to the skin and soft tissue. Notably, due to the instability of the spinal cord, even minor manipulations can further exacerbate the damage, potentially leading to severe outcomes like paraplegia. Although the current clinical guidelines provide instructive recommendations for standard position, there remains no specific protocols for intraoperative repositioning in patients with spine fracture and dislocation. With a concern for the lack of clinical studies on positioning techniques, risk prevention, and operational norms for special patients, no applicable guidelines or standards are available. A consensus was required to provide clinical reference, meet the requirements of surgical treatment, and minimize the safety risks of patients caused by improper placement of positions. Professional Committee of Operating Room Nursing of Shaanxi Nursing Association organized experts in nursing management and operating room nursing from major hospitals across China to formulate Expert consensus on intraoperative repositioning for patients with spinal fracture and dislocation ( version 2025). The consensus provides 11 recommendations covering pre-repositioning preparation, intraoperative maneuvers, and post-repositioning observation, aiming to provide references for clinical standardization of the intraoperative repositioning process and protection of patients′ safety.

Objective To explore the effect of galangin(GAL)on bone metabolism by regulating Hippo/Yes associated protein(YAP)signaling pathway in rats with diabetic osteoporosis(DOP).Methods 90 female SD rats were randomly divided into normal control(NC)group,model(Mod)group,low-dose GAL(GAL-L)group,high-dose GAL(GAL-H)group,and high-dose GAL+YAP inhibitor Verteporfin(GAL-H+Verteporfin)group,with 18 rats in each group.Dual energy X-ray was used to detect bone mineral density(BMD).Three-point bending assay was used to evaluate the biomechanics of femur.HE staining was used to test the pathological changes in femoral tissue.ELISA was used to detect serum levels of osteocalcin(OC),alkaline phosphatase(ALP),and tartaric-resistant acid phosphatase(TRAP).Western blot was used to evaluate the expression of YAP protein in femoral tissue.Results Compared with NC group,the BMD,maximum load,elastic modulus,OC,ALP,and YAP protein expression of femur were reduced(P<0.05),and the TRAP was increased in Mod group(P<0.05).Compared with Mod group,BMD,maximum load,elastic modulus,OC,ALP and YAP protein expressions of femur were increased(P<0.05),while TRAP was decreased in GAL-L and GAL-H groups(P<0.05),and the improvement was better in GAL-H group.Compared with GAL-H group,femur BMD,maximum load,elastic modulus,OC,ALP and YAP protein expressions of femur were decreased(P<0.05),while TRAP was increased in GAL-H+Verteporfin group(P<0.05).Conclusions GAL may regulate the Hippo/YAP signaling pathway,increase the expression of YAP,regulate bone metabolism in DOP rats,and inhibit bone resorption.

Objective To explore whether creatine therapy regulates neuronal ferroptosis by inhibiting the activation of STAT1 signaling pathway associated with suppressor of cytokine signaling 1(SOCS1)in Alzheimer's disease.Methods Immunohistochemical staining and counting of positive results using paraffin sections of human brain frontal lobes were employed to determine the trend of changes in the target proteins.Further validation was performed by immunofluorescence and Western blotting.STAT1 phosphorylation was inhibited by creatine injection using eleven FAD4T mice and by cerebellar medullary pool puncture,and the expression of target proteins was examined by immunohistochemistry and immunofluorescence after postmortem sampling.Results Compared with the age controls,interferon-γ(IFN-γ),an activating cytokine of the STAT1 signaling pathway,and SOCS1,a negative regulator of STAT1 activation,were both significantly up-regulated,STAT1 phosphorylation was enhanced,and the ferroptosis markers ferritin light chain(FTL)and cystine/glutamate transporter(xCT)increased markedly in the cortex of AD human brains;Creatine treatment of FAD4T mice resulted in a reduction of both IFN-γ and SOCS1,and a significant decrease in the ferroptosis markers FTL and xCT(SLC7A11).Conclusion Creatine ameliorates neuronal ferroptosis in AD model mice by reducing neuronal STAT1-SOCS1 signalling activation.

Osteoarthritis (OA), the most prevalent joint disease of late life, is closely linked to cellular senescence. Previously, we found that the senescence of fibroblast-like synoviocytes (FLS) played an essential role in the degradation of cartilage. In this work, single-cell sequencing data further demonstrated that cartilage acidic protein 1 (CRTAC1) is a critical secreted factor of senescent FLS, which suppresses mitophagy and induces mitochondrial dysfunction by regulating SIRT3 expression. In vivo, deletion of SIRT3 in chondrocytes accelerated cartilage degradation and aggravated the progression of OA. Oppositely, intra-articular injection of adeno-associated virus expressing SIRT3 effectively alleviated OA progression in mice. Mechanistically, we demonstrated that elevated CRTAC1 could bind with NRF2 in chondrocytes, which subsequently suppresses the transcription of SIRT3 in vitro. In addition, SIRT3 reduction could promote the acetylation of FOXO3a and result in mitochondrial dysfunction, which finally contributes to the degradation of chondrocytes. To conclude, this work revealed the critical role and underlying mechanism of senescent FLSs-derived CRTAC1 in OA progression, which provided a potential strategy for the OA therapy.

Objective To design a novel bromodomain-containing protein 4(BRD4)and histone deacetylase(HDAC)dual-target inhibitor(11b),and to elucidate its therapeutic efficacy and mechanisms in suppressing prostate cancer through epigenetic regulation.Methods BRD4 and HDAC expression levels were assessed via immunohistochemistry(IHC)using prostate cancer tissue microarrays.The inhibitory activity of 11b was screened across three prostate cancer cell lines,with the half-maximal inhibitory concentration(IC50)determined by CCK-8 assay.Western blot was employed to analyze changes in the expression of target proteins,including BRD4,c-Myc proto-oncogene protein(c-Myc),and Ac-H3K27,with parallel comparisons to single-target agents,including suberoylanilide hydroxamic acid(SAHA),a HDAC inhibitor,and JQ-1,a BRD4 inhibitor.Cell invasion and proliferation were evaluated using Transwell and colony formation assays,and the autophagy mechanism was validated using 3-methyladenine(3-MA),an autophagy inhibitor.A PC-3 xenograft model was established in nude mice.Then,11b(7.5 mg/kg or 15 mg/kg),normal saline,SAHA,and JQ-1 were administered via intraperitoneal injection,and their tumor growth inhibition effects were observed.The percentage of target protein-positive cells and the expression levels of target genes were quantified via IHC and RT-PCR,respectively.Results BRD4 and HDAC expression levels were both higher in tumor tissues than those in normal tissues(P<0.01).11b exhibited the strongest inhibitory activity against PC-3 cells(IC50=8.28 μmol/L),outperforming SAHA(22.61 μmol/L)and JQ-1(22.09 μmol/L).Treatment with 11b reduced BRD4 and c-Myc expression by(41.58±3.28)%and(63.21±6.91)%,respectively(P<0.01),and increased the Ac-H3K27 level to 6.52-fold that of the negative control(NC)group(P<0.01),demonstrating greater modulation than either SAHA or JQ-1 did.The in vitro experiment showed that 8 μmol/L 11b treatment reduced PC-3 colony formation and migration by 97.5%and 96.3%,respectively(P<0.001),and co-treatment with 3-MA reversed its cytotoxic effects.The in vivo experiment showed that 11b at both 7.5 mg/kg and 15 mg/kg significantly reduced tumor volume and weight compared with the control,SAHA,and JQ-1 groups(all P<0.01),with the proportion of percentage of target protein-positive cells and the expression of target genes showing trends consistent with in vitro findings.Conclusion The dual-target inhibitor 11b exerts potent antitumor effects in prostate cancer by synergistically modulating the BRD4/HDAC pathways.11b demonstrates therapeutic efficacy superior to that of the single-target agents SAHA and JQ-1 in suppressing prostate cancer progression,highlighting its potential for clinical translation.

Objective To analyze the effect of Hsa-circ-0101216 on gemcitabine(GEM)chemotherapy resistance in pancreatic cancer and its mechanism.Methods Differentially expressed circRNAs between GEM-resistant pancreatic cancer cells and parent cells were screened using the GEO database.Pancreatic cancer GEM resistant cell lines(BxPC-3-GEM and Capan-1-GEM)were constructed by intermittent concentration gradient method.qRT-PCR was used to detect the expression of Hsa-circ-0101216 in cells.GEM resistant pancreatic cancer cell lines were taken and divided into sh-circ-0101216 group(knockdown of circ-0101216),sh-NC group(transfected with sh-NC),and blank control group(untreated).CCK-8 assay and EdU proliferation assay were used to detect the half inhibitory concentration(IC50)of GEM and proliferation ability of cells in each group.Western blotting was performed to detect the expression of multidrug resistance-related protein 1(MRP1),breast cancer resistance protein(BCRP),and human equilibrative nucleoside transporter-1(hENT-1).A subcutaneous xenograft tumor model of human pancreatic cancer in nude mice was constructed,and sh-NC+GEM group and sh-circ-0101216+GEM group(n=6)were set up.The volume and weight of xenograft tumor in nude mice were compared between the two groups.Western blotting and immunohistochemistry were used to detect the expression of MRP1,BCRP,and hENT-1 proteins in xenograft tumor tissues,and EDU proliferation assay was used to detect the proliferation ability of tumor cells.Results The GEO database screening showed that Hsa-circ-0101216 was up-regulated in GEM-resistant pancreatic cancer cell lines.Pancreatic cancer GEM-resistant cell lines were successfully constructed,and the expression levels of Hsa-circ-0101216 and the IC50 value in GEM-resistant pancreatic cancer cells BxPC-3-GEM and Capan-1-GEM were significantly higher than those in parental cells(P<0.05).In sh-circ-0101216 group,the IC50 values of GEM,cell viability,EdU positivity rate,and the expression levels of MRP1 and BCRP proteins in GEM-resistant pancreatic cancer cells BxPC-3-GEM and Capan-1-GEM were significantly lower than those in blank control group and sh-NC group,while the expression level of hENT-1 protein was significantly higher(P<0.05 or P<0.001).In sh-circ-0101216+GEM group,the weight and volume of subcutaneous xenograft tumors in nude mice,the expression levels and positive expression rates of MRP1 and BCRP proteins in tumor tissues,and the EdU positive rate were significantly lower than those in sh-NC+GEM group,while the expression level and positive expression rate of hENT-1 protein were significantly higher(P<0.05).Conclusions Hsa-circ-0101216 is highly expressed in GEM-resistant pancreatic cancer cell lines.Its knockdown can inhibit the proliferation of pancreatic cancer cells and enhance the chemosensitivity of pancreatic cancer cells to GEM.The mechanism may be related to the regulation of transmembrane transporter protein expression.

Objective To identify risk factors for postoperative respiratory failure(PORF)in cardiovascular surgery patients using machine learning algorithms and to construct a specific risk prediction model.Methods A retrospective cohort was conducted on 1 623 patients undergoing cardiovascular surgery between 2011 and 2020 from the INSPIRE database.Following data quality analysis,multiple imputation was employed to handle missing data,and the Boruta algorithm was used for feature selection.Eight machine learning models were constructed based on the selected features,including Gradient Boosting Machine(GBM),Generalized Linear Model(GLM),Extreme Gradient Boosting(XGBoost),K-Nearest Neighbors(KNN),Neural Network(NNET),Naive Bayes(NB),Support Vector Machine(SVM),and Random Forest(RF).Model performance was evaluated using metrics including the area under the curve(AUC),sensitivity,and specificity.Variables significantly influencing PORF were identified using the permutation importance algorithm.Results The overall incidence of PORF was 27.05％(439/1 623).The in-hospital mortality rate was significantly higher in the PORF group than the non-PORF group(12.98％vs 1.60％,P<0.001).Among the developed models,the SVM model demonstrated the best performance,achieving an AUC of 0.705 in the testing set,with a sensitivity,specificity,positive predictive value(PPV),and negative predictive value(NPV)of 0.481,0.825,0.504,and 0.812,respectively.Based on feature importance analysis,the top 10 variables most predictive of PORF were anesthesia duration,arterial partial pressure of carbon dioxide(PaCO?),calcium level,lymphocyte percentage,cardiopulmonary bypass duration,intraoperative blood loss,age,creatinine level,aspartate aminotransferase(AST)level,and activated partial thromboplastin time(aPTT).Conclusion A predictieon model for PORF following cardiovascular surgery is successfully developed.This model can identify high-risk patients and estimate their probability of developing respiratory failure,thereby facilitating data-driven clinical decision-making.