As a key technology for the integration of biological intelligence and machine intelligence, brain-computer interface provide breakthrough solutions in medical service fields such as brain disease diagnosis and treatment, neural rehabilitation, and mental health. However, it still faces numerous risks and challenges. To guide and standardize the ethical review of clinical research involving brain-computer interface in medical institutions in Beijing, improve the quality of ethical review, protect the rights and interests of research participants, and promote responsible innovation, a multidisciplinary ethical review guideline for brain-computer interface clinical research has been formulated on the basis of the  laws, regulations, and policy documents. It carefully elaborates on aspects such as review elements, protection of specific groups, declaration of conflicts of interest, and review procedures.

Early diagnosis of urologic neoplasms is pivotal for delivering precision therapy and optimizing patient outcomes. In recent years, artificial intelligence (AI) has demonstrated remarkable potential in medical-image analysis, histopathologic image recognition, biomarker discovery, and prognostic prediction. This article systematically reviews the current status and advances of AI applications in the diagnosis of the three most common urologic cancers, including prostate cancer, bladder cancer, and renal cell cancer. By enhancing diagnostic efficiency, alleviating physicians' workload, and optimizing clinical decision-making, AI offers broad prospects. With continuous algorithmic refinement and the accumulation of multicentric data, AI is expected to play an even greater role in the precision management of urologic tumors.

Objective  To investigate the inhibitory effects and molecular mechanisms of the small molecule drug WP1066 on MYCN amplified neuroblastoma (NB) cells. Methods  Among 26 pediatric drugs approved by the Food and Drug Administration (FDA) or in clinical trials, WP1066 demonstrated the most potent cytotoxic effect against MYCN amplified NB cells SK-N-BE(2). After treatment with different concentration gradients of WP1066, cell proliferation and viability were detected with CellTiter-Glo, crystal violet staining, and colony formation assays in MYCN amplified NB cells SK-N-BE(2) and IMR32, MYCN non-amplified NB cells SH-SY5Y and SK-N-AS, and human retinal pigment epithelial cells hTERT RPE-1. Apoptosis was detected with Caspase3/7 assay. The expression levels of signal transducer and activator of transcription 3(STAT3) and p-STAT3 proteins were detected with Western blotting, and the expression level of the anti-apoptotic molecule Bcl-2 mRNA was detected with real-time quantitative reverse transcription polymerase chain reaction (RT-qPCR). Results  CellTiter-Glo results showed that WP1066 had a significant killing effect on MYCN-amplified NB cells SK-N-BE(2) and IMR32(P<0.05), but had no significant effect on MYCN non-amplified NB cells SH-SY5Y and SK-N-AS, and human retinal pigment epithelial cells hTERT RPE-1 at the same concentration. Crystal violet staining and colony formation experiments also showed the same results. Caspase3/7 apoptosis assay showed that WP1066 significantly promoted apoptosis in MYCN amplified NB cells SK-N-BE(2) (P<0.05), but had no significant effect on MYCN non-amplified NB cells SH-SY5Y. At the mechanism level, the small molecule drug WP1066 affected the activity of NB cells by inhibiting the p-STAT3 level in SK-N-BE(2) cells and regulating the expression level of Bcl-2(P<0.05), an anti-apoptotic molecule downstream of p-STAT3. Conclusion  WP1066 has a significant inhibitory effect on the proliferation of MYCN amplified NB cells and is expected to become a candidate therapeutic drug for MYCN amplified NB.

Objective  To investigate the role and molecular mechanisms of Rac GTPase-activating protein 1 (RACGAP1) in resistance to cyclin-dependent kinase 4/6 (CDK4/6) inhibitors, and to determine whether targeting RACGAP1 can synergistically enhance the efficacy of CDK4/6 inhibitors and reverse drug resistance phenotypes, thereby providing a novel therapeutic target strategy for overcoming resistance in breast cancer and other malignancies.  Methods  A Ribociclib-resistant MCF-7 sub-line was established by long-term exposure. Whole-cell pellets were subjected to RNA-seq to identify differentially expressed transcripts between parental and resistant cells. Genes consistently up-regulated across multiple CDK4/6 inhibitor models were prioritized. Public breast cancer data from The Cancer Genome Atlas (TCGA) were interrogated using the R package clusterProfiler to perform gene set enrichment analysis (GSEA) and map downstream pathways.  Results  Both RACGAP1 was markedly elevated at the mRNA and protein levels in resistant cells and in TCGA tumors, and their high expression correlated with poor response to Ribociclib. Genetic knockdown of RACGAP1 restored sensitivity to CDK4/6 inhibitors and synergistically inducing apoptosis and suppressing clonogenicity.  Conclusion  Elevated RACGAP1 drive CDK4/6 inhibitor resistance by modulating cell-cycle progression and microtubule dynamics. Targeting these genes re-sensitizes resistant breast cancer cells, offering a clinically implementable strategy to overcome CDK4/6 inhibitor resistance.

Objective  To make use of single-cell RNA sequencing (scRNA-seq) technology to conduct deep analysis on glioblastoma (GBM) tumor microenvironment, identify key driver genes that have specific expression in malignant tumor cells, and assess their potential as novel therapeutic targets and prognostic biomarkers. Methods  Tumor tissues and adjacent normal tissues from three clinical GBM patients were collected for scRNA-seq. After strict data quality control, integration, normalization, and batch effect correction, cells were clustered and annotated according to cell type. Differentially expressed genes that have specific upregulation in tumor cells were screened. Loss-of-function experiments (colony formation, Transwell assays, etc.) were carried out in vitro via the GBM cell line (LN229) treated with an inhibitor (NAZ2329), so as to verify the target gene's effects on cell proliferation, viability, invasion, and migration. Protein-protein interaction networks were analyzed by use of the STRING database, and pathway enrichment analysis was implemented through Gene Set Enrichment Analysis（GSEA）. Public databases such as the Cancer Genome Atlas（TCGA） and Gene Expression Profiling Interactive Analysis（ GEPIA） were used for expression profiling and survival analysis, and immunohistochemical staining  was employed to validate target protein expression in clinical tissue samples. Results  scRNA-seq analysis identified four major cell populations: T cells, macrophages, malignant tumor cells, and oligodendrocytes. Differential expression analysis revealed that the receptor-type tyrosine phosphatase receptor-type tyrosine-protein phosphatase zeta（PTPRZ1） was one of the most significantly and specifically upregulated genes in malignant tumor cells, which was validated in an independent single-cell dataset (GSE131928). TCGA data analysis indicated that high expression of PTPRZ1 was specific to glioma. In vitro functional experiments proved that inhibition of PTPRZ1 obviously suppressed the proliferation, viability, invasion, and migration capacities of GBM cells. Bioinformatics analysis indicated that PTPRZ1 has close association with its ligand PTN, thus it may promote tumor progression via activating pathways related to nervous system development. Clinical analysis confirmed that PTPRZ1 protein has high expression in GBM tissues, and it significantly correlated with patients' poor overall survival. Conclusion  PTPRZ1 is a key molecule that has specific high expression in malignant GBM cells, it obviously promotes malignant phenotypes of GBM cells, and its high expression is associated with a poor clinical outcomes. Hence, these findings demonstrate that PTPRZ1 is a potential diagnostic biomarker.

Objective  To investigate the incidence of adverse pathological features (APF) after radical prostatectomy (RP) in prostate cancer (PCa) patients, evaluate the predictive value of preoperative clinical indicators for APF, and explore the association between APF and postoperative biochemical failure.Methods  Clinical data of PCa patients who underwent RP at Beijing Friendship Hospital, Capital Medical University from July 2016 to July 2024 were retrospectively collected, including general characteristics, imaging and laboratory examinations, biopsy and postoperative pathology，and follow-up data. APF was determined based on pathological findings. Univariate and multivariate Logistic regression analyses were performed to identify independent predictors of APF and to construct a nomogram, while Cox regression analysis was used to identify predictors of biochemical failure. Results  A total of 352 patients were included. The incidence of APF after RP was 66.76% (235 cases), including positive surgical margin in 174 cases (49.43%), extraprostatic extension in 102 cases (28.98%), and seminal vesicle invasion in 51 cases (14.49%). Biochemical failure occurred in 39.77% of patients. The APF group had significantly higher rates of biochemical failure，with a shorter time to biochemical recurrence (28.0 months vs not reached，P<0.001). Multivariate analysis revealed that elevated body mass index (BMI), increased prostate-specific antigen density (PSAD) and advanced clinical stage were independent predictors of APF, and Cox regression analysis showed that  APF （HR=1.75，95% CI: 1.13-2.72，P=0.012） and higher International Society of Urological Pathology (ISUP) grade（HR=1.50，95%CI: 1.06-2.14，P=0.023）   were independent risk factors for biochemical failure. Conclusion  APF is closely associated with biochemical failure after RP. Preoperative BMI, PSAD and clinical stage can serve as valuable indicators for predicting APF.

Objective  To explore pathological features that might affect biochemical recurrence in patients with prostate cancer following radical prostatectomy, and to establish a risk prediction model for biochemical recurrence. Methods  A total of 237 prostate cancer patients who underwent radical prostatectomy were retrospectively enrolled. Clinical and pathological data were retrieved. Biochemical recurrence data were collected from outpatient follow-up records, and Kaplan-Meier analysis was performed to assess the influence of different pathological features on biochemical recurrence-free survival (BRS). Cox regression analyses were performed to identify risk factors for BRS. A prediction model and nomogram for 12-month BRS were established with these risk factors. Results  Pathological stage,  International Society of Urological Pathology (ISUP) grade group, positive basal and bladder neck margin, and phosphatase and tensin homolog (PTEN) deletion were independent risk factors for BRS. Based on these factors, a prediction model and nomogram for 12-month BRS were built, and showed good discrimination (C-index = 0.810). Conclusion  The biochemical recurrence prediction model for prostate cancer based on pathological features provides an easily accessible personalized prognostic assessment tool for clinical practice, which helps guide postoperative adjuvant treatment decisions and the formulation of intensive surveillance protocols.

The neddylation of proteins, which involves tagging substrate proteins with neural precursor cell-expressed developmentally down-regulated protein 8 (NEDD8), is one of the most important post-translational modifications. It has been shown to play significant roles in various biological processes such as cell growth, apoptosis, and signal transduction. Recent research has found a close association between protein neddylation and the occurrence and development of inflammatory diseases. This article begins by reviewing the neddylation cascade, including its biochemical processes and regulation, and further expounds on its effects by regulating key proteins in inflammatory signaling pathways, discovering that it acts as a crucial regulator for the characteristics and functions of innate immune cells (neutrophils, macrophages, and dendritic cells) as well as adaptive immune cells. Subsequently, we focus on reviewing the roles and mechanisms of protein neddylation in various inflammatory diseases such as inflammatory bowel disease, rheumatoid arthritis, liver fibrosis, pancreatitis, atherosclerosis, and acute lung injury. The potential of protein neddylation as a therapeutic target is discussed. Finally, we discussed the significance and potential clinical values of current small-molecule neddylation inhibitors (particularly MLN4924 and TAS4464) as an promising therapeutic approach in the treatment of inflammation, further, we proposed possible future research directions and key issues to be addressed. 

Ubiquitin-like modification (ULM) is defined as a reversible post-translational modification that modulates protein function through the conjugation of ubiquitin-like proteins (UBLs). Numerous studies have documented the regulatory role of ULM in cancer immunity by helping immune cell, cytokine, and tumor microenvironment cellular functionality. This paper analyzes the constituent and modification mechanisms of some common ULM systems, and examines UBLs like neural precursor cell expressed developmentally down-regulated 8 (NEDD8), small ubiquitin-related modifier (SUMO), human  leukocyte antigen-F adjacent transcript 10 (FAT10) and ubiquitin-fold modifier 1 (UFM1) and their tumor immune regulatory role in tumor immunity alongside their prospective therapeutic role in cancer.

Objective  To investigate the effects of the zinc ion chelator N,N,N′,N′-tetrakis(2-pyridylmethyl)ethylenediamine (TPEN) on the expression levels of key pyroptosis pathway proteins following cerebral ischemia-reperfusion in rats, including  nucleotide-binding domain leucine-rich repeat containing protein 3 (NLRP3), cleaved caspase-1, and the key execution protein gasdermin D (GSDMD). This study designed to evaluate the impact of zinc ions on the cellular pyroptosis pathway, providing a novel theoretical basis for the development of zinc-targeted therapeutic strategies for ischemic-reperfusion injury. Methods  Healthy male rats were randomly divided into three groups: Sham, middle cerebral artery occlusion (MCAO), and TPEN+MCAO. The MCAO model was established using the modified suture method, with 90 min of ischemia followed by reperfusion upon suture removal. The TPEN+MCAO group received an intraperitoneal injection of TPEN at 30 min before ischemia, while the Sham and MCAO groups received an equal volume of solvent. The ischemic hemisphere tissue was isolated at 6 h and 24 h after reperfusion. Immunofluorescence staining was performed to observe the co-localization of NLRP3 and the neuronal marker NeuN. Western blotting was used to detect the protein expression levels of NLRP3, cleaved caspase-1, and GSDMD. Results  ①NLRP3 was co-localized with the neuronal marker NeuN in the ischemic brain tissue of MCAO rats at 6 h and 24 h after reperfusion.  ②Compared to Sham group, the protein expression of NLRP3 increased to 1.8-fold at 6 h and 2.2-fold at 24 h after reperfusion in the ischemic tissue of MCAO group (P<0.01). TPEN treatment significantly reduced the protein expression of NLRP3 in the ischemic tissue at 24 h after reperfusion (P<0.05).  ③Compared to Sham group, the expression of cleaved caspase-1 increased at 24 h after reperfusion in ischemic tissue of MCAO group rats (P<0.01), and this increase was attenuated by TPEN treatment (P<0.01). ④Compared to Sham group, the protein expression of GSDMD increased to 3.5-fold and 2.0-fold at 6 h and 24 h after reperfusion, respectively, in the ischemic tissue of MCAO group rats (P<0.001). TPEN treatment significantly reduced the protein expression of GSDMD in the ischemic tissue at 24 h after reperfusion (P<0.001). Conclusion  The present study  reveals that neuronal pyroptosis and inflammatory response were significantly increased in the ischemic tissue following cerebral ischemia-reperfusion injury in rats. Chelating zinc  with TPEN was able to alleviate neuronal pyroptosis and inflammatory response,.It provides new scientific evidence for targeting zinc ions as a therapeutic strategy for cerebral ischemic-reperfusion injury.

Objective To investigate the effect of disrupted neuronal zinc homeostasis on the expression of histone deacetylase 2 (HDAC2) and O-GlcNAc transferase (OGT), as well as their potential interaction in brain tissue following cerebral ischemia/reperfusion (I/R), in order to elucidate whether zinc dyshomeostasis participates in the synergistic epigenetic regulatory mechanisms during cerebral I/R injury. Methods  Adult Sprague-Dawley rats were subjected to transient middle cerebral artery occlusion (MCAO) for 90 min, followed by reperfusion for 6 h or 24 h. The animals were randomly divided into the Sham, MCAO, and MCAO + N,N,N′,N′-tetrakis (2-pyridylmethyl)ethylenediamine（TPEN） groups (n=6 per group). Protein expression levels of HDAC2 and OGT in brain tissue were analyzed by Western blotting. Protein-protein docking between HDAC2 and OGT was performed using the HDOCK server, and the interaction interface was visualized with PyMOL. Results  ①Compared with the Sham group, HDAC2 protein expression in rat ischemic brain tissue was significantly downregulated at 6 h and 24 h after reperfusion. ②TPEN treatment significantly upregulated HDAC2 expression in rat ischemic brain tissue at both 6 h and 24 h after reperfusion.③Compared with the Sham group, OGT protein expression in rat ischemic brain tissue was markedly reduced at 24 h after reperfusion.④TPEN treatment significantly increased OGT expression in rat ischemic brain tissue at both 6 h and 24 h after reperfusion. ⑤ Molecular docking analysis revealed high-confidence binding conformations between HDAC2 and OGT, suggesting a potential protein-protein interaction based on structural complementarity. Conclusion  Cerebral ischemia-reperfusion leads to a marked downregulation of HDAC2 and OGT expression in rat ischemic brain tissue, which is closely associated with excessive zinc accumulation. The potential protein-protein interaction between OGT and HDAC2 further suggests that zinc overload after ischemia may simultaneously alter their expression levels and disrupt their interaction, thereby impairing neuronal epigenetic regulatory processes.

Objective  To investigate whether the ferroptosis inhibitor ferrostatin-1 (Fer-1) attenuates cerebral edema 24 h after middle-cerebral-artery occlusion-reperfusion (MCAO/R) in mice and to explore the underlying mechanisms focusing on nuclear factor kappa B (NF-κB), matrix metalloproteinase-9 (MMP-9) and aquaporin-4 (AQP4) polarity. Methods  Adult male C57BL/6J mice were randomly allocated to Sham, MCAO/R + vehicle, and MCAO/R + Fer-1 groups (n=10－13 per group). Sixty-minute filament occlusion was followed by reperfusion. Fer-1 (0.8 mg·kg-1) or equal-volume vehicle was administered intravenously at the onset of reperfusion. Twenty-four hours later, brain water content was quantified by the dry-wet weight method; Western blotting was employed to detect total NF-κB, MMP-9 and AQP4 levels as well as the AQP4-M23/M1 isoform ratio; and immunofluorescence co-labelling of AQP4 with CD31 was performed to assess perivascular AQP4 polarization. Image J was used for densitometric analysis of Western blotting bands and quantitative assessment of fluorescence intensity. Results  ① Brain water content was markedly elevated in the MCAO/R group compared with Sham (P<0.01), and this increase was significantly attenuated by Fer-1 (P<0.05). ②The protein expression levels of NF-κB, MMP-9 and total AQP4 were up-regulated in the ischemic hemisphere after MCAO/R (P<0.05 versus Sham); Fer-1 treatment substantially decreased NF-κB and MMP-9 expression (P<0.01) and moderately down-regulated total AQP4 (P<0.05). ③The AQP4-M23/M1 ratio, an index of AQP4 polarization, was significantly decreased after MCAO/R (P<0.01 versus Sham) and was restored by Fer-1 (P<0.05).④ In the ischemic hemisphere, the peak-to-background fluorescence ratio of perivascular AQP4 was lower in MCAO/R mice than that in Sham mice (P<0.05); Fer-1 administration reversed this deficit (P<0.05). Conclusion  Fer-1 attenuates early cerebral edema following MCAO/R by suppressing NF-κB and MMP-9 signaling, down-regulating total AQP4 abundance and preserving perivascular AQP4 polarization. These findings highlight ferroptosis inhibition as a potential therapeutic strategy for ischemia－reperfusion-induced brain edema.  

Objective  To explore the association between the novel composite metabolic index triglyceride-high density lipoprotein-cholesterol-glucose body index(TyHGB) and the risk of stroke incidence in the middle-aged and elderly population in China. Methods  Based on the China Health and Retirement Longitudinal Study (CHARLS), 7 064 middle-aged and elder adults aged ≥ 45 years with no prior history of stroke were enrolled and followed up for 9 years，with additional validation performed using a hospital-based clinical cohort (n=204). The Cox proportional hazards regression model was employed to evaluate the association between TyHGB and the incidence of stroke. Subgroup analyses and restricted cubic spline (RCS) models were utilized to investigate potential interactions and nonlinear dose-response relationships. Additionally, receiver operating characteristic (ROC) curves were used to assess the predictive value of TyHGB in relation to stroke risk. Results  Following multivariable adjustment, each 1-unit increase in TyHGB was associated with an 18% elevated risk of stroke in the CHARLS cohort (HR=1.18, 95% CI: 1.11－1.25, P<0.001) and a 38% increased risk in the hospital validation cohort (HR=1.38, 95% CI: 1.09－1.75, P =0.008). RCS analysis revealed population heterogeneity in the association pattern, showing a nonlinear relationship in the CHARLS cohort but an approximately  linear trend in the hospital cohort. Nevertheless, both cohorts consistently supported a positive association between TyHGB and stroke risk. ROC curves suggested that TyHGB had moderate capability in predicting stroke risk among middle-aged and elder Chinese adults, with area under the curve (AUC) of 0.578 in the CHARLS cohort and 0.753 in the hospital cohort. TyHGB was significantly superior to the conventional TyG (triglyceride-glucose) index in both cohorts (both P<0.05). The positive association between TyHGB and incident stroke risk remained robust across various demographic and clinical subgroups. Conclusion  TyHGB is significantly positively associated with stroke risk in middle-aged and elder Chinese adults, and it exhibits superior predictive efficacy compared to the conventional TyG index in both the nationally representative CHARLS cohort and the hospital-based clinical cohort. The nonlinear association observed in the community population, combined with its robustness in the clinical cohort, collectively suggests that TyHGB serves as a reliable and convenient preliminary screening tool for stroke risk assessment. It is applicable for population risk evaluation and primary prevention strategy development across different scenarios.

Objective  To investigate the expression of paired immunoglobin like type 2 receptor beta (PILRB) in prostate cancer (PCa), and to evaluate its effects on the proliferation, migration, as well as the underlying mechanisms.  Methods  Small interfering RNA (siRNA) was used to knock down PILRB expression in prostate cancer cells. Quantitative real-time polymerase chain reaction (qPCR) was performed to verify the mRNA expression level. Immunohistochemistry (IHC) staining and Western blotting(WB) were employed to detect the expression of PILRB and related proteins. Cell counting kit-8 (CCK-8) assay, scratch wound healing assay, immunofluorescent staining (IF) and Transwell chamber assay were conducted to assess the proliferation, migration, and invasion capabilities of prostate cancer cells in vitro. The tumor-promoting role of PILRB in vivo was investigated using immunodeficient nude mice.  Results  PILRB protein expression was notably elevated in PCa tissues exhibiting high Gleason scores relative to those with low scores. Suppression of PILRB expression markedly inhibited the proliferation （22RV1：1.054±0.054 vs 1.959±0.032，t=40.574，P＜0.001；PC3：1.606±0.535 vs 2.178±0.479，t=22.497，P＜0.01；DU145：1.290±0.184 vs 2.147±0.597，t=38.750，P＜0.01）, transwell invasion assay (unit：n per field) （siPILRB-2：11.500±3.271 vs 101.667±12.909，t=16.584，P＜0.001） and migration （siPILRB-2：67.125±1.178 vs 81.588±1.454，t=21.855，P＜0.001；si-CCL2：63.100±3.019 vs 81.588±1.454，t=15.602，P＜0.001） of prostate cancer cells in vitro. Knockdown of PILRB effectively suppressed the secretion of  C-C motif chemokine ligand 2 (CCL2） and  C-C motif chemokine ligand 5 (CCL5） (pg/mL), as determined by ELISA （CCL2：82.450±3.075 vs 92.061±4.925，t=4.966，P＜0.01；CCL5：796.558±11.606 vs 816.300±19.965，t=2.564，P＜0.05；CSF-1：92.771±5.276 vs 106.787±10.016，t=3.714，P＜0.05）. This finding was further supported at the intracellular relative protein   expression level by WB, which showed a significant downregulation of CCL2 （PILRB：0.305±0.007 vs 0.706±0.016，t=54.668，P＜0.05；CCL2：0.149±0.005 vs 0.522±0.204，t=43.221，P＜0.05）and a modest decrease in CCL5 （CCL5：0.204±0.005 vs 0.220±0.014，t=2.468，P＜0.05）in siPILRB-2-transfected cells relative to the si-Control. Subcutaneous xenograft tumors formed from PILRB-knockdown cells displayed significantly reduced tumor volumes in vivo （shPILRB：585.920±117.582 vs.1 314.462±234.633，t=6.207，P＜0.001）.  Conclusion  Elevated expression of PILRB in prostate cancer cells promotes the progression of prostate cancer by enhancing the secretion of CCL2 and CCL5, which modulates the differentiation of monocytes and macrophages towards the M2 phenotype. Therefore, PILRB may serve as a potential therapeutic target for suppressing prostate cancer progression.

Objective  To explore the changes in adipokines and inflammatory factors in rats under subclinical hypothyroidism conditions. Methods  This study established an animal model of thyroidectomy to simulate the characteristics of subclinical hypothyroidism patients in clinical practice. Combined with molecular biology methods, the expression changes of key molecules in thyroid biology processes and the relationship between hormones and inflammatory factors secreted by fat and liver were investigated. Results  The results showed that the serum leptin content in the  subclinical hypothyroidism model group was significantly higher than that in the normal group (P<0.001), and the adiponectin content was significantly higher than that in the normal group (P<0.01). In addition, the levels of interleukin-6 ( IL-6 )and tumor necrosis factor-α (TNF-α) in serum were significantly higher than those in the normal group (P<0.05). The levels of IL-6 and TNF-α in the liver were significantly higher than those in the normal group (P<0.01). The Western blotting of adipose tissue showed that the expression levels of thyroid hormone receptor α(TRa), TRβ and TR in the subclinical hypothyroidism model group increased compared to the normal group, and the elevated expression of thyrotropin receptor (TSHR) was observed. Conclusion  This study preliminarily confirms that subclinical hypothyroidism leads to abnormal fat accumulation and distribution in rats, which in turn induces disorders in leptin and adiponectin secretion, accompanied by elevated levels of inflammatory factors such as IL-6 and TNF-α. These changes participate in the regulation of local energy metabolism by modulating the secretion of thyrotropin-releasing hormone (TRH) and thyroid stimulating hormone (TSH), laying an experimental foundation for elucidating the intrinsic relationship between subclinical hypothyroidism and obesity.

Objective  To summarize the clinical characteristics and outcomes associated with Legionella pneumophila pneumonia, thereby enhancing clinicians' understanding of this disease. Methods  A retrospective analysis of the clinical characteristics and prognostic outcomes of patients diagnosed with Legionella pneumophila pneumonia at The First Hospital of Changsha from October 2021 to July 2024. Results  The study included 50 male and 21 female participants, with an average age of (62.6±15.9) years. Common symptoms included cough (n =58), expectoration (n= 51), Dyspnea (n=34), fever (n=33), headache (n =13), fatigue (n= 9), and myalgia (n=8). Dyspnea was the only clinical symptom that showed a significant difference between the severe and non-severe pneumonia groups. The levels of procalcitonin (PCT), C-reactive protein (CRP), D-dimer, creatine kinase (CK), and CK-myocardial band (CK-MB) were significantly higher in the severe pneumonia group compared to the non-severe group. Conversely, lymphocyte count, platelet (PLT) count, and albumin levels were significantly lower in the severe group (P<0.05). Common computed tomography (CT) manifestations included flake-like high-density shadows (n = 62, 87.3%), small pulmonary nodules (n = 23, 32.4%), pleural effusion (n=18, 25.4%). Common complications included electrolyte disorders (n=26), type I respiratory failure (n=22), acute liver injury (n=20), sepsis (n=13), acute renal impairment (n=11), septic shock (n=6), multiple organ dysfunction syndrome (MODS) (n=4), and acute respiratory distress syndrome (ARDS) (n=2). The rate of intensive care unit (ICU) admission was 22.5% and the overall mortality rate during hospital was 4.2%(n=3). The majority of patients received treatment with quinolones (59 out of 71, 83.1%). Specifically, 38 patients were treated exclusively with quinolones, while 3 patients received azithromycin alone. A total of 7 patients received invasive ventilation treatment, while 11 patients were treated with non-invasive ventilation. Unfortunately, 3 patients in the severe pneumonia group died due to sepsis and multiple organ failure. Conclusion  If Legionella pneumophila infections are not diagnosed promptly, patients may experience severe pneumonia, multiple organ failure, or even fatal outcomes. The early initiation of quinolones or combination therapy with other medications has shown significant therapeutic benefits for patients suffering from Legionella pneumophila pneumonia.

Objective  To develop and validate a nomogram model based on a physical examination follow-up cohort to predict the risk of incident impaired fasting glucose (IFG) within 3 and 5 years among older adults with normal blood glucose at baseline. Methods  A retrospective cohort study was conducted using data from the health examination database of Ruici Medical Group (2010－2016). Older adults aged ≥60 years with normal baseline fasting plasma glucose (FPG) and complete data were included and randomly split into a training set and a validation set at a 7:3 ratio. Univariate screening and multivariable modeling were performed using the Cox proportional hazards model to identify independent predictors of IFG and construct a nomogram. Model discrimination and calibration were assessed using the concordance index (C-index), receiver operating characteristic (ROC) curves, and calibration plots. Results  A total of 21 914 participants were included (15 340 in the training set and 6 574 in the validation set). During follow-up, 1 411 incident IFG cases occurred in the training set and 602 in the validation set. Multivariable analysis showed that age, body mass index, baseline FPG, triglycerides, and alanine aminotransferase were independently associated with the risk of IFG, and a nomogram was developed accordingly. The model demonstrated good discrimination in both the training and validation sets (C-index: 0.767 and 0.763, respectively), and calibration plots indicated good agreement between predicted probabilities and observed incidence. Conclusion  The IFG risk nomogram constructed from routinely collected health examination indicators is simple and feasible, with good predictive performance, and can be used for early risk stratification and screening management in health check-up settings.

Objective  To investigate the relationship between intrauterine adhesions (IUA) detected under hysteroscopy during retained products of conception (RPOC) removal and postoperative reproductive outcomes, including postoperative IUA, pregnancy rate, and mode of conception, and to explore factors affecting postoperative live birth. A predictive model for reproductive outcomes  was also established.Methods  Clinical data of 400 patients who underwent hysteroscopic RPOC removal at Fuxing Hospital, Capital Medical University from January 2017 to December 2023 were retrospectively analyzed. Patients were divided into adhesion (n=150) and non-adhesion (n=250) groups according to intraoperative hysteroscopic findings. Baseline characteristics and postoperative reproductive outcomes were compared. Multivariate Logistic regression was used to identify factors associated with postoperative live birth, and a predictive model was evaluated using receiver operating characteristic (ROC) curve analysis.Results  The adhesion group had significantly higher rates of previous curettage and prior IUA history than the non-adhesion group (P<0.05). Postoperative pregnancy rate was lower in the adhesion group (54.7% vs 79.2%, P<0.001). Among pregnant patients, the live birth rate was lower in the adhesion group than in the non-adhesion group ［72.0% (59/82) vs 83.3% (165/198), P=0.043］, and median time to conception was prolonged ［9 (6－15) months vs 5 (3－9) months, P<0.001］. Multivariate Logistic analysis showed that intraoperative IUA (adjusted OR=0.520, 95% CI: 0.353－0.774, P<0.001) and postoperative IUA (adjusted OR=0.571, 95% CI: 0.372－0.880, P=0.012) were independent risk factors for reduced live birth, while postoperative anti-adhesion therapy exerted protective effect (adjusted OR=1.492, 95% CI: 1.021－2.173, P=0.038). The RPOC fertility prediction model predicted postoperative live birth with an area under the curve (AUC) of 0.656, indicating moderate discriminative ability.Conclusion  In RPOC patients, intraoperative IUA is associated with lower postoperative pregnancy and live birth rates but longer time to conception. Both intraoperative and postoperative adhesions reduce live birth rates, whereas postoperative anti-adhesion therapy may improve reproductive outcomes.

Objective  To provide a reference for the clinical characteristics, type, treatment and prognosis of abdominal wall endometriosis (AWE). Methods  This was a retrospective study of 227 AWE patients from January 2015 to December 2021. According to different depth of lesions, the enrolled patients were divided into four types and the clinical characteristics were analyzed. Results  The average age of onset for AWE patients was (35.2±4.6) years, the average number of pregnancies was (1.9±1.2) times, and the average number of deliveries was (1.2±0.5) times. Among them, 225 cases (99.1%) had a previous history of cesarean section, 1 case (0.4%) had only a history of laparoscopic ovarian endometriosis cystectomy, and 1 case (0.4%) was spontaneous AWE. The average latency period of onset was (4.3±3.5) years, and the average duration of the disease was (2.6±2.8) years. The average preoperative CA125 of 129 patients was (37.8±42.7) U/mL, and 42 cases had elevated results (＞35 U/mL). In 16 patients, the incision tension was relatively large after resection of the lesion. Among them, 13 cases underwent artificial mesh placement, and 3 cases underwent autologous tissue repair. All patients underwent postoperative pathological examination, which all indicated AWE, among which 2 cases were malignant. According to the different invasion depths of AWE lesions, they were classified into type I (56 cases, 24.7%), type Ⅱ (91 cases, 40.1%), type Ⅲ (37 cases, 16.3%), and type Ⅳ (43 cases, 18.9%). The comparison results of clinical characteristics in the four types showed that there were statistically significant differences in the number of pregnancies, the number of deliveries, the number of intraoperative lesions, the maximum diameter of the lesion, the mesh implantation rate, and the length of hospital stay (P＜0.05). Excluding the 2 patients with malignant AWE, the average follow-up time after surgery for the 225 AWE patients was (62.2±23.3) months, the symptom relief rate was 99.1% (223/225), the recurrence rate was 7.1% (16/225), and the average recurrence interval was (16.5±9.5) months. There were statistically significant differences in the postoperative recurrence rate and recurrence-free time among the patients of the four types (P＜0.05). In the type Ⅳ group, the recurrence rate was significantly increased, and the recurrence-free time was significantly reduced. Conclusion  AWE can be diagnosed according to the typical clinical manifestations. AWE should be treated immediately once confirmed and taken measures to prevent recurrence. Surgical treatment is the best choice, with high symptom remission rate and low recurrence rate. Malignant transformation of AWE is rare and the prognosis is poor.

Objective  To investigate the prevalence of neuropsychiatric symptoms in patients with persistent olfactory loss (POL) and analyze the influencing factors.Methods  Patients diagnosed with POL at the Smell and Taste Disorder Clinic of Beijing Anzhen Hospital, Capital Medical University, from July 2023 to June 2025 were enrolled. Demographic and clinical data, including age, sex, etiology, and disease duration, were collected. Olfactory function was assessed using the Sniffin' Sticks test, while anxiety and depression were evaluated with the Self-Rating Anxiety Scale (SAS) and Self-Rating Depression Scale (SDS), respectively. Cognitive function and sleep quality were measured using the Montreal Cognitive Assessment (MoCA) and Pittsburgh Sleep Quality Index (PSQI). All participants underwent structural magnetic resonance imaging scans, and volumes of the bilateral hippocampus and amygdala were extracted using a region of interest (ROI)-based approach. Univariate and multivariate Logistic regression analyses were performed to identify influencing factors, and receiver operating characteristic (ROC) curves were used to evaluate the predictive value of these factors.Results  A total of 84 POL patients were enrolled in the study. The prevalence rates of anxiety, depression, cognitive impairment, and insomnia were 46.43%, 32.14%, 26.19%, and 9.52%, respectively. Univariate analysis revealed that etiology, hippocampal volume, and amygdala volume were significantly associated with the occurrence of neuropsychiatric symptoms (P<0.05). Multivariate Logistic regression analysis indicated that hippocampal volume (OR=0.763, 95% CI=0.622-0.932) and amygdala volume (OR=0.786, 95% CI=0.656-0.979) were protective factors against neuropsychiatric dysfunction in POL patients (P<0.05). The area under the curve (AUC) of ROC analysis showed that both hippocampal volume (AUC=0.874, 95% CI=0.802-0.946) and amygdala volume (AUC=0.912, 95% CI=0.852-0.973) had predictive value for neuropsychiatric symptoms. The combination of these two factors achieved an AUC of 0.944 (95% CI=0.898-0.989), with a sensitivity of 88.9% and specificity of 87.2%.Conclusion  POL patients exhibit a relatively high prevalence of anxiety and depression. Reduced volumes of the hippocampus and amygdala are significant influencing factors for neuropsychiatric symptoms in POL patients. In clinical practice, special attention should be paid to the assessment and follow-up of neuropsychiatric status in POL patients with atrophy of the hippocampus and amygdala.

In response to the core bottleneck issue of the significantly low conversion rate of medical science and technology achievements in China, in this article we deeply analyze the root cause which lie in the serious lack of industrialization orientation, especially the insufficient efficient screening in the proof-of-concept (PoC) stage. The research proposes to build a new type of medical PoC platform system oriented towards industry as the solution. This system takes market demand as the anchor point, and through establishing a pre-demand assessment mechanism, building a vertical professional platform matrix covering core and frontier fields, and innovatively designing a dynamic benefit-sharing and risk-sharing mechanism of “five-party linkage of government, industry, academia, research and medicine”. The platform integrates core functional modules such as intelligent assessment and incubation, capital collaboration, technology acceleration, dual drive of clinical and market, compliance risk control, and industrial ecosystem. It is expected to significantly enhance the efficiency of medical technology transfer, shorten the industrialization cycle, and drive the incubation of compound talents and the construction of an industrial collaborative ecosystem, providing a systematic solution for breaking through the “first mile” of medical technology transfer.