Objectives:To investigate the expression of signal-induced proliferation-associated 1 (SIPA1) in colorectal cancer tissues and its relationship with patient prognosis. To explore the effects of SIPA1 on proliferation and migration abilities, as well as the possible molecular mechanisms.Methods:Using The Cancer Genome Atlas (TCGA) database to analyze the differential expression of SIPA1 and conduct survival analysis. Then, plotting receiver operating characteristic curve (ROC) and prognosis calibration curve analysis to assess the predictive capability and accuracy of SIPA1 for patient prognosis. Subsequently, verifying the expression levels of SIPA1 in tumor tissues and adjacent normal tissues using immunohistochemistry (IHC) and western blot (WB) assays(from March 1, 2023, to May 1, 2024, pathological specimens of five colorectal cancer patients were selected from the tissue bank of affiliated hospital of Nantong University. tissue microarrays were constructed using both cancerous tissues and adjacent normal tissues), and exploring the correlation between SIPA1 and clinical pathological parameters. Next, establishing SIPA1 stable knockdown cell lines in colorectal cancer cell lines DLD1 and HCT116, and assessing the biological behavior changes of tumor cells after SIPA1 knockdown through cell proliferation, invasion, and migration experiments. Validating the impact of SIPA1 on colorectal cancer cell proliferation in vivo through subcutaneous xenograft experiments in nude mice. Exploring the potential pro-tumor mechanisms of SIPA1 through pathway enrichment analysis, and confirming these using WB experiments. The proliferation, invasion and migration of tumor cells were detected after adding PI3K activator. Lastly, conducting correlation analysis between SIPA1 and immune checkpoint, as well as the association with immune cells in the tumor microenvironment. Results:Differential analysis showed that mRNA expression of SIPA1 in colorectal cancer tissues was significantly higher than that in adjacent normal tissues ( P＜0.05). Prognostic analysis indicated that patients with high expression of SIPA1 had poor overall survival ( P＜0.001), and the expression level of SIPA1was correlated with lymph node invasion ( P＜0.001) and N stage ( P＜0.05). ROC curve and prognosis calibration curve suggest that SIPA1 can effectively predict five-year survival rate of patients (AUC=0.7), and the predictive performance of the model is relatively accurate ( P＜0.001). WB experiments showed a significant increase in the expression level of SIPA1 protein in colorectal cancer specimens ( P＜0.001). Immunohistochemistry results indicated higher staining scores of SIPA1 in tumor tissues. In vitro experiments demonstrated that SIPA1 knockdown significantly inhibited the proliferation, invasion, and migration capabilities of colorectal cancer cells. In DLD1 and HCT116 cells, the SIPA1-knockdown group exhibited significantly lower absorbance compared to the control group (0.89±0.01 vs. 1.57±0.02 and 0.72±0.01 vs. 1.31±0.03, respectively, both P＜0.001). The SIPA1-knockdown group also demonstrated a reduced number of migrated cells relative to the control group (197.93±16.64 vs. 518.48±29.15 and 171.83±12.49 vs. 446.00±21.81, respectively, both P＜0.001). Furthermore, the cell wound-healing rate was significantly lower in the SIPA1-knockdown group than that in the control group [(0.32±0.01)% vs. (0.61±0.01)% and (0.28±0.01)% vs. (0.75±0.01)%, respectively, both P＜0.001]. In vivo animal experiments suggested that SIPA1 knockdown could inhibit tumor growth [(460.35±57.47) mm3 vs (1 177.55±208.24)mm3, (0.76±0.11)g vs (1.43±0.08)g, P＜0.05]. Pathway enrichment analysis revealed significant enrichment of the receptor tyrosine kinase signaling pathway, and SIPA1 knockdown could inhibit the activation of the phosphatidylinositide 3-kinases (PI3K)/protein kinase B (PKB)/glycogen synthase kinase-3β (GSK3β) signaling pathway. The PI3K activator reversed the inhibitory effect of SIPA1 silencing on tumor cell proliferation, invasion and migration. Correlation analysis indicated that high expression of SIPA1 was associated with immune checkpoints and various immunosuppressive cells (all P＜0.05). Conclusions:SIPA1 is highly expressed in colorectal cancer and associated with poor prognosis. SIPA1 may affect the proliferation and migration abilities of tumor cells by regulating the PI3K/AKT/GSK3β signaling pathway.

ObjectiveTo evaluate the effectiveness of stone needle thermocompression and massage compared to flurbiprofen gel patch in relieving chronic musculoskeletal pain in the shoulder and back， and to explore the potential mediating mechanism through muscle elasticity. MethodsA total of 120 patients with chronic musculoskeletal pain in the shoulder and back were randomly assigned to either stone needle group or flurbiprofen group， with 60 patients in each. The stone needle group received stone needle thermocompression and massage for 30 minutes， three times per week； the flurbiprofen group received flurbiprofen gel patch twice daily. Both groups were treated for 2 weeks. Pain improvement， as the primary outcome， was assessed using the Global Pain Scale （GPS） at baseline， after 2 weeks of treatment， and again 2 weeks post-treatment. To explore potential mechanisms， a mediator analysis was conducted by measuring changes in superficial and deep muscle elasticity using musculoskeletal ultrasound at baseline and after the 2-week treatment period. ResultsThe stone needle group showed significantly greater pain relief than the flurbiprofen group 2 weeks post-treatment. After adjusting for confounders related to pain duration， the between-group mean difference was -8.8 ［95% CI （-18.2， -0.7）， P＜0.05］. Part of the therapeutic effect was mediated by changes in deep muscle elasticity， with a mediation effect size of -1.5 ［95% CI （-2.0， -0.9）， P = 0.024］， accounting for 17.9% of the total effect. ConclusionStone needle thermocompression and massage can effectively relieve chronic musculoskeletal pain in the shoulder and back， partly through a mediating effect of improved deep muscle elasticity.

Objective To observe the clinical efficacy of regulating conception vessel and unblocking governor vessel electroacupuncture in the treatment of cancer-related fatigue(CRF)of middle-to-advanced stage cervical cancer,and to explore its effect on inflammatory factors.Methods A total of 122 patients with a definitive diagnosis of CRF of middle-to-advanced stage cervical cancer admitted to the wards and outpatient clinics of Cangzhou Central Hospital from August 2021 to August 2023 were selected for the study.The patients were randomly divided into the control group and the observation group according to the random number table method,with 61 cases in each group.The patients in both groups were given conventional symptomatic treatments such as gastric protection and anti-vomiting since the day of action of chemotherapy.The control group was treated with Dexamethasone Tablets,and the observation group was treated with regulating conception vessel and unblocking governor vessel electroacupuncture on the basis of the control group,the course of treatment covered 21 days.After three weeks of treatment,the clinical efficacy of the two groups was evaluated.The changes in the traditional Chinese medicine(TCM)syndrome scores,Piper's Fatigue Scale(PFS)scores,Karnofsky Performance Status(KPS)scores,and Functional Assessment of Cancer Therapy-General(FACT-G)scores of the patients in the two groups before and after treatment were observed.The changes in interleukin 6(IL-6),hypersensitive C-reactive protein(hs-CRP),tumor necrosis factor α(TNF-α),and T-lymphocyte subsets indicators[CD3+,CD4+,CD8+,CD4+/CD8+]were compared between the patients in the two groups before and after treatment.Results(1)The total effective rate was 95.08%(58/61)in the observation group and 77.05%(47/61)in the control group.The efficacy of the observation group was superior to that of the control group,the difference being statistically significant(P<0.05).(2)After treatment,the TCM syndrome scores of patients in the two groups were significantly improved(P<0.05),and the improvement in the observation group was significantly superior to that in the control group,the difference being statistically significant(P<0.05).(3)After treatment,the PFS scores of patients in the two groups were improved significantly(P<0.05),and the improvement in the observation group was significantly superior to that in the control group,the difference being statistically significant(P<0.05).(4)After treatment,the serum IL-6,hs-CRP,and TNF-α levels of patients in the two groups were significantly improved(P<0.05),and the improvement in the observation group was significantly superior to that in the control group,the difference being statistically significant(P<0.05).(5)After treatment,the CD3+,CD4+,CD8+,CD4+/CD8+of patients in the two groups were significantly improved(P<0.05),and the improvement in the observation group was significantly superior to that in the control group,the difference being statistically significant(P<0.05).(6)After treatment,the KPS scores and FACT-G scores of patients in the two groups were significantly improved(P<0.05),and the improvement in the observation group was significantly superior to that in the control group,the difference being statistically significant(P<0.05).Conclusion Regulating conception vessel and unblocking governor vessel electroacupuncture in the treatment of CRF of middle-to-advanced stage cervical cancer can effectively alleviate the fatigue of patients,inhibit the release of inflammatory factors,regulate the immune function,and improve the physical condition of patients,so as to improve the quality of life of patients.

Type 2 diabetes (T2D) is an independent risk factor for cognitive impairment. The dysregulation of hypoxia inducible factor (HIF) signaling in T2D patients results in impaired adaptive responses to hypoxia, thereby accelerating the progression of complications. However, limited knowledge is available regarding its precise function in diabetes-associated cognitive impairment (DACI). Here, elevated HIF-1α levels were observed in brain endothelial cells (ECs) of db/db mice. Functionally, brain ECs-specific knockdown of H if1 a significantly ameliorated T2D-induced memory loss and neuronal damage. Glycolysis in brain ECs was inhibited in this process, as indicated by RNA-seq, leading to decreased hippocampal lactate production through reduced LDHA expression. Notably, T2D patients showed increased cerebrospinal fluid lactate levels, which were strongly associated with their cognitive dysfunction. Intrahippocampal injection of lactate accelerated cognitive dysfunction and impaired adult hippocampal neurogenesis (AHN) in db/db mice. Conversely, reducing hippocampal lactate levels through the intrahippocampal injection of oxamate delayed the onset of memory deficits. Furthermore, asiatic acid was discovered to protect db/db mice from cognitive impairment by decreasing brain endothelial HIF-1α expression and subsequently reducing hippocampal lactate-induced AHN damage. Overall, this study elucidates the inhibiting role played by endothelial HIF-1α-driven lactate in AHN and highlights a potential tactic of targeting HIF-1α in brain ECs for treating cognitive impairment.

BACKGROUND:Bile acid metabolism plays a crucial role in the development and progression of Crohn's disease.There is no research on changes in bile acid metabolism and key target genes following treatment with biological agents.OBJECTIVE:To investigate the expression characteristics of bile acid metabolism-related genes in patients with Crohn's disease,identify key genes associated with response to biological agents.METHODS:Transcriptome data were obtained through the GEO database to analyze differentially expressed genes between inflammation-control groups and inflammation-treatment groups.GO,KEGG,and GSEA enrichment analyses were used to evaluate the effects of biological agent therapy on bile acid metabolism.Protein-protein interaction network and WGCNA algorithm were employed to analyze differentially expressed genes,identifying modules closely related to biological agent treatment response,which led to the determination of UGT2A3 as a key gene in bile acid metabolism.In the inflammation group of the GSE186582 dataset,samples were divided into high and low expression groups based on UGT2A3 levels to study its relationship with immune infiltration and explore the interaction between UGT2A3 and the immune microenvironment.Clinical characteristics and intestinal manifestations were compared between high and low expression groups,and correlations between UGT2A3 and clinical indicators(C-reactive protein,erythrocyte sedimentation rate,Crohn's disease activity index,and Crohn's disease endoscopic activity score)were investigated.The competing endogenous RNA regulatory network of UGT2A3 was constructed,and its upstream miRNA was functionally enriched to explore the molecular mechanism of UGT2A3 in bile acid metabolism.Single-cell analysis and clustering were performed using high-throughput sequencing data of GSE134809 to observe the expression of UGT2A3 in different samples and cell populations.Colon tissue samples from untreated and biologic-treated Crohn's disease patients and healthy colon tissue samples from patients with intestinal polyps were collected,and UGT2A3 expression was detected by immunohistochemistry,qRT-PCR,and western blot assay.Fresh feces from Crohn's disease patients and healthy controls were collected to detect bile acid levels,and the relationship between UGT2A3 and fecal bile acid levels was analyzed.RESULTS AND CONCLUSION:A total of 11 bile acid metabolism-related genes were screened,showing significant changes in gene expression after biological agent therapy.GO and KEGG enrichment analyses revealed that intestinal nutrient absorption and metabolic processes normalized after treatment,while leukocyte chemotaxis and inflammatory response pathway activity decreased.GSEA analysis revealed significant enrichment of bile acid metabolism-related pathways after treatment.Protein-protein interaction network construction and WGCNA analysis identified UGT2A3 as a key gene closely associated with treatment response.UGT2A3 expression was significantly decreased in inflamed tissues of Crohn's disease patients and returned to normal levels after biological agent therapy.This result was confirmed in clinical specimens.UGT2A3 expression levels showed significant negative correlations with C-reactive protein,erythrocyte sedimentation rate,Crohn's Disease Activity Index,and Crohn's Disease Endoscopic Index of Severity.Receiver Operating Characteristic curve analysis demonstrated that UGT2A3 has good diagnostic value(Area Under Curve AUC=0.801 0)and effectively reflects treatment outcomes.Immune infiltration analysis showed significantly increased infiltration of various immune cells in samples with low UGT2A3 expression,and its expression levels negatively correlated with immune scores,microenvironment scores,and stromal scores.Compared with the low UGT2A3 expression group,patients with high expression showed less fecal occult blood and penetrating inflammation,with milder intestinal strictures and general condition severity.Fecal bile acid analysis revealed that UGT2A3 expression strongly negatively correlated with primary bile acid content and strongly positively correlated with secondary bile acid content.

BACKGROUND:Bile acid metabolism plays a crucial role in the development and progression of Crohn's disease.There is no research on changes in bile acid metabolism and key target genes following treatment with biological agents.OBJECTIVE:To investigate the expression characteristics of bile acid metabolism-related genes in patients with Crohn's disease,identify key genes associated with response to biological agents.METHODS:Transcriptome data were obtained through the GEO database to analyze differentially expressed genes between inflammation-control groups and inflammation-treatment groups.GO,KEGG,and GSEA enrichment analyses were used to evaluate the effects of biological agent therapy on bile acid metabolism.Protein-protein interaction network and WGCNA algorithm were employed to analyze differentially expressed genes,identifying modules closely related to biological agent treatment response,which led to the determination of UGT2A3 as a key gene in bile acid metabolism.In the inflammation group of the GSE186582 dataset,samples were divided into high and low expression groups based on UGT2A3 levels to study its relationship with immune infiltration and explore the interaction between UGT2A3 and the immune microenvironment.Clinical characteristics and intestinal manifestations were compared between high and low expression groups,and correlations between UGT2A3 and clinical indicators(C-reactive protein,erythrocyte sedimentation rate,Crohn's disease activity index,and Crohn's disease endoscopic activity score)were investigated.The competing endogenous RNA regulatory network of UGT2A3 was constructed,and its upstream miRNA was functionally enriched to explore the molecular mechanism of UGT2A3 in bile acid metabolism.Single-cell analysis and clustering were performed using high-throughput sequencing data of GSE134809 to observe the expression of UGT2A3 in different samples and cell populations.Colon tissue samples from untreated and biologic-treated Crohn's disease patients and healthy colon tissue samples from patients with intestinal polyps were collected,and UGT2A3 expression was detected by immunohistochemistry,qRT-PCR,and western blot assay.Fresh feces from Crohn's disease patients and healthy controls were collected to detect bile acid levels,and the relationship between UGT2A3 and fecal bile acid levels was analyzed.RESULTS AND CONCLUSION:A total of 11 bile acid metabolism-related genes were screened,showing significant changes in gene expression after biological agent therapy.GO and KEGG enrichment analyses revealed that intestinal nutrient absorption and metabolic processes normalized after treatment,while leukocyte chemotaxis and inflammatory response pathway activity decreased.GSEA analysis revealed significant enrichment of bile acid metabolism-related pathways after treatment.Protein-protein interaction network construction and WGCNA analysis identified UGT2A3 as a key gene closely associated with treatment response.UGT2A3 expression was significantly decreased in inflamed tissues of Crohn's disease patients and returned to normal levels after biological agent therapy.This result was confirmed in clinical specimens.UGT2A3 expression levels showed significant negative correlations with C-reactive protein,erythrocyte sedimentation rate,Crohn's Disease Activity Index,and Crohn's Disease Endoscopic Index of Severity.Receiver Operating Characteristic curve analysis demonstrated that UGT2A3 has good diagnostic value(Area Under Curve AUC=0.801 0)and effectively reflects treatment outcomes.Immune infiltration analysis showed significantly increased infiltration of various immune cells in samples with low UGT2A3 expression,and its expression levels negatively correlated with immune scores,microenvironment scores,and stromal scores.Compared with the low UGT2A3 expression group,patients with high expression showed less fecal occult blood and penetrating inflammation,with milder intestinal strictures and general condition severity.Fecal bile acid analysis revealed that UGT2A3 expression strongly negatively correlated with primary bile acid content and strongly positively correlated with secondary bile acid content.

Objectives:To investigate the expression of signal-induced proliferation-associated 1 (SIPA1) in colorectal cancer tissues and its relationship with patient prognosis. To explore the effects of SIPA1 on proliferation and migration abilities, as well as the possible molecular mechanisms.Methods:Using The Cancer Genome Atlas (TCGA) database to analyze the differential expression of SIPA1 and conduct survival analysis. Then, plotting receiver operating characteristic curve (ROC) and prognosis calibration curve analysis to assess the predictive capability and accuracy of SIPA1 for patient prognosis. Subsequently, verifying the expression levels of SIPA1 in tumor tissues and adjacent normal tissues using immunohistochemistry (IHC) and western blot (WB) assays(from March 1, 2023, to May 1, 2024, pathological specimens of five colorectal cancer patients were selected from the tissue bank of affiliated hospital of Nantong University. tissue microarrays were constructed using both cancerous tissues and adjacent normal tissues), and exploring the correlation between SIPA1 and clinical pathological parameters. Next, establishing SIPA1 stable knockdown cell lines in colorectal cancer cell lines DLD1 and HCT116, and assessing the biological behavior changes of tumor cells after SIPA1 knockdown through cell proliferation, invasion, and migration experiments. Validating the impact of SIPA1 on colorectal cancer cell proliferation in vivo through subcutaneous xenograft experiments in nude mice. Exploring the potential pro-tumor mechanisms of SIPA1 through pathway enrichment analysis, and confirming these using WB experiments. The proliferation, invasion and migration of tumor cells were detected after adding PI3K activator. Lastly, conducting correlation analysis between SIPA1 and immune checkpoint, as well as the association with immune cells in the tumor microenvironment. Results:Differential analysis showed that mRNA expression of SIPA1 in colorectal cancer tissues was significantly higher than that in adjacent normal tissues ( P＜0.05). Prognostic analysis indicated that patients with high expression of SIPA1 had poor overall survival ( P＜0.001), and the expression level of SIPA1was correlated with lymph node invasion ( P＜0.001) and N stage ( P＜0.05). ROC curve and prognosis calibration curve suggest that SIPA1 can effectively predict five-year survival rate of patients (AUC=0.7), and the predictive performance of the model is relatively accurate ( P＜0.001). WB experiments showed a significant increase in the expression level of SIPA1 protein in colorectal cancer specimens ( P＜0.001). Immunohistochemistry results indicated higher staining scores of SIPA1 in tumor tissues. In vitro experiments demonstrated that SIPA1 knockdown significantly inhibited the proliferation, invasion, and migration capabilities of colorectal cancer cells. In DLD1 and HCT116 cells, the SIPA1-knockdown group exhibited significantly lower absorbance compared to the control group (0.89±0.01 vs. 1.57±0.02 and 0.72±0.01 vs. 1.31±0.03, respectively, both P＜0.001). The SIPA1-knockdown group also demonstrated a reduced number of migrated cells relative to the control group (197.93±16.64 vs. 518.48±29.15 and 171.83±12.49 vs. 446.00±21.81, respectively, both P＜0.001). Furthermore, the cell wound-healing rate was significantly lower in the SIPA1-knockdown group than that in the control group [(0.32±0.01)% vs. (0.61±0.01)% and (0.28±0.01)% vs. (0.75±0.01)%, respectively, both P＜0.001]. In vivo animal experiments suggested that SIPA1 knockdown could inhibit tumor growth [(460.35±57.47) mm3 vs (1 177.55±208.24)mm3, (0.76±0.11)g vs (1.43±0.08)g, P＜0.05]. Pathway enrichment analysis revealed significant enrichment of the receptor tyrosine kinase signaling pathway, and SIPA1 knockdown could inhibit the activation of the phosphatidylinositide 3-kinases (PI3K)/protein kinase B (PKB)/glycogen synthase kinase-3β (GSK3β) signaling pathway. The PI3K activator reversed the inhibitory effect of SIPA1 silencing on tumor cell proliferation, invasion and migration. Correlation analysis indicated that high expression of SIPA1 was associated with immune checkpoints and various immunosuppressive cells (all P＜0.05). Conclusions:SIPA1 is highly expressed in colorectal cancer and associated with poor prognosis. SIPA1 may affect the proliferation and migration abilities of tumor cells by regulating the PI3K/AKT/GSK3β signaling pathway.

Objective To investigate the expression of centromere protein U(CENPU)in the intestinal tissues of patients with colon cancer,and to analyze the effect of CENPU expression level on the prognosis of patients with colon cancer combined with bioinformatics.Methods Firstly,the expression of CENPU in cancer tissues and normal tissues of colon cancer patients was analyzed by the expression of CENPU in tissues was further verified by real-time quantitative real time polymerase chain reaction(qRT-PCR),Western blot(WB)and immunohistochemistry(IHC).Combined with clinical data,univariate and multivariate Cox regression are used to analyze the correlation between CENPU expression and clinical case parameters of colon cancer patients.Then,the predictive effect of CENPU expression on the prognosis of colon cancer patients are explored by drawing receiver operating characteristic(ROC)curve and Kaplan-Meier survival curve.Finally,the possible molecular mechanism of the effect of CENPU expression on the progression of colon cancer are analyzed by bioinformatics.Results By qRT-PCR,WB and IHC experiments,we find that compared with normal tissues,the expression of CENPU in cancer tissues of colon cancer patients is significantly increased.Cox regression analysis show that the expression of CENPU is significantly correlated with the age and TNM stage of patients,and is a risk factor affecting the prognosis of patients.Kaplan-Meier survival curve analysis show that colon cancer patients with high CENPU expression has significantly lower survival rates.ROC curve show that the model based on CENPU expression has a high predictive power for the prognosis of colon cancer patients area under the curve(AUC=0.832).Bioinformatics analysis show that CENPI,CENPN,CENPD,CENPK,CENPP,CENPM,CENPQ,CENPH,NDC80 and ITGB3BP have significant interaction with CENPU gene.CENPU is involved in DNA repair,MYC/TARGETS/V1 and PI3K/AKT/MTOR signaling pathways.Conclusion High expression of CENPU in cancer tissues of patients with colon cancer is significantly associated with poor prognosis of patients,suggesting that CENPU is expected to be a potential target for early diagnosis and prognosis prediction of patients with colon cancer.

Objective To develop a nomogram model based on the clinical features and the radiomics texture analysis of multimodal magnetic resonance imaging(MRI),so as to predict the tumor response in patients with advanced hepatocellular carcinoma(HCC)3 months after receiving transcatheter arterial chemoembolization(TACE).Methods A total of 105 patients with advanced HCC,whose diagnosis was pathologically-confirmed at the Suzhou Municipal Ninth People's Hospital between January 2017 and December 2021,were enrolled in this study.The patients were randomly divided into training group(n=63)and verification group(n=42).Before chemotherapy,T1WI,T2WI,dynamic contrast-enhanced(DCE)scan,and diffusion-weighted imaging(DWI)were performed by using a 3.0T MRI scanner.A.K.software was used to extract the texture.Three months after chemotherapy,according to the modified Response Evaluation Criteria in Solid Tumors(mRECIST)the patients were divided into response group(n=63)and non-response group(n=42).Results Compared with the response group,in the non-response group the percentage of Child-Pugh grade B and BCLC stage C was obviously higher and the serum alpha fetoprotein(AFP)level was remarkably elevated(P＜0.05).A.K.software extracted 396 MRI texture features,and LASSO regression analysis screened out 6 optimal predictors.The radiation score(Rad-score)was calculated by ROC.The AUC of Rad-score for predicting tumor non-response after TACE by ROC in the training group and verification group were 0.842 and 0.803 respectively.Multivariate logistic regression model analysis showed that AFP≥50 ng/mL(OR=1.568,95%CI=1.234-1.902,P=0.003),Child-Pugh grade B(OR=1.754,95%CI=1.326-2.021,P=0.001),BCLC stage C(OR=1.847,95%CI=1.412-2.232,P=0.001)and Rad-score(OR=2.023,95%CI=1.569-2.457,P＜0.001)were the independent risk factors for tumor non-response.Clinico-radiomics combination had the highest AUC value for predicting tumor non-response.The correction curve showed that the nomogram model had a good agreement.Conclusion The quantitative score of radiomics texture analysis of multimodal MRI has a certain value in predicting tumor non-response in advanced HCC patients 3 months after TACE,and the nomogram model,which is constructed if combined with clinical factors,carries good practical potential.(J Intervent Radiol,2024,32:63-68)

Objective:To investigate the clinical characteristics and offer diagnostic and therapeutic approaches for adult-onset idiopathic hypogonadotropic hypogonadism(AIHH).Methods:Clinical, laboratory, and imaging data, as well as follow-up information, of three male patients diagnosed with AIHH at the Department of Endocrinology and Metabolism of Nanfang Hospital, Southern Medical University, were systematically reviewed and analyzed.Results:All three patients were male, with a median age of 39 years(range, 22 to 40). Two patients reported symptoms of enlarged breasts and reduced sexual function, while one case solely reported a decline in sexual function. Physical examination showed that the median length of the penis was 6 cm(range, 5 to 6 cm), and the bilateral testicular volume was 7.96 mL(4.70-8.82 mL). Basal hormone levels at the time of initial visit to our hospital as follows: the median testosterone level was 0.32 ng/mL(0.24-2.96 ng/mL), median follicle stimulating hormone(FSH) level was 0.56 mIU/mL(0.1-0.75 mIU/mL), and the median luteinizing hormone(LH) level was 0.69 mIU/mL(0.1-1.03 mIU/mL). The levels of other hormones secreted by the anterior pituitary gland were normal. Hypothalamic-pituitary magnetic resonance imaging(MRI) showed that 1 patient had a pituitary microadenoma. Three patients were treated with pulsatile GnRH or gonadotropins, one of which had hypothalamic-pituitary-gonadal(HPG) axis function reversal after GnRH pulse pump therapy and lasted for 1 year, but then still had irreversible reduction.Conclusion:AIHH is marked by adult-onset disease and idiopathic hypogonadism. Enhancing fertility remains a critical requirement for these patients. Pulsatile GnRH treatment or gonadotropin therapy, as viable treatments, exhibit therapeutic effects, albeit with occasional fluctuations. Therefore, the emphasis lies in the timely consideration of fertility preservation.