Objective To analyze the MSCT features of subepithelial lesions of the urinary bladder.Methods Thirty-one patients with subepithelial lesions of the urinary bladder proved by pathology were enrolled in this study.The MSCT findings were analyzed. Results Among the 3 1 cases with subpeithelial lesions of the urinary bladder,7 cases were non-epithelial tumors (including 3 cases of leiomyomas,2 cases of paragangliomas,1 case of hemangioma and 1 case of granulocytic sarcoma),and other 24 cases were inflammatory/reactive lesions,all as cystitis glandularis.MSCT findings were as follows:paragangliomas were solitary masses with homogeneous density,smooth border and wide base,with rapid wash-in and wash-out enhancement pattern and peak enhancement in the arterial phase.Hemangiomas and leiomyomas both presented as single round mass with slight enhancement.Granulocytic sarcoma appeared as diffuse bladder wall thickening with pebble-like projections,and slight enhancement.Cystitis glandularis was characterized by local thickening of the bladder wall with nodular or aquatics-like uplift,and was also characterized by diffuse thickening,with slight and progressive enhancement in 22 cases,and significant enhancement in venous phase in 2 cases.Conclusion The subepithelial lesions of urinary bladder may present with tumor-like appearance.The key characteristic feature for cystitis glandularis is local thickening of the bladder wall with nodular or aquatics-like uplift.Rapid wash-in and wash-out enhancement pattern is considered to be diagnostically significant for paragangliomas.However,the rest of the lesions overlap in the imaging appearances,and the diagnosis should be combined with clinical manifestations to improve the accuracy of preoperative diagnosis.

Objective ToexplorethevalueofspectralCTimaginginmultiGparameterquantitativeanalysisoflungcancerwithdifferent pathologicaltypes.Methods SpectralCTimagesof72patientswithlungcancerprovedbypathologywereanalyzed,includingadenocarcinoma (ADC)in44cases,squamouscellcarcinoma(SQCC)in23casesandsmallcelllungcancer(SCLC)in5cases.Theslopeof40－100keVspectralattenuationcurve(λH),effectiveatomicnumber(EffectiveGZ),Calciumconcentration,hydroxyapatite(HAP)concentration, normalizediodineconcentration(NIC)and Waterconcentration were measuredandcomparedrespectively.The O n eG W a y analysisof variance (ANOVA ) was used and a value of P＜0.05 was considered statistically significant.Results (1 )O n plain C T ,there were statisticallysignificantdifferencesinEffectiveGZandλHamongthreeGdiseasegroups(F＝3.423,P＝0.04,F＝3.476,P＝0.038,respectively). (2)IncontrastGenhancedarterialphase,theWaterconcentrationandλHshowedstatisticallysignificantdifferencesamongthreegroups (F＝6.303,P＝0.003,F＝5.833,P＝0.005,respectively).(3)Invenousphase,thedifferenceinNICandλH wasstatisticallysignificant amongthegroups(F＝3.974,P＝0.023,F＝6.766,P＝0.002,respectively).(4)Apairwisecomparisonshowedtherewerestatistically significantdifferencesinallquantitativeparametersofspectralCTbetweenADCandSQCCgroups.ROCcurveanalysisshowedthat thosequantitativeparametersinvenousphaseappearedtohavehighdiagnosticefficiencyindifferentiatingADCfromSQCC,especiallyfor theλHinVP,withaAUCof0.754,sensitivityof79.5%,specificityof69.6%andthresholdvalueof1.78.Conclusion CTSpectral multiGparameterimagingprovidesanewsupplementarymethodforpreoperativediagnosisofADCandSQCC,andλHinvenousphase hasthehighestvalueindifferentiatingADCfromSQCC.

Lung adenocarcinoma (LUAD) is a global malignancy with significant chemoresistance impacting patient prognosis. The pro-tumorigenic role of hyaluronan-mediated motility receptor (HMMR) in LUAD is recognized. This study was designed to investigate the underlying mechanisms by which HMMR affects chemoresistance in LUAD. Bioinformatics presented the expression patterns of HMMR in LUAD patients and the association between HMMR levels and patient survival, followed by qRT-PCR to verify HMMR expression in LUAD tissues and cells. Further, bioinformatics was leveraged to identify the signaling pathways enriched by HMMR and its relevance to glycolytic genes, we also analyzed changes in the glycolytic activity of LUAD cells by manipulating HMMR expression. Stemness was evaluated through cell aggregation assays and Western blot, and drug responsiveness was gauged using CCK-8 assays, alongside flow cytometry for apoptosis analysis. HMMR was highly expressed in LUAD tissues and cells, and this overexpression correlated with poorer prognoses in patients. GSEA showed that HMMR was notably enriched in the glycolysis and gluconeogenesis pathways, correlating positively with the expression of key glycolytic genes. Cellular experiments confirmed that HMMR knockdown notably suppressed aerobic glycolysis in LUAD cells. Moreover, overexpression of HMMR could further enhance the stemness and cisplatin resistance of LUAD cells by stimulating glycolysis. In brief, this study has validated that high levels of HMMR in LUAD are predictive of poor patient prognosis, and that overexpression of HMMR can catalyze aerobic glycolysis, thus promoting stemness and chemoresistance in LUAD cells. Thus, HMMR could be a target for improving chemosensitivity in LUAD.

Lung adenocarcinoma (LUAD) is a global malignancy with significant chemoresistance impacting patient prognosis. The pro-tumorigenic role of hyaluronan-mediated motility receptor (HMMR) in LUAD is recognized. This study was designed to investigate the underlying mechanisms by which HMMR affects chemoresistance in LUAD. Bioinformatics presented the expression patterns of HMMR in LUAD patients and the association between HMMR levels and patient survival, followed by qRT-PCR to verify HMMR expression in LUAD tissues and cells. Further, bioinformatics was leveraged to identify the signaling pathways enriched by HMMR and its relevance to glycolytic genes, we also analyzed changes in the glycolytic activity of LUAD cells by manipulating HMMR expression. Stemness was evaluated through cell aggregation assays and Western blot, and drug responsiveness was gauged using CCK-8 assays, alongside flow cytometry for apoptosis analysis. HMMR was highly expressed in LUAD tissues and cells, and this overexpression correlated with poorer prognoses in patients. GSEA showed that HMMR was notably enriched in the glycolysis and gluconeogenesis pathways, correlating positively with the expression of key glycolytic genes. Cellular experiments confirmed that HMMR knockdown notably suppressed aerobic glycolysis in LUAD cells. Moreover, overexpression of HMMR could further enhance the stemness and cisplatin resistance of LUAD cells by stimulating glycolysis. In brief, this study has validated that high levels of HMMR in LUAD are predictive of poor patient prognosis, and that overexpression of HMMR can catalyze aerobic glycolysis, thus promoting stemness and chemoresistance in LUAD cells. Thus, HMMR could be a target for improving chemosensitivity in LUAD.

Lung adenocarcinoma (LUAD) is a global malignancy with significant chemoresistance impacting patient prognosis. The pro-tumorigenic role of hyaluronan-mediated motility receptor (HMMR) in LUAD is recognized. This study was designed to investigate the underlying mechanisms by which HMMR affects chemoresistance in LUAD. Bioinformatics presented the expression patterns of HMMR in LUAD patients and the association between HMMR levels and patient survival, followed by qRT-PCR to verify HMMR expression in LUAD tissues and cells. Further, bioinformatics was leveraged to identify the signaling pathways enriched by HMMR and its relevance to glycolytic genes, we also analyzed changes in the glycolytic activity of LUAD cells by manipulating HMMR expression. Stemness was evaluated through cell aggregation assays and Western blot, and drug responsiveness was gauged using CCK-8 assays, alongside flow cytometry for apoptosis analysis. HMMR was highly expressed in LUAD tissues and cells, and this overexpression correlated with poorer prognoses in patients. GSEA showed that HMMR was notably enriched in the glycolysis and gluconeogenesis pathways, correlating positively with the expression of key glycolytic genes. Cellular experiments confirmed that HMMR knockdown notably suppressed aerobic glycolysis in LUAD cells. Moreover, overexpression of HMMR could further enhance the stemness and cisplatin resistance of LUAD cells by stimulating glycolysis. In brief, this study has validated that high levels of HMMR in LUAD are predictive of poor patient prognosis, and that overexpression of HMMR can catalyze aerobic glycolysis, thus promoting stemness and chemoresistance in LUAD cells. Thus, HMMR could be a target for improving chemosensitivity in LUAD.

Lung adenocarcinoma (LUAD) is a global malignancy with significant chemoresistance impacting patient prognosis. The pro-tumorigenic role of hyaluronan-mediated motility receptor (HMMR) in LUAD is recognized. This study was designed to investigate the underlying mechanisms by which HMMR affects chemoresistance in LUAD. Bioinformatics presented the expression patterns of HMMR in LUAD patients and the association between HMMR levels and patient survival, followed by qRT-PCR to verify HMMR expression in LUAD tissues and cells. Further, bioinformatics was leveraged to identify the signaling pathways enriched by HMMR and its relevance to glycolytic genes, we also analyzed changes in the glycolytic activity of LUAD cells by manipulating HMMR expression. Stemness was evaluated through cell aggregation assays and Western blot, and drug responsiveness was gauged using CCK-8 assays, alongside flow cytometry for apoptosis analysis. HMMR was highly expressed in LUAD tissues and cells, and this overexpression correlated with poorer prognoses in patients. GSEA showed that HMMR was notably enriched in the glycolysis and gluconeogenesis pathways, correlating positively with the expression of key glycolytic genes. Cellular experiments confirmed that HMMR knockdown notably suppressed aerobic glycolysis in LUAD cells. Moreover, overexpression of HMMR could further enhance the stemness and cisplatin resistance of LUAD cells by stimulating glycolysis. In brief, this study has validated that high levels of HMMR in LUAD are predictive of poor patient prognosis, and that overexpression of HMMR can catalyze aerobic glycolysis, thus promoting stemness and chemoresistance in LUAD cells. Thus, HMMR could be a target for improving chemosensitivity in LUAD.

Objective To explore the feasibility of predicting expression level of Ki-67 in lung adenocarcinoma via multi-parameter of spectral CT.Methods The data of 226 patients with lung adenocarcinoma confirmed by pathology were analyzed retrospectively.The conventional and spectral CT parameters of the lesions were analyzed.According to Ki-67 expression level,all patients were divided into low expression group and high expression group.The parameters with statistical significance were identified as independent variables for multivariate logistic regression analysis to establish a logistic regression model for predicting the expression level of Ki-67.Receiver operating characteristic(ROC)curve was used to assess the diagnostic performance for each model,respectively.Results There were significant differences in the clinical factors of gender,smoking and chest pain between high and low Ki-67 expression groups.In spectral CT parameters,CT40 keV,CT100 keV,Z-effective(Zeff)and iodine concentration(IC)in the high expression group in arterial phase were significantly higher than those in the low expression group.Logistic regression analysis showed that CT100 keV was the independent risk factor for Ki-67 expression level.Both the spectral CT model and the combined model had high value in predicting the expression level of Ki-67 in lung adenocarcinoma,and the combined model had better diagnostic efficacy.Conclusion Spectral CT parameters combined with clinical factors have a certain value in predicting the expression level of Ki-67 in lung adenocarcinoma.

Lung adenocarcinoma (LUAD) is a global malignancy with significant chemoresistance impacting patient prognosis. The pro-tumorigenic role of hyaluronan-mediated motility receptor (HMMR) in LUAD is recognized. This study was designed to investigate the underlying mechanisms by which HMMR affects chemoresistance in LUAD. Bioinformatics presented the expression patterns of HMMR in LUAD patients and the association between HMMR levels and patient survival, followed by qRT-PCR to verify HMMR expression in LUAD tissues and cells. Further, bioinformatics was leveraged to identify the signaling pathways enriched by HMMR and its relevance to glycolytic genes, we also analyzed changes in the glycolytic activity of LUAD cells by manipulating HMMR expression. Stemness was evaluated through cell aggregation assays and Western blot, and drug responsiveness was gauged using CCK-8 assays, alongside flow cytometry for apoptosis analysis. HMMR was highly expressed in LUAD tissues and cells, and this overexpression correlated with poorer prognoses in patients. GSEA showed that HMMR was notably enriched in the glycolysis and gluconeogenesis pathways, correlating positively with the expression of key glycolytic genes. Cellular experiments confirmed that HMMR knockdown notably suppressed aerobic glycolysis in LUAD cells. Moreover, overexpression of HMMR could further enhance the stemness and cisplatin resistance of LUAD cells by stimulating glycolysis. In brief, this study has validated that high levels of HMMR in LUAD are predictive of poor patient prognosis, and that overexpression of HMMR can catalyze aerobic glycolysis, thus promoting stemness and chemoresistance in LUAD cells. Thus, HMMR could be a target for improving chemosensitivity in LUAD.