ABSTRACT
BACKGROUND@#Positive surgical margins are independent risk factor for biochemical recurrence, local recurrence, and distant metastasis after radical prostatectomy. However, limited predictive tools are available. This study aimed to develop and validate a preoperative nomogram for predicting positive surgical margins after laparoscopic radical prostatectomy (LRP).@*METHODS@#From January 2010 to March 2016, a total of 418 patients who underwent LRP without receiving neoadjuvant therapy at Peking University Third Hospital were retrospectively involved in this study. Clinical and pathological results of each patient were collected for further analysis. Univariable and multivariable logistic regression (backward stepwise method) were used for the nomogram development. The concordance index (CI), calibration curve analysis and decision curve analysis were used to evaluate the performance of our model.@*RESULTS@#Of 418 patients involved in this study, 142 patients (34.0%) had a positive surgical margin on final pathology. Based on the backward selection, four variables were included in the final multivariable regression model, including the percentage of positive cores in preoperative biopsy, clinical stage, free prostate specific antigen (fPSA)/total PSA (tPSA), and age. A nomogram was developed using these four variables. The concordance index (C-index) of the nomogram was 0.722 in the development cohort and 0.700 in the bootstrap validations. The bias-corrected calibration plot showed a limited departure from the ideal line with a mean absolute error of 2.0%. In decision curve analyses, the nomogram showed net benefits in the range from 0.2 to 0.7.@*CONCLUSION@#A nomogram to predict positive surgical margins after LRP was developed and validated, which could help urologists plan surgical procedures.
Subject(s)
Aged , Humans , Male , Middle Aged , Laparoscopy , Methods , Margins of Excision , Nomograms , Prostatectomy , Methods , Prostatic Neoplasms , General Surgery , ROC Curve , Retrospective StudiesABSTRACT
Objective To investigate the effect of knockout of IgG receptor( FcγRIIB) on systemic and adipose tis-sue inflammation and fat tissue lipid metabolism treated with high-fat diet ( HFD) . Methods We used 10 male mice with IgG receptor FcγRIIB knockout ( FcγRIIB-/-) and another 10 male FcγRIIB+/+mice as control, and trea-ted them with HFD. At the end of the 17th week, mice were weighed, the blood was taken by cardiac puncture af-ter sacrifice. Adipose tissue was collected to measure inflammation and lipid metabolism. Results Compared with FcγRIIB+/+mice, FcγRIIB-/-mice had significantly increased levels of inflammatory cytokines, IL-6, TNF-α, and IFN-γ in the serum, and increased macrophage infiltration in adipose tissue. M1 polarization gene MCP-1 and TNF-α increased ( P＜0.05) and M2 polarization gene ARG and IL-10 did not differ significantly. However, there was no significant difference in body mass, adipocyte size and expression of lipid metabolism related genes PPARG, CEBPα, FASn, HSL, ATGL, UCP-1 and GLUT4. Conclusions Under HFD treatment, knocking out the IgG re-ceptor FcγRIIB aggravates the inflammatory response of the whole body and adipose tissue, but cannot influence lipid metabolism of adipose tissue and body weight.
ABSTRACT
<p><b>OBJECTIVE</b>To explore the pathogenesis mechanism of hypertrophic scar (HS) and the effective means for its clinical treatment, the difference of the gene expressions between HS and normal skin was compared.</p><p><b>METHODS</b>The differentially expressed genes between HS and normal skin were obtained by mining PubMed. The dysregulated genes in HS were analyzed by a series of bioinformatics methods, including protein-protein interaction networks, pathways, Gene Ontology and functional annotation clustering analysis.</p><p><b>RESULTS</b>A total of 55 dysregulated genes in HS was identified (46 up-regulated genes and 9 down-regulated genes). Fifty-one genes were found to encode proteins with interaction network, including up-regulated genes TGFB1, FN1, JUN, COL1A1, CTGF, VEGFA, FOS, COL3A1, IGF1, IL4, PELO, SMAD2, TIMP1, PCNA, and ITGA4 and down-regulated genes ITGB1 and DCN as the central nodes for this network. The dysregulated genes in HS involved in a variety of biological pathways, such as focal adhesion formation, integrin signal transduction, and tumor formation. Furthermore, the dysregulated genes in HS played the important roles in biological processes of cell surface receptor linked signal transduction, tissue development, cell proliferation and apoptosis, and macromolecule biosynthetic process, as well as in molecular function of calcium ion binding, double-stranded DNA binding, heparin binding, promoter binding and MAP kinase activity. The results of functional annotation clustering analysis revealed that the dysregulated genes in HS involved in epidermis development, angiogenesis, and apoptosis.</p><p><b>CONCLUSION</b>Such key genes as TGFB1, FN1, and JUN, along with the pathways, biological processes and molecular functions involving epidermis development, angiogenesis, and extracellular matrix-integrin-focal adhesion signal transduction may play the important roles in the development of HS. The investigations of the dysregulated genes in HS could provide the new targets for clinical treatment.</p>