ABSTRACT
【Objective】 To explore the feasibility, safety and clinical application value of laparoscopic radical rectal cancer surgery with natural orifice specimen extraction (NOSE) by comparing the postoperative pathological data, surgery-related variables and postoperative recovery between laparoscopic radical rectal cancer surgery with NOSE and laparoscopic-assisted radical rectal cancer surgery. 【Methods】 A retrospective analysis was conducted on 74 patients who underwent radical rectal cancer surgery with anus preservation in the Department of General Surgery of The First Affiliated Hospital of Xi’an Jiaotong University from July 2017 to April 2022. Among them, 38 cases underwent surgery with specimen extraction through an abdominal auxiliary incision (auxiliary incision group), and 36 cases underwent surgery with specimen extraction through a natural orifice (NOSES group). The differences in the efficacy of the two surgeries were evaluated by comparing the postoperative pathological data, surgical variables, and postoperative recovery of the two groups. 【Results】 There were no statistically significant differences in general data and postoperative pathological data between the two groups (all P>0.05). The NOSES group exhibited significantly shorter operative time, time to first flatus, time to first oral intake postoperatively, and postoperative hospital stay compared to the auxiliary incision group (all P0.05). 【Conclusion】 Laparoscopic surgery with NOSE for rectal cancer is safe and feasible with minimally invasive and accelerated recovery, which is worth promoting and applying in clinical practice.
ABSTRACT
Objective:To investigate the relationship between transcription factors (TFs) and the prognosis of colon cancer, and to construct a prognosis model through TCGA and GEO dual databases, so as to quantify the risk of patients and guide clinical treatment decisions.Methods:The transcriptome and clinical data of colon cancer in TCGA and GEO databases were used in this study. The transcriptome data were annotated and the gene expression was calculated. The difference analysis of TFs in TCGA and GEO (log2FC > 1, P-value (Fdr) < 0.05) was performed. The difference TFs of double data intersection were used for correlation prognosis analysis ( P<0.01). The risk coefficient and risk value of prognosis-related TFs were calculated by COX multivariate analysis, and the prognosis model of TFs was constructed by COX model with "survival" and "glmnet" package. The survival curve ( P<0.001) and ROC curve (AUC>0.75) of the sequence set and verification set were drawn, and the distribution of risk value was visualized. After grouping according to risk value, GSEA enrichment analysis was calculated, gene set grid was constructed, target genes were predicted, and finally, pathway enrichment analysis of GO and KEGG was carried out. Results:387 TFs with different expressions in TCGA and GEO databases were used to draw heat map, volcanic map and TFs-related forest map, and the prognosis model of colon cancer was constructed according to COX multivariate analysis=0.310×HSF4+0.137×IRX3-0.127×ATOH1+0.290×OVOL3+0.137×HOXC6+0.155×SIX2+0.092×ZNF556-0.444×CXXC5+0.429×TIGD1+0.413×TCF7L1. Through enrichment analysis, our results showed that these prognostic factors may directly or indirectly act on cancer pathways, such as basic cell carcinoma and cancer signaling pathway, local tissue-cell adhesion, and extracellular matrix.Conclusions:The constructed TFs prognosis model of colon cancer can quantify the prognostic risk of colon cancer, and its high-risk group is an independent risk factor of colon cancer prognosis. This model is a new way to evaluate the prognosis of colon cancer.
ABSTRACT
Objective@#To examine the proliferating cell nuclear antigen (PCNA) expression in submandibular gland of diabetic mice and to investigate the influence of fibroblast growth factor 1 (FGF-1) on PCNA expression and its possible mechanism.@*Methods@#Sixteen db/db diabetic male mice were randomly divided into diabetic group and diabetic-FGF-1 group (n=8). Eight age-matched db/m mice served as a control group. After FGF-1 was administered intraperitoneally to diabetic-FGF-1 group continuously for 16 weeks, blood glucose and body weight of each mouse in the three groups were detected at 0, 4, 8, 12, 16 weeks. Then the flow rate of saliva in three groups was compared at 0, 8, 16 weeks. At 16 week, bilateral submandibular glands were resected. Then HE staining was performed to observe the histological morphology of submandibular gland and PCNA expression was examined by immunohistochemical staining.@*Results@#Four weeks after administration, the blood glucose in diabetic-FGF-1 group decreased markedly, close to the control group (P>0.05). Weight loss in diabetic-FGF-1 group was noticeable at 8 weeks after administration, but still higher than that in the control group (P<0.05). The flow rate of saliva in diabetic-FGF-1 group increased gradually after administration, which was higher at 8, 16 weeks ([260.1±43.3], [308.5±34.0] mg·min-1·kg-1) respectively than that in the diabetic group at the same time point ([181.8±37.5], [194.9±49.8] mg·min-1·kg-1) (P<0.05). Compared with the control group, submandibular glands in diabetic group significantly atrophied and the glandular atrophy in diabetic-FGF-1 group was alleviated. The submandibular gland index in the control group, diabetic group and diabetic-FGF-1 group were (7.45±0.63), (2.23±0.26), (3.97±0.15) mg/g, respectively (P<0.05). HE staining showed that the histological morphology of submandibular gland in diabetic-FGF-1 group was clearer, and acinar and ductal atrophy were less significant than diabetic group. Immunohistochemistry showed that the rate of PCNA-positive cells in the control group, diabetic group and diabetic-FGF-1 group were (45.23±7.78)%, (11.50±1.69)%, (36.98±6.53)% respectively (P<0.05).@*Conclusions@#FGF-1 can up-regulate the expression of PCNA in submandibular gland of diabetic mice. This effect may be one of the important mechanisms of FGF-1 reversing the structural atrophy and dysfunction of submandibular gland caused by diabetes mellitus.