Objective To investigate the clinical application of skin bridge preopening window drainage in enhanced recovery of mixed hemorrhoids surgically treated with external dissection and internal ligation.Methods A total of 620 patients with mixed hemorrhoids surgically treated with external dissection and internal ligation were retrospectively analyzed from March 1,2021-February 28,2022.Patients were divided into the observation group(n=304)and the control group(n=316)according to the single and even numbers randomly generated at the time of admission.In the observation group,on the basis of conventional operation and drug treatment in the control group,most of them chose to implement preopening window drainage of the skin bridge according to the intraoperative evaluation of the anal skin bridge according to the unified evaluation criteria.Symptom-sign scoring scale used to evaluate the anal edema and pain after the operation.To compare and analyze differences in anal edema,anal pain and the postoperative hospital stay between the observation group and the control.Results The average daily edema scores of the observation group and the control group were 0.56 and 1.2 points,respectively.The average daily edema score of the observation group was lower than that of the control group,with the statistically significant differences(P＜0.05).The average daily pain scores of the observation group and the control group were 0.6 and 1.201+0.289 points,respectively.The average daily pain score of the observation group was lower than that of the control group,with the statistically significant differences(P＜0.05).The average hospitalization days of the observation group and the control group were 8 days and 10 days,respectively.The average length of stay in the observation group was less than that in the control group,with the statistically significant differences(P＜0.05).Conclusion Skin bridge preopening window drainage can effectively relieve the degree of anal edema and pain in patients with mixed hemorrhoids surgically treated with external dissection and internal ligation,improve clinical efficacy,shorten the postoperative hospital stay.It has practical value and clinical significance for enhanced recovery.

Objective To investigate the clinicopathological characteristics of colorectal cancer patients with different mismatch repair (MMR) statuses and their correlation with KRAS/NRAF/BRAF (KNB) gene mutations. Methods The clinicopathological data of 477 patients with colorectal cancer were collected, and MMR, microsatellite instability (MSI), and KNB status were detected via immunohistochemistry (IHC), PCR–capillary electrophoresis, and next-generation sequencing (NGS), respectively. The clinicopathological features of patients with different MMR statuses and correlations with KNB mutations were analyzed. Results Compared with the patients in the pMMR group, the patients in the classical dMMR group were younger, included more females, and exhibited more tumors in the right colon, mostly mucinous adenocarcinoma and poorly differentiated tumors (all P<0.05). The tumors in the nonclassical dMMR group were commonly found in the right colon and were prone to special histologic types (all P<0.05). MLH1-PMS2 codeletion, BRAF mutation, and KRAS G13 codon mutation were common in patients in both the classical and the nonclassical dMMR groups (both P<0.05). The results of MMR IHC (100%) were highly consistent with those of MSI PCR (99.1%). Patients in the classical dMMR group with KRAS mutations were younger, included more males, and were prone to specific histologic types, but distant metastasis was rare (all P<0.05). Conversely, lymph node metastasis was rare in patients in the nonclassical dMMR group with KRAS mutations (P=0.005). The mutation rate of the MSH6 gene was relatively high in the nonclassical dMMR group (P=0.002), and all patients presented complete deletion of MLH1-PMS2 combined with nonclassical expression of MSH6 (100%). Five patients with medullary carcinoma components had complete deletions of MLH1-PMS2. Among the five patients, three had combined nonclassical expression of MSH2/MSH6. Two of the three patients carried the MSH6 gene c.3261 locus mutation. Conclusion The clinicopathologic features of patients with classical/nonclassical dMMR colorectal cancer differ from those of patients with pMMR, and MMR IHC could be used to predict effectively the MSI status. The clinicopathologic features differ between classical and nonclassical dMMR colorectal cancer patients with KRAS mutations, but both groups present codeletion of MLH1-PMS2, BRAF mutation, and KRAS G13 codon mutation. In patients with nonclassical dMMR, complete deletion of MLH1-PMS2 combined with nonclassical expression of MSH6 is common. Mutations in the MSH6 gene may play a key role in the development of colorectal cancer with medullary carcinoma components.

Objective To explore the correlation of MET status in patients with advanced prostatic acinar adenocarcinoma with the clinical pathological parameters and prognosis. Methods The specimen from 135 patients with advanced prostatic acinar adenocarcinoma was included. The expression of c-MET protein was detected via immunohistochemistry, and MET gene amplification was assessed by fluorescence in situ hybridization. The relationships of c-MET expression and gene amplification with clinicopathological features and prognosis were analyzed. Results The positive expression rate of c-MET was 52.60% (71/135). Compared with the c-MET expression in adjacent tissues, that in tumor tissues showed lower heterogeneous expression. Among the cases, 1.71% (2/117) exhibited MET gene polyploidy, but no gene amplification was detected. Positive c-MET expression was significantly correlated with high Gleason scores and grade groups (P=0.0073). However, no significant relationship was found between c-MET expression and progression-free survival or post-treatment t-PSA levels. Conclusion c-MET protein is expressed at a relatively low level in advanced prostatic acinar adenocarcinoma, suggesting that c-MET may not be a viable target for ADC drug development in prostatic acinar adenocarcinoma.