Thymectomy is a major surgical procedure for patients with non-thymomatous myasthenia gravis，and can enhance their symptomatic remission rate and cure rate. There is still much controversy about appropriate surgical approach and extent of resection of thymectomy. The majority of thoracic surgeons believe that the completeness of thymectomy is closely associated with clinical symptom improvement，and perform complete resection of encapsulated thymus and surroun-ding fat tissues via mid-sternotomy. But minimally invasive thymectomies are often more acceptable by patients. On the contrary，in view of common existence of ectopic thymus tissue，some thoracic surgeons advocate a combination of cervical incision and sternotomy in order to further completely remove all thymus tissue.
Abstract： Appropriate prophylactic administration of antibiotics for thoracic and cardiovascular surgical procedure can reduce postoperative morbidity and decrease the overall cost due to infections. Prophylactic antibiotics should be given within 30 minutes preceding incision intravascularly. Serum levels of free drug above the minimal inhibitory concentration (MIC) for common contaminating bacteria should be maintained for the entire surgical period. Prophylactic antibiotics after operation are useless for patients without risk factors predisposing to postoperative infection. Heart and(or) lung transplant patients should be given antiviral and antifungal prophylaxis. Selection of antibiotics must be based on the pharmacokinetic, pharcodynamic and pharmacoeconomic properties of antibiotics and features of surgery. The policy of antibiotic prophylaxis must be modified in response to alterations in antibiotic resistance pattern which is constantly changing in hospital.
Objective The objective of this study is to find individualized, evidence-based treatment for a patientwith extensive small cell lung cancer, malignant pleural effusion, and liver metastasis.Methods According to the PICO (patient intervention comparison outcome) principle, evidence was collected and critically assessed. The patient’s preference was also taken into consideration in the decision making process. Results We included 10 randomized controlled trials, 13 systematic reviews and meta-analyses, and three clinical guidelines. The evidence indicated that chemotherapeutic treatment prolongs survival in patients with extensive small cell lung cancer and AiDi injections could relieve adverse effects caused by chemotherapy or radiotherapy. Cisplatin and etoposide are considered major standard cytotoxic drugs for small cell lung cancer. We drained the pleural cavity and infused Bleomycin into the pleural cavity. We also used an EP regimen of chemotherapy after the patient’s condition had improved. This patient survived longer than the average survival time for small cell lung cancer patients and has enjoyed a higher quality of life. Conclusion Chemotherapy is the main medical treatment for patients with extensive small cell lung cancer, backed up by symptomatic treatment and supportive care. Prophylactic cranial irradiation decreases brain metastases incidence and improves survival in complete response small cell lung cancer patients.
ObjectiveTo identify genes associated with resistance to programmed cell death protein 1 (PD-1) inhibitors in colorectal cancer and elucidate their underlying mechanisms using bioinformatics approaches. MethodsGenes expression datasets were downloaded from the Gene Expression Omnibus (GEO) database to screen hypoxia-related genes (HRGs) and differentially expressed genes (DEGs). The intersection of HRGs and DEGs was defined as hypoxia-related differentially expressed genes (HDGs). The gene expression data of patients with colorectal cancer from The Cancer Genome Atlas (TCGA) were analyzed using Pearson correlation to identify the PD-1-related genes, further the STRING analysis (minimum interaction score was greater than 0.7) and Cytoscape were subsequently employed to screen the key PD-1-related genes. The relation between the screened key PD-1-related genes and the prognosis of colorectal cancer patients was analyzed to screen out the target genes. The real-time fluorescence reverse transcription quantitative polymerase chain reaction was used to analyze the expression of the target genes in the cancer tissues and their corresponding adjacent tissues of 20 patients with colorectal cancer. The Kaplan-Meier Plotter database and the ROC Plotter database were used to analyze the relation between the high and low expression of the target genes and the prognosis in different patients. The significance level was set as α=0.05. ResultsA total of 651 HRGs and 329 DEGs were screened out. By taking the intersection of these two sets, 37 HDGs were obtained for subsequent analysis. Through Pearson correlation analysis, 25 key PD-1-related genes were screened out and 10 and 14 key PD-1-related genes were screened out by the MCC algorithm and the MCODE algorithm respectively. By taking the intersection of these three sets, 3 key PD-1-related genes were obtained, then survival analysis, the Aurora kinase A (AURKA) gene was finally screened out as the target gene. The expression level of the AURKA gene in the pan-cancer patients who responded to PD-1 inhibitor treatment was significantly higher than that in non-responders (P＜0.001), and was significantly lower in the six colorectal cancer cells treated with hypoxia than in six colorectal cancer cells treated with normoxia (P＜0.001). The AURKA expression in the colorectal cancer tissues was significantly higher than that in the corresponding adjacent colorectal tissues (P=0.008). The overall survival of pan-cancer patients with high AURKA expression was better than that of those with low AURKA expression [HR (95%CI)=0.67 (0.49, 0.93), P=0.015]. Among the colorectal cancer patients with MMR deficiency, the patients with low AURKA gene expression had worse overall survival [HR (95%CI)=2.596 (1.028, 6.332), P=0.043] and recurrence-free survival [HR (95%CI)=4.201 (1.092, 16.150), P=0.037] as compared with those with high AURKA gene expression. The low AURKA expression was associated with significantly worse overall survivals in the colorectal cancer patients harboring wild-type or mutant TP53, BRAF, and KRAS as compared with high AURKA expression (P＜0.05), while no statistically significant difference was found in the overall survival of the normal MMR patients between with high AURKA expression and low AURKA expression (P=0.307). ConclusionThe results of this bioinformatics analysis suggest that hypoxia down-regulated AURKA expression, and low AURKA expression is associated with worse prognosis in colorectal cancer patients, and worse reactivity and prognosis in patients treated with PD-1 inhibitors.
ObjectiveTo systematically evaluate the effect of mucin 1 (MUC1) expression on the prognosis and clinicopathologic characteristics of patients with colorectal cancer.MethodsThe cohort studies on the relationship between MUC1 expression and the prognosis of colorectal cancer patients were retrieved from PubMed, Embase, Web of Science, Cochrane Library, CNKI, China Biology Medicine, WanFang, VIP, and other databases from the establishment of the database to December 2020. The two researchers screened the literatures according to the inclusion and exclusion criteria, extracted relevant data, and performed meta analysis using Stata 12.0 software.ResultsA total of 17 eligible studies comprising 2 516 patients with colorectal cancer were included. The results of meta-analysis showed that the overall survival (OS) of patients with high MUC1 expression was worse than that with low MUC1 expression [HR=1.51, 95%CI (1.33, 1.71), P<0.001], but not statistically significant with disease-free survival [HR=1.39, 95%CI (0.41, 4.68), P=0.565]. Subgroup analysis results showed the same results as the overall analysis regardless of analysis method (multivariate or survival curve), different ethnic groups (Asian or Caucasian), and different sample sizes (≥100 or <100). The results of clinicopathologic analysis showed that the high expression of MUC1 was correlated with lymph node metastasis, distant metastasis, depth of invasion, and TNM stage (P<0.05), but not correlated with gender, age, degree of tumor differentiation, and tumor location (P>0.05).ConclusionsHigh expression of MUC1 is closely associated with poor prognosis, lymph node metastasis, distant metastasis, tumor invasion depth, and TNM stage in patients with colorectal cancer, which is expected to be an important reference indicator for disease monitoring and prognosis judgment of colorectal cancer.
ObjectiveTo explore the significance of mesenchymal epithelial transition factor (MET) as a clinical prognostic evaluation index for patients with pancreatic cancer based on bioinformatics analysis.MethodsThe GSE28735 and GSE62452 gene chips from GEO database were downloaded and the difference of MET gene expression between cancer and adjacent cancerous tissues were analyzed by bioinformatics. We downloaded pancreatic cancer gene chip from TCGA database to analyze the correlation between MET gene expression and clinicopathological features of pancreatic cancer patients and prognosis risk. Finally, the possible molecular mechanism of MET involved in pancreatic carcinogenesis was analyzed by GO and KEGG enrichment analysis.ResultsThe expression level of MET gene in pancreatic cancer tissues was significantly higher than that in adjacent cancerous tissues (P<0.001). The overall survival and disease-free survival of pancreatic cancer patients in the high MET gene expression group were lower than those in the low expression group (P<0.001). The expression level of MET gene was related to the age of pancreatic cancer patients, T stage, and histological grading of tumors (P<0.05), and high MET gene expression, age >65 years, and N1 stage were independent risk factors affecting the prognosis of pancreatic cancer patients. KEGG enrichment analysis showed that MET was mainly related to PI3K/AKT signaling pathway, FAK signaling pathway, and cancer transcription dysregulation and so on.ConclusionMET may be a valuable tumor marker for pancreatic cancer and can predict the poor prognosis of patients with pancreatic cancer.
Objective To summarize the key roles of cancer-associated fibroblasts (CAFs) in the pathogenesis, development, therapeutic resistance, and immune microenvironment modulation of colorectal cancer (CRC). MethodsThrough a systematic review of existing literature, this article summarizes the origin and heterogeneity of CAFs, their mechanisms of action in CRC occurrence and progression, and reviews potential CAFs-targeting therapeutic strategies. ResultsCAFs are heterogeneous with respect to both origin and function. As a critical ingredient in tumor microenvironment, CAFs drive CRC progression by promoting tumor proliferation, invasion, metastasis, angiogenesis. CAFs can mediate therapy resistance by regulating cancer stem cell properties and suppress antitumor immunity by regulating immune checkpoint molecules. Targeting specific CAFs subsets or their key signaling pathways demonstrat tumor-suppressive effects. ConclusionsCAFs are key regulators of CRC progression. Developing targeted therapeutic strategies against their origins, heterogeneity, and functional mechanisms holds the potential to providing new directions in CRC treatment.
ObjectiveTo systematically evaluate the correlation of amplification of human epidermal growth factor receptor 2 (HER2) with the clinicopathological characteristics and prognosis of colorectal cancer patients.MethodsPubMed, EMbase, Cochrane Library, Chinese Biomedical Literature Database (CBM), Wanfang, and other databases were searched, and cohort studies focused on the relationship between HER2 amplification and clinicopathological characteristics and prognosis of colorectal cancer patients were included. The retrieval time limit was from October 2020, and RevMan 5.4 software was used for meta-analysis.ResultsA total of 9 studies (11 cohorts) were included for meta-analysis of 7 209 patients with colorectal cancer. Results of the meta-analysis showed that HER2 amplification was not associated with overall survival [HR=1.10, 95%CI (0.98, 1.24), P=0.11]. HER2 amplification was not correlated with gender [OR=0.98, 95%C1 (0.74, 1.31), P=0.90] and tumor differentiation [OR=0.80, 95%C1 (0.49, 1.32), P=0.39], but correlated with the tumor location [OR=1.85, 95%C1 (1.01, 3.37), P=0.04], RAS wild-type gene [OR=6.36, 95%C1 (3.41, 11.87), P<0.000 01], TNM stage [OR=0.45, 95%C1 (0.32, 0.64), P<0.000 01], lymph node metastasis [OR=1.54, 95%C1 (1.12, 2.13), P=0.008], and the depth of tumor invasion [OR=0.17, 95%C1 (0.05, 0.55), P=0.003].ConclusionCurrent evidence shows that HER2 amplification is not associated with OS in patients with colorectal cancer, but associated with tumor infiltration, lymph node metastasis, TNM stage, tumor site, and RAS genotype.
Objective
To investigate association between –174C/G genetic polymorphism of interleukin-6 (IL-6) and susceptibility to gastric cancer by conducting a meta-analysis.
Methods
Such databases as PubMed, Embase, The Cochrane Library, Web of Science, CNKI, VIP, and Wanfang Data were searched from inception to January 2017 to collect case-control studies about the correlation between the –174C/G genetic polymorphism of IL-6 and susceptibility to gastric cancer. For the population genotype distributions of both the gastric cancer group and the control group, their odds ratios (OR) and 95% confidence intervals (CI) were taken as the effect indexes were applied to conduct meta-analysis in the homozygote model (CC vs. GG), heterozygote model (GC vs. GG), dominant model (CC+CG vs. GG), recessive model (CG+GG vs. CC), and allelic genetic model (C vs. G). Two reviewers independently screened the literatures, extracted the data, and evaluated the quality of the included studies. The meta-analysis was performed using Stata 12.0 software.
Results
Thirteen articles were included in the final meta-analysis, covering a total of 2 062 gastric cancer cases and 3 152 controls. The results of meta-analysis showed that there was no correlation between the IL-6 –174C/G genetic polymorphism and the risk of gastric cancer〔CC vs. GG: OR=1.33, 95% CI (0.92, 1.94); GC vs. GG: OR=1.32, 95% CI (0.96, 1.82); CC+CG vs. GG: OR=1.32, 95% CI (0.97, 1.80); CG+GG vs. CC: OR=0.89, 95% CI (0.67, 1.17); C vs. G: OR=1.22, 95% CI (0.98, 1.54)〕. But the results of the subgroup analysis showed there was a significant association between the IL-6 –174 C/G genetic polymorphism and the risk of gastric cancer in Asians〔CC vs. GG: OR=1.80, 95% CI (1.29, 2.50); GC vs. GG: OR=1.51, 95% CI (1.20, 1.90); CC+CG vs. GG: OR=1.60, 95% CI (1.30, 1.96); CG+GG vs. CC: OR=0.60, 95% CI (0.44, 0.83); C vs. G: OR=1.59, 95% CI (1.24, 2.03)〕. However, no association was found in Europeans〔CC vs. GG: OR=1.11, 95% CI (0.90, 1.39); GC vs. GG: OR=1.16, 95% CI (0.98, 1.37); CC+CG vs. GG: OR=1.12, 95% CI (0.96, 1.32); CG+GG vs. CC: OR=1.07, 95% CI (0.88, 1.30); C vs. G: OR=1.04, 95% CI (0.78, 1.41)〕 .
Conclusion
IL-6 –174C/G genetic polymorphism is associated with susceptibility to gastric cancer in Asians, which is not associated with susceptibility to gastric cancer in Europeans.
Bone remodeling requires an intimate cross-talk between osteoclasts and osteoblasts and is tightly coordinated with regulatory proteins that interact through complex autocrine/paracrine processes. Osteocytes, bone lining cells, osteomacs and vascular endothelial cells also regulate bone remodeling in the basic multicellular unit (BMU) via cell signaling networks of ligand-receptor complexes. In addition, through secreted and membrane-bound factors in the bone microenvironment, T and B lymphocytes mediate bone homeostasis for osteoimmunology. Osteoporosis and other bone diseases occur because multicellular communication within the BMU is disrupted. This review focuses on the roles of the cells in the BMU and the interaction between these cells and the factors involved in regulating bone remodeling at the cellular level. Understanding the process of bone remodeling and related genes could help us to lay the foundation for drug development against bone diseases.
