The Relationship between the Permanent Trigeminal Artery and Cerebrovascular Disease: A Meta-Analysis.

Background: We aimed to analyze the variability of the permanent trigeminal artery (PTA) and its relationship with cerebrovascular disease. Methods: To analyze the variability of the PTA and its relationship with cerebrovascular disease by using the terms "primitive trigeminal artery", "persistent primitive trigeminal artery", " persistent trigeminal artery variant", "PPTA", "PTAV", "carotid- basilar anastomoses", "carotid-vertebrobasilar anastomoses", "persisting embryonic vessels" were used as keywords, and the English-language literature related to PTA and cerebrovascular diseases published in PubMed, EMBAS, and Web of Science databases from 2000 to 2022 were searched by using "subject terms + free words". A meta-analysis of the collected data was performed using stata14.0 statistical software to assess the relationship between the immortal trigeminal artery and cerebrovascular-related diseases. Results: A total of 1908 relevant articles were initially retrieved for this study. Ten papers were initially screened according to the inclusion and exclusion criteria, while the literature was then read one by one to exclude duplicates, reviews, case reports, and conference abstracts, and six papers were finally included for meta-analysis. The six papers included in this paper were all cross-sectional studies with 39,355 subjects, of which 206 subjects had PTA, with a variation rate of approximately 0.52%, including 77 males and 129 females, 117 left-sided variants and 87 right-sided variants. In contrast, of the 206 subjects with a PTA, 52 had cerebrovascular disease, with an overall prevalence of approximately 25.24%. Conclusion: The PTA could influence the development of cerebrovascular disease.

Diagnostic value of SHOX2, RASSF1A gene methylation combined with CEA level detection in malignant pleural effusion.

AIM: To investigate the diagnostic value of combined detection of SHOX2 and RASSF1A gene methylation with carcinoembryonic antigen (CEA) level in diagnosing malignant pleural effusion. METHODS: Between March 2020 and December 2021, we enrolled 68 patients with pleural effusion admitted to the Department of Respiratory and critical care medicine of Foshan Second People's Hospital. The study group included 35 cases of malignant pleural effusion and 33 cases of benign pleural effusion. Methylation of the short homeobox 2 genes (SHOX2) and RAS-related region family 1A gene (RASSF1A) in pleural effusion samples were detected by real-time fluorescence quantitative PCR, and the level of carcinoembryonic antigen (CEA) in pleural effusion samples was detected by immune flow cytometry fluorescence quantitative chemiluminescence. RESULTS: SHOX2 or RASSF1A gene methylation was detected in 5 cases in the benign pleural effusion group and 25 patients in the malignant pleural effusion group. The positive rate of SHOX2 or RASSF1A gene methylation in the malignant pleural effusion group was significantly higher than in the benign pleural effusion group (71.4% vs. 15.2%, P < 0.01). Positive CEA (CEA > 5 ng/m) was detected in 1 case in the benign pleural effusion group and 26 patients in the malignant pleural effusion group. The CEA-positive rate in the malignant pleural effusion group was significantly higher than in the benign pleural effusion group (74.3% vs. 3%, P < 0.01). When SHOX2 and RASSF1A gene methylation was combined with CEA detection, 6 cases were positive in the benign pleural effusion group, and 31 patients were positive in the malignant pleural effusion group. The positive rate of combined detection in the malignant pleural effusion group was significantly higher than in the benign pleural effusion group (88.6% vs. 18.2%, P < 0.01). The sensitivity, specificity, accuracy, positive predictive value, negative predictive value, and Youden's index of SHOX2, RASSF1A gene methylation combined with CEA in diagnosing malignant pleural effusion were 88.6%, 81.8%, 85.3%, 83.8%, 87.1% and 0.7 respectively. CONCLUSION: The combined detection of SHOX2 and RASSF1A gene methylation with CEA level in pleural effusion has a high diagnostic value for malignant pleural effusion.

Dezocine Has the Potential to Regulate the Clinical and Biological Features of Tumors.

Cancer is the second leading cause of death following ischemic heart disease in the world and the primary clinical, social and economic burden. Surgical resection is the main measure for the treatment of the vast majority of solid tumors. However, the recurrence and metastasis of tumors occur at different periods after surgery in many cases undergoing radical tumor surgery, which is the main cause of death of tumor patients. Moreover, tumor patients are prone to suffer from mental depression, which may increase the morbidity and mortality of tumors. Tumors have a series of clinical biological signs with the following five main features: postoperative pain and cancerous pain; suppression of antitumor immunity; angiogenesis in tumors; proliferation, growth and metastasis of tumors; and mental depression. Surgery is the first treatment in the majority of cancer patients with solid tumors. Opioids are required for anesthesia and postoperative analgesia. For cancerous pain control, patients undergo surgery, and their quality of life of is improved. However, traditional opioids, such as morphine, may inhibit antitumor immunity, induce vascular growth of tumors and promote the proliferation, invasion and migration of cancer cells, and traditional opioids can induce a risk of somatic dependence. However, studies have found that not all opioids share the effects of immunosuppression, tumor proliferation promotion and angiogenesis induction. Dezocine, a novel opioid with specific pharmacological mechanisms, has been demonstrated to regulate the five clinical and biological features of tumors. We reviewed the preclinical and clinical studies of dezocine on postoperative pain and cancer pain in tumor patients as well as the immune system, tumor angiogenesis, tumor proliferation, tumor growth, tumor metastasis and mental depression. We proposed that dezocine may be the best choice of opioids for anesthesia and analgesia in cancer patients.

Identification of heterogeneous nuclear ribonucleoprotein as a candidate biomarker for diagnosis and prognosis of hepatocellular carcinoma.

BACKGROUND: Hepatocellular carcinoma (HCC) is the most common type of liver cancer with a high mortality rate. However, spliceosomal genes are still lacking in the diagnosis and prognosis of HCC. METHODS: Identification of differentially expressed genes (DEGs) was performed using the limma package in R software. Modules highly related to HCC were obtained by weighted gene co-expression network analysis (WGCNA), and the module genes were analyzed using the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway. The biomarker for diagnosing HCC was determined by receiver operating characteristic (ROC) curve analysis, and the effect of the biomarker in the diagnosis of HCC was evaluated by performing five-fold cross-validation with logistic regression. HCC specimens from preoperatively treated patients were tested for biomarker by real-time quantitative polymerase chain reaction (RT-qPCR). Kaplan-Meier analysis was used to assess the relationship between biomarker and patient survival. The role of biomarker was evaluated using ESTIMATE analysis in the tumor microenvironment. RESULTS: In this study, 389 DEGs were screened out from three Gene Expression Omnibus (GEO) datasets. We also found that the turquoise module of 123 genes from The Cancer Genome Atlas (TCGA) data was the key module with the highest correlation with HCC traits. Then, 123 genes were analyzed using the KEGG enrichment pathway, and eight genes were found to be most significantly related to the spliceosome pathway. We selected 8 genes and 389 DEGs shared genes, and finally got the only gene, heterogeneous nuclear ribonucleoprotein (hnRNPU). The high expression of hnRNPU was associated with poor prognosis of HCC, and hnRNPU was a biomarker for diagnosing HCC. In the tissues of patients with excellent HCC treatment hnRNPU messenger RNA (mRNA) was lower than in the tissues of patients with poor HCC treatment. High expression of hnRNPU was significantly increased in HCC patients with low stromal (P<0.05), low immune (P<0.05), and low estimation scores (P<0.05), and with high tumor purity (P<0.05) and high malignant progression (P<0.05) of the HCC. CONCLUSIONS: The hnRNPU gene identified in this study may become a new biomarker for the diagnosis and prognosis of HCC.

The construction and analysis of ceRNA network and patterns of immune infiltration in lung adenocarcinoma.

BACKGROUND: Competitive Endogenous RNA (ceRNA) may be closely associated with tumor progression. However, studies on ceRNAs and immune cells in LUAD are scarce. METHOD: The profiles of gene expression and clinical data of LUAD patients were extracted from the TCGA database. Bioinformatics methods were used to evaluate differentially-expressed genes (DEGs) and to form a ceRNA network. Preliminary verification of clinical specimens was utilized to detect the expressions of key biomarkers at the tissues. Cox and Lasso regressions were used to identify key genes, and prognosis prediction nomograms were formed. The mRNA levels of 9 genes in the risk score model in independent clinical LUAD samples were detected by qRT-PCR. The interconnection between the risk of cancer and immune cells was evaluated using the CIBERSORT algorithm, while the conformation of notable tumor-infiltrating immune cells (TIICs) in the LUAD tissues of the high and low risk groups was assessed using the RNA transcript subgroup in order to identify tissue types. Finally, co-expression study was used to examine the interconnection between the key genes in the ceRNA networks and the immune cells. RESULT: A ceRNA network of 115 RNAs was established, and nine key genes were identified to construct a Cox proportional-hazard model and create a prognostic nomogram. This risk-assessment model might serve as an independent factor to forecast the prognosis of LUAD, and it was consistent with the preliminary verification of clinical specimens. Survival analysis of clinical samples further validated the potential value of high risk groups in predicting LUAD prognosis. Five immune cells were identified with significant differences in the LUAD tissues of the high and low risk groups. Besides, two pairs of biomarkers associated with the growth of LUAD were found, i.e., E2F7 and macrophage M1 (R = 0.419, p = 1.4e- 08) and DBF4 and macrophage M1 (R = 0.282, p < 2.2 e- 16). CONCLUSION: This study identified several important ceRNAs, i.e. (E2F7 and BNF4) and TIICs (macrophage M1), which might be related to the development and prognosis of LUAD. The established risk-assessment model might be a potential tool in predicting LUAD of prognosis.

SESN2 correlates with advantageous prognosis in hepatocellular carcinoma.

BACKGROUND: SESN2 plays important roles in the regulation of cell survival, cell protection, and tumor suppression. However, the relationship between SESN2 expression and the clinicopathological attributes of hepatocellular carcinoma (HCC) is barely investigated. METHODS: One-step quantitative reverse transcription PCR, Western blotting analysis in 15 fresh HCC tissues, and immunohistochemistry (IHC) analysis in a tissue microarray (TMA) containing 100 HCC cases were performed to examine SESN2 expression. Survival analyses by Cox regression method and Kaplan-Meier curve were performed to describe the overall survival of 100 HCC patients. RESULTS: The SESN2 expression in HCC tissues declined dramatically compared with the corresponding noncancerous tissues, and SESN2 expression was remarkably associated with HBV infection (p = 0.019), HCV infection (p = 0.001), and lymph node metastasis (p = 0.033). Survival analysis further demonstrated that SESN2 expression could serve as an independent prognostic biomarker for overall survival in univariate (p = 0.001) and multivariate analyses (p = 0.003). CONCLUSION: The data are the first to indicate that SESN2 might be a novel prognostic marker for HCC and that elevated SESN2 expression predicts advantageous outcomes in HCC patients.

[Clinical implications of serum amyloid A level in patients with obstructive sleep apnea].

OBJECTIVE: To detect the levels of serum amyloid A (SAA) and explore the pathogenesis of cardiovascular diseases in patients with obstructive sleep apnea syndrome (OSAS). METHODS: Polysomnography was performed in 80 patients with OSAS and 20 control subjects matched for age and body mass index. The patients with OSAS were divided into mild OSAS group (n=22), moderate OSAS group (n=23) and severe OSAS group (n=35) according to the apnea hypopnea index (AHI). Serum amyloid A levels were measured in all the subjects by enzyme-linked immunosorbent assay for correlation analysis. RESULTS: Serum amyloid A levels in mild OSAS group (1.66-/+0.73 microg/ml), moderate OSAS group (2.72-/+1.12 microg/ml) and severe OSAS group (4.08-/+1.85 microg/ml) were significantly higher than those in the control group (0.66-/+0.59 microg/ml) (P<0.05). SAA levels also differed significantly between the 3 OSAS groups (P<0.01), increasing with the severity of OSAS. Correlation analysis indicated that SAA level was positively correlated to AHI (r=0.649, P<0.01) and TSaO(2)<90% (r=0.491, P<0.01), but inversely yo miniSaO(2) (r=-0.499, P<0.01). After 3 months of nCPAP therapy, SAA levels were significantly decreased in the 20 patients with severe OSAS (4.13-/+2.27 microg/ml vs 5.14-/+2.30 microg/ml, P<0.01). CONCLUSION: SAA levels are elevated in OSAS patients in close correlation to the severity of OSAS, which may contribute to the vulnerability of the patients to cardiovascular diseases. nCPAP therapy help reduce the risk for cardiovascular diseases in OSAS patients.