Linkage of CDC42 and T-helper cell ratio with anxiety, depression and quality of life in ST-elevation myocardial infarction.

Objective: To investigate the correlations between CDC42 and T-cell subsets concerning anxiety, depression and quality of life in ST-elevation myocardial infarction patients undergoing percutaneous coronary intervention. Methods: Sera from 156 participants were analyzed for CDC42 levels and Th1, Th2, Th17 and Treg cells. Results: CDC42 correlated with reduced Th1/Th2 and Th17/Treg ratios, lower anxiety and depression, and higher EuroQol visual analog scale (EQ-VAS) score. The Th17/Treg ratio correlated with elevated anxiety, depression, EuroQol-5 dimensions score and decreased EQ-VAS score. The Th1/Th2 ratio was positively related to the EQ-VAS score. Conclusion: CDC42 correlates with reduced Th1/Th2 and Th17/Treg ratios, reduced anxiety and depression, and improved quality of life in ST-elevation myocardial infarction patients undergoing percutaneous coronary intervention.

CDC42 is a protein that regulates immune cells and negative mood. This study enrolled 156 patients with ST-elevation myocardial infarction (a severe type of coronary artery disease) who had percutaneous coronary intervention (a treatment that improves coronary blood flow). Their blood was collected for detecting CDC42 and specific immune cells, including Th1, Th2, Th17 and Treg cells. Their feelings of anxiety, depression and quality of life (QoL) were assessed using relevant questionnaires. The results showed that if a patient presented with reduced CDC42, they would have a high probability of anxiety and depression and poor QoL, as well as increased Th1 and Th17 cells. The study also found that patients with increased Th17 cells or decreased Treg cells would have a high possibility of anxiety and depression, as well as bad QoL. In addition, if a patient had increased Th2 cells, they would have a high probability of poor QoL. In summary, the detection of CDC42 can help ST-elevation myocardial infarction patients who have percutaneous coronary intervention better observe anxiety and depression.

Association Between IL-17 and Chronic Obstructive Pulmonary Disease: A Systematic Review and Meta-Analysis.

Background: Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory disease characterized by neutrophils airway infiltration. It is currently known that Interleukin-17 (IL-17) is an important pro-inflammatory factor. It can promote the accumulation of neutrophils and participate in the chronic inflammatory process of COPD. However, the value of IL-17 levels in the diagnosis and assessment of COPD remains controversial. In view of this, we conducted a systematic review and meta-analysis to assess its relevance. Methods: We searched databases such as PubMed, Web of Science, Cochrane Library and Embase to extract original research. Results: A total of 10 studies with 2268 participants were included in this meta-analysis. The results showed that the level of serum IL-17 in patients with stable COPD was significantly higher than that in healthy controls (standard mean difference SMD, 1.59, 95% CI 0.84-2.34; p<0.001). Compared with the stable COPD group, the serum IL-17 level in acute exacerbation (AECOPD) was significantly higher (SMD, 1.78, 95% CI 1.22-2.33; p<0.001). The level of IL-17 in sputum of COPD patients was also higher than that of healthy controls (SMD, 2.03, 95% CI 0.74-3.31; p<0.001). Conclusion: Our results showed that IL-17 levels were elevated in serum and sputum in COPD patients compared with healthy controls, and IL-17 levels increased with disease progression. IL-17 serves as a potential biomarker to indicate the persistence of neutrophilic inflammation and exacerbation of COPD.

Role of Th17 cells, Treg cells, and Th17/Treg imbalance in immune homeostasis disorders in patients with chronic obstructive pulmonary disease.

Chronic obstructive pulmonary disease (COPD) is the third leading cause of death worldwide, following strokes and cardiovascular diseases. Chronic lung inflammation is believed to play a role in the development of COPD. In addition, accumulating evidence shows that the immune system plays a crucial role in the pathogenesis of COPD. Significant advancements have been made in research on the pathogenesis of immune diseases and chronic inflammation in recent years, and T helper 17 (Th17) cells and regulatory T (Treg) cells have been found to play a crucial role in the autoimmune response. Th17 cells are a proinflammatory subpopulation that causes autoimmune disease and tissue damage. Treg cells, on the other hand, have a negative effect but can contribute to the occurrence of the same disease when their antagonism fails. This review mainly summarizes the biological characteristics of Th17 cells and Treg cells, their roles in chronic inflammatory diseases of COPD, and the role of the Th17/Treg ratio in the onset, development, and outcome of inflammatory disorders, as well as recent advancements in immunomodulatory treatment targeting Th17/Treg cells in COPD.

Chest X-ray features facilitate screening for pulmonary hypertension caused by fibrosing mediastinitis.

Background: Misdiagnosis and underdiagnosis of pulmonary hypertension caused by fibrosing mediastinitis (PH-FM) are considerably prevalent due to unspecific symptoms and as well as the lack of awareness of this fatal disease. Objectives: The aim of this study was to evaluate the diagnostic accuracy of the chest X-ray (CXR) for screening the patients with PH-FM from those with pulmonary hypertension (PH). Design: This was a retrospective observational cohort study. Methods: The patients with suspected PH were recruited between October 2014 and October 2020. All the clinical data and CXR findings were collected. The sensitivity, specificity, and likelihood ratio of the CXR features were calculated. Logistic regression was used to identify the factors associated with the CXR characteristics and FM and to generate a prediction model. Finally, the diagnostic efficiency of the prediction model was evaluated using nomogram and internal validation. Results: The patients with PH-FM (n = 36) and PH caused by the diseases other than FM (PH-non-FM, n = 62) were enrolled. The CXR features, including atelectasis, pleural effusion, consolidation, nodules, calcification, interlobular septal thickening, and interstitial reticulation, were more prevalent in patients with PH-FM than in those with PH-non-FM (all p < 0.05). Atelectasis had a specificity of 97%, a sensitivity of 50%, and a greater accuracy for diagnosing of PH-FM [area under the curve (AUC) = 0.720; 95% CI: 0.634-0.806] than the other factors did. The combination of tuberculosis, natural logarithmic NT-proBNP (lnBNP), atelectasis, pleural effusion, and prominent right heart border constituted a prediction model to distinguish the PH-FM from the PH-non-FM, with a sensitivity of 91.7% and a specificity of 83.9%. The model demonstrated good prediction performance by showing an AUC of 0.922 (95% CI: 0.861-0.983) in the internal validation. Conclusion: In this study, atelectasis was the most specific and accurate CXR characteristic for identifying PH-FM in the PH patients. The combination of atelectasis, pleural effusion, prominent right heart border, tuberculosis, and lnBNP constituted a prediction model that distinguished the PH-FM patients from the PH-non-FM ones with good performance.

Pulmonary Hypertension Caused by Fibrosing Mediastinitis.

Pulmonary hypertension (PH) is a progressive and severe disorder in pulmonary hemodynamics. PH can be fatal if not well managed. Fibrosing mediastinitis (FM) is a rare and benign fibroproliferative disease in the mediastinum, which may lead to pulmonary vessel compression and PH. PH caused by FM (PH-FM) is a pathologic condition belonging to group 5 in the World Health Organization PH classification. PH-FM has a poor prognosis because of a lack of effective therapeutic modalities and inappropriate diagnosis. With the development of percutaneous pulmonary vascular interventional therapy, the prognosis of PH-FM has been greatly improved in recent years. This article provides a comprehensive review on the epidemiology, pathophysiologic characteristics, clinical manifestations, diagnostic approaches, and treatment modalities of PH-FM based on data from published reports and our medical center with the goal of facilitating the diagnosis and treatment of this fatal disease.

The role of the inflammasome and its related pathways in ovarian cancer

Ovarian cancer (OC) is the most lethal tumor of the female reproductive tract and one of the most prevalent causes of death among female cancer patients. The absence of suitable procedures for early diagnosis, chemoresistance, and limited surgical debulking are all contributing to poor survival in patients. Despite aggressive treatments, the majority of patients have a recurrence within 16–22 months. Inflammasomes are multimeric protein complexes that play a major role in the innate immune system and inflammation. The overexpression of inflammasome-related pathways, including NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3), Absent in melanoma 2 (AIM2), caspase-1, and Interleukin (IL)-1 have been reported in OC patients and in vitro cell lines. Therefore, inflammasome-related genes and protein might have a role in OC pathogenesis. Considering the potential relationship between inflammasome and OC, this study aimed to provide a literature-based review to explain the role of inflammasome and inflammation in cancer progression in OC. (AU)

The role of the inflammasome and its related pathways in ovarian cancer.

Ovarian cancer (OC) is the most lethal tumor of the female reproductive tract and one of the most prevalent causes of death among female cancer patients. The absence of suitable procedures for early diagnosis, chemoresistance, and limited surgical debulking are all contributing to poor survival in patients. Despite aggressive treatments, the majority of patients have a recurrence within 16-22 months. Inflammasomes are multimeric protein complexes that play a major role in the innate immune system and inflammation. The overexpression of inflammasome-related pathways, including NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3), Absent in melanoma 2 (AIM2), caspase-1, and Interleukin (IL)-1 have been reported in OC patients and in vitro cell lines. Therefore, inflammasome-related genes and protein might have a role in OC pathogenesis. Considering the potential relationship between inflammasome and OC, this study aimed to provide a literature-based review to explain the role of inflammasome and inflammation in cancer progression in OC.

Evaluation of risk factors and effective factors in determining the prognosis of ovarian cancer.

Ovarian cancer is still one of the leading causes of death from reproductive system cancers. Despite recent advances in treating this cancer, ovarian cancer is the fourth cause of death in women. Knowing the risk factors of ovarian cancer and the factors affecting the prognosis of this tumor can be helpful. This study investigates risk factors and practical factors in determining the prognosis of ovarian cancer. In the present study, we searched through various databases such as Wiley Online Library, Google Scholar, PubMed, and Elsevier with the keywords Polycystic Ovarian, Ovarian Estrogen-Dependent Tumors Syndrome Chronic Inflammation, Prognosis of Ovarian Cancer, among published articles from 1996 to 2022. Based on these studies, we investigated the age of menstruation, age of menopause, number of pregnancies, family history of ovarian cancer and genital tract cancer, use of birth control pills, histological type of tumor, degree of cell differentiation, type of surgery, and post-surgery treatments, and examination of the serum level of tumor marker CA12, as well as the role of polycystic ovary syndrome in the development of ovarian cancer. In general, infertility was one of the most important risk factors and the serum level of tumor marker CA125 was one of the most important determinants of ovarian cancer prognosis.

Prognostic implications of ST-segment elevation in lead aVR in patients with acute coronary syndrome: A meta-analysis.

BACKGROUND: ST-segment elevation (STE) in lead aVR is a useful tool in recognizing patients with left main or left anterior descending coronary obstruction during acute coronary syndrome (ACS). The prognostic implication of STE in lead aVR on outcomes has not been established. METHODS: We performed a systematic search for clinical studies about STE in lead aVR in four databases including PubMed, EMBASE, Cochrane Library, and Web of Science. Primary outcome was in-hospital mortality. Secondary outcomes included in-hospital (re)infarction, in-hospital heart failure, and 90-day mortality. RESULTS: We included 7 studies with a total of 7,700 patients. The all-cause in-hospital mortality of patients with STE in lead aVR during ACS was significantly higher than that of patients without STE (OR: 4.37, 95% CI 1.63 to 11.68, p = .003). Patients with greater STE (>0.1 mV) in lead aVR had a higher in-hospital mortality when compared to lower STE (0.05-0.1 mV) (OR: 2.00, 95% CI 1.11-3.60, p = .02), However, STE in aVR was not independently associated with in-hospital mortality in ACS patients (OR: 2.72, 95% CI 0.85-8.63, p = .09). The incidence of in-hospital myocardial (re)infarction (OR: 2.77, 95% CI 1.30-5.94, p = .009), in-hospital heart failure (OR: 2.62, 95% CI 1.06-6.50, p = .04), and 90-day mortality (OR: 10.19, 95% CI 5.27-19.71, p < .00001) was also noted to be higher in patients STE in lead aVR. CONCLUSIONS: This contemporary meta-analysis shows STE in lead aVR is a poor prognostic marker in patients with ACS with higher in-hospital mortality, reinfarction, heart failure and 90-day mortality. Greater magnitude of STE portends worse prognosis. Further studies are needed to establish an independent predictive role of STE in aVR for these adverse outcomes.

A rare case of severe right heart failure due to pulmonary artery lymphomatoid granulomatosis.

Lymphomatoid granulomatosis is a rare, vascular-centric, and vessel-destroying lymphoproliferative disease that hardly involves the pulmonary arteries. Herein, we report a case with severe right heart failure and pulmonary arterial stenosis caused by pulmonary artery lymphomatoid granulomatosis. This case was diagnosed by percutaneous transluminal pulmonary artery biopsy and was effectively treated with stent implantation and steroid administration.

GST null polymorphisms may affect the risk of coronary artery disease: evidence from a meta-analysis.

BACKGROUND: Whether glutathione S-transferase (GST) null polymorphisms, namely GSTM1 null, GSTP1 null and GSTT1 null polymorphisms, influence the risk of coronary artery disease (CAD) or not remains unclear. Thus, the authors performed a meta-analysis to more robustly estimate associations between GST null polymorphisms and the risk of CAD by integrating the results of previous publications. METHODS: Medline, Embase, Wanfang, VIP and CNKI were searched comprehensively for eligible studies, and 45 genetic association studies were finally selected to be included in this meta-analysis. RESULTS: We found that GSTM1 null polymorphism was significantly associated with the risk of CAD in overall population (OR = 1.37, p = 0.003) and mixed population (OR = 1.61, p = 0.004), GSTP1 null polymorphism was significantly associated with the risk of CAD in overall population (OR = 1.23, p = 0.03), whereas GSTT1 null polymorphism was significantly associated with the risk of CAD in overall population (OR = 1.23, p = 0.02), Caucasians (OR = 1.23, p = 0.02) and East Asians (OR = 1.38, p < 0.0001). CONCLUSIONS: This meta-analysis demonstrated that GSTM1 null, GSTP1 null and GSTT1 null polymorphisms were all significantly associated with an increased risk of CAD.

Salvianolic acid B protects against sepsis-induced liver injury via activation of SIRT1/PGC-1α signaling.

Liver injury occurs frequently during sepsis, which leads to high mortality and morbidity. A previous study has suggested that salvianolic acid B (SalB) is protective against sepsis-induced lung injury. However, whether SalB is able to protect against sepsis-induced liver injury remains unclear. The present study aimed to investigate the effects of SalB on sepsis-induced liver injury and its potential underlying mechanisms. Sepsis was induced in mice using a cecal ligation and puncture (CLP) method. The mice were treated with SalB (30 mg/kg intraperitoneally) at 0.5, 2 and 8 h after CLP induction. Pathological alterations of the liver were assessed using hematoxylin and eosin staining. The serum levels of alanine transaminase (ALT), aspartate aminotransferase (AST), tumor necrosis factor (TNF)-α and interleukin (IL)-6 were measured. The hepatic mRNA levels of TNF-α, IL-6, Bax and Bcl-2 were also detected. The results suggested that treatment with SalB ameliorated sepsis-induced liver injury in the mice, as supported by the mitigated pathologic changes and lowered serum aminotransferase levels. SalB also decreased the levels of the inflammatory cytokines TNF-α and IL-6 in the serum and the liver of the CLP model mice. In addition, SalB significantly downregulated Bax expression and upregulated Bcl-2 expression, and upregulated the expression levels of SIRT1 and PGC-1α. However, when sirtuin 1 (SIRT1) small interfering RNA was co-administered with SalB, the protective effects of SalB were attenuated and the expression levels of SIRT1 and PGC-1α were reduced. In summary, these results indicate that SalB mitigates sepsis-induced liver injury via reduction of the inflammatory response and hepatic apoptosis, and the underlying mechanism may be associated with the activation of SIRT1/PGC-1α signaling.

Meta-analysis of right ventricular function in patients with aortic stenosis after transfemoral aortic valve replacement or surgical aortic valve replacement.

BACKGROUND: Right ventricular function (RVF) is an independent predictor of prognosis for patients undergoing aortic valve replacement: transcatheter aortic valve replacement (TAVR) or surgical aortic valve replacement (SAVR). The effect of transfemoral aortic valve replacement (TF-TAVR) on RVF is uncertain. We aimed to perform a meta-analysis of the effect of TF-TAVR on RVF in patients with aortic stenosis (AS) and compare the effect of TF-TAVR with SAVR. METHODS: We searched relevant studies from PubMed, Embase, Cochrane Library databases, and Web of Science. Furthermore, two reviewers (Wang AQ and Cao YS) extracted all relevant data, which were then double checked by another two reviewers (Zhang M and Qi GM). We used the forest plot to present results. Tricuspid annular plane systolic excursion (TAPSE) was the primary outcome. RESULTS: This meta-analysis included 11 studies. There were 353 patients who underwent TF-TAVR, and 358 patients who were subjected to SAVR. There was no significant difference in TAPSE at 1 week and 6 months as well as right ventricular ejection fraction (RVEF) at <2 weeks and 6 months after TF-TAVR. For the SAVR group, TAPSE at 1 week and 3 months as well as fractional area change (FAC) at 3 months post procedure were significantly aggravated, while RVEF did not change significantly. Moreover, TAPSE post-TF-TAVR was significantly improved as compared with post-SAVR. The △TAPSE, the difference between TAPSE post-procedure and TAPSE prior to procedure, was also significantly better in the TF-TAVR group than in the SAVR group. CONCLUSION: RVF was maintained post TF-TAVR. For SAVR, discrepancy in the measured parameters exists, as reduced TAPSE indicates compromised longitudinal RVF, while insignificant changes in RVEF implicate maintained RVF post procedure. Collectively, our study suggests that the baseline RV dysfunction and the effect of TF-TAVR versus SAVR on longitudinal RVF may influence the selection of aortic valve intervention.

ETS2 and microRNA-155 regulate the pathogenesis of heart failure through targeting and regulating GPR18 expression.

Heart failure (HF) is a global pandemic cardiovascular disease with increasing prevalence, but the pathogenesis remains to be elucidated. The present study aimed to investigate the underlying mechanism in heart failure (HF) using bioinformatics and experimental validation. A HF-associated dataset GSE84796 was downloaded from the Gene Expression Omnibus database and differentially expressed genes (DEGs) were screened for using Bayes method in the Limma package. Kyoto Encyclopedia of Genes and Genomes pathway analysis was used to perform pathway enrichment analysis of these DEGs using The Database for Annotation, Visualization and Integrated Discovery. A protein-protein interaction (PPI) network of DEG-encoded proteins was subsequently constructed using the Search tool for the Retrieval of Interacting Genes/Proteins, and a transcription factor (TF)/miRNA-target network was constructed according to the WEB-based Gene SeT AnaLysis Tookit. The expression levels of microRNA (miRNA/miR)-155, G-protein coupled receptor 18 (GRP18) and E26 transformation-specific transcription factor 2 (ETS2) were analyzed in clinical HF samples, and functional validations were performed in H9c2 (2-1) cells. A total of 419 DEGs were identified, including 366 upregulated genes and 53 downregulated genes. The upregulated DEGs were significantly enriched in the pathways of 'cytokine-cytokine receptor interaction', 'natural killer cell mediated cytotoxicity' and 'primary immunodeficiency'. A total of two functional modules were identified in the PPI network: Module A was enriched in 3 KEGG pathways and module B was enriched in 15 KEGG pathways. Furthermore, a total of three miRNAs and eight TFs were identified in the TF/miRNA-target network. Specifically, GPR18 was discovered to be targeted by both ETS2 and miR-155. Clinical validation revealed that the expression levels of miR-155 were significantly decreased in the HF samples, whereas the expression levels of ETS2 and GPR18 were significantly increased in HF samples. In conclusion, the present study suggested that GPR18 may be a target of ETS2 and miR-155, and miR-155 may regulate cell viability and apoptosis in H9c2 (2-1) cells through targeting and regulating GPR18.

MiR-3150b inhibits hepatocellular carcinoma cell proliferation, migration and invasion by targeting GOLPH3.

BACKGROUND: In this study, we aimed to explore the potential involvement of miR-3150b in hepatocellular carcinoma (HCC) carcinogenesis. METHODS: The expression of miR-3150b and Golgi phosphoprotein 3 (GOLPH3) was determined in HCC cell lines. Cell proliferation, migration and invasion were estimated by Cell Counting Kit-8, wound healing and Transwell assays. The association between miR-3150b and GOLPH3 was verified by luciferase assay. RESULTS: MiR-3150b was downregulated, while GOLPH3 was remarkably upregulated in HCC cells. Furthermore, miR-3150b inhibited HCC cell proliferation, migration and invasion. MiR-3150b directly targeted and negatively regulated GOLPH3. CONCLUSION: MiR-3150b suppressed HCC cell proliferation, invasion and migration by targeting GOLPH3.