Objective: Angiographic slow/no-reflow during emergency percutaneous coronary intervention (PCI) in patients with ST-elevated acute myocardial infarction (AMI) may result in unfavorable outcomes. The aim of our study was to investigate the clinical factors and angiographic findings that predict slow/no-reflow phenomenon and the long-term prognosis of AMI patients with angiographic slow/no-reflow. Methods: A total of 210 consecutive AMI patients, who underwent primary PCI within 12 hours of symptom onset were divided into a normal flow group (thrombolysis in myocardial infarction [TIMI] flow grade 3, n = 169) and a slow/no-reflow group (≤TIMI flow grade 2, n = 41), based on cineangiograms performed during PCI. Results: A total of 41 patients (19.5%) developed slow/no-reflow phenomenon. Univariate analysis showed that delayed reperfusion, high thrombus burden on baseline angiography, and acute hyperglycemia all correlated with slow/no-reflow (P < 0.05 for all). Multivariate analysis revealed that hyperglycemia on admission (≥10 mmol/L; odds ratio [OR]: 1.7, 95% confidence interval [CI]: 1.423-2.971, P = 0.012), reperfusion time (≥6 h; OR:1.4, 95% CI: 1.193-1.695, P = 0.040), and high thrombus burden (OR: 1.6, 95% CI: 1.026-2.825, P = 0.031) were significant and independent predictors of angiographic slow/no-reflow. The 6-month mortality and incidence of major adverse cardiac and cerebrovascular events (MACCE) were significantly higher in the slow/no-reflow group than in the normal flow group. Angiographic slow/no-reflow was independently predictive of MACCE (hazard ratio [HR]: 2.642, 95% CI: 1.304-5.932, P = 0.028). Conclusion: Delayed reperfusion, high thrombus burden on baseline angiography, and blood glucose level on admission can be used to stratify AMI patients into a lower or higher risk for angiographic slow/no-reflow during PCI. In addition, angiographic slow/no-reflow predicts an adverse outcome in AMI patients. IntroductionThe aim of treatment for ST-elevation acute myocardial infarction (AMI) is to restore full antegrade blood flow into the infarct-related artery (IRA) and minimize ischemic damage to the myocardium. Thrombolytic therapy is an option, but primary emergency percutaneous coronary intervention (PCI) is the treatment of choice, based on lower rates of recurrent ischemia or infarction and good success rates in restoring antegrade blood flow in the IRA. 1,2 The beneficial effects of stents for patients with AMI have been reported, 3 but these effects have been limited because of a 14% to 25% incidence of slow/no-reflow phenomenon detected during angiography. 4,5 Several studies have demonstrated that AMI patients with angiographic slow/no-reflow have poor functional recovery and more frequently manifest post-AMI complications in comparison to those with good flow. 4,6 -9
We investigated the relationship between platelet to lymphocyte ratio (PLR) and contrast-induced nephropathy (CIN) in patients with ST-segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (pPCI). We enrolled 5719 patients in 3 tertiary hospitals from January 2005 to December 2010. The PLR was calculated as the ratio of platelet to lymphocyte counts on admission. Serum creatinine level was measured before and within 72 hours after contrast medium administration. To evaluate the relation between PLR and CIN, the 5719 patients were divided into a CIN group and a non-CIN group. Contrast-induced nephropathy occurred in 252 (4.4%) patients. Patients in the CIN group had significantly higher PLR than those in the non-CIN group (173.8 [62.3] and 116.2 [51.7], respectively; P < .001). In logistic regression analysis, PLR was an independent predictor of CIN (odds ratio: 1.432, 95% confidence interval: 1.205-1.816, P = .031), along with age, diabetes mellitus, creatinine, estimated glomerular filtration rate, and neutrophil to lymphocyte ratio. In conclusion, a higher PLR was an independent risk factor for the development of CIN in patients with STEMI undergoing pPCI.
Objectives: Recent studies have reported increased red blood cell distribution width (RDW) has been associated with adverse outcomes in heart failure and stable coronary disease. We investigated the association between RDW and risk of all-cause mortality in patients with ST-elevation myocardial infarction (STEMI) who were free of heart failure at baseline. Methods: We enrolled 691 patients with STEMI who were free of heart failure at baseline confirmed by coronary angiography in Beijing Friendship Hospital from January 2007 to December 2008. According to the median RDW at baseline (13.0%) on admission, the patients were divided into two groups: a low-RDW group (RDW <13.0%, n = 329) and a high-RDW group (RDW ≥13.0%, n = 362). All-cause mortality rates were compared between groups. Mean duration of follow-up was 41.8 months. The relation between RDW and clinical outcomes after hospital discharge were tested using Cox regression models, adjusting for clinical variables. At the same time, the sensitivity and specificity of RDW were analyzed by ROC analysis. Results: Forty-seven patients (6.8%) died during follow-up. The cumulative incidence of all-cause death was significantly higher in the high-RDW group than in the low-RDW group (log-rank p = 0.007). Multivariate analysis revealed that high RDW was associated with all-cause mortality (hazard ratio: 3.43; 95% confidence interval: 1.17-8.32; p = 0.025). The area under the ROC curve was 0.562. Conclusion: From the statistical point of view, increased RDW is associated with all-cause and cardiac mortality rates in patients with STEMI who were free of heart failure at baseline. But RDW is a marker with a very low prognostic accuracy that does not seem to be clinically helpful.
We investigated the association between platelet-to-lymphocyte ratio (PLR) and clinical outcomes (including all-cause mortality, recurrent myocardial infarction, heart failure, serious cardiac arrhythmias and ischemic stroke) in patients with ST-segment elevation myocardial infarction (STEMI). Based on PLR quartiles, 5886 patients with STEMI were categorized into 4 groups: <98.8 (n = 1470), 98.8 to 125.9 (n = 1474), 126.0 to 163.3 (n = 1478), >163.3 (n = 1464), respectively. We used Cox proportional hazards models to examine the relation between PLR and clinical outcomes. Mean duration of follow-up was 81.6 months, and 948 patients (16.1%) died during follow-up. The lowest mortality occurred in the lowest PLR quartile group ( P = 0.006), with an adjusted hazard ratio of 1.18 (95% confidence interval [CI], 1.04-1.55), 1.31 (95% CI, 1.18-1.64), and 1.59 (95% CI, 1.33-1.94) in patients with PLR of 98.8 to 125.9, 126.0 to 163.3, >163.3, respectively. Higher levels of PLR were also associated with recurrent myocardial infarction ( P = .023), heart failure ( P = .018), and ischemic stroke ( P = .043). In conclusion, a higher PLR was associated with recurrent myocardial infarction, heart failure, ischemic stroke, and all-cause mortality in patients with STEMI.
As a newly discovered cytokine, interleukin 9 was initially considered a T-lymphocyte growth factor. Interleukin 9 affects target cells by binding to a member of the γc-family of receptors and is involved in inflammation, autoimmune diseases, and other ailments. In recent years, mounting evidence reveals that interleukin 9 exerts antitumor effects, which has attracted considerable attention. Many previous studies were performed in vivo by establishing a mouse model of melanoma. Here, interleukin 9 protein and messenger RNA expression levels were both low in colon carcinoma tissue specimens, as assessed by immunohistochemistry and quantitative real-time polymerase chain reaction. In addition, interleukin 9 expression in these samples was correlated with TNM staging, Dukes staging, lymph node metastasis, and good prognosis, but not with gender, age, tumor size, tumor differentiation, and hepatic metastasis. In vivo, by establishing a mouse subcutaneous allograft model, we found that interleukin 9 overexpression inhibited tumor growth and resulted in longer survival time. Then, antitumor immune responses were increased by interleukin 9 as demonstrated by flow cytometry. Furthermore, interleukin 9 was shown to exert antitumor effects by regulating T-cell function and killing tumor cells in the tumor microenvironment. Overall, this study revealed that interleukin 9 exerts robust antitumor effects in colon cancer and transforms the tumor microenvironment in vivo.
ObjectiveThis study aimed to investigate the role of B7-H3 in chemotherapy resistance of pancreatic cancer cells and discover the potential signal transduction pathway and molecular targets involved.MethodsImmunohistochemical staining and real-time polymerase chain reaction (PCR) were used to determine the expression of B7-H3 in clinical specimens. Clinical data were applied to survival analysis. Phosphoprotein was purified from cultured Patu8988 cells using the Phosphoprotein Purification Kit. Cell apoptosis was detected using propidium iodide–Annexin V staining to investigate the relation between the expression of B7-H3 and Patu8988 cells treated with gemcitabine. Western blot was used to determine the effect of B7-H3 on the expression of proteins including extracellular signal–regulated kinase (ERK)1/2, epidermal growth factor receptor (EGFR), and Inhibitor of NF-κB(IκB) in Patu8988 cells; B7-H3 was activated by 4H7, which as an agonist monoclonal antibody to B7-H3.ResultsThe expression of B7-H3 was found to be higher in tumor tissues than in normal tissues of pancreatic carcinoma. Survival analysis revealed that patients in the low-B7-H3 expression group were likely to have a longer overall survival compared with those in the high-expression group (P < 0.05). B7-H3 activated by 4H7 could reduce gemcitabine-induced apoptosis in Patu8988 cells. Activation of B7-H3 by 4H7 induced variations in p-ERK1/2, EGFR, and IκB protein levels. When B7-H3 was upregulated, the expression levels of EGFR and p-ERK1/2 proteins significantly increased (P < 0.05), but the expression level of IκB significantly decreased (P < 0.05), especially in the gemcitabine-treated group.ConclusionThis study demonstrated that B7-H3 could deliver signals to pancreatic cancer cells to combat apoptosis induced by gemcitabine.
Metastasis is an important factor contributing to poor prognosis in patients with gastric cancer; yet, the molecular mechanism leading to this cell behavior is still not well understood. In this study, we explored the role of cysteine protease inhibitor SN (Cystatin SN, CST1) in promoting gastric cancer metastasis. We hypothesized that CST1 could regulate gastric cancer progression by regulating GPX4 and ferroptosis. Whole transcriptome sequencing suggested that the expression of CST1 was significantly increased in metastatic cancer, and high CST1 expression was correlated with a worse prognosis. Our data further confirmed that the overexpression of CST1 may significantly promote the migration and invasion of gastric cancer cells in vitro and enhance liver, lung, and peritoneal metastasis of gastric cancer in nude mice. Meanwhile, high expression of CST1 promoted the epithelial-mesenchymal transition (EMT) of gastric cancer cells. Mechanistically, a co-immunoprecipitation experiment combined with mass spectrometry analysis confirmed that CST1 could interact with GPX4, a key protein regulating ferroptosis. CST1 relieves GPX4 ubiquitination modification by recruiting OTUB1, improving GPX4 protein stability and reducing intracellular reactive oxygen species (ROS), thereby inhibiting ferroptosis and, in turn, promoting gastric cancer metastasis. Moreover, clinical data suggested that CST1 is significantly increased in peripheral blood and ascites of gastric cancer patients with metastasis; multivariate Cox regression model analysis showed that CST1 was an independent risk factor for the prognosis of gastric cancer patients. Overall, our results elucidated a critical pathway through which high CST1 expression protects gastric cancer cells from undergoing ferroptosis, thus promoting its progression and metastasis. CST1 may be used as a new oncological marker and potential therapeutic target for gastric cancer metastasis.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.