Data_Sheet_1_The predictive value of CatLet© angiographic scoring system for long-term prognosis in patients with acute myocardial infarction presenting > 12 h after symptom onset.docx

BackgroundWe have recently developed the Coronary Artery Tree description and Lesion EvaluaTion (CatLet©) angiographic scoring system, which is capable of accounting for the variability in coronary anatomy, and risk-stratifying patients with coronary artery disease. This study aimed to clarify whether the CatLet score had a predictive value for long-term prognosis in patients with acute myocardial infarction (AMI) presenting > 12 h after symptom onset.Materials and methodsThe CatLet score was calculated for 1,018 consecutively enrolled AMI patients, who were divided into 3 groups according to the CatLet score tertiles. The primary endpoint was major adverse cardiac events (MACEs), defined as a composite of myocardial infarction, cardiac death, and ischemia-driven revascularization; secondary endpoints were all-cause death, cardiac death, myocardial infarction, and ischemia-driven revascularization.ResultsThe CatLet score was capable of predicting long-term prognosis at a median 4.9-year follow-up alone or after adjustment for risk factors. Multivariable-adjusted hazard ratios (95% CI)/unit higher score were 1.06 (1.05–1.08) for MACEs, 1.05 (1.03–1.07) for all-cause death, 1.06 (1.04–1.09) for cardiac death, 1.06 (1.04–1.08) for myocardial infarction, and 1.06 (1.04–1.08) for revascularization. The univariate model showed good calibration (χ2 = 8.25, P = 0.4091) and good discrimination (area under ROC curve = 0.7086) for MACEs.ConclusionThe CatLet score is an independent predictor of long-term clinical outcomes of patients with AMI presenting > 12 h after symptom onset (http://www.chictr.org.cn; Registry Number: ChiCTR2000033730).</p

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<p>Streptococcus agalactiae and Candida albicans often co-colonize the female genital tract, and under certain conditions induce mucosal inflammation. The role of the interaction between the two organisms in candidal vaginitis is not known. In this study, we found that co-infection with S. agalactiae significantly attenuated the hyphal development of C. albicans, and that EFG1-Hwp1 signal pathway of C. albicans was involved in this process. In a mouse model of vulvovaginal candidiasis (VVC), the fungal burden and the levels of pro-inflammatory cytokines, IL-1β, IL-6 and TNF-α showed a increase on co-infection with S. agalactiae, while the level of TH17 T cells and IL-17 in the cervicovaginal lavage fluid were significantly decreased. Our results indicate that S. agalactiae inhibits C. albicans hyphal development by downregulating the expression of EFG1-Hwp1. The interaction between S. agalactiae and C. albicans may attenuate host vaginal mucosal TH17 immunity and contribute to mucosal colonization by C. albicans.</p

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<p>Streptococcus agalactiae and Candida albicans often co-colonize the female genital tract, and under certain conditions induce mucosal inflammation. The role of the interaction between the two organisms in candidal vaginitis is not known. In this study, we found that co-infection with S. agalactiae significantly attenuated the hyphal development of C. albicans, and that EFG1-Hwp1 signal pathway of C. albicans was involved in this process. In a mouse model of vulvovaginal candidiasis (VVC), the fungal burden and the levels of pro-inflammatory cytokines, IL-1β, IL-6 and TNF-α showed a increase on co-infection with S. agalactiae, while the level of TH17 T cells and IL-17 in the cervicovaginal lavage fluid were significantly decreased. Our results indicate that S. agalactiae inhibits C. albicans hyphal development by downregulating the expression of EFG1-Hwp1. The interaction between S. agalactiae and C. albicans may attenuate host vaginal mucosal TH17 immunity and contribute to mucosal colonization by C. albicans.</p

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<p>Streptococcus agalactiae and Candida albicans often co-colonize the female genital tract, and under certain conditions induce mucosal inflammation. The role of the interaction between the two organisms in candidal vaginitis is not known. In this study, we found that co-infection with S. agalactiae significantly attenuated the hyphal development of C. albicans, and that EFG1-Hwp1 signal pathway of C. albicans was involved in this process. In a mouse model of vulvovaginal candidiasis (VVC), the fungal burden and the levels of pro-inflammatory cytokines, IL-1β, IL-6 and TNF-α showed a increase on co-infection with S. agalactiae, while the level of TH17 T cells and IL-17 in the cervicovaginal lavage fluid were significantly decreased. Our results indicate that S. agalactiae inhibits C. albicans hyphal development by downregulating the expression of EFG1-Hwp1. The interaction between S. agalactiae and C. albicans may attenuate host vaginal mucosal TH17 immunity and contribute to mucosal colonization by C. albicans.</p