Navegando por Palavras-chave "remodeling"
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- ItemSomente MetadadadosRelaxation of the mouse pubic symphysis during late pregnancy is not accompanied by the influx of granulocytes(Wiley-Blackwell, 2008-03-01) Rosa, Renata Giardini; Badin Tarsitano, Christiane Aparecida; Hyslop, Stephen; Yamada, Aureo Tatsumi; Toledo, Olga Maria S. [UNIFESP]; Joazeiro, Paulo Pinto; Universidade Estadual de Campinas (UNICAMP); Universidade Federal de São Paulo (UNIFESP)In some animals, such as mice and guinea pigs, a hormonally controlled mechanism increases the flexibility of the pubic symphysis and enhances the cervical remodeling necessary for safe delivery. Cervical ripening during pregnancy is associated with a paradoxical influx of leukocytes. However, the changes in cell metabolism during relaxation of the mouse pubic symphysis for delivery have not been extensively studied. in this work, we used light microscopy and transmission and scanning electron microcopy, as well as immunohistochemistry and Western blotting for MMP-8, to investigate the involvement of granulocytes or resident stromal cells in the relaxation of the virgin pubic symphysis during late pregnancy (days 18 and 19, before delivery) in vivo and in explanted joints. MMP-8 was studied because this collagenase is a hallmark for cervical ripening associated with the influx of granulocytes during late pregnancy. Extensive dissolution and disorganization of the extracellular matrix was seen around fibroblastic-like cells in late pregnancy. in contrast to the cervix (positive control), morphological and immunohistochemical analyses revealed that there was no characteristic cellular inflammatory response in the interpubic tissue. Staining for MMP-8 was observed in chondroid and fibroblastic-like cells of virgin and relaxed interpubic ligament, respectively. However, no granulocytes were seen during the extensive remodeling of the pubic joint in late pregnancy. These results indicate that constitutive stromal cells may have an important role in tissue relaxation during remodeling of the pubic symphysis in pregnancy.
- ItemSomente MetadadadosSleep Duration and Quality as Related to Left Ventricular Structure and Function(Lippincott Williams & Wilkins, 2018) Lee, Jae-Hon; Park, Sung Keun; Ryoo, Jae-Hong; Oh, Chang-Mo; Kang, Jeong Gyu; Mansur, Rodrigo B. [UNIFESP]; Alfonsi, Jeffrey E.; Lee, Yena; Shin, Sun-Han; McIntyre, Roger S.; Jung, Ju YoungObjective Inadequate sleep is associated with increased risk of cardiovascular events; however, the associations between sleep duration or quality and cardiac function or structure are not well understood. This cross-sectional study was conducted to investigate to what extent sleep duration and quality are associated with left ventricular (LV) diastolic dysfunction or structural deterioration. Methods A total of 31,598 healthy Korean adults who received echocardiography and completed the Pittsburg Sleep Quality Index were enrolled in this study. Participants were stratified into three groups by self-reported sleep duration (i.e., <7, 7-9, >9 hours) and into two groups by subjective sleep quality. Sleep duration was also assessed as a continuous variable. The odds ratios for impaired LV diastolic function, increased relative wall thickness, and LV hypertrophy (LVH) were compared between groups using multivariable logistic regression analyses. Results After adjustment for confounding variables (e.g., age, smoking, body mass index), there was a statistically significant association between short sleep duration (<7 hours) and greater LVH (fully adjusted odds ratio = 1.32 [95% confidence interval {CI} = 1.02-1.73]). Short sleep duration was also significantly associated with greater LVH (0.87 per hour [95% CI = 0.78-0.98]) and increased relative wall thickness (0.92 [95% CI = 0.86-0.99]), but there was no significant association between sleep and LV diastolic function. Among individuals with normal sleep duration, poor quality of sleep was not associated with adverse cardiac measures. Conclusions These results indicate that short sleep duration (<7 hours) is associated with unfavorable LV structural characteristics. The association of insufficient sleep with adverse cardiovascular health outcomes may be mediated in part by adverse changes in cardiac structure and function.
- ItemSomente MetadadadosXanthine oxidoreductase inhibition causes reverse remodeling in rats with dilated cardiomyopathy(Lippincott Williams & Wilkins, 2006-02-03) Minhas, K. M.; Saraiva, Roberto Magalhães [UNIFESP]; Schuleri, K. H.; Lehrke, S.; Zheng, M. Z.; Saliaris, A. P.; Berry, C. E.; Vandegaer, K. M.; Li, D. C.; Hare, J. M.; Johns Hopkins Med Inst; Universidade Federal de São Paulo (UNIFESP)Increased reactive oxygen species (ROS) generation is implicated in cardiac remodeling in heart failure (HF). As xanthine oxidoreductase (XOR) is 1 of the major sources of ROS, we tested whether XOR inhibition could improve cardiac performance and induce reverse remodeling in a model of established HF, the spontaneously hypertensive/HF (SHHF) rat. We randomized Wistar Kyoto (WKY, controls, 18 to 21 months) and SHHF ( 19 to 21 months) rats to oxypurinol (1 mmol/L; n = 4 and n = 15, respectively) or placebo (n = 3 and n = 10, respectively) orally for 4 weeks. At baseline, SHHF rats had decreased fractional shortening (FS) (31 +/- 3% versus 67 +/- 3% in WKY, P < 0.0001) and increased left-ventricular (LV) end-diastolic dimension (9.7 +/- 0.2 mm versus 7.0 +/- 0.4 mm in WKY, P < 0.0001). Whereas placebo and oxypurinol did not change cardiac architecture in WKY, oxypurinol attenuated decreased FS and elevated LV end-diastolic dimension, LV end-systolic dimension, and LV mass in SHHF. Increased myocyte width in SHHF was reduced by oxypurinol. Additionally, fetal gene activation, altered calcium cycling proteins, and upregulated phospho-extracellular signal-regulated kinase were restored toward normal by oxypurinol (P < 0.05 versus placebo-SHHF). Importantly, SHHF rats exhibited increased XOR mRNA expression and activity, and oxypurinol treatment reduced XOR activity and superoxide production toward normal, but not expression. On the other hand, NADPH oxidase activity remained unchanged, despite elevated subunit protein abundance in treated and untreated SHHF rats. Together these data demonstrate that chronic XOR inhibition restores cardiac structure and function and offsets alterations in fetal gene expression/Ca2+ handling pathways, supporting the idea that inhibiting XOR-derived oxidative stress substantially improves the HF phenotype.