Ohio Business College is a private for-profit junior college with multiple locations in Ohio. It is owned by Tri-State Educational Systems, Inc. with corporate headquarters located in Middletown, Ohio. Currently, Ohio Business College operates three campuses in Ohio with career education focused around information technology, business administration, allied health, and CDL training.
Women face a disproportionate burden of stroke mortality and disability. Biologic sex and sociocultural gender both contribute to differences in stroke risk factors, assessment, treatment, and outcomes. There are substantial differences in the strength of association of stroke risk factors, as well as female-specific risk factors. Moreover, there are differences in presentation, response to treatment, and stroke outcomes in women. This review outlines current knowledge of impact of sex and gender on stroke, as well as delineates research gaps and areas for future inquiry.
Calmodulin (CaM) mutants are associated with severe arrhythmias (calmodulinopathy). While dysregulation of Ca 2+ handling proteins (RyR2, Ca V 1.2) are known mediators of calmodulinopathy, the role of Na + channels (Na V s) remains unclear. Interestingly, effects on Ca V 1.2 do not fully explain action potential (AP) prolongation by the long QT syndrome CaM mutant D96V. We investigated Na V dysregulation by D96V-CaM and its arrhythmogenic impact. In wild-type (WT) murine cardiomyocytes (CM) dialysis of D96V-CaM (6.5 μM) via a patch pipette prolonged AP, induced early and delayed afterdepolarizations (EADs and DADs) and increased Ca 2+ waves compared to WT-CaM. The effects of D96V-CaM were abrogated by a Na V 1.6 blocker, 4,9-anhydrotetrodotoxin (4,9ahTTX, 300 nM; Fig. 1A ). Dialysis of D96V-CaM dysregulated inactivation of 4,9ahTTX-sensitive Na + current (I Na ) promoting late I Na in WT murine CM ( Fig. 1B ) and in Chinese Hamster Ovary (CHO) cells expressing Na V 1.6 but not Na V 1.5. D96V-CaM, but not WT-CaM, also promoted late I Na in human induced pluripotent stem cell (iPSC) - derived ventricular myocytes, underscoring translational relevance ( Fig. 1C ). To examine the arrhythmia potential of Na V 1.6 dysregulation by D96V-CaM, we generated mice with cardiac-specific expression of D96V-CaM (cD96V; tgD96V-CaM x β-MHC-Cre). cD96V mice exhibited increased late I Na and Ca 2+ waves resembling those in D96V-CaM-dialyzed WT CMs. In vivo cD96V mice evidenced prolonged QTc intervals and ventricular tachycardia (VT) during bradycardia (carbachol 0.5 mg/kg intraperitoneal). Cardiac-specific Na V 1.6 knockout protected cD96V mice from impaired I Na inactivation and arrhythmogenic Ca 2+ waves on cellular level as well as long QT and VT in vivo ( Fig. 1D, E ). In summary, D96V-CaM promotes arrhythmias by dysregulating Na V 1.6 and thereby, facilitating aberrant Ca 2+ release. Importantly, Na V 1.6 may be a therapeutic target for management of CaM-related arrhythmias.
BACKGROUND & AIMS:Previous studies have suggested that cocoa products, which are rich sources of flavonoids, may lower blood pressure, serum cholesterol, fasting blood glucose and improve endothelial function. However, it is unclear whether consumption of cocoa products including chocolate influences the risk of metabolic syndrome (MetS). In a cross-sectional design, we sought to examine the association between chocolate consumption and the prevalence of MetS. METHODS:We studied 4098 participants from the National Heart, Lung, and Blood Institute (NHLBI) Family Heart Study aged 25-93 years. Chocolate consumption was assessed using a semi-quantitative food-frequency questionnaire. MetS was defined using the NCEP III criteria. Generalized estimating equations were used to estimate prevalence odds ratios of MetS according to frequency of chocolate intake. RESULTS:Of the 4098 participants (mean age 51.7 y) included in the analyses, 2206 (53.8%) were female. The prevalence of metabolic syndrome in our population was 30.2%. Compared with those who did not consume any chocolate, multivariate adjusted odds ratios (95% CI) for MetS were 1.26 (0.94, 1.69), 1.15 (0.85, 1.55), and 0.99 (0.66, 1.51) among women who reported chocolate consumption of 1-3 times/ month, 1-4 times/week, and 5+ times/week, respectively. Corresponding values for men were: 1.13 (0.82, 1.57), 1.02 (0.74, 1.39), and 1.21 (0.79, 1.85). CONCLUSION:These data do not support an association between chocolate intake and the prevalence of MetS in US adult men and women.
A structured abstract of no more than 150 words should contain the following major headings: Ⅲ Objective(s): Reflects the purpose of the study (the hypothesis that is being tested).Ⅲ Study Design: The setting for the study, the subjects (number and type), the treatment or intervention, and the type of statistical analysis used.Ⅲ Results: The outcome(s) of the study and, if appropriate, its/their statistical significance. Ⅲ Conclusion(s):The significance of the results.
