No abstract

Exercise-induced LV growth in young males is strongly associated with the ACE I/D polymorphism.

Our work elucidates the ability to cell electrospin primary cells as highly concentrated cellular suspensions. The post-cell electrospun organisms are viable over long periods of time, demonstrating a significant active cell population when compared with controls.

Restenosis after angioplasty is due predominantly to accumulation of vascular smooth muscle cells (VSMCs). The resistance of restenosis to pharmacological treatment has prompted investigation of genes involved in VSMC proliferation. We have examined the effect on VSMC proliferation of blocking expression of the c-myc proto-oncogene with antisense oligodeoxynucleotides, both in vitro and in a rat carotid artery injury model of angioplasty restenosis. Antisense c-myc oligodeoxynucleotides reduced average cell levels of c-myc mRNA and protein by 50-55% and inhibited proliferation of VSMCs when mitogenically stimulated from quiescence or when proliferating logarithmically (IC5o = 10 ug/ml). Corresponding sense c-myc, two-basepair mismatch antisense c-myc, antisense a-actin or glyceraldehyde phosphate dehydrogenase oligodeoxynucleotides did not suppress c-myc expression or inhibit VSMC proliferation. Antisense c-myc inhibition was relieved by overexpression of an exogenous c-myc gene. After balloon catheter injury, peak cmyc mRNA expression occurred at 2 h. Antisense c-myc applied in a pluronic gel to the arterial adventitia reduced peak c-myc expression by 75% and significantly reduced neointimal formation at 14 d, compared with sense c-myc and gel application alone. We conclude that c-myc expression is required for VSMC proliferation in vitro and in the vessel wall. C-myc is a therefore a potential target for adjunctive therapy to reduce angioplasty restenosis. (J. Clin. Invest. 1994. 93:820-828.

Objective: To investigate the role of vigorous physical exertion and anger as triggers of acute coronary syndromes (ACS) and to identify the clinical and sociodemographic correlates of triggering. Design: Prospective observational clinical cohort study. Setting: Four coronary care units in the London area. Patients: 295 men and women with electrocardiographically and biochemically verified ACS. Main outcome measures: Physical exertion in the 1 h and anger in the 2 h before symptom onset were assessed with structured interviews. Control periods were the equivalent hours one day earlier and usual rates over the past six months. Data were analysed by case-crossover methods. Results: Physical exertion was reported by 10% and anger by 17.4% of patients in the hazard period. The risk of ACS onset after physical exertion compared with light or no activity was 3.50 (95% confidence interval (CI) 1.37 to 10.6). The risk of onset with anger was 2.06 (95% CI 1.12 to 3.92). Physical exertion during the hazard period was related to an absence of premonitory symptoms, presentation with an ST elevation myocardial infarction (STEMI), low socioeconomic deprivation and higher future cardiovascular risk. Anger during the hazard period was more common in younger, socioeconomically deprived patients who presented with a STEMI. Conclusions: Triggers are relevant across the spectrum of ACS. The distinct clinical and sociodemographic factors associated with physical exertion and anger suggest that different pathophysiological processes may be involved.