Strength of cardiac conditioned responses with varying unconditioned stimulus durations.
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BACKGROUND/RATIONALE: Support groups of peers were designed to convey support specific to stressful situations encountered by persons with a first-time myocardial infarction and by their spouse or partners. There were no previous published support intervention studies focused on the couple. Survivors and spouses (n=28) participated in a pilot study which tested the effect of a 12-week support group intervention. DESIGN: The support groups for couples were cofacilitated by a peer and professional. The facilitators recorded field notes, while participants completed weekly diaries about the intervention activities. Following the intervention, participants were interviewed individually and facilitators were interviewed jointly about the perceived effect of the intervention and influencing factors. This article focuses on the facilitators' and participants' perceptions of intervention processes and outcomes. FINDINGS: Support processes in the group included social comparison, social learning, and social exchange. Three types of support--emotional, information, and affirmation--were provided. All participants were satisfied with the support intervention and referred to the positive effect on their coping, confidence, outlook, and spousal relationship. Factors that influenced the intervention effect were participant input, cofacilitation, similarity of group members, and the provision of information and support. CONCLUSIONS: Future interventions could consider similarity of peers, leadership, and optimum timing and duration.
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BACKGROUND: Myocardial expression of endothelin-1 (ET-1) and its receptors ET(A) and ET(B) is increased in heart failure. However, the role of ET-1 and its signaling pathways in the pathogenesis of myocardial diseases is unclear. METHODS AND RESULTS: Human ET-1 cDNA was placed downstream of a promoter responsive to a doxycycline (DOX)-regulated transcriptional activator (tTA). This line (ET+) was bred with one harboring cardiac myocyte-restricted expression of tTA (alphaMHC-tTA). Myocardial ET-1 peptide levels were significantly increased in binary transgenic (BT, ET+/tTA+) compared with nonbinary transgenic (NBT, ET+/tTA-; ET-/tTA+; ET-/tTA-) or DOX-treated BT littermates (40.1+/-4.7 versus 2.6+/-1.2 fmol/mL, P<0.003). BT mice demonstrated progressive mortality between 5 and 11 weeks after DOX withdrawal, associated with left ventricular dilatation and contractile dysfunction (peak +dP/dT, 4673+/-468 versus 5585+/-658 mm Hg/s, P<0.05). An interstitial inflammatory infiltrate, including macrophages and T lymphocytes, was evident in the myocardium of BT mice, associated with sequential increases in nuclear factor-kappaB translocation and expression of tumor necrosis factor-alpha, interferon-gamma, interleukin-1 and interleukin-6. Significant prolongation of survival was observed with the combined ET(A)/ET(B) antagonist LU420627 (n=8, P<0.05) in BT mice but not the ET(A)-selective antagonist LU135252 (n=5, P=0.9), consistent with an important role for ET(B) in this model. CONCLUSIONS: These are the first data to demonstrate that cardiac overexpression of ET-1 is sufficient to cause increased expression of inflammatory cytokines and an inflammatory cardiomyopathy leading to heart failure and death.
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