Percutaneous insertion of an IABP through the left axillary artery is a feasible and relatively well-tolerated strategy to bridge patients with end-stage heart failure to heart transplantation. This form of mechanical-device treatment permits upright sitting and ambulation in those requiring extended support.

Hatching success in olive ridley mass nesting arribada beaches is typically low. We conducted a short study to understand whether incubation temperature in dry months accounts for exceedingly low hatching success at Ostional Beach, Costa Rica, a mass nesting rookery. We measured in situ incubation temperatures in nests from 4 arribadas recorded in October to December 2008, and January 2009. Mean incubation temperatures for all months exceeded the upper lethal limit of 35°C, and no nests produced hatchlings when incubated at this or higher temperatures. Embryo development was inversely related to mean incubation temperature. Hatching success was low (2%) for the study period, and only 5 of 37 marked nests produced hatchlings. Mean incubation temperature for successful nests was < 35°C. Since incubation temperatures of 32°C and higher recorded during the gonadal thermosensitive period were above the mean pivotal temperature of 30.5°C, the few hatchlings produced were presumably female. Incubation temperatures were significantly higher during the second and third trimesters of incubation during all months as a result of metabolic heating. However, during January to March when embryos did not develop, higher incubation temperatures of in situ nests relative to controls indicated that heating was a result of microbial activity associated with egg decomposition. Our study demonstrates that after the onset of the dry season, incubation temperatures at this beach become lethal.

BackgroundLimited information exists on the role of B‐cell‐dependent mechanisms in the progression of heart failure (HF). However, in failing human myocardium, there is evidence of deposition of activated complement components as well as anticardiac antibodies. We aimed to determine the contribution of B‐cells in HF progression using a nonsurgical mouse model of nonischemic cardiomyopathy (CMP).Methods and Results CMP protocol involved the use of l‐NAME and NaCl in the drinking water and angiotensin‐II infusion for 35 days. At day 35, mice were analyzed by cardiac magnetic resonance imaging, gene expression, and histology. Mice (12 weeks old) were divided into 4 groups, all in C57BL/6 background: wild‐type (WT) CMP; severe combined immunodeficiency (SCID) CMP (T‐ and B‐cell deficient); CD22− CMP (B‐cell depleted); and Nude CMP (T‐cell deficient), with their respective controls. We performed B‐cell depletion and reconstitution protocols. The protective effect of B‐cell depletion was demonstrated by a significant reduction of cell hypertrophy and collagen deposition and a preserved ejection fraction in the CD22− CMP group compared to WT CMP. Once SCID mice underwent B‐cell reconstitution with isolated CMP B‐cells, the CMP phenotype was restored. Furthermore, deposition of IgG3 and apoptosis in the myocardium follows the development of CMP; in addition, in vitro studies demonstrated that activated B‐cells stimulate collagen production by cardiac fibroblasts.ConclusionsThe absence of B‐cells in this model of HF resulted in less hypertrophy and collagen deposition, preservation of left ventricular function, and, in association with these changes, a reduction in expression of proinflammatory cytokines, immunoglobulin G deposition, and apoptosis in the myocardium. Taken together, these data suggest that B‐cells play a contributory role in an angiotensin‐II‐induced HF model.

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