Magnetic-Field Immunity Examination and Evaluation of Transcutaneous Energy-Transmission System for a Totally Implantable Artificial Heart

Transcutaneous energy transmission (TET) is the most promising noninvasive method for supplying driving energy to a totally implantable artificial heart. Induction-heating (IH) cookers generate a magnetic flux, and if a cooker is operated near a transcutaneous transformer, the magnetic flux generated will link with its external and internal coils. This will affect the performance of the TET and the artificial heart system. In this paper, we present the design and development of a coil to be used for a magnetic immunity test, and we detail the investigation of the magnetic immunity of a transcutaneous transformer. The experimental coil, with five turns like a solenoid, was able to generate a uniform magnetic field in the necessary bandwidth. A magnetic-field immunity examination of the TET system was performed using this coil, and the system was confirmed to have sufficient immunity to the magnetic field generated as a result of the conventional operation of induction-heating cooker.

Targeted overexpression of ornithine decarboxylase enhances β-adrenergic agonist-induced cardiac hypertrophy

These studies were designed to determine the consequences of constitutive overexpression of ornithine decarboxylase (ODC) in the heart. Induction of ODC is known to occur in response to agents that induce cardiac hypertrophy. However, it is not known whether high ODC levels are sufficient for the development of a hypertrophic phenotype. Transgenic mice were generated with cardiac-specific expression of a stable ODC protein using the α-myosin heavy-chain promoter. Founder lines with > 1000-fold overexpression of ODC in the heart were established, resulting in a 50-fold overaccumulation of putrescine, 4-fold elevation in spermidine, a slight increase in spermine and accumulation of large amounts of cadaverine compared with littermate controls. Despite these significant alterations in polyamines, myocardial hypertrophy, as measured by ratio of heart to body weight, did not develop, although atrial natriuretic factor RNA was slightly elevated in transgenic ventricles. However, stimulation of β-adrenergic signalling by isoproterenol resulted in severe hypertrophy and even death in ODC-overexpressing mice without further altering polyamine levels, compared with only a mild hypertrophy in littermates. When β1-adrenergic stimulation was blocked by simultaneous treatment with isoproterenol and the β1 antagonist atenolol, a significant, although reduced, hypertrophy was still present in the hearts of transgenic mice, suggesting that both β1 and β2 adrenergic receptors contribute to the hypertrophic phenotype. Therefore these mice provide a model to study the in vivo co-operativity between high ODC activity and activation of other pathways leading to hypertrophy in the heart.

An inductive role for the endoderm in Xenopus cardiogenesis

Heart induction in Xenopus has been thought to be dependent primarily on the interaction of the heart primordia with the Spemann organizer. We demonstrate, however, that signals derived from the deep dorsoanterior endoderm during early gastrulation are also essential for heart formation. The presence of deep endoderm dramatically enhances heart formation in explants of heart primordia, both in the presence and absence of organizer. Likewise, extirpation of the entire endoderm can decrease the frequency of heart formation in embryos that retain organizer activity. Finally, we show that the combined presence of both endoderm and organizer is necessary and sufficient to induce heart in ventral mesoderm explants that would not otherwise form heart tissue. Xenopus heart induction, therefore, may be a multistep process requiring separate dorsalization and cardiogenic signalling events. This is the first demonstration of a heart-inducing role for the endoderm in Xenopus, indicating that the mechanism of heart formation may be similar in most vertebrates.