Abstract: In accordance with the present invention, there are provided targeted loss of function mutant mice which express less than endogenous levels of at least one member of the steroid/thyroid superfamily of receptors in at least one specific tissue type. For example, mutations in the RXR&agr; gene in mouse germlines are lethal in the embryonic stage between E13.5 and E16.5 when bred to homozygosity. The major defect responsible for this lethal effect is hypoplastic development of the ventricular chambers of the heart, which is manifest as a grossly thinned ventricular wall with concurrent defects in ventricular septation. This phenotype is identical to a subset of the effects of embryonic vitamin A deficiency, and therefore establishes RXR&agr; as a genetic component of the vitamin A signaling pathway in cardiac morphogenesis.

Abstract: Combinations and methods for inducing a semi-synchronous wave of liver cell proliferation in vivo and combinations and methods for inducing a semi-synchronous wave of liver cell proliferation and achieving transduction of proliferating liver cells in vivo are disclosed.

Abstract: The present invention provides a method for treating ischemic tissue in a mammal which comprises injecting said tissue with an effective amount of a nucleic acid capable of expressing an angiogenic protein. The method of the present invention may be used to treat any ischemic tissue, i.e., a tissue having a deficiency in blood as the result of an ischemic disease. Such tissues can include, for example, muscle, brain, kidney and lung. Ischemic diseases include, for example, cerebrovascular ischemia, renal ischemia, pulmonary ischemia, limb ischemia, ischemic cardiomyopathy and myocardial ischemia.