The Pattern of Stem Cell Repopulation in Heavily Irradiated Mice Receiving Transplants of Fetal Liver

Pluripotential cells derived from fetal liver had a lower plating efficiencythan adult marrow cells, but estimates of the generation time derived fromthe growth curve are significantly shorter and may account for the earliererythroid population.

Submitted on June 18, 1969 Accepted on August 12, 1969     

Echocardiographic Aspects of Restrictive Cardiomyopathy

Background and Methods: We studied 17 patients with restrictive cardiomyopathy; eight had biventricular restriction (type A), four had left ventricular restriction (type B), and five had only right ventricular restriction (type C). Results: Type A disease was characterized by pulmonary and systemic venous congestion. The restrictive pattern was found in the inlet of both ventricles. Both atria were enormous, with small or normal-size ventricles. Differential diagnosis included constrictive pericarditis and systolic pump dysfunction. Type B restriction disease was characterized by venous pulmonary congestion, pulmonary hypertension, and important dilatation of the left atrium and right cavities with a small or normal-size left ventricle; the restrictive pattern was found only in the affected left ventricle. Conclusions: The clinical picture resembles that of rheumatic mitral valve disease with right ventricular failure. Type C disease had restriction only in the inlet of right ventricle, with giant right atrium, systemic venous hypertension with low flow, and normal pressure of pulmonary artery and left heart. Differential diagnosis included Ebstein's anomaly of tricuspid valve. The etiology of type A disease was amyloid, endomyocardial fibrosis of ventricles and idiopathic interstitial fibrosis. Asymmetric types were always caused by Davies' disease.     

VIRUSES AND THE TYPE I INTERFERON ANTIVIRAL SYSTEM: INDUCTION AND EVASION

The type I interferon (IFN) system responds to viral infection and induces an "antiviral state" in cells, providing an important first line of defense against virus infection. Interaction of type I IFNs (IFNα and IFNβ) with their receptor induces hundreds of cellular genes. Of the proteins induced by IFN, the antiviral function of only a few is known, and their mechanisms of action are only partly understood. Additionally, although viral-encoded mechanisms that counteract specific components of the type I IFN response have been known for some time, it has recently become clear that many (if not most) viruses encode some form of IFN-antagonist. Understanding the interplay between viral-encoded IFN antagonists and the interferon response will be essential if the therapeutic potential of IFNs is to be fully exploited.