Members of the SNF2 (Sucrose Non-Fermenter) family of chromatin-remodeling proteins function in processes ranging from DNA repair to transcription to methylation. Using differential display, we recently identified a novel member of the SNF2 family that is highly expressed at the mRNA level in proliferating cells and is down-regulated during apoptosis. We have named this gene PASG (Proliferation-Associated SNF2-like Gene). Northern blot analysis of adult mouse tissues shows PASG to be highly expressed in proliferating organs such as thymus, bone marrow, and testis and absent from nonproliferative tissues such as brain and heart. In situ hybridization analysis of mouse embryos shows that PASG is differentially expressed during development, with highest expression in developing face, limbs, skeletal muscle, heart, and tail. In vitro, PASG expression correlates with a shift from a quiescent to a proliferative state. Mice null for PASG (also known as LSH or Hells) are reported to die perinatally, although the mechanism for lethality is unclear (Geiman and Muegge, 2000). To test the hypothesis that PASG functions in cell proliferation, we compared 5-bromodeoxyuridine (BrdU) incorporation in C33A cells transiently transfected with PASG versus empty vector and found that PASG transfected cells showed a significant decrease in the amount of BrdU incorporation. These findings suggest that PASG plays a role in cell proliferation and may function in the development of multiple cell lineages during murine embryogenesis.
Thrombotic coronary arterial occlusion, and myocardial infarction, are rare in the newborn. We report such a happening presenting shortly after birth with cardiogenic shock, no left ventricular output and a systemic circulation dependent on flow from a patent arterial duct.
Case reportThe patient was the 2.88 kg product of an uncomplicated 42-week gestation. The placenta weighed 315g and was histologically normal. Hypotension and bradycardia were present at birth with Apgar scores of 2, 4, and 6 at 1, 5 and 10 minutes respectively. Physical exam revealed an irregular tachycardia of 150-190 beats per minute, a single second heart sound and no murmurs. The chest radiograph was normal. The electrocardiogram demonstrated 4-6mm ST depression in leads VI-V4, and 3^m m ST elevation and qS pattern in leads V5 &V6, suggestive of infero-lateral myocardial injury.Echocardiogram and Doppler evaluation showed a large, dilated, poorly contractile left ventricle. The leaflets of the aortic valve were thin but immobile with no antegrade flow. There was however, a continuous jet of regurgitant flow across the aortic valve, indicating that the valve was not atretic. The mitral valve was severely regurgitant,
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