An unusually accentuated diastolic anterior motion of the mitral valve in aortic insufficiency.

A 55-year-old woman was diagnosed with endocarditis involving the aortic valve and resulting in moderate aortic insufficiency. Transesophageal and transthoracic echocardiography demonstrated an unusually accentuated diastolic anterior motion of the anterior mitral valve leaflet toward the interventricular septum. The anterior leaflet remained within a few millimeters of the septum throughout diastole, with a narrow jet of aortic insufficiency separating the anterior leaflet from the septum.

Pharmacological and genetic reversal of age-dependent cognitive deficits attributable to decreased presenilin function.

Alzheimer's disease (AD) is the leading cause of cognitive loss and neurodegeneration in the developed world. Although its genetic and environmental causes are not generally known, familial forms of the disease (FAD) are attributable to mutations in a single copy of the Presenilin (PS) and amyloid precursor protein genes. The dominant inheritance pattern of FAD indicates that it may be attributable to gain or change of function mutations.

Age-dependent cognitive impairment in a Drosophila fragile X model and its pharmacological rescue.

Fragile X syndrome afflicts 1 in 2,500 individuals and is the leading heritable cause of mental retardation worldwide. The overriding clinical manifestation of this disease is mild to severe cognitive impairment. Age-dependent cognitive decline has been identified in Fragile X patients, although it has not been fully characterized nor examined in animal models.

Independent association of rheumatoid arthritis with increased left ventricular mass but not with reduced ejection fraction.

Objective: Rheumatoid arthritis (RA) is a chronic inflammatory disease associated with premature atherosclerosis, vascular stiffening, and heart failure. This study was undertaken to investigate whether RA is associated with underlying structural and functional abnormalities of the left ventricle (LV).

Methods: Eighty-nine RA patients without clinical cardiovascular disease and 89 healthy matched controls underwent echocardiography, carotid ultrasonography, and radial tonometry to measure arterial stiffness.