Influence of left ventricular mass on the diagnostic accuracy of myocardial perfusion imaging using positron emission tomography with dipyridamole stress.

This study assesses the influence of left ventricular hypertrophy (LVH) on the accuracy of myocardial perfusion imaging using pharmacologic coronary vasodilation. Seventy-five patients without previous infarction, and with known coronary anatomy, were studied by echocardiography and PET. LVH (defined by mass greater than 131 g/m2 in males or greater than 100 g/m2 in females) was identified in 25 patients; this group did not differ significantly from the remainder in terms of clinical or angiographic parameters. Twenty patients with hypertrophy had significant coronary artery stenoses, which were identified correctly by PET in 11 (55%), in contrast to 29 of 34 patients (85%, p = 0.03) with coronary disease but normal LV mass. Normal perfusion images were obtained in three of five patients (60%) with hypertrophy but no coronary disease; in contrast, 14 of 16 patients without either coronary disease or hypertrophy (88%, p = ns) had normal scans. The accuracy of PET was 14/25 (56%) in those with hypertrophy, and 43/50 (86%, p = 0.01) in patients with normal LV mass. In this group, the presence of hypertrophy was associated with reduction in the diagnostic accuracy of PET using dipyridamole stress. These findings may account for the phenomenon of "dipyridamole nonresponsiveness" in some patients.     

6－甲氧基正丁苯酞在大鼠肝微粒体中的代谢研究

报道了用ＧＣ／ＭＳ方法及衍生化技术研究６甲氧基正丁苯酞（ＭＢＰ）在大鼠肝微粒体中的代谢转化结果。６甲氧基正丁苯酞在苯巴比妥（ＰＢ）诱导的大鼠肝微粒体中主要转化为３羟基、γ羟基取代物，６羟基正丁苯酞与一个环氧化代谢产物     

Improvement of left ventricular function by lifestyle intervention in obesity: contributions of weight loss and reduced insulin resistance

Aims/hypothesis  

Weight excess and insulin resistance mediate the link between obesity and left ventricular dysfunction. We investigated the effect and mechanisms of lifestyle modification on left ventricular function changes in obese patients.     

The relationship between CR3 deficiency and neutrophil actin assembly

Polymorphonuclear leukocytes (PMN) with a deficiency of the complement receptor type 3 (CR3) membrane glycoprotein family have impairments in the ability to adhere to surfaces as well as chemotactic and phagocytic defects, processes that require a functional contractile apparatus. PMN from the patient with neutrophil actin dysfunction (NAD) displayed similar functional characteristics to those with CR3 deficiency suggesting the two disorders may be the same disease. In order to evaluate the relationship between CR3 deficiency and actin assembly, actin filament assembly was measured in PMN from six previously reported homozygotes (two severe and four moderate CR3-deficient patients) as well as five heterozygotes for CR3 deficiency. PMN from all patients had normal unstimulated concentrations of F-actin and after exposure to the chemotactic peptide FMLP (5 x 10(-7) mol/L for 5 to 40 seconds at 25 degrees C) assembled actin normally. Pretreatment of normal PMN with concentrations of monoclonal anti-alpha CR3 antibody, capable of blocking PMN adherence, also failed to impair FMLP- induced actin filament assembly. CR3 glycoprotein expression was measured in PMNs from the mother, father, and older sister of the NAD patient (N Engl J Med 291:1093, 1974). Actin filament assembly was recently shown to be defective in PMNs from all three family members. The total concentrations of the alpha and beta CR3 subunits were below normal in PMN detergent extracts from the mother (25% of simultaneous controls) and older sister (56% of control). PMN surface expression of these two subunits was also found to be depressed (mother, 50%; older sister, 63% of control). These findings suggest these two NAD family members are heterozygote carriers for CR3 deficiency as well as NAD. Simultaneous studies of the father, however, demonstrated normal total concentrations of both the alpha and beta CR3 subunits (126% of controls) as well as normal surface expression of both subunits after phorbol myristate acetate stimulation and incubation at 37 degrees C (mean, 112% of controls) but slightly lower than normal levels after FMLP stimulation (mean, 83%). These findings indicate that CR3 deficiency generally is not associated with defective actin filament assembly and support the conclusion that NAD represents a unique kindred in which PMN actin function differs from previously reported genotypes of CR3 deficiency.