Relative complement-fixing activity of antibodies to nuclear antigens, including DNA, were determined in serums of 15 patients with, and 65 patients without, active lupus nephritis, by comparing titers obtained in two methods. High complement-fixing activity of antibody was found in the nephritis group and low activity in the others. Results with immunoglobulin G fractions were similar.

Antibodies, Antinuclear↗

PubMedDate not supplied

Prediction of functional recovery in acute myocardial infarction: comparison between sestamibi reverse redistribution and sestamibi/BMIPP mismatch.

BACKGROUND: It has been known that Tc 99m sestamibi/iodine 123 betamethyliodophenylpentadecanoic (123I-BMIPP) (sestamibi/BMIPP) mismatch is an indicator of viable myocardium in acute myocardial infarction (AMI). We have reported that reverse redistribution of sestamibi in AMI indicates the patency of infarct-related artery and a preserved left ventricular function in the chronic stage. In this study we investigated the relationship between reverse redistribution of sestamibi and sestamibi/BMIPP mismatch in patients with AMI. METHODS: Twenty-three patients with AMI who received direct percutaneous transluminal coronary angioplasty underwent both BMIPP and sestamibi SPECT within 2 weeks after onset. Sestamibi images were obtained 1 hour (early) and 3 hours (delayed) after injection of sestamibi. BMIPP imaging was carried out 30 minutes after injection. The left ventricle was divided into 17 segments, and regional myocardial uptakes of the tracers in each segment were scored from 0 (normal) to 3 (no activity). A reverse redistribution pattern was defined as an increase of > or =1 in the regional score at the delayed images. More reduced BMIPP uptake than sestamibi uptake in each segment was determined as sestamibi/BMIPP mismatch. Contrast left ventriculography was performed soon after revascularization and repeated 1 month later. RESULTS: Of 15 patients with sestamibi reverse redistribution, sestamibi/BMIPP mismatch was observed in 14 patients (93%), whereas mismatch was seen in only one of seven patients (14%) without reverse redistribution (p < 0.01). In patients with sestamibi reverse redistribution, regional scores of BMIPP agreed with those of early and delayed images of sestamibi in 51 segments (46%) and in 92 segments (83%), respectively. In the chronic stage, both regional wall motion and left ventricular ejection fraction improved in patients with sestamibi reverse redistribution (wall motion score: 6.7 +/- 2.4 vs 2.7 +/- 2.1, p < 0.01; ejection fraction: 56% +/- 7% vs 64% +/- 8%, p < 0.01), but not in those without reverse redistribution. CONCLUSION: Both reverse redistribution of sestamibi and sestamibi/BMIPP mismatch reflect the recovery of left ventricular function and thus imply myocardial viability in AMI. Because the presence of reverse redistribution of sestamibi agreed with that of sestamibi/BMIPP mismatch, additional BMIPP images can be replaced by the delayed images after a single injection of sestamibi.

Aged↗

PubMedDate not supplied

Marker antibodies in systemic autoimmune diseases.

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Antibodies, Antinuclear↗

PubMedDate not supplied

Gizzard erosion in broiler chicks by group I avian adenovirus.

Incidences of mortality without any clinical signs occurred in growing chicks in a broiler flock. Five 17-day-old dead broilers with gizzard erosions were investigated pathologically. Macroscopically, the gizzards were found to be dilated with bloody fluids. The koilin layer of the gizzards showed multifocal black patches (erosions). Histologically, there was necrosis of the koilin layer, degeneration and depletion of the gizzard glandular epithelium with intranuclear inclusion bodies, and hyperplasia of the macrophages in the lamina propria. An immunohistochemical analysis revealed intranuclear inclusion bodies in the degenerating gizzard glandular epithelial cells that stained positively for group I avian adenovirus antigen. Ultrastructurally, numerous viral particles (an average of 72 nm in diameter, from 63 to 88 nm) were in the intranuclear inclusions of glandular epithelium. This study suggests that the gizzard erosions may have been caused by group I avian adenovirus. In addition, the degeneration and depletion of gizzard glands secreting koilin substances, by adenovirus, may induce a reduction of koilin substances, which may then cause gizzard erosion (focal loss of the koilin layer).

Adenoviridae Infections↗

PubMedDate not supplied

Thrombocytopenia responsive to warfarin in a patient with systemic sclerosis--systemic lupus erythematosus overlap.

We report a patient with overlapping systemic sclerosis-systemic lupus erythematosus who developed refractory thrombocytopenia and recurrent thromboses. Coagulation and platelet labeling studies revealed that platelets were being consumed by the thrombus formation, and anticoagulation with warfarin dramatically increased the platelet count. This case report suggests that platelet consumption due to thrombus formation is one of the causes of thrombocytopenia in patients with rheumatic disease.

Blood Platelets↗

PubMedDate not supplied

Protection against lipid peroxidation induced during preservation of lungs for transplantation.

The questions of whether oxygen-derived free radicals are induced during preservation of lungs and, if so, how such radicals might relate to reperfusion injury were investigated by means of an isolated canine lung model. Lungs were obtained from 16 mongrel dogs and divided into groups 1 (n = 6), 2 (n = 5), and 3 (n = 5). The lungs of groups 1, 2, and 3 were flushed through the pulmonary artery with Euro-Collins solution alone, the solution with superoxide dismutase (120,000 U/L), and the solution with allopurinol (1 mmol/L), respectively, at 4 degrees C and then stored for 4 hours in the respective solutions at 4 degrees C with clamped bronchi. They were then reperfused for 2 hours by means of an isolated lung model. Lung lipid peroxidation was sequentially determined. The lung functional status was assessed by systolic pulmonary arterial pressure and end-inspiratory airway pressure. The lung edema was assessed by lung wet/dry weight ratio. Lipid peroxidation was induced after 1 hour of preservation and the first 30 minutes of the reperfusion in group 1 and only 2 hours of the reperfusion in group 2, whereas no induction was observed in group 3. Values for systolic pulmonary arterial pressure and end-inspiratory pressure in group 1 were significantly higher than those in group 3 (p < 0.05). The lung wet/dry weight ratio in group 1 was significantly higher than that in groups 2 and 3 (p < 0.05). The present results indicate that the administration of free radical scavengers in the preservation may effectively improve conditions for lung transplantation.

Airway Resistance↗