Biomedical subjects
Publications and source records attributed to M Greenwald.
Undiagnosed myocardial infarction of the right ventricle presented as Dressler's syndrome. Radioisotopic diagnostic procedures including first-pass and multigated acquisition nuclear angiography ( MUGA ) and thallium-201 perfusion studies enabled a retroactive diagnosis of myocardial infarction, showed it to be in the right ventricle, and clarified the aetiology of the unexplained fever and pleuropericarditis.
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A 47-year-old woman underwent thoracoplasty for tuberculosis on the right apex of the lung. A heavily scarred area remained asymptomatic. Both the long interval after surgery and the histology of the tumor are unusual.
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Serum colchicine levels were determined by radioimmunoassay after a 1-mg bolus injected intravenously in 4 patients with familial Mediterranean fever and in 6 normal subjects. Mean elimination half-life (t1/2) (+/- SEM) was 157 +/- 20 min in the patients and 65 +/- 15 min in the normal subjects (p less than 0.005). Total clearance was 239 +/- 50 ml/min in the patients and 601 +/- 155 ml/min in the normal subjects (p less than 0.05). Volume of distribution (Vdarea) was 76 +/- 16 and 49 +/- 91 and did not differ significantly. In 8 patients receiving colchicine prophylactically with good clinical response, serum colchicine ranged from 0.3 to 2.4 ng/ml after daily doses of 1 mg orally. In 2 responding patients 2-mg doses orally induced levels from 4 to 10 ng/ml, and in one (a nonresponder) a 3-mg dose induced levels of 7.5 to 13 ng/ml. Of 3 patients receiving 2 mg daily with unsatisfactory clinical responses, serum levels were not detectable in one and in the low range of 1.5 to 5.4 ng/ml in the others. It is suggested that lack of response to colchicine orally in some nonresponders could result from inadequate absorption or altered disposition of colchicine.
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Dimethyl sulfoxide was administered intravenously for 60 days to twenty mice with casein-induced amyloidosis. Partial or total disappearance of amyloid deposits occurred in all treated animals. The urine of these animals contained a substance from which amyloid fibrils could be synthesized. A control group of mice with casein-induced amyloidosis given saline injections showed massive amyloid deposition in the liver and in the spleen at the end of the experiment. Neither the urine of these mice nor the urine of normal control mice treated with dimethyl sulfoxide contained substances from which amyloid fibrils could be synthesized. It is our assumption that dimethyl sulfoxide treatment of mice with amyloidosis resulted in a break up of amyloid fibres into small subunits which were excreted in the urine.
AA protein constitutes 50 to 60% of the amyloid fibrils from livers of ducks developing spontaneous amyloidosis and has a m.w. of about 12,000. The sequence of the first 73 residues was established by automatic Edman degradation of the whole molecule and isolated cyanogen bromide fragments, and corroborated by placement of tryptic peptides. The sequence from position 76-80 was tentatively derived from a peptide that was homologous to that region of human and monkey AA proteins. Carboxypeptidase digestion showed the carboxy terminal sequence to be Ala, Arg, with some heterogeneity (Ser, Arg). Compared to human AA protein, there were five additional residues at the amino terminus. In view of the m.w. and the existence of additional peptides an extension at the C-terminal end seems likely. Sequence homologies to other AA proteins are discussed.
Swiss white and C57/BL/6J mice inoculated repeatedly with either Nocardia asteroides or Nocardia brasiliensis organisms developed amyloidosis over a 7-month period. Amyloidosis also developed in these mice within 6 weeks following a single large inoculum of either organism, but not in other in-bred mouse strains, suggesting a genetic influence in the pathogenesis of this form of secondary amyloidosis.
Colchicine was found to inhibit the first phase of casein-induced synthesis of murine amyloid. When mice were treated with colchicine during the first 7 days of an amyloid induction regimen or when colchicine was given to the donor mice in a transfer model, the amyloidogenic stimulus of casein was blocked completely. Amyloid synthesis was however, not interrupted by the administration of colchicine during the last 7 days of the casein regimen nor by colchicine treatment of recipient mice in a transfer model.
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We prospectively ascertained gestational cocaine use by neonatal urine and hair tests in 600 mother infant pairs in 3 nurseries in Toronto. The 37 (6.25%) babies who tested positive for cocaine and their mothers were compared to the 563 nonexposed with regard to pregnancy outcome and neonatal complications. Mothers using cocaine were not different in their ages, racial distribution, and obstetric history from those nonexposed. Cocaine-using women had significantly higher risk for vaginal bleeding (16% vs 6%, P < 0.05), hepatitis B carrier state (8% vs 0.8%, P < 0.005), and perhaps more urinary tract infections (8% vs 2.5%, P = 0.08). Cocaine-using mothers were significantly more likely to smoke cigarettes (29% vs 10%, P < 0.001). Infants exposed to cocaine in utero were of lower birth weight (3162 +/- 645 [SD] g vs 3391 +/- 573, P < 0.05) and birth length (49.9 +/- 2.9 cm vs 51.1 +/- 3.1 cm, P < 0.05). Further stratification of babies exposed to cocaine by maternal cigarette smoking suggests that cigarette smoking accounted for most of this variability [birth weight of babies exposed to cocaine and cigarettes 2899 +/- 7.50 g (and 50% of them weighed less than 2500 g), vs 3423 +/- 612 (and only 8% less than 2500 g) in those exposed to cocaine only (P < 0.05)]. Babies exposed to cocaine in utero were significantly more likely to need initial medical support or resuscitation (52% vs 30%, P < 0.05). We conclude that gestational exposure to cocaine, ascertained by a sensitive biologic marker, is associated with substantial perinatal risks.(ABSTRACT TRUNCATED AT 250 WORDS)
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The implications of gestational cocaine use are widely documented. There is evidence that cocaine crosses the placenta in animals and humans; however, the fetal distribution of the drug and its metabolites has not been documented. We describe the distribution of cocaine and benzoylecgonine (BE) in the fetus of a cocaine user mother. Cocaine and BE were detected in brain, scalp, liver, kidney, heart, placenta, blood, and hair. The liver contained substantially more cocaine than other tissues, whereas the brain had more BE than any other sample.
Four patients with microphthalmos with cyst were examined and evaluated by computed tomography (CT). Each patient had a different clinical presentation, which varied according to the appearance of the anterior segment and the size and location of the orbital cyst. All had very poor vision in the involved eye. CT was of great value in the diagnosis and definition of this condition. The differentiation of microphthalmos with cyst from coloboma and from other orbital masses by means of CT is discussed.