Biomedical subjects
Publications and source records attributed to M Richardson.
Pushed to expand psychobehavioral services to meet the mental health needs of all their patients, hospitals must set policies that are strong enough to weather the 'medical-behavioral explosion'.
Although community mental health centers appear to have a mandate to serve mentally retarded children, adults, and their families, there is little evidence that adequate treatment actually is being provided. In a survey of the CMHCs in the state of Washington in 1979, the authors found that only about 1,500 of the estimated 22,500 retarded individuals with a potential for emotional disorder were actually being treated in the centers. Moreover, very few of the centers kept records of the intellectual ability of clients, and only about half had a staff specialist in retardation. The barriers to increasing the scope and frequency of services are discussed, as is the potential of continuing education training to improve mental retardation services in the mental health system.
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A subacute toxicity study on 99m Tc stannous glucoheptonate was performed with rats, dogs and rabbits, injected intravenously at ten to 100 times the human dose on a body weight basis. There were no abnormalities in the clinical status of any of the animals. No changes were found in urinalysis, blood chemistry or hematology in the rabbit nor in gross examination, renal histology or bone marrow smears in the rats and rabbits. Hepatic histology was also done. A focal area of necrosis in a liver of one rabbit that had been injected with 100 times the human dose was observed using light microscopy. Examination by electron microscopy in another group of rats and rabbits was prompted by the observation of that lesion. This revealed vacuolated and dilated smooth endoplasmic reticulum and degranulated and vesiculated rough endoplasmic reticulum in all the test livers. X-ray microanalysis indicates that the ultrastructural changes are linked to the deposition of tin.
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(1) Third molar genesis may occur up to the age of sixteen years, although the possibility of their appearance after the age of twelve years is reduced. (2) When third molar genesis is delayed beyond the age of ten years, the possibility of all four third molars developing is reduced by about fifty percent. (3) The intraindividual variability in stage of development of third molars increase when genesis is delayed beyond ten years of age. (4) There is no significant difference in size of early and late developing third molars.
The glycosaminoglycan (GAG), content of rabbit aortic wall was assayed morphometrically using ruthenium red-stained sections viewed by transmission electron microscopy. Two types of ruthenium red-positive granules were identified in the intercellular matrix. Large granules (20 to 50 nm. in diameter) with interconnecting fibrils were removed by digestion of the tissue with testicular hyaluronidase or chondroitinase ABC. Smaller granules (20 nm). were localized mainly in endothelial basement membrane and were resistant to digestion by these enzymes. Both types of granules were removed from the tissue by the action of nitrous acid. At intervals of 11 to 17 weeks after a single balloon deendothelialization of the aortas of normolipemic rabbits, there were significantly more granules of both types in areas where endothelium had regenerated over the neointima than in areas not covered by endothelium. Lipid also accumulated preferentially in the endothelium-covered neointima. Compared to normal aortas, there is an increase in the large granule content in the reendothelialized areas and a decrease in both large and small granule content in the nonendothelialized areas. It is suggested that GAG may trap low density lipoproteins. The low GAG content of the nonendothelialized neointima may account for the low lipid content; additionally, the lack of endothelial cover may allow diffusion of GAG out of these areas carrying low density lipoprotein into the blood stream in the form of GAG-low density lipoprotein complexes or low density lipoprotein removal may be facilitated by high density lipoprotein.
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We have quantified the accumulation of 51Cr-labeled washed rabbit platelets on the subendothelium of rabbit aortae following injury with a balloon catheter. The amount of radioactivity that became associated with the damaged wall within 10 minutes of the injury did not change appreciably during the following 24 hours, indicating that there was little turnover of platelets on the injured vessel wall. In addition, by injecting 51Cr-labeled platelets into rabbits at different times after injury, it was possible to estimate the reactivity of the exposed surface to newly injected platelets. Scanning electron microscopy showed that a monolayer of platelets initially formed on the injured surface; the number of platelets associated with the surface decreased over the 7-day observation period. The amount of 51Cr associated with the injured vessel wall also diminished during this period. The ability of the damaged surface to attract fresh platelets gradually decreased during the 7 days following injury. Platelet survival in rabbits was not significantly reduced following the removal of the aortic endothelium (balloon catheter injury 66.3 +/- 12.2 hours, sham operated 72.1 +/- 7.2 hours, untreated controls 76.2 +/- 3.8 hours). Thus, in rabbits, it cannot be assumed that platelet survival provides an estimate of endothelial injury in all circumstances.
Hypercholesterolemia was induced in pigs by feeding a chow diet supplemented with 1.5% cholesterol and 19.5% lard for periods up to 12 weeks. The aortic intima from areas of spontaneously differing permeability to proteins, as demarcated by their uptake of Evans blue dye, was examined using light microscopy and both scanning and transmission electron microscopy to describe the earliest detectable changes in intimal morphology induced by the diet. After 2, 4, and 6 weeks of feeding, cholesterol/lardfed pigs demonstrated monocyte adherence to the endothelium in areas of enhanced permeability (blue areas) in 86% of samples examined, as compared to 52% in areas of lesser permeability (white areas) and 17% in control animals. Similarly, the number of monocytes in the intima was higher in blue areas than in adjacent white areas or blue areas from control animals. After 12 weeks of feeding, all blue areas showed intimal monocytes, with fewer seen in white areas. Aortic endothelial cells in hypercholesterolemic pigs were normal in ultrastructural appearance, except they contained more lysosomes and cytoplasmic filaments than those from control animals. No lesions were observed at 2, 4, and 6 weeks, although plasma cholesterol levels were substantially elevated (200-400 mg/dl) at these times. A marked hyper-beta-lipoproteinemia was evident from 4 weeks onward, but no elevation of serum triglycerides was evident at any stage. Plasma phospholipid concentrations increased but not in direct proportion to cholesterol levels. At 12 weeks, foam cell lesions were observed in areas of enhanced permeability but not in adjacent areas of normal permeability. Lesion foam cells appeared to be derived from the monocytes which adhered to and penetrated the endothelium at earlier stages, since no intimal involvement, or lipid engorgement, by medial smooth muscle cells was observed.
Stable nonhemolytic small colony variants were isolated in pure culture from nine of 30 Staphylococcus aureus clinical strains after incubation of log10 7.0 cfu for 48 hr in MH broth containing 1.0 microgram/ml gentamicin. The variants resembled Staphylococcus epidermidis on blood agar, but they were positive for tube coagulase and thermostable nuclease at 24 hr and fermented mannitol slowly. The infectivity and virulence of four variants were compared to four parent S. aureus and three S. epidermidis strains in a rabbit model of endocarditis. Log10 5.0 cfu of the variant S. aureus, parent S. aureus, or S. epidermidis strains were injected intravenously into rabbits with intracardiac catheters. Quantitative culture of vegetations demonstrated endocardial infection in 47 of 49 (96%) animals injected with S. aureus variants, 44 of 44 injected with S. aureus parent strains, and four of 21 (19%) S. epidermidis-injected animals. The mortality rate in untreated animals within 4 days was five of 49 (10%) for variant S. aureus, 33 of 44 (75%) for parent S. aureus, and 0 of 21 for S. epidermidis. Small colony variants of S. aureus may be mistaken for S. epidermidis, but the variants are significantly more infective than S. epidermidis and are more likely to cause endocarditis. Gentamicin-induced S. aureus small colony variants are as infective but less virulent than their parent S. aureus strains.
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