A longitudinal study comparing apically repositioned flaps, with and without osseous surgery.
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Biomedical subjects
Publications and source records attributed to C T Olsen.
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(NZB x NZW)F1 hybrid (B/W) female mice were treated intermittently with dactinomycin beginning at 6--6.5 months of age. Survival was greatly prolonged relative to control mice. IgG antibody to DNA did not decline significantly in the treated mice until they were more than 18 months old, but circulating levels of the first complement component (Cl) rose during the first 4 weeks of treatment and were back into the normal range after 8 weeks. Thus these two humoral indexes of disease activity varied independently, and only Cl reflected the improved status of the treated mice.
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Dactinomycin treatment a of group of (NZB X NZW)F1 hybrid female mice was delayed until the age of 6-6 1/2 months, by which time the immune complex disease was well established. Three animals of the original twenty-eight had already died, ten had heavy proteinuria and a few were oedematous. The dactinomycin dose was 3.5 microgram per day, which was suspended when significant weight loss occurred. Twelve of the thirteen experimental mice were alive at 12 months of age, eleven at 15 months, but only eight by 20 months, whereas all twelve control animals had died by the age of 11 months. These results and the supporting data on body weight and renal function indicate that dactinomycin can at least arrest the disease process and may improve it. The mechanism is not known, but it may be the result of a reduced availability of DNA or an alteration in its properties following combination with dactinomycin.
Sera from periodic bleedings of B/W female mice were assayed for C1 hemolytic activity. It peaked at 3 to 4 months of age and declined to very low levels by 6 to 7 months. Activity remained low even in long-lived animals.
Three groups of female (NZB X NZW)F1 hybrid mice were treated with an intermittent regimen of dactinomycin (actinomycin D), 3.5 microgram. daily. Median survival was doubled in two of the groups and increased by more than 75 per cent in the third. Most of the treated animals never had significant proteinuria. When kidneys from 14 treated mice, which died between the ages of 11 and 20 months, were examined by light and fluorescence microscopy, most showed the lesions of normal aged CBA and C57BL/6 mice, some expansion of the mesangial matrix and increased cellularity, consistent with deposition of immunoglobulins and complement components in the mesangium, generally sparing the capillary loops. Four of the 14 animals, three of them long-lived, had advanced renal glomerular disease. These data indicate that dactinomycin, by whatever therapeutic mechanism, permits very extended survival of B/W female mice, the large majority of them without significant renal disease.
(NZB X NZW)F1 hybrid female mice were transfused fortnightly with 1 ml of packed buffy-coat-poor syngeneic erythrocytes, beginning at 3--4 months of age, in an effort to suppress erythropoiesis selectively and perhaps limit availabiliity of DNA for immune complex formation. The mean increase in survival was about 8 weeks (P less than 0-05). Repeatedly phlebotomized donor female mice tended to sicken earlier and die at younger ages. This is initial support for the hypothesis that erythroblast DNA may be involved in this SLE-like disease.
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