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Biomedical subjects

A E Gabrielsen

Publications and source records attributed to A E Gabrielsen.

At least 19 recordsLinked to original sources
PubMed1981

Late treatment of murine lupus erythematosus with dactinomycin. II. C1 and antibody to DNA.

(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.

Age Factors↗
PubMed1979

Late treatment of murine lupus erythematosus with dactinomycin (actinomycin D). I. Course and longevity.

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.

Animals↗
PubMed1978

Dactinomycin treatment of murine lupus erythematosus. I. Renal disease and longevity.

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.

Animals↗
PubMed1977

C4 in glomerular lesions of NZB/NZW mice.

Antisera to human C4 can discriminate circulating Ss protein (C4) levels in mice. Since there has been no information on early complement components (C1, C4, C2) in the renal lesions of B/W mice, we applied the indirect immunofluorescence technique to post-mortem sections of kidney from B/W female mice with advanced renal disease. C4 was present in fifteen of the sixteen specimens, usually in a distribution similar to that of IgG or C3. Specificity was demonstrated by differential absorptions with high-Ss serum from C57BL/6 male mice and low-Ss serum from C3H/HeJ female mice. High-Ss-absorbed antiserum did not stain, while low-Ss-absorbed antibody retained much of its activity. This finding parallels the demonstration of early complement components in lesions of clinical lupus nephritis, and is consistent with classic complement pathway activation in B/W disease.

Animals↗
PubMed1977

Prolonged survival of hypertransfused NZB/NZW mice.

(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.

Animals↗
PubMed1975

Combined immunodeficiency disease: an inborn error of purine metabolism.

The recently discovered association of adenosine deaminase (ADA) deficiency and combined immune deficiency (CID) has emphasized the critical role of purine salvage in the function of lymphoid tissue. Known enzymatic properties of ADA are presented. In addition, known phenotypic data and possible genetic mechanisms for the occurrence of ADA deficiency in CID are discussed. A hypothesis based on considerations of known metabolic pathways in human erythrocytes is proposed to account for the selectivity of ADA deficiency for lymphoid tissue. Finally, some inhibitors of ADA are discussed as well as some immunosuppressive agents.

Adenine↗
PubMed1975

Immune complexes in skin of NZB/NZW mice.

Skin biopsies were performed on female (NZB X NZW)F1 mice (B/W) at ages ranging from 1 to 12 months. The control strain was the C57B1/6. Immunoglobulin G and beta 1C globulin deposition was sought using the indirect immunofluorescence method. Both globulins were detected consistently at the dermal-epidermal junction from the age of 6 months. The pattern of staining was granular, and progressed from focal deposition to confluent and diffuse involvement of the basement membrane at 9-10 months of age. No staining was observed in any of the C57B1/6 mice up to 14 months of age. These findings increase the resemblance of B/W disease to human systemic lupus erythematosus.

Animals↗