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Biomedical subjects

D Potter

Publications and source records attributed to D Potter.

At least 109 records · Page 6Linked to original sources
PubMed1978

Growth and glucocorticoids in children with kidney disease.

Glucorticoid therapy inhibits statural growth. Alternate-day therapy causes less growth suppression than does daily therapy, and, in experimental animals and children with asthma, it has been associated with normal growth. Although catch-up growth may occur after cessation of steroid therapy, this is not always the case, especially when therapy has been prolonged. In children treated with steroids for glomerulonephritis or nephrotic syndrome and especially in children after renal transplantation, factors other than steroid therapy may contribute to growth retardation. Steroids may suppress growth by direct action on cell metabolism, by inhibition of growth hormone or somatomedin and/or by effects on calcium and phosphorus metabolism. Present knowledge of mechanisms of action and dose-response relationships is complete, and it is difficult to prescribe therapy which will achieve a predictable therapeutic effect without inhibiting growth.

Animals↗
PubMed1978

Deletion of the long arm of chromosome 20 [del(20)(q11)] in myeloid disorders.

Detailed clinical and cytogenetic studies were performed in five patients who had abnormal hematopoiesis and an acquired deletion of an F-group chromosome. Cytogenetic analyses, with banding techniques, of cells from bone marrow, spleen, or unstimulated peripheral blood showed a partial deletion of the long arm of one chromosome 20 [del(20)(q11)] in all five patients. Three patients had myeloproliferative disorders of uncertain classification, the fourth had possible preleukemia, and the fifth had acute myelomonocytic leukemia. Although the five cases showed certain similarities, the clinical and hematologic findings seen with the 20q- abnormality were not specific. None of the patients showed evidence of polycythemia vera or idiopathic acquired refractory sideroblastic anemia, two diseases previously associated with the 20q-. Our studies indicate that the 20q- abnormality is not limited to diseases primarily affecting erythropoiesis but that it can be found in the broader spectrum of myeloid disorders. In polycythemia vera, the 20q- has sometimes been regarded as a possible result of previous therapy with cytotoxic agents; however, four of our patients were untreated when the deletion was first noted.

Aged↗
PubMed1977

Further evidence for a non-random chromosomal abnormality in acute promyelocytic leukemia.

We have previously reported on two patients with acute promyelocytic leukemia (APL) who had what appeared to be a deletion of chromosome No. 17. We now describe a third patient with APL. All three patients had a structural rearrangement involving No. 15 and No. 17. Our current interpretation of the chromosomal abnormality is that it is a reciprocal translocation, t (15;17) (q22; q21). Evidence that this is a consistent rearrangement associated with APL comes not only from our three patients, but also from two other published cases of APL, studied with banding, who also had an identical abnormality.

Adult↗
PubMed1976

Improved patient survival in renal transplantation.

Patient and graft survival in 655 consecutive renal transplants performed at the University of California, San Francisco, was analyzed in two separate groups to assess the results of the low-dose immunosuppressive regimen established in September, 1972. These results show that graft survival is not jeopardized by adopting a policy of low-dose immunosuppressive therapy, but, in fact, that patient survival is improved significantly. This study also shows that cadaver renal transplantation can be performed with a mortality rate comparable to or better than that in patients on chronic hemodialysis.

Cadaver↗
PubMed1976

Chromosomal banding patterns in acute nonlymphocytic leukemia.

Bone marrow chromosomes obtained from 50 of 55 consecutive adult patients with acute nonlymphocytic leukemia were analyzed with quinacrine fluorescence. Twenty-five patients showed a normal karyotype and 25 an abnormal karyotype on the initial samples available for analysis. Among the 25 patients with abnormalities, the marrow cells contained 48 chromosomes in one case, 47 in two, 46 in ten, 45 in nine, 43 in two, and 42 chromosomes in one case. Seven of the ten patients with 46 chromosomes had abnormalities, primarily balanced translocations, that were not detected with the standard Giemsa stains. The analysis of all of the data available revealed the presence of nonrandom chromosome changes such as the addition of No. 8, the loss of No. 7, and a gain or loss of one No. 21. the most frequent structural rearrangement was the translocation between the long arm of No. 8 and No. 21, which may also be associated with the loss of a sex chromosome. Chromosomal abnormalities decreased or disappeared during remission; the same abnormality recurred in relapse. Chemotherapy did not appear to produce a stable clone of aberrant cells. Evolution of the karyotype occurred in eight patients, in five of whom an additional No. 8 was observed. This pattern of chromosomal evolution in patients with acute leukemia was very similar to that observed in patients with chronic myelogenous leukemia in the blast phase.

Acute Disease↗