On the fine structure of rat liver ribosome small subunits.
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Animals↗
Biomedical subjects
M Platzer
Publications and source records attributed to M Platzer.
Prediction of therapeutic response to radioactive iodine in Graves' disease using TSH-receptor antibodies and HLA-status.
We have examined the combined usefulness of TSH-receptor antibody detection and HLA status on the therapeutic response to standard doses of radioactive iodine (RAI) in forty-three hyperthyroid Graves' patients. Twenty-three patients had detectable TSH-receptor antibodies as measured by 125I-TSH binding-inhibition (TBI) prior to administration of 7 mCi RAI. Eighteen (78%) of these patients were rendered euthyroid within 3 months. In contrast, twenty patients were TBI negative prior to RAI and sixteen (80%) of these individuals remained hyperthyroid at 3 months and required two, or more, doses of RAI to control their thyroid function. DR3 status alone was not strongly associated with resistance to RAI. However, of sixteen patients without detectable TBI activity and who required two or more doses of RAI, ten patients were DR3 positive (62%) compared with 25% in a control population. Only one patient who was both TBI and DR3 negative required more than one dose of RAI. These data indicate that TBI may be an accurate predictor of the therapeutic response to RAI in patients with hyperthyroid Graves' disease. Investigation of HLA status alone was of limited value, although it appeared that the combination of TBI and DR3 may be of additional help in developing an overall strategy for the treatment of hyperthyroid Graves' disease.
Adolescent↗
The perifused Leydig cell: system characterization and rapid gonadotropin-induced desensitization.
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Animals↗
UHX1 and PCTK1: precise characterisation and localisation within a gene-rich region in Xp11.23 and evaluation as candidate genes for retinal diseases mapped to Xp21.1-p11.2.
The gene for ubiquitin hydrolase on the X chromosome (UHX1), cloned and mapped to Xp21.2-p11.2, is a candidate gene for retinal diseases. We used fine mapping techniques to localise UHX1 between markers DXS1266 and DXS337, where congenital stationary night blindness (XICSNB) and retinitis pigmentosa type 2 (RP2) are also located. Reevaluation of the UHX1 gene structure demonstrated five new exons, for a total of 21 exons and a predicted protein product of 963 amino acids. Evaluation of patients revealed no UHX1 mutations using SSCP (10 CSNB1 and 20 XLRP) or deletion screening with cDNA hybridisation (13 CSNB1 and 43 XLRP). Likewise, no aberrations were found in the nearby PCTAIRE1 (PCTK1) gene in 13 CSNB1 and 43 XLRP patients by deletion screening. Thus mutations of UHX1, and probably PCTK1, do not appear to cause common X-linked eye diseases. UHX1's role in patients with mental retardation may be appropriate for further investigations into UHX1 function.
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