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T E Parry

Publications and source records attributed to T E Parry.

At least 37 records · Page 2Linked to original sources
PubMed1978

Electron microscope autoradiographic studies of the erythroblasts of a case of congenital dyserythropoietic anaemia, type II.

The bone marrow cells of a patient with congenital dyserythropoietic anaemia, type II, were incubated with 3H-thymidine, 3H-uridine or 3H-leucine for 1 h and studied using the technique of electron microscope autoradiography. Several of the erythroblasts which either displayed the characteristic subsurface double membranes or showed various non-specific abnormalities of the nuclear membrane were found to be actively engaged in DNA, RNA and protein synthesis. Both members of some pairs of erythroblasts which were joined together by a spindle bridge were found to be engaged in DNA synthesis, indicating that some spindle bridges persist for a period longer than the duration of the G1 phase. A small proportion of mononucleate and binucleate late (non-dividing) erythroblasts showed a marked depression or arrest of protein synthesis and some or all of such cells were presumably destined to be phagocytosed by the bone marrow macrophages.

Anemia↗
PubMed1976

Serum "uracil+uridine" levels in pernicious anaemia.

The serum "uracil+uridine" level, expressed as uracil, has been measured in 21 cases of vitamin B12 deficiency, in which the serum folate was normal, and compared with the level in 97 normal subjects. The level in the vitamin B12 deficient group (11.9 mumol/1). was significantly lower than in the controls (15.7 mumol/1., P less than 0.005). Nine of the former were complicated by stystemic illness but the clinical and haematological features in the remaining 12 were consistent with the diagnosis of pernicious anaemia in relapse. The serum uracil level in this group was even lower (10.21 mumol/1., P less than 0.01). This finding is unexpected in view of the generally accepted indirect role of vitamine B12 in the methylation of deoxyuridine monophosphate to deoxythymidine monophosphate. Reasons are given for not accepting these results as reflecting the main biochemical lesion in vitamin B12 deficiency. Although they do not give direct support to an impairment in the methylation of deoxyuridine monophosphate, they do not exclude it as they test only one possible metabolic pathway and moreover they could represent the result of more than one action of vitamin B12 on uracil metabolism. They do show, however, that some aspect of uracil metabolism other than methylation is affected in vitamin B12 deficiency in man.

Anemia, Pernicious↗
PubMed1976

Serum "uracil+uridine" levels before and after vitamin B12 therapy in pernicious anaemia.

The serum "uracil+uridine" levels, expressed as uracil, have been measured in 10 cases of pernicious anaemia both before and after treatment, and compared with the levels in 97 normal subjects. The mean pre-treamtent value (8.82 mumol/1., range 6.0-12.0 mumol/1.) differed significantly from that of the normal controls (15.7 mumol/1., range 5.7-40.5 mumol/1., t = 8.8, P less than 0.001). This confirms the low serum uracil level previously reported in pernicious anaemia relapse. The level rose progressively after treatment, reaching a maximum on the fourth day (mean 17.85 mumol/1., range 9.3-23.4 mumol/1.). This was not significantly different from the mean of the normal control group. The difference between the pre- and post-treatment levels was significant on days 3,4 and 5 (P less than 0.005, P less than 0.001 and P less than 0.005 respectively) and the rise preceded the reticulocyte response by 24 h. A further case was treated with pysiological doses of vitamin B12 (2 mug daily for 6 d) and a similar rise in the serum uracil level noted. These results are not explained by any of the known functions of vitamin B12. They are, however, similar to the changes in the serum methionine levels previously reported in pernicious anaemia. The latter were readily explained by the known action of vitamin B12 on "de novo" methionine synthesis and it is suggested that the synthesis of uracil, like that of methionine, might be influenced by vitamin B12 in man.

Anemia, Pernicious↗
PubMed1976

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Dental Assistants↗
PubMed1974

Serum 'uracil plus uridine' levels in normal subjects and their possible significance.

A microbiological method for the assay of uracil is described. The growth of the test organism is supported by uracil and also by uridine but not by uridylic acid. The method therefore measures uracil and uridine together. The ;uracil + uridine' level, expressed as uracil, has been measured in blood from 144 normal subjects ranging in age from cord blood to the eighth decade. The mean level of 22 mu mol/l (0.25 mg%) in cord blood decreases to 15 mumol/l (0.17 mg%) in adults over the age of 20. There is no difference between the sexes. Uracil is of interest because (a) it is a constituent base of RNA, (b) it is the precursor of two of the bases thymine and cytosine that enter into the composition of DNA, and (c) under certain circumstances it has mutagenic properties. The last is dependent upon the existence of two tautomeric forms of uracil, the common keto form which pairs normally with adenine and the rare enol form which pairs with guanine. A mistake in base pairing which allows uracil in its enol form to enter the DNA molecule and pair with guanine can result in a G = C --> A = T base transition in the DNA molecule. The molecular mechanism involved as well as the possible bearing on somatic mutation are discussed.

Age Factors↗
PubMed1972

Microbiological assay of amino acids in serum: valine, leucine, and methionine.

A microbiological method for the assay of valine, leucine, and methionine in serum is described and its accuracy and reproducibility are assessed. Under the conditions specified the L-isomers only of the three amino acids are measured. The serum levels of the three amino acids in 60 normal subjects are presented.

Adolescent↗
PubMed1972

Congenital dyserythropoietic anaemia with erythroblastic multinuclearity.

A case of congenital dyserythropoietic anaemia with erythroblastic multinuclearity in a 36-year-old woman is described and the literature reviewed. The syndrome is characterized by a protracted clinical course, a relatively mild anaemia, a low reticulocyte count, slight hyperbilirubinaemia, splenomegaly, pronounced erythroid hyperplasia with reversal of the myeloid erythroid ratio, and in particular by the presence of multinucleated erythroblasts in the marrow. The picture of ineffective erythropoiesis is confirmed by erythrokinetic studies. The present case is the forty-first to be described in the literature and is the third from Britain. Thirty-one of these have occurred in seven families but a family history has been lacking in the remaining ten. The onset of anaemia occurred in childhood in 21 of the 41 cases.

Adult↗