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Biomedical subjects

J M Bridges

Publications and source records attributed to J M Bridges.

At least 73 records · Page 4Linked to original sources

An estimation of beta-glucuronidase and N-acetyl-beta-D-glucosaminidase activity in normal and chronic lymphocytic leukaemia lymphocytes.

The lysosomal enzymes beta-glucuronidase (EC 3.2.1.31) and N-acetyl-beta-D-glucosaminidase (EC 3.2.1.30) were estimated by biochemical and cytochemical means in the circulating lymphocytes of 20 control subjects, 19 cases of B cell and one case of T cell chronic lymphocytic leukaemia. Significantly lower levels of activity were observed both biochemically and cytochemically for each enzyme in B cell chronic lymphocytic leukaemia lymphocytes, whereas the values obtained for the T cell chronic lymphocytic leukaemic patient fell within the normal range. The absence of staining reaction for both enzymes in the majority of B cell chronic lymphocytic leukemia lymphocytes contrasted with the uniform pattern of polar positivity obtained in T cell chronic lymphocytic leukaemia lymphocytes.

Acetylglucosaminidase↗

N-Acetyl-beta-D-glucosaminidase activity in normal and chronic lymphocytic leukaemic lymphocytes.

N-Acetyl-beta-D-glucosaminidase (EC 3.2.1.30) activity was measured fluorimetrically in: (a) lymphocytes from 20 normal donors, (b) enriched B and T lymphocyte populations prepared by E rosette sedimentation from 8 normal subjects, (c) lymphocytes from 15 untreated B cell chronic lymphocytic leukaemic patients. The pH profiles and optima (4.7) were similar in all preparations. Normal B lymphocytes had higher activity than normal T lymphocytes and both these preparations and normal unfractionated lymphocytes had significantly higher activity than chronic lymphocytic leukaemic lymphocytes. The apparent Michaelis constants were similar in normal unfractionated, B enriched and T enriched lymphocytes, whereas a reduced affinity for the enzyme was observed in the leukaemic lymphocytes. The difference in enzyme content between normal and chronic lymphocytic leukaemic lymphocytes cannot therefore be explained on the basis of a high B cell percentage in patients with chronic lymphocytic leukaemia.

Acetylglucosaminidase↗

Changes in granulopoiesis detected by in vitro colony formation in acute lymphatic leukaemia.

Patients with acute lymphatic leukaemia (ALL) could be divided into two groups at diagnosis--those whose peripheral blood and/or bone marrow exhibited in vitro colony formation and those in whom it did not, but this finding did not appear to correlate with any clinical or haematological parameter, or with prognosis. The colonly-forming potential of patients with ALL in their first full remission, early relapse or second remission did not deviate significantly from previously established normal values, but the colony-forming potential of patients in early remission was very significantly reduced. No loss of colony-forming potential of normal marrow cells was noted when they were cultured with cells from patients with ALL.

Adolescent↗

Inhibition of normal human in vitro colony forming cells by cells from leukaemic patients.

Co-culture in agar of normal bone marrow cells from different individuals gave granulocyte macrophage colony counts that were expected from counts made when the marrows were cultured separately. Co-culture of normal marrow with normal peripheral blood leucocytes (which did not themselves give rise to colonies) caused inhibition of colony growth only when the ratio of peripheral blood to bone marrow cells was of the order of 4 : 1. Peripheral blood or bone marrow cells from 7 of 9 patients with acute myelomonocytic leukaemia, which did not give rise to colonies, caused a marked reduction in the number of colonies obtained from normal marrow cells when cultured with them. This inhibitory effect of leukaemic cells was found when ratios of leukaemic to normal cells were as low as 1 : 4. Additional evidence that the inhibition of normal colony formation was related to the leukaemic process was obtained from follow-up studies on one of the patients whose cells lost the capacity to inhibit normal colony formation during remission and became inhibitory again on relapse.

Adolescent↗

Fanconi's aplastic anaemia with short stature. Absence of response to human growth hormone.

A patient with idiopathic marrow hypoplasia associated with short stature and other anomalies (Fanconi's anaemia) is described: treatment with human growth hormone for one year did not accelerate his growth rate or significantly affect his anaemia: androgen treatment considerably improved both features. Endocrine studies suggest that though he had poor and insufficient production of endogenous growth hormone to insulin-induced hypoglycaemia, the major defect in this syndrome is determined more at the end-organ than at the pituitary or gonadal level.

Anemia, Aplastic↗

Reactivation of scabies rash by methotrexate.

A 13-year-old female was on maintenance therapy for acute lymphoblastic leukemia. On three occasions she received methotrexate orally and each time this was associated with reactivation of scabies rash. The mechanisms for this phenomenon are discussed.

Adolescent↗

Characteristics of colony growth from normal human bone marrow.

The number of granulocyte/macrophage colonies grown in vitro from bone marrow cells obtained from 90 rib segments and 30 ;normal' bone marrow aspirates was found to be highly variable. Considerable variation was also noted in the relationship between colony number and the number of cells cultured in both groups. The aspirate group was found to have a significantly greater ability to form colonies without the addition of colony-stimulating factor to the culture medium at low cell concentrations.

Biopsy↗