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Biomedical subjects

H Parry

Publications and source records attributed to H Parry.

30 records · Page 2Linked to original sources
PubMed1984

Acute lymphoblastic leukemia supervening in a case of chronic lymphocytic leukemia after continuous 3-year treatment with chlorambucil.

A case is presented of a patient with classical chronic lymphatic leukemia (CLL) treated with continuous chlorambucil for 3 years who presented with a picture of acute leukemia. The peripheral blood still showed a prevalence of mature lymphocytes with a few blast cells, whereas the bone marrow showed a predominant population of blast cells possessing a null acute lymphoblastic leukemia phenotype. Karyotype analysis showed a prevalent hyperdiploid clone of 67 to 68 chromosomes with endoreduplication and marker chromosomes. The coexistence of a CLL-type population with the blastic, undifferentiated cell clone suggests a second malignancy superimposed on the previous leukemic process, and possibly brought about by the continuous chlorambucil treatment.

Aged↗
PubMed1982

Prostaglandin E2-mediated enhancement of human plasma cell differentiation.

Addition of prostaglandin E2 (PGE2) to blood mononuclear cell cultures containing pokeweed mitogen (PWM) enhances plasma cell (PC) differentiation measured by intracytoplasmic immunoglobulin 7 days later. T-cell mitogenesis to concanavalin A is inhibited using the same concentrations of PGE2. PGE2 failed to enhance the PC differentiation of lymphocytes from patients with systemic lupus erythematosus (SLE). Indomethacin, on the other hand, either had no effect or suppressed PC differentiation. The data is discussed in terms of the effect of PGE2 on human suppressor T-cell function.

Adult↗
PubMed1982

A plasma factor inhibiting prostacyclin-like activity in thrombotic thrombocytopenic purpura.

The plasma from a patient with thrombotic thrombocytopenic purpura contained a low molecular weight dialysable factor which inhibited the synthesis and release or activity of prostacyclin-like activity from vascular tissue. This factor was not an immunoglobulin or complement component. Following fresh plasma infusions the ability of the patient's plasma to stimulate the release of prostacyclin-like activity returned but no clinical improvement occurred.

Adult↗
PubMed1981

Rapidly fatal respiratory failure and angioimmunoblastic lymphadenopathy: possible contributions of immunoblastic leukaemia, chemotherapy, and multiple antibodies directed against mature blood cells.

A patient with angioimmunoblastic lymphadenopathy, immunoblastic leukaemia, pulmonary immunoblastic infiltration, and multiple antihaemocytic antibodies in his serum deteriorated rapidly after chemotherapy due to severe progressive respiratory of dysfunction. The haematological and immunological changes that accompanied this are described and discussed in the light of the pulmonary changes observed at necropsy of pulmonary oedema, fibrinous thrombi within venules, and immunoblastic infiltration of these thrombi and the venule walls. A pathophysiological mechanism is postulated in an attempt to rationalise these findings, and to act as a guide for the future assessment and management of similar cases.

Blood Cells↗
PubMed1980

Reduced prostacyclin activity in systemic lupus erythematosus.

When fresh rabbit aorta is incubated with plasma, prostacyclin, a potent inhibitor of platelet aggregation, is normally released. Plasma obtained from 2 patients with systemic lupus erythematosus (SLE) inhibited prostacyclin activity, while plasma from 22 other patients with SLE and 40 normal control subjects showed normal activity. Absence of prostacyclin activity did not appear to correlate with the clinical severity of the underlying disease. The possible association of this finding and the presence of thrombotic lesions in both patients is discussed.

Adult↗
PubMed1979

Cation transport across the guinea-pig placenta perfused in situ.

1. The guinea-pig placenta perfused in situ via the umbilical circulation has been used to measure unidirectional fluxes of Na from mother to fetus, and in the reverse direction, with 24Na and 22Na. There was no significant difference between the two fluxes, each being 22 mumole.min-1. 2. Ouabain 10(-5) M in the perfusion fluid had no detectable effect on radioisotopic movements of Na in either direction. 3. Unidirectional fluxes of 42K in both directions were approximately equal at 1.7 mumole.min-1 mother fetus and 1.8 mumole.min-1 in the reverse direction, despite a K concentration of 3.4 mM on the maternal side and 5.0 mM on the fetal side of the placenta. 4. Extraction of 42K and 86Rb from the perfusion fluid was inhibited by 43% by 10(-5) M-ouabain in the fluid. This effect was largely due to a reduction of isotope uptake by the placental tissue. 5. The relative permeabilities of the placenta, mother to fetus, were Rb approximately K (3.2) greater than Na (1.0) greater than Li (0.55). 6. Under the experimental conditions, the electrical potential difference between perfusion fluid and maternal blood was 6 mV (fetus negative). It was shifted towards the positive by a low Na fluid. 7. The results suggest the presence of a dominant Na-K pump (active component towards mother) sited at the maternal-facing membrane of the syncytiotrophoblast together with a subsidiary pump oriented in the opposite direction and probably sited together with a subsidiary pump oriented in the opposite direction and probably sited at the fetal-facing membrane of the syncytiotrophoblast. 8. A high proportion of Na movement particularly towards the fetus is probably passive, occurring through water-filled spaces, whilst K movement is more dependent on active transport.

Animals↗