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T C Morris

Publications and source records attributed to T C Morris.

At least 55 records · Page 3Linked to original sources
PubMed1991

Lactoferrin-inducible monocyte cytotoxicity for K562 cells and decay of natural killer lymphocyte cytotoxicity.

Monocyte-enriched and lymphocyte-enriched fractions of peripheral blood from three healthy volunteers were obtained by percoll density gradient centrifugation. The cytotoxic activity of each fraction against 51Cr-labelled K562 cells was quantified in a 2-h assay using freshly isolated cells of each fraction and cells of each fraction which had been incubated with and without lactoferrin in complete medium for 18 h before performing the assay. We have thereby shown that cytotoxicity was not demonstrable in the lymphocyte fraction (containing 7.3 +/- 2% large granular lymphocytes) after 18 h in medium, whereas the cytotoxicity of the monocyte fraction (containing 3 +/- 0.4% large granular lymphocytes) was still significantly increased (P less than or equal to 0.01) and that lactoferrin had no effect on lymphocyte fraction cytotoxicity while producing an 11-fold increase in the cytotoxicity of the monocyte fraction. It is therefore possible to perform a relatively simple test of monocyte cytotoxicity using lactoferrin as a stimulant in a 2-h 51Cr-labelled K562 assay system by allowing 18 h to elapse for lymphocyte natural killer cytotoxicity to decay.

Cell Separation↗
PubMed1991

Normal unstimulated lymphocytes produce granulopoietic inhibitory activity.

Normal unstimulated lymphocytes cocultured with normal bone marrow will inhibit day-7 colony- forming units in culture. We have shown that this phenomenon has a molecular basis and attempted to characterize it further. Using specific assays and neutralizing monoclonal antibodies we have found that this granulopoietic inhibitory activity (GIA) is not due to alpha- or gamma-interferon, tumor necrosis factor, or acidic or basic isoferritins. Biochemical studies suggest that it is a glycoprotein with a molecular weight greater than 100,000 daltons. It appears to act on cells in S phase, although it may not be S-phase specific. GIA represents a novel inhibitor that merits further investigation.

Bone Marrow↗
PubMed1990

Prospective in vitro testing for drug-induced neutropenia in a patient requiring anti-malarial prophylaxis: confirmation of findings on exposure of patient to drug.

A patient with moderate pancytopenia thought to be due to chloroquine ingestion was shown to have granulocyte progenitors (CFU-G) which were abnormally sensitive in vitro to chloroquine. As he required further anti-malarial prophylaxis, his marrow was prospectively tested in vitro with proguanil and its metabolite cycloguanil. The patient's CFU-G were also abnormally sensitive to these agents and predicted neutropenia was verified when the patient had a trial course of proguanil. We believe this is the first instance of in vivo confirmation of in vitro CFU-G drug sensitivities.

Agranulocytosis↗
PubMed1990

Monocyte esterase deficiency in malignant neoplasia.

A survey of the incidence of monocyte esterase deficiency in 4000 inpatients (including 808 with malignant neoplastic disease) and 474 normal controls was performed using an automated esterase method. A highly significant excess of patients with malignant disease and the deficiency was evident when compared with normal controls or all other patients. Within the group of patients with malignant disease the demonstrable excess occurred in B chronic lymphocytic leukaemia, non-Hodgkin's and Hodgkin's lymphoma, and carcinoma of the gastrointestinal tract. There was also a significant excess of patients with the deficiency attending the renal unit, both among patients who had had renal transplants and those who had not. A familial incidence of monocyte esterase deficiency was found in 19 (35%) of first degree relatives of those patients in whom family studies were done. It is suggested that the reason for the increased prevalence of the anomaly in these disorders might be that the diminution of esterase activity has a role in their development.

Esterases↗
PubMed1990

Tartrate resistant acid phosphatase positive splenic lymphoma: a relatively benign condition occurring in a time-space cluster?

Conventional light and electron microscopic studies, together with cytochemical and immunocytochemical staining procedures, were carried out to ascertain whether the lymphomata of four elderly female patients living within 10 kilometers of each other, who presented within a short space of time with massive splenomegaly and varying cytopenia, belonged to any particular subgroup of lymphoma. In each case the lymphoma had a diffuse pattern and mature B cell phenotype. The malignant cells were of uniform cell type, slightly larger than admixed polymorphonuclear leucocytes, and showed minimal nuclear irregularity and positivity for tartrate resistant acid phosphatase (TRAP) staining. Their clinical and morphological features were compared with those of other lymphoproliferative disorders, but while sharing some features in common with each condition, this small group of patients seemed to have a unique combination of findings. The cytopenias of all four responded well after removal of the spleen and their disease has not been aggressive. It is concluded that these patients have a distinct subgroup of lymphoma, which it is important to recognise so that inappropriate use of aggressive cytotoxic drugs can be avoided.

Acid Phosphatase↗
PubMed1989

Immunoglobulin light chains in common acute lymphoblastic leukaemia.

A single immunoglobulin light chain lambda was identified in the blast cells of two out of 12 patients with common acute lymphoblastic leukaemia (C-ALL) using the alkaline phosphatase/anti-alkaline phosphatase (APAAP) technique. Inhibition at the cell surface proved that the reaction was a genuine anti-lambda reaction. Immunoglobulin mu chain was not identified in these patients. Results of immunoglobulin typing in 103 patients with B chronic lymphocytic leukaemia (B-CLL) are cited to show the increased sensitivity of the APAAP technique as compared to the indirect immunoperoxidase technique for cellular immunoglobulin identification.

Female↗
PubMed1989

CFU-GM inhibitors in neutropenia.

Peripheral blood lymphocytes from 20 patients with neutropenia not consistent with aplastic anaemia were tested for their ability to inhibit the proliferation of normal granulopoietic precursor cells (CFU-GM) in agar culture. Two patients, both with features of an autoimmune disorder, had lymphocytes which were more inhibitory than normal lymphocytes to both normal and their own CFU-GM. Two other patients had lymphocytes which were more inhibitory than normal lymphocytes to either their own CFU-GM or normal CFU-GM but not both. Eight patients had lymphocytes which were significantly less inhibitory than normal lymphocytes to either normal or their own CFU-GM, but only one showed this feature against both normal and their own CFU-GM. One patient had a highly potent plasma inhibitor of CFU-GM--this patient had received multiple transfusions and had a leucocyte antibody of a broad specificity. No clinical or haematological features were common to any of these groups of patients which reflects the heterogeneity of patients studied and stresses the importance of controls.

Adolescent↗
PubMed1987

Evidence following splenic radiotherapy for a highly dynamic traffic of CFU-GM between the spleen and other organs in chronic granulocytic leukaemia.

Five patients with Ph1 +ve chronic granulocytic leukaemia and massive splenomegaly were given induction therapy with splenic irradiation, and their peripheral blood leucocyte count and granulocyte macrophage progenitor (CFU-GM) concentration monitored during the following six hours. In each patient there was a greater fall in CFU-GM than would have been expected from the fall in leucocyte count, but no evidence of a plasma inhibitor was found to explain the disproportionate reduction in CFU-GM. The difference between the estimated and observed decrease in CFU-GM/1 following splenic irradiation indicates a highly dynamic traffic of CFU-GM from the spleen to other organs in chronic granulocytic leukaemia.

Adult↗
PubMed1987

The CFU-C assay in patients with neutropenia and, in particular, drug associated neutropenia.

One-hundred and four patients with a diagnosis of aplastic anaemia (28) or neutropenia (76) referred to our laboratory for assessment of granulopoiesis were studied. Bone marrow myeloid progenitor cell (CFU-C) frequency was measured and in 85 patients, inhibitor studies with either in-vitro drug addition or plasma co-culture were performed. Of 28 patients with aplastic anaemia, 22 (79%) had low numbers of CFU-C, while four (14%) had numbers within the normal range and two (7%) had elevated progenitor cell frequency. In contrast, of the 76 patients with neutropenia who were studied only 29 (38%) had low CFU-C numbers, 33 (43%) had a CFU-C frequency within the normal range and 14 (18%) had elevated CFU-C numbers. Thirty-nine patients had ingested potentially myelotoxic drugs and in eight of these it was possible to demonstrate drug associated inhibition of CFU-C proliferation in vitro. The drugs most commonly associated on a historical basis with myelosuppression were chloramphenicol, antimalarials, sulphonamides, anticonvulsants and nonsteroidal anti-inflammatory agents.

Agranulocytosis↗
PubMed1987

Pathology of the heart and conduction system in lymphoma and leukaemia.

The clinical and pathological findings in two patients with non-Hodgkin's lymphoma and two patients with T helper cell prolymphocytic leukaemia affecting the heart are described. All four patients had extensive malignant disease, with infiltration of multiple organs. Cardiac infiltration varied from microscopic foci in one case, to grossly identifiable tumour deposits destroying and replacing normal heart structures in three cases. Two patients with infiltration of the conduction system had abnormal electrocardiograms and cardiac dysfunction: one died suddenly, and the other died in heart failure. A third patient with widespread cardiac lymphoma did not show any electrocardiographic abnormalities or dysfunction. Clinicians should be aware of the possibility of cardiac and conduction system disease, particularly in the light of the evolution of specific antitumour chemotherapeutic agents.

Aged↗
PubMed1987

T-lymphocyte colony formation by lymphocytes from patients with aplastic anaemia.

T-lymphocyte colonies were cultured using lymphocytes from patients with aplastic anaemia and normal donors to assess their respective proliferative activities. Colony numbers from aplastic patient's cells were lower than from normal donors', though this was not significant. When lymphocytes from patients were co-cultured with normal lymphocytes, inhibition of T-colony formation was observed in 8 out of 12 experiments. As the degree of inhibition was greater than if patient cells grew no colonies, then, clearly, normal T-colony formation was inhibited. This ability of patients' lymphocytes to suppress lymphopoiesis might account for the low levels of patient T-colony formation, as well as low in vivo numbers of lymphocytes found in patients with aplastic anaemia. The role of patients' lymphocytes in causing marrow aplasia was investigated. Although the incorporation of patients' lymphocytes in normal granulocyte-macrophage (GM) colony-forming systems inhibited colony growth, in only 1 out of 8 patients was this inhibition significantly greater than that caused by the addition of normal lymphocytes to GM colony systems. Therefore, lymphocytes may not be the primary cause of aplastic anaemia, except for a few rare cases.

Adolescent↗
PubMed1987

Monocyte esterase? A factor involved in the pathogenesis of lymphoproliferative neoplasia.

Monocyte esterase activity was studied in 1,000 doctor-attending patients with normal hematological indices and in 56 patients with non-Hodgkin's lymphoma (NHL) or B chronic lymphocytic leukemia (CLL). The incidence of esterase deficiency was significantly greater in the NHL-CLL patients (7.1%) than in the population group (1.7%; p less than 0.05). In the NHL-CLL group, study of the families showed the esterase deficiency to be a familial characteristic. We postulate that the presence of the anomaly may be either a factor predisposing to the development of the NHL or CLL or a factor indicating a predisposition to these disorders.

Esterases↗
PubMed1986

Concurrent familial myeloma in Northern Ireland.

Three families are presented containing two members of each family with myeloma over a 13-year period in Northern Ireland. In all three families, the disease was concurrent, and the first reported cases of concurrent myeloma in a father and son and also identical twins are included. This incidence represents a greater frequency than would be expected and gives credence to the idea of an etiologic agent in this disease.

Aged↗