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Biomedical subjects

M Greaves

Publications and source records attributed to M Greaves.

At least 91 records · Page 5Linked to original sources
PubMed1997

Sea-blue histiocytosis and pancytopaenia associated with chronic total parenteral nutrition administration.

A 22-year-old female on chronic total parenteral nutrition for short bowel syndrome presented for investigation of pancytopaenia and hepatosplenomegaly. Bone marrow examination revealed an infiltrate of sea-blue histiocytes and cytochemistry confirmed these to be lipid laden macrophages. The total amount of fat in the feeding regimen was subsequently reduced, and there has been a partial haematological improvement. The occurrence of sea-blue histiocyte syndrome complicating the fat emulsion component of chronic total parenteral nutrition has been reported recently. To our knowledge this report is the first where reduction in the lipid content of the feeding regimem has resulted in an improvement in the degree of pancytopaenia.

Adult↗
PubMed1996

A concept-based retrieval system for thoracic radiology.

Current digital information systems in radiology are insufficient to accommodate the retrieval needs of academicians. Significant efforts are required in retrieving clinical cases for teaching and research. We describe a prototype system that supports intelligent case retrieval based on a combined specification of patient demographics, radiologic findings, and pathologic diagnoses. The documents for these cases can be distributed among multiple heterogeneous data bases. The system features automatic indexing of radiology and pathology reports, a comprehensive lexicon for thoracic radiology, an interface to a hospital information system, radiology information system, and picture archiving and communication systems, and a graphical user interface for query formulation and results visualization. The prototype system was developed within the domain of thoracic radiology involving patients with lung cancer.

Abstracting and Indexing↗
PubMed1996

Discordant clinical presentation and outcome in infant twins sharing a common clonal leukaemia.

We report the different presentation features and clinical outcome between two identical infant twins with acute lymphoblastic leukaemia with a shared clonal disease and MLL gene rearrangement. One twin relapsed and died, but the other is in complete remission > 4 years after diagnosis. These data, and similar observations on other twin infants with leukaemia, suggest that despite a common clonal in utero, post-natally these leukaemias can evolve independently, at different rates, in the twinned individuals, and that the usually fatal leukaemia associated with t(4;11) MLL gene rearrangement can be effectively treated when the leukaemic burden is small.

Bone Marrow↗
PubMed1996

Antibodies to membranes of endothelial cells and fibroblasts in scleroderma.

Anti-endothelial and other cell membrane-reactive antibodies in scleroderma were characterized by immunoblotting sera with membrane and cytosol preparations of human umbilical vein endothelial cells (HUVEC), dermal fibroblasts and a T cell lymphoma HUT78. Antibodies reactive with HUVEC membranes were found in 17 of 20 patients with scleroderma (33 bands) in contrast to only two of 20 controls (two bands; P < 0.01) and three of 11 patients with myocardial infarction (four bands). Eleven of the 20 patients possessed antibodies that were specific for HUVEC membrane and did not cross-react with other cell lines. Analysis of patient subgroups showed that HUVEC membrane antibodies were present in nine of 11 patients with systemic sclerosis and in all nine with the CREST syndrome, and were HUVEC-specific in five and six of these cases, respectively. Although considerable heterogeneity was seen, antibodies to an 18-19-kD membrane epitope were found in 11 of the 20 patients but in none of the controls (P < 0.01). This antibody which reacted particularly with HUVEC (n = 9) and HUT78 membranes (n = 9) was associated with CREST syndrome rather than systemic sclerosis (9/9 versus 1/11; P < 0.01), and after elution was shown to possess anticentromere activity. In addition, antibodies reactive with both fibroblast (n = 11; 18 bands) and HUT78 membranes (n = 18; 42 bands) were detected and were specific for either fibroblast or HUT78 membranes in nine and 14 patients, respectively. There was no significant difference in the incidence of these fibroblasts and HUT78 membrane antibodies in the two patient subgroups. These findings support the concept that membrane-reactive antibodies, including anticentromeric antibodies, may play a central role in the pathogenesis of scleroderma, through their ability to react with endothelial cells.

Aged↗
PubMed1996

Further characterization of anti-endothelial cell antibodies in systemic lupus erythematosus by controlled immunoblotting.

Anti-endothelial cell antibodies in systemic lupus erythematosus were further characterized by controlled immunoblotting studies with EN4 defined membrane and cytosol preparations of human umbilical vein endothelial cells. Antibodies to endothelial cell membranes, some of which reacted with the membranes of both dermal fibroblasts and T-cell lymphoma HUT78, were detected in 26/33 patients (78%), but in only 4/34 normal controls (P < 0.001) and 3/11 patients with a recent myocardial infarction. Although the antibody response was very heterogeneous against epitopes ranging from 17 to 205 kDa, there was a tendency to detect particular membrane epitopes at 31-33 kDa (15 cases), 72-78 kDa (eight cases), 66-68 kDa (seven cases) and 17-19 kDa (five cases). No correlations between antibodies to particular epitopes and disease manifestations were observed nor was a relationship to disease activity detected in a retrospective analysis. However, the possibility that anti-endothelial cell antibodies may be pathogenically important was supported by prospective serial studies in two cases with nephritis who showed diminution and disappearance of anti-endothelial cell antibodies as their active disease was treated into remission.

Adult↗
PubMed1996

Haemoglobin Hallamshire (beta146 HIS --> TYR): a new high oxygen affinity haemoglobin responsible for familial erythrocytosis.

A new high oxygen affinity haemoglobin with the beta chain mutation beta146 HIS --> TYR is described. This variant was detected in a fit 34-year-old man with true erythrocytosis. The abnormal haemoglobin was identified as an extra band on cellulose acetate electrophoresis at pH 6.3 and was later confirmed by beta globin gene sequencing and oxygen dissociation studies. Whole blood containing Haemoglobin Hallamshire has a P50 of 18 mmHg. This newly described haemoglobin variant was also responsible for erythrocytosis in the mother and maternal half cousin of the index case. The identification of Haemoglobin Hallamshire provides confirmatory evidence of the important role of the C-terminal end of the chain in haemoglobin function.

Adult↗
PubMed1996

The microvasculature in myeloproliferative disease. A study using retinal fluorescein angiography.

Microvascular occlusion is known to be a feature of myeloproliferative diseases. Acute manifestations are well documented in individuals causing a variety of symptoms. However, it is not known whether ongoing microvascular changes are present in asymptomatic individuals. We investigated this further by using retinal intravenous fluorescein angiography to image the microvasculature in patients with myeloproliferative disease. In our group of patients fluorescein angiography did not show any ongoing microvascular damage. There appears to be no intrinsic retinal vasculopathy in patients with myeloproliferative disease, suggesting that acute symptomatic events are caused by microemboli in an otherwise normal vascular tree.

Adult↗
PubMed1995

The stem cell antigen CD34 functions as a regulator of hemopoietic cell adhesion.

Although the CD34 antigen is widely used in the identification and purification of hemopoietic stem and progenitor cells, its function within hemopoiesis is unknown. We have investigated this issue by ectopically expressing human (hu) CD34 on the surface of murine hemopoietic cells. Forced expression of hu-CD34 in the thymocytes of transgenic mice did not appear to affect the development, maturation, or distribution of murine T cells but did significantly increase their ability to adhere to bone marrow stromal layers of human but not mouse origin. Ectopic expression of hu-CD34 on murine 416B cells, a multipotential progenitor that expresses murine CD34, yielded similar results. In both cases hu-CD34-dependent adhesion was enhanced by molecular engagement of the hu-CD34 protein using anti-CD34 antibodies. These results provide evidence that CD34 promotes the adhesive interactions of hemopoietic cells with the stromal microenvironment of the bone marrow thereby implicating CD34 in regulation and compartmentalization of stem cells. We propose that CD34 regulates these processes in part via an indirect mechanism, signaling changes in cellular adhesion in response to molecular recognition of an as yet unidentified stromal CD34 counterreceptor or ligand.

Animals↗
PubMed1995

A radiation hybrid panel for human chromosome 6q.

A panel of 63 radiation-reduced hybrids has been derived from a mouse cell line containing a neo-marked human Chromosome (Chr) 6, primarily to provide a resource for higher resolution localization of new markers. Hybrids were generated with radiation doses of 40-400 Gy, selected in G418, and were shown by PCR to contain the neo gene. PCR was also used to score the retention of 15 loci that map from 6q13 to q25.2 of the current consensus map, plus six other loci assigned to 6q26-q27. An average retention frequency of 27.8% was observed, with the highest frequencies at D6S313 and D6S280 (63.5%) located near the centromere at 6q13, and at D6S283 (68.5%) at 6q16.3-q21, presumably close to the neo integration site. Lowest frequencies (4.8%) were observed for telomeric markers. All markers segregated independently except D6S297 and D6S193. Agreement and some improvement to the current consensus map of 6q was made by mapping 12 loci by the non-parametric statistical method of Falk. In addition, deletion mapping with informative hybrids allowed the ordering of six loci from 6q26 to q27 and permitted some integration of maps of this region.

Animals↗
PubMed1995

Livedo reticularis associated with hereditary protein C deficiency and recurrent thromboembolism.

We report the occurrence of livedo reticularis in a patient with symptomatic hereditary type 1 protein C deficiency. Antithrombin III deficiency and the antiphospholipid syndrome may also be associated with livedo reticularis, and we suggest that a thrombophilia screen may be a useful investigation in a patient with otherwise unexplained livedo, particularly if there is a personal or family history of thromboembolism.

Adult↗
PubMed1995

Characterization and specificity of anti-endothelial cell membrane antibodies and their relationship to thrombosis in primary antiphospholipid syndrome (APS).

Immunoblotting was used to detect antibodies reacting with membrane and cytosol preparations of human umbilical vein endothelial cells (HUVEC), fibroblasts and a T lymphoma line HUT78 in 18 patients with anticardiolipin antibodies (ACA) (14 of whom had had a thrombotic event), 11 patients with a recent myocardial infarction and 17 controls. Multiple membrane-specific antibodies to HUVEC were found in 10 of the patients with ACA (28 bands) and in nine of the patients with thromboses (27 bands) in contrast to only three of the patients with myocardial infarction (four bands) and one control (one band). The most frequently recognized HUVEC membrane epitopes were at 33 kD (four sera), 61-63 kD (five sera) and 76-79 kD (four sera). Although cross-reactivity with fibroblast and/or HUT78 membranes was seen at 33 kD, binding at 61-63 kD and 76-79 kD was specific for endothelial membranes. Although no correlations with the presence and titre of ACA were seen, HUVEC membrane-specific antibodies showed a correlation with venous thrombotic events.

Antibodies, Anticardiolipin↗