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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fourier analysis, previously introduced by Liquori et al. (1983, 1986), has been applied to the primary structures of two core proteins of human T-lymphotropic leukemia retroviruses HTLV-I and HTLV-II. The resulting autocorrelation functions display striking patterns that can be interpreted in terms of an approximately fourfold quasi-periodicity of the primary structures. Self-alignments of the amino acid sequences containing a few gaps are consistent with the above finding and suggest that the tertiary structure of these two homologous core proteins contains alpha-helical and delta-helical segments, the latter being characteristic of the threefold helix present in collagen structure.
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PMID:Quasi-periodic primary structures of core proteins of human T-lymphotropic leukemia retroviruses. 283 59

Multiple visceral aneurysms complicating periarteritis nodosa are considered characteristic, though not pathognomonic, on arteriography. This arteriographic pattern has been described with hairy-cell leukemia, collagen vascular disorders, and atrial myxoma, but, to our knowledge, has not been previously reported with subacute bacterial endocarditis. A patient with enterococcal endocarditis sustained separate intra-abdominal hemorrhages, 24 hours apart, from aneurysms of the middle colic and left colic arteries. Sterile vessel cultures with inflammatory infiltrates, decreased complement levels, positive rheumatoid factor, and arteriographic evidence of multiple visceral aneurysms suggest the vasculitis was immunologically mediated and not mycotic. Antibiotic therapy after control of hemorrhage controlled abdominal symptoms.
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PMID:Multiple mesenteric aneurysms complicating subacute bacterial endocarditis. 288 83

Human hemopoietic blast colony-forming cells (BI-CFCs) recognize and adhere to the extracellular matrix (ECM) produced by marrow-derived stromal cells in vitro. We have investigated the requirements for this interaction by testing the capacity of BI-CFCs to adhere to ECM components under a variety of conditions. Binding was prevented completely by prior treatment of stromal ECM with nitrous acid, in large part by treatment with heparitinase or hyaluronidase, and slightly by treatment with chondroitinases. Whereas heparan sulfate isolated from marrow stromal cultures effectively blocked binding, heparan sulfate from bovine kidney did not. Chondroitin sulfate and hyaluronic acid did not have any effect in this test. In contrast, collagen was not sufficient for the interaction because dishes coated with collagen type I or IV did not act as adhesive surfaces for BI-CFCs. Ligands for integrin receptors (e.g., fibronectin) did not participate in BI-CFC binding because the synthetic pentapeptide glycine-arginine-glycine-asparagine-serine did not compete with stroma in binding BI-CFCs. These findings indicate that heparan sulfate in the bone marrow microenvironment is necessary for BI-CFC binding to ECM and may contribute to localizing hemopoietic stem cells in hemopoietic tissue.
Leukemia 1988 Dec
PMID:Heparan sulfate is necessary for adhesive interactions between human early hemopoietic progenitor cells and the extracellular matrix of the marrow microenvironment. 297 4

Filamentous aggregates of collagen are distinct structures in the pathological dermis. These aggregates are distinguishable from fibrous long-spacing collagen (in vitro and at biopsy) and the Luse body. The aggregates are produced from dermal collagen fibrils by clostridial collagenase and culture-medium extract, which supposedly contains cellular collagenase at a neutral pH, as well as by organ cultures. In vitro experiments showed that carrageenan granuloma contains fibrous long-spacing collagen and segment long-spacing collagen. The granuloma also contains the aggregates. The aggregates were found in skin biopsies from syphilitic chancres, acrosclerotic scleroderma, morphea, mycosis fungoides, myeloid leukemia, mastocytosis and malignant melanoma. These findings indicate that the aggregates are products of the in situ degradation of collagen fibrils by some collagenolytic factor. This factor may originate in fibroblast-like cells, reticulum cells, leukemia cells, mast cells and melanoma cells.
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PMID:Filamentous aggregates of collagen. Ultrastructural evidence for collagen-fibril degradation in situ. 299 Mar 57

Human T-cell leukaemia virus (HTLV1/ATLV), which causes adult T cell leukaemia (ATL), is an infectious, lymphotrophic retrovirus unique for humans. The present study was undertaken to determine whether HTLV1 had any pathogenetic role for systemic lupus erythematosus (SLE). The incidence of antibodies to ATL cell-associated antigens (ATLA) in sera from patients with SLE and other collagen diseases was investigated by an indirect immunofluorescent cytoplasmic staining of an HTLV1-infected cell line (MT-1). A radioimmunoassay was also performed to detect antibodies to HTLV1 protein and crude membrane fraction derived from an HTLV1-producing cell line MT-2. Furthermore, an Epstein-Barr virus (EBV)-transformed B cell line (ES-1) was constructed from an SLE patient, which produced a monoclonal antibody (IgG, lambda) reactive to an HTLV1-related cell-membrane antigen expressed on MT-1 and MT-2 cells. The specific reactivity of the monoclonal antibody was analysed by an indirect immunofluorescent cell-membrane staining and a microcytotoxicity test. The incidence of anti-ATLA antibodies was not different among SLE and other collagen diseases. The monoclonal antibody produced by ES-1 stained and killed HTLV1-infected cell lines specifically, but did not react with other human lymphoid cell lines. This monoclonal antibody failed to react with peripheral blood mononuclear cells (PBMC), mitogen-induced T cell blasts, and iododeoxyuridine-treated T cells from SLE patients. Thus, a possible role of HTLV1 in the aetiology of SLE was not established.
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PMID:Production of a monoclonal antibody to a membrane antigen of human T-cell leukaemia virus (HTLV1/ATLV)-infected cell lines from a systemic lupus erythematosus (SLE) patient: serological analyses for HTLV1 infections in SLE patients. 299 59

This study demonstrates the potential usefulness of a flow cytometric technique to measure platelet survival time in cats utilizing autologous platelets labeled in vitro with fluorescein isothiocyanate (FITC). When compared with a 51Cr method, no significant differences in estimated survival times were found. Both the 51Cr and FITC-labeling procedures induced similar changes in platelet shape and collagen-induced aggregation. Platelets labeled with FITC had significantly greater volumes compared with those of glutaraldehyde-fixed platelets. These changes were primarily related to the platelet centrifugation and washing procedures rather than the labels themselves. This novel technique potentially has wide applicability to cell circulation time studies as flow cytometry equipment becomes more readily available. Problems with the technique are discussed. In a preliminary study of the platelet survival time in feline leukemia virus (FeLV)-infected cats, two of three cats had significantly reduced survival times using both flow cytometric and radioisotopic methods. These data suggest increased platelet turnover in FeLV-infected cats.
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PMID:Flow cytometric and radioisotopic determinations of platelet survival time in normal cats and feline leukemia virus-infected cats. 300 46

It is difficult to study the regulation and interactions of the connective tissue macromolecules in vivo. However, studies of genetically determined diseases of the connective tissues have yielded a large amount of new information in these areas. Specific molecular defects can then be correlated with the functional and pathological changes in the tissues. We have concentrated on this approach which takes advantage of the large number of families with genetic diseases who come to our Hospital from all parts of Australasia and also takes advantage of developments in molecular biology in our Unit which were initiated with a RACS John Mitchell Crouch Fellowship. In addition to these studies on naturally occurring mutations we are also studying specific mutations that we are able to produce in specific regions of the collagen molecule. Another approach takes advantage of a unique model culture system developed in our Unit. These studies will be supplemented by various collaborative projects such as current ones involving smooth muscle cells in atherosclerosis, bone cells metabolism and myelofibrosis in leukaemia.
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PMID:Regulation and organization of connective tissues. 307 87

A patient is described who presented a thrombocytopenia with thrombocytopathy followed by the development of a leukaemia. The disorder was characterized by decreased aggregation in the presence of ADP, and a lack of aggregation in the presence of arachidonic acid, natural endoperoxide or collagen. In parallel, 14C-serotonin release was severely decreased or nil in response to these inducers. Thrombin induced a slightly decreased aggregation and a normal 14C-serotonin release. Thromboxane B2 (T X B2) synthesis was normal after stimulation by arachidonic acid, natural endoperoxide or thrombin showing a normal arachidonate metabolism. In addition, the mepacrine test showed no significant decrease of the number of dense bodies with an average of 4.6 per platelet (versus 5.4 +/- 0.8 sd in controls). Stimulation by ionophore A 23187 failed to induce aggregation, 14C-serotonin release, or T X B2 synthesis. Furthermore, in the presence of EDTA, A 23187 did not provoke activation as reflected by 14C-serotonin release or T X B2 synthesis. Thus, in this case of thrombocytopathy, the hypothesis of abnormal intracellular Ca++ fluxes responsible for the defective platelet release phenomenon, was suggested.
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PMID:Thrombocytopenia with thrombocytopathy possibly related to abnormalities of intracellular Ca++ fluxes and followed by the development of leukaemia. 308 7

The etiology of alkylator-induced leukemia is obscure, but may be due in part to alternations in the bone marrow stromal microenvironment. Marrow extracellular matrix, including collagen, glycosaminoglycans/proteoglycans, and glycoproteins, may play a crucial role in the control of normal and abnormal hematopoiesis. Twenty-four hours after seeding, confluent human bone marrow stromal cell cultures were exposed for 3 h to 15 micrograms/ml of 1,3-bis-(2-chloroethyl)-1-nitrosourea (BCNU), an alkylating agent with leukemogenic potential. On the eighth day of culture, [35S]sulfate was added and radiolabeled glycosaminoglycan(s) (GAGs) was harvested 24 h later. BCNU treatment resulted in a 104% increase of the radiolabel incorporation into cetylpyridinium chloride precipitable GAG. In addition, spectrophotometric measurement of total GAG in treated cells revealed a similar GAG increase. However, BCNU treatment did not alter compartmental GAG distribution or GAG species. Our results demonstrate a profound quantitative change in the production of important extracellular matrix components by bone marrow stromal cells after exposure to a nitrosourea. This increase may be a factor in microenvironmental alterations leading to bone marrow toxicity following alkylator exposure.
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PMID:BCNU-induced increase in sulfated glycosaminoglycan production by human bone marrow stromal cells. 313 51

Atrophie blanche is a syndrome of painful vasculitic infarctive lesions of the lower extremities that heal leaving characteristic atrophic, porcelain white scars. The syndrome may occur as an idiopathic entity or associated with various hematologic and collagen vascular disorders. We present the first recognized case of atrophie blanche in a patient with chronic myelogenous leukemia. This presentation may be part of the expanding spectrum of nonspecific cutaneous manifestations of leukemia (leukemids).
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PMID:Atrophie blanche in chronic myelogenous leukemia. 316 50


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