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

The cells of a patient with chronic lymphocytic leukaemia (CLL) showed a peculiar phenomenon of nuclear blebbing and nuclear extrusion, observed by transmission (TEM) and scanning (SEM) electron microscopy. Protein synthesis of the lymphocytes was 3 times higher than that of cells of other 3 patients with CLL, but was lower than the synthesis of cells from a patient with acute lymphoblastic leukaemia (ALL). Similar results were observed when RNA synthesizing activity of the cells was examined. On the other hand, thymidine incorporation proceeded in a similar rate in the patient's and the ALL lymphocytes, whereas in those CLL patients it was merely detected. The morphological findings and the synthesizing activities of the cells suggest that the patient's disease represents an intermediate form between CLL and ALL.
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PMID:Ultrastructural and functional studied on the lymphocytes of a patient with chronic lymphocytic leukaemia and nuclear extrusion. 9 56

The effect of temperature shiftdown on the assembly of ts3 virions was investigated by both scanning (SEM) and transmission (TEM) electron microscopy. Ts3 is a spontaneous temperature-sensitive mutant of Moloney murine leukemia virus (Mo-MuLV) which previous studies indicated to be defective in assembly or release of the virions. In the present study, both SEM and TEM revealed the following: (i) there were more cell-associated virions in ts3-infected cells grown at the nonpermissive temperature (39 degrees C) than either in cells grown at the permissive temperature (34 degrees C) or in wild-type MuLV-infected cells grown at 39 degrees C; (ii) there were more normal single particles than multiploids (virions with two or more pieces of genomic RNA) in ts3-infected cells grown at the nonpermissive temperature; (iii) there were more multiploids in ts3-infected cells grown at the nonpermissive temperature than either in cells grown at the permissive temperature or in wild-type MuLV-infected cells grown at the nonpermissive temperature; (iv) upon temperature shift from 39 to 34 degrees C, about 90% of the cell-associated virions dissociated from the cell surface. TEM studies also indicated that upon temperature shiftdown, virion assembly rapidly occurred. The above observations suggest that faulty assembly, which results in the production of multiploids, may not be the reason why ts3 virions accumulate on the cell surface at the nonpermissive temperature. The relatively higher proportion of multiploids found in ts3-infected cells grown at 39 degrees C compared with those grown at 34 degrees C may be due to the higher density of budding virions at the cell surface at the nonpermissive temperature, which increases the possibility of two or more particles assembling close to one another. The accumulation of ts3 virions in all stages of assembly at the nonpermissive temperature, together with the fact that rapid assembly and release of ts3 virions occurred on temperature shiftdown, indicates that virion assembly is restricted after it has been initiated. The probable role of altered glycoprotein(s) in restricting virion assembly is discussed.
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PMID:Electron microscopic characterization of the defectiveness of a temperature-sensitive mutant of Moloney murine leukemia virus restricted in assembly. 19 76

In two cases of trichocellular leukaemia, specimens of blood, bone marrow and the spleen were evaluated not only by means of SEM and TEM but also with a view to their phagocytic and immunological properties. While immunological investigation rather suggested a B lymphocytic aetiology of the process, phagocytosis of Ferrocide (not, however, of latex) seemed to justify, in one case, also histoendothelial aetiology.
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PMID:[Trichocellular leukemia--ultrastructural study of tumor cells and various functional parameters]. 30 67

The present resolution (75-100 A) of the conventional scanning electron microscope (SEM) and its ability to image the surfaces of large numbers of whole cells in situ permits the approach of problems such as viral and cell surface antigen localization by immunological labeling with visual markers. Identification of virus and cell surface antigens in situ has been accomplished in indirect reactions by conjugated and unconjugated markers. Hemocyanin (Hcy) from whelk, Busycon canniculatum, has been developed as an immunospecific marker for virion and cell surface labeling in the electron microscope. Its size (approximately 30 x 50 nm) and distinct cylindrical shape permit easy visualization in the SEM and TEM. The Hcy method involves the preparation of antisera to Hcy in appropriate hosts for use in an unlabeled antibody macromolecular procedure based exclusively on antigen-antibody affinity to couple the macromolecule to the antigen site. Further correlative data from fluorescence microscopy can be obtained from similarly labeled samples by binding fluorescein to the bridging antibodies used in the Hcy technique. The usefulness of the Hcy marker system was demonstrated using antisera to the major envelope and cell surface glycoprotein (gp70) of Rauscher murine leukemia virus (R-MuLV), a type C retrovirus. The antiserum was shown to bind to the virion and cell surfaces of virus-infected cells in the homologous virus-infected cell system. It also demonstrated the expression of R-MuLV gp70-related antigens on a murine cell line Mm5mt/c1 which produces mouse mammary tumor virus (MuMTV), A type B retrovirus. Furthermore, when used in the Hcy marker system this antiserum was able to distinguish type B from type C budding virus on the same cell. Examples of other marker systems (ferritin, peroxidase, colloidal gold, and latex) used to show anti-gp70 serum reactivity will be presented to demonstrate their applicability to cell surface labeling studies. Methods for the preparation of immunoreagents and labeling of cells are discussed.
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PMID:Immunologic techniques for the identification of virion and cell surface antigens by correlative fluorescence, transmission electron and scanning electron microscopy. 39 19

The peripheral blood cells of a patient with acute plasma cell leukemia were examined with transmission (TEM) and scanning (SEM) electron microscopes. The TEM features of the immature plasma cells comprised lobulated and irregulary shaped nuclei, with scanty heterochromating and bizarre nucleoli, parallel arrays of endoplasmic reticulum, cytoplasmic fibrils and numerous polymorphic mitochondria. SEM examination of the cells showed long, thin irregular ruffles, or round blebs on the cell surface, with appearance different from this observed on other types of leukemia. A remarkable clinical and hematological remission was achieved with administration of melphalan and steroids.
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PMID:Transmission and scanning electron microscopy study on plasma cell leukemia. 89 Jan 42

An isolate of Klebsiella oxytoca from the blood culture of a child with leukemia was found to produce two beta-lactamases, at least one of which conferred resistance to ceftazidime. Genes encoding both enzymes were located on a single self-transmissible 100-kb plasmid, pOZ201. This plasmid was introduced into Escherichia coli UB5201 (pACYC184), and the gene encoding one beta-lactamase was transposed onto plasmid pACYC184 by exploiting a gene dosage effect. The transposable gene was found to encode a TEM-12 enzyme as determined by nucleotide sequencing. This gene was subsequently transposed onto plasmid pUB307. The transposable element encoding the TEM-12 enzyme has been designated Tn841. Both plasmids pACYC184::Tn841 and pUB307::Tn841 were shown to encode a beta-lactamase with the same isoelectric point and substrate profile as the TEM-12 beta-lactamase. Transposon Tn841, at approximately 7 kb, is larger than TnA (4.8 kb) and transposes at a lower frequency. Although it produced a resolvase which can complement the resolvase of Tn3, its transposase function was not able to complement the transposition of a TnA element which lacked transposase. The occurrence of a gene encoding an extended-spectrum beta-lactamase on a transposable element in a clinically significant bacterium is potentially a cause for concern for the spread of resistance to the extended-spectrum cephalosporins.
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PMID:Transposition of the gene encoding a TEM-12 extended-spectrum beta-lactamase. 132 36

Hemocyanin (Hcy) from whelks, Busycon canniculatum has been developed as a visual marker for the identification of virus and cell surface antigens by the correlative techniques of fluorescence microscopy, TEM and SEM. A series of hybridomas producing monoclonal antibodies that allow the identification of type-, group-, and class-specific antigenic determinants on the major envelope glycoprotein of mouse mammary tumor virus (MMTV) gp 52 and two group-specific monoclonal antibodies to MMTV gp 36 have been developed. We used these antibodies in the unlabeled antibody Hcy bridge for immunoelectron microscopy (IEM) and found that each gp 52 antigenic determinant was expressed on virus during all stages of morphogenesis and on the infected cell surface while the gp 36 determinants were not detected. The positive labeling of gp 52 by IEM correlated well with immuno-experiments using the 125I Staph protein A plate binding assay (125IPA). The anti-gp 36 monoclonals in contrast, however, gave positive results only in the 125IPA assay. Hybridomas to murine and primate type C virion envelope proteins [gp 70 and p15(E)] have also been developed. None of the monoclonal antibodies to murine type C virus gp 70 or p15(E) gave positive labeling by IEM when tested with Rauscher murine leukemia virus but two were positive by the 125IPA assay. Monoclonal antibodies to the gp 70 of a baboon type C virus, M-7 were positive in IEM, labeling both the cell surface and viral envelope and reacted with virus in the 125IPA assay. Since monoclonal antibodies provide a much better resolution of the molecular structure and antigenic differences of viruses, interpretations of labeling results are thoroughly discussed. Methods for testing the specificity and titer of monoclonals are presented. The unlabeled antibody Hcy bridge technique and recent advances in methodology are reviewed.
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PMID:Monoclonal antibodies as immunospecific probes for virus and cell surface antigen localization with the unlabeled antibody hemocyanin bridge: a review. 617 45

This review is based on the findings of multiparameter studies performed on cells obtained from over 200 cases of leukemia and illustrates the wide range of laboratory tests currently available for cell phenotype identification. Immunological techniques are not discussed and the review deals mainly with light and electron microscopic cytochemistry, transmission (TEM) and scanning electron microscopy (SEM). The importance of light microscopic cytochemistry is clearly demonstrated. In particular, paranuclear acid phosphatase, non-specific esterase (NSE) and diaminopeptidase staining are recommended as reliable T-cell markers. Ultrastructural identification of unclassified leukemic cells using techniques to detect myeloperoxidase, acid phosphatase, platelet peroxide (PPO) and NSE, is shown to be of great importance in cases of early myelo-monoblastic differentiation with negative light microscopic cytochemistry. SEM is also shown to be a reliable means of distinguishing lymphoid and non-lymphoid leukemia when some degree of differentiation is present. However SEM does not appear to contribute in the diagnosis of unclassified leukemia. The new scanning immunoelectron microscopy (SIEM) technique employing heteroantisera or monoclonal antibodies conjugated to latex microspheres (immunolatex) to detect surface receptors and specific antigens is also illustrated. This technique displays the topography of surface antigens on the cell surface of leukemic cells in 3-dimension and facilitates simultaneous visualization of the surface architecture of the labelled cells.
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PMID:Cytochemistry and ultrastructure in lymphoma and leukemia: utility in the diagnosis of different leukemias and the recognition of subtypes of lymphoproliferative disorders. 637 13

11 patients with plasma cell leukaemia (PCL) are reported. Diagnostic clinical, haematological, immunological, biochemical and electron microscopical (TEM) data were analysed and compared to the largest series of PCL cases reported in the literature. Special attention was paid to four facets of this disease: (a) the clinical picture at admission; (b) the frequency of PCL; (c) the production of M components in relation to the maturity and type of the asynchronous plasma cells, and (d) the diagnostic problems of this entity of acute leukaemia of the afferent limb of the B lymphocyte transformation. In this series PCL emerges as a distinct clinical entity: patients are severely anaemic, hepatosplenomegaly is prominent, bone lessions are uncommun, but if present are usually non-osteolytic, and the response to treatment with an alkylating agent and glucocorticoid is poor. The diagnosis is difficult since the circulating plasma cells may have morphological features which only allows the diagnosis to be made after the TEM examination. If the peripheral blood of cases of acute leukaemias and immunocytic dyscrasias is routinely examined by TEM, PCL appears to be a not uncommon variant of plasma cell dyscrasia--in the present study it was 11%.
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PMID:Plasma cell leukaemia. Diagnostic problems in our experience with 11 cases. 676 79

Three cefoxitin-resistant Escherichia coli isolates from stool specimens of a patient with leukemia were either resistant, intermediate, or sensitive to imipenem. Conjugation experiments showed that cefoxitin resistance, but not imipenem resistance, was transferable. All isolates were shown by isoelectric focusing to produce two beta-lactamases with isoelectric points of 5.4 (TEM-1, confirmed by sequencing of a PCR product) and >8.5 (consistent with a class C beta-lactamase). The gene coding for the unknown beta-lactamase was cloned and sequenced and revealed an enzyme which had 99.9% sequence identity with the plasmid-determined class C beta-lactamase CMY-2. The cloned beta-lactamase gene differed from blaCMY-2 at one nucleotide position that resulted in an amino acid change, tryptophan to arginine at position 221. We propose that this enzyme be designated CMY-4. Both the imipenem-resistant and -intermediate isolates lacked a 38-kDa outer membrane protein (OMP) that was present in the imipenem-sensitive isolate. The lack of an OMP alone did not explain the difference in carbapenem susceptibilities observed. However, measurement of beta-lactamase activities (including measurements under conditions where TEM-1 beta-lactamase was inhibited) indicated that the imipenem-intermediate isolate expressed six- to eightfold less beta-lactamase than did the other isolates. This study illustrates that carbapenem resistance in E. coli can arise from high-level expression of plasmid-mediated class C beta-lactamase combined with an OMP deficiency. Furthermore, in the presence of an OMP deficiency, the level of expression of a plasmid-mediated class C beta-lactamase is an important factor in determining whether E. coli isolates are fully resistant to carbapenems.
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PMID:Carbapenem resistance in Escherichia coli associated with plasmid-determined CMY-4 beta-lactamase production and loss of an outer membrane protein. 1022 37


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