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Biomedical subjects

E Kondo

Publications and source records attributed to E Kondo.

At least 109 records · Page 6Linked to original sources
PubMed1994

bcl-2 regulation in normal resting lymphocytes and lymphoblasts.

Expression of the bcl-2 protein and bcl-2 mRNA at the individual cell level was semiquantitatively examined in normal quiescent peripheral blood lymphocytes and pokeweed mitogen- or concanavalin A and interleukin-2-induced lymphoblasts in vitro by microscopic fluorometry using immunofluorescence and fluorescein-labeled in situ hybridization. Approximately 90% of normal quiescent T and B lymphocytes expressed bcl-2 protein at a level which was compatible with that of bcl-2 mRNA. On the contrary, most mitogen-induced lymphoblasts showed a posttranscriptional suppression of bcl-2 protein expression. However, bcl-2 protein was not downregulated by the posttranscriptional suppression in all lymphocytes activated in vitro, but approximately 15% of the lymphoblasts still expressed bcl-2 protein at a higher level than nontransformed quiescent small lymphocytes; thus bcl-2 protein expression in lymphoblasts showed a distinct bimodal pattern. Furthermore, it was supposed that lymphoblasts with no detectable bcl-2 protein might fall into apoptosis but the remainder, expressing high levels of bcl-2 protein, could escape apoptosis. Thus, the bcl-2 gene may play an important role as a regulator of apoptosis in the human immune system.

Apoptosis↗
PubMed1994

HTLV-II non-integrated malignant lymphoma induction in Japanese white rabbits following intravenous inoculation of HTLV-II-infected simian leukocyte cell line (Si-IIA).

Lymphoma induction in rabbits by an unknown factor derived from an HTLV-II-producing simian (Cynomolgus) leukocyte cell line (Si-IIA) is reported. Thirteen of 17 male Japanese white rabbits (76%) inoculated intravenously with Si-IIA cells developed malignant lymphoma including Hodgkin-like lymphoma between 62 and 167 days after inoculation. Histologically, there was extensive diffuse or nodular infiltration of either large cell type or mixed type lymphoma cells in many organs, frequently involving the spleen, liver, lymph nodes and kidneys, and less frequently the thymus, bone marrow, lungs, heart, skin and gastrointestinal tract. Hodgkin-like lymphoma was also observed in two rabbits. Chromosomal analysis of five cell lines established from tumor-bearing rabbits revealed the male rabbit karyotype. The immunophenotype of these tumor cells was usually T-cell (CD5+ or -, RT1+, RT2+ or -, CD45+, CD4-, RABELA- and MHC class II-DQ+) except for Hodgkin-like lymphoma cells which expressed only CD45. However, integration of the HTLV-II provirus genome could not be demonstrated in the tumor tissues or any of the rabbit cell lines by polymerase chain reaction or Southern blot analysis. Moreover, no lymphoma was induced by inoculation of HTLV-IIC, MOT (other HTLV-II-producing human cell lines) or TALL-1 (control). Two of four rabbits injected with cell-free pellets from Si-IIA cultures died of malignant lymphoma (15-20 days). Five irradiated rabbit cell lines were inoculated but only one (Ra-SLN) induced lymphoma in 1 of 3 rabbits at 27 days. Neither Herpesvirus saimiri nor Herpesvirus ateles (simian oncogenic viruses) was detected in Si-IIA cells by immunofluorescence testing. These data suggest that the high rate of lymphoma induction in rabbits may be caused not by only HTLV-II or well known simian oncogenic viruses, but rather by an unknown passenger agent derived from Si-IIA or HTLV-IIA, with which Si-IIA was established.

Animals↗
PubMed1994

Aberrant expression of the monocyte/macrophage phenotype in a human T cell line immortalized by HTLV-I and an adult T cell leukemia/lymphoma cell line.

An HTLV-I-immortalized human T cell line (JP-2), a N-methyl-N'-nitro-N-nitrosoguanidine-treated JP-2 line (JP-2T), and an adult T cell leukemia cell line (ATL-1T) were examined morphologically and phenotypically. All of these cell lines expressed some T cell markers, including CD4, and showed rearrangement of T cell receptor (TCR) genes, but they lacked CD3 and TCR antigens and expressed some myelomonocytic markers (CD68, HL-21, CD15, CD16). JP-2 cells grew in suspension, but JP-2T and ATL-1T cells, which mostly adhered to the surface of culture vessels, showed macrophage-like morphological features and expressed more monocyte/macrophage markers (lysozyme, alpha 1-antitrypsin) and fibronectin. ATL-1T cells transplanted into SCID mice lost the macrophage features. These results suggest that HTLV-I infected T cells can express some macrophage features and that these cells may provide a model that will be useful in elucidating the phenotypic variability of T cell lymphomas.

Animals↗
PubMed1994

Expression of Bcl-2 protein and Bcl-2 mRNA in normal and neoplastic lymphoid tissues.

The bcl-2 gene is a unique proto-oncogene that blocks apoptosis; its product is localized on the inner mitochondrial membrane. In non neoplastic human lymphoid tissues, bcl-2 protein is strongly expressed in the small recirculating lymphocytes of the follicular mantle zone; it is expressed less intensely in T-cell areas, and is almost absent from germinal center cells. Bcl-2 mRNA, in contrast to bcl-2 protein, is strongly expressed on most of the latter cells, a similar phenomenon also being observed in peripheral blood lymphocytes (PBL). Resting PBL express both bcl-2 mRNA and protein, while most lymphoblasts in mitogen-stimulated PBL cultures lose bcl-2 protein and become apoptotic, despite expressing higher levels of mRNA. Posttranscriptional regulation of the bcl-2 gene may cause this paradoxical down-regulation of bcl-2 protein and may play an important role in the clonal selection of lymphocytes. Bcl-2 protein is frequently expressed in follicular lymphomas bearing the t(14;18) chromosomal translocation, but it is also widely expressed in many other B- and T-cell lymphomas without bcl-2 rearrangement, showing that mechanisms other than t(14;18) translocation may deregulate bcl-2 expression. Many lymphoid and myeloid cell lines also express bcl-2 protein with no correlation being shown with differentiation stage. Thus, it is conceivable that bcl-2 protein may play a role in the oncogenesis of many hematolymphoid malignancies by interfering with programmed cell death, in concert with other oncogenes or tumor suppressor genes.

Cell Line↗
PubMed1994

Expression of Bcl-2 protein and Fas antigen in non-Hodgkin's lymphomas.

Expression of Bcl-2 protein and Fas antigens was analyzed in 12 cases of follicular lymphoma and 32 cases of diffuse lymphoma, including 22 B-cell and 10 T-cell lymphomas. It was shown that 75% of follicular lymphomas had clear expression of both Bcl-2 protein and Fas antigen. Thus, follicular lymphomas may have a growth advantage due to their high expression of Bcl-2 protein, which tended to impede apoptosis mediated by Fas antigen. On the other hand, diffuse lymphomas showed various patterns; 28% were double positive, 16% were only Bcl-2 protein-positive, 28% were only Fas antigen-positive, and 28% were double negative or equivocal. Cytocidal assay of seven leukemia/lymphoma cell lines using anti-human Fas monoclonal antibody revealed that overexpression of Bcl-2 protein tended to impede apoptosis mediated by Fas antigen. However, this inhibitory effect of Bcl-2 protein was incomplete and its effect might be dependent upon cell type.

Antibodies, Monoclonal↗
PubMed1994

Effects of tunicamycin on the pH-activity pattern of acid phosphatase in Pseudomonas pseudomallei.

The liquid culture of Pseudomonas pseudomallei shows a complex feature in in the pH-activity pattern of acid phosphatase, not a single peak curve. There was an evident tendency that the higher activity shifted to the higher pH range with the growth of culture. The culture in the presence of tunicamycin (20 micrograms/ml) showed a decreased activity selectively in the higher pH range, while the activity in the lower pH was more heat-labile. The bacterial cells grown on agar plates containing tunicamycin were more heat-labile than the untreated control cells. The glucosidase-treatment reduced the enzymatic activity (of the phosphatase-active fractions from the living cells) with the shift of the optimum pH to lower pH. These observations together with some collateral findings suggest that the pH-activity pattern of acid phosphatase in P. pseudomallei is associated with the development of precursor enzyme proteins to mature glycoproteins.

Acid Phosphatase↗
PubMed1994

Separation of antigenic glycoprotein fractions from cell-free homogenate of Pseudomonas pseudomallei and characterization as tyrosine phosphatase.

Cell-free extracts were prepared from Pseudomonas pseudomallei cells by freezing-thawing, sonication, and differential ultracentrifugation. The extracts were subjected to column chromatography with DEAE-sepharose to obtain glycoprotein fractions. The fractions showed acid phosphatase activity to p-nitrophenyl phosphate, tyrosine phosphate, serine phosphate, but not to threonine phosphate. They were highly antigenic when tested by immunofluorescence assay with the sera of melioidosis patients.

Animals↗
PubMed1994

Refined mapping of a gene responsible for Fukuyama-type congenital muscular dystrophy: evidence for strong linkage disequilibrium.

Fukuyama-type congenital muscular dystrophy (FCMD), the second most common form of childhood muscular dystrophy in Japan, is an autosomal recessive severe muscular dystrophy associated with an anomaly of the brain. After our initial mapping of the FCMD locus to chromosome 9q31-33, we further defined the locus within a region of approximately 5 cM between loci D9S127 and CA246, by homozygosity mapping in patients born to consanguineous marriages and by recombination analyses in other families. We also found evidence for strong linkage disequilibrium between FCMD and a polymorphic microsatellite marker, mfd220, which showed no recombination and a lod score of (Z) 17.49. A "111-bp" allele for the mfd220 locus was observed in 22 (34%) of 64 FCMD chromosomes, but it was present in only 1 of 120 normal chromosomes. This allelic association with FCMD was highly significant (chi 2 = 50.7; P < .0001). Hence, we suspect that the FCMD gene could lie within a few hundred kilobases of the mfd220 locus.

Chromosome Mapping↗
PubMed1994

[A clinical study of fulminant Legionnaires' disease].

Seven cases of fulminant Legionnaires' disease treated at Kitasato University Hospital between 1985 and 1992 were reviewed. These patients were male with a mean age of 55.9 years (range, 37-67 yrs), and five were heavy alcohol drinkers. All seven patients required mechanical ventilation. Four patients recovered (group 1) and three expired due to respiratory failure (group 2). The mean interval from initial symptoms to the development of respiratory failure was 8.8 days in group 1 and 6.0 days in group 2, except in the one patient with lung cancer (case 6). The progression of pneumonia was more rapid in group 2. The mean intervals from admission to administration of erythromycin were 1.5 days and 3.5 days, respectively, in groups 1 and 2. In group 1, pulmonary infiltrates and respiratory insufficiency worsened for the first few days after erythromycin administration but improved thereafter. The average duration of ventilatory care in group 1 was 13.3 days. The administration of rifampicin combined with erythromycin may be useful for the treatment of fulminant Legionnaires' disease. When fulminant pneumonia is encountered in a middle-aged or elderly male alcoholic, Legionnaires' disease should be suspected and erythromycin administration with rifampicin should be initiated as early as possible.

Adult↗
PubMed1993

Expression of muscarinic and nicotinic receptor mRNA in the salivary gland of rats: a study by in situ hybridization histochemistry.

Expression of muscarinic receptor mRNA subtypes (m1-5) and nicotinic receptor subunits (alpha 2-4, and beta 2) was examined in the rat submandibular gland by in situ hybridization histochemistry, using oligonucleotide probes for the muscarinic receptor and RNA probes for the nicotinic receptors. m2, alpha 3, and beta 2 mRNA were strongly expressed in the submandibular ganglion, and m3, alpha 2, alpha 3, alpha 4, and beta 2 were expressed in the striated and interlobular duct cells. Both muscarinic and nicotinic receptors were coexpressed in the same ganglion neurons, while none of these mRNA were detected in the terminal secretory units.

Animals↗
PubMed1993

A human T cell line with an abnormal trisomy 2 karyotype established by coculture of peripheral lymphocytes with an HTLV-II-infected simian leukocyte cell line.

A new human T cell line with a chromosomal abnormality (47,XY,+2), designated AS-IIA, was established by coculturing peripheral blood leukocytes of a healthy adult male with a lethally irradiated human T lymphotropic virus type II (HTLV-II)-infected simian leukocyte cell line (Si-IIA). A polymerase chain reaction method showed that this interleukin-2 (IL-2)-dependent cell line possessed the HTLV-II provirus genome; the cells also reacted with HTLV-II-positive human sera, anti-HTLV-I/II p24, and anti-HTLV-II gp46 antibodies. AS-IIA cells expressed the suppressor/cytotoxic T cell markers CD3+, CD4-, CD8+, CD25+, and HLA-DR+, with later conversion to CD8-. These cells showed better proliferation than other human HTLV-II-infected cell lines with normal karyotypes, but were not transplantable into severe combined immunodeficiency mice. Virus production from AS-IIA was confirmed not only by electron microscopic examination, which revealed mature and immature type C virus particles, but also by the capacity of the line to immortalize human T cells. These results suggest that HTLV-II shows broad tropism for T cells including CD4+ or CD8+, and that not only Si-IIA, but also AS-IIA, are good sources of HTLV-II. The authors of the present study believe that AS-IIA may be a useful human T cell line for the investigation of HTLV-II in comparison with HTLV-I.

Adult↗
PubMed1993

Application of indirect immunofluorescence microscopy to colony identification of Pseudomonas pseudomallei.

Indirect immunofluorescence microscopy was used as a colony identification method of Pseudomonas pseudomallei isolates. The antisera against lipopolysaccharide and protein fractions of P. pseudomallei were prepared in guinea pigs and rabbits. With these antisera and fluorescence-labelled anti-guinea pig IgG and anti-rabbit IgG prepared in sheep (goat), indirect immunofluorescence microscopy was conducted on the colonies of P. pseudomallei and other species of bacteria. The overall results indicated that this method is efficient, rapid and specific for identification of P. pseudomallei colonies from clinical specimens.

Animals↗
PubMed1993

[Clinical significance of dystrophin test for patients with various neuromuscular diseases--immunofluorescence and immunoblot analyses of dystrophin abnormalities].

The dystrophin test was performed on skeletal muscle specimens from 81 cases with various neuromuscular diseases by using two new monoclonal antibodies. The results were compared with those obtained by using four polyclonal antibodies. These monoclonal and polyclonal antibodies were raised against various portions of the dystrophin molecule. On immunohistochemical analysis, the two new monoclonal antibodies showed the same staining pattern as the four polyclonal antibodies. Non-specific immunostaining of the cytoplasm, often seen with polyclonal antibodies, was not observed with monoclonal antibodies. With the application of monoclonal antibodies, the connective tissue sometimes showed non-specific immunostaining which originated from the second fluorescent antibody. On immunoblot analysis, one of the two monoclonal antibodies, antibody 4-4 C 5, showed weak immunoreactivity, and the 400 kDa dystrophin band was not detected. Three cases out of 15 with Duchenne muscular dystrophy (DMD), and one case out of 3 with limb-girdle type muscular dystrophy which had previously been diagnosed on the basis of clinical data, were found to have non-dystrophin-related muscular dystrophy, and Becker muscular dystrophy (BMD), respectively. Three and two of five cases were diagnosed as DMD and BMD, respectively, though clinical diagnosis had not been possible because they were too young. Clinical diagnosis of congenital muscular dystrophy was confirmed in 9 patients by the dystrophin test. Only one of three certain DMD carriers had a so-called mosaic staining pattern. We conclude that all six antibodies are useful tools for the diagnosis of neuromuscular diseases, because of their high specificity for dystrophin.

Adolescent↗
PubMed1993

[Molecular genetics of Duchenne/Becker muscular dystrophy].

The X-linked gene responsible for Duchenne muscular dystrophy (DMD)/Becker muscular dystrophy (BMD) encodes dystrophin, a high-molecular-weight cytoskeletal protein. The identification of the dystrophin gene through positional cloning, and the subsequent description of its protein product have opened several new fields of research and genetic diagnosis. Studies in our laboratory revealed that 26 out of 47 (55%) cases of DMD and nine out of 12 (75%) cases of BMD exhibited genomic deletion. The DMD phenotype is associated with mutations that shift the reading frame of the message, whereas the BMD phenotype is associated with mutations that maintain the reading frame. Immunofluorescence microscopy has established dystrophin's distribution on the plasma membrane of muscles. DMD patients demonstrate a lack of dystrophin on their muscle cell membrane, whereas BMD patients produce a limited amount of protein or abnormally sized protein. Extensive studies on dystrophin and the gene may lead to an understanding of the cause for this and may allow development of a rational treatment for DMD to be developed.

Animals↗
PubMed1992

Detection of bcl-2 protein and bcl-2 messenger RNA in normal and neoplastic lymphoid tissues by immunohistochemistry and in situ hybridization.

bcl-2 protein has been detected in surgical specimens and cultured permanent cell lines of non-Hodgkin's lymphomas and leukemias using enzyme immunohistochemistry and immunofluorescence with anti-bcl-2 monoclonal antibodies. Of 40 surgical specimens, bcl-2 protein was expressed in 50% of B-cell and 41% of T-cell lymphomas, both with and without the bcl-2 gene rearrangement. In investigations of 38 hematopoietic cell lines, bcl-2 protein was detected not only in lymphoid cell lines but also in myeloid cell lines. In situ hybridization and immunohistochemical analysis of reactive lymph nodes showed that lymphocytes in mantle zones and paracortical areas expressed bcl-2 protein consistent with the messenger RNA distribution and that germinal center cells showed abundant bcl-2 transcript, despite the absence of detectable bcl-2 protein. These results suggest that bcl-2 protein is broadly expressed in various hematopoietic neoplasms not restricted in t(14; 18) lymphomas and that germinal center cells may be involved in some arrest of bcl-2 protein expression at the posttranscriptional level.

Blotting, Northern↗
PubMed1992

Infectivity of human T-lymphotropic virus type I to human nervous tissue cells in vitro.

Infectivity of human T-lymphotropic virus type I (HTLV-I) to human nervous tissue cells was explored using co-cultivation with X-irradiated, HTLV-I-producing MT2 cells. Examined cells included normal cerebellar cells, brain tumor cells (astrocytoma, medulloblastoma, meningioma, hemangioblastoma, and schwannoma), and various cell lines (astrocytoma, ependymoma, oligodendroglioma, medulloblastoma, and neuroblastoma). Successful HTLV-I infection was confirmed immunohistochemically using monoclonal antibodies to HTLV-I p19, p24, and pX product. All cell lines and primary cultures from normal cerebellar tissues and brain tumors could be infected with HTLV-I. Double immunostaining showed that glial fibrillary acidic protein-, S-100 protein- or vimentin-positive cells were susceptible to infection. Neurofilament- or neuron-specific enolase-positive cells in medulloblastoma could also be infected. Reverse-transcriptase assay revealed the productive infection in U251-MG (astrocytoma) and KG-IC (oligodendroglioma) lines. Co-cultivated U251-MG cells formed syncytial polykaryons after serial passages, and polymerase chain reaction assay detected HTLV-I genome in U251-MG syncytial polykaryons and p19+ mononuclear cells. HTLV-I viral RNA was also detected in infected U251-MG cells by in situ hybridization. These data show that HTLV-I may have a wide spectrum of infectivity in human nervous tissues.

Base Sequence↗