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Biomedical subjects

M Abe

Publications and source records attributed to M Abe.

At least 541 records · Page 30Linked to original sources
PubMed1996

The relationship between the gene mutation of p53 and the protein expression of p53 and Ki-67 in non-Hodgkin's lymphomas.

The relationship between the mutation of the p53 gene and the expression of the p53 protein and the Ki-67 antigen has been investigated in 115 cases with non-Hodgkin's lymphoma, using the immunohistochemical double staining technique, single-strand conformational polymorphism and DNA sequencing methods. Eighteen cases showed more than 10% of p53+ cells and the others showed a few p53+ cells presented sporadically. Alterations in the p53 gene were detected in six cases with B cell type, consisting of five cases with point mutation and one case with point mutation and 15 base pairs deletion. These six cases showed a high percentage of p53+ cells and five cases revealed that the percentage of p53+ cells was higher than that of Ki-67+ cells (p53+ cells > Ki-67+ cells). Excluding the six cases with mutation of the p53 gene, all cases revealed that the percentage of p53+ cells was less than that of Ki-67+ cells (p53+ cells < Ki-67+ cells). Moreover, there was a positive correlation between expression of the p53 protein and of the Ki-67 antigen in histologic types of B cell lymphomas and of T cell lymphomas, respectively, except in small non-cleaved (Burkitt's) and lymphoblastic types. Therefore, sporadic cases showing p53+ cells > Ki-67+ cells revealed alteration of the p53 gene, and expressed abnormal p53 protein (mutant form). Most cases showing p53+ cells < Ki-67+ cells expressed normal p53 protein (wild type), and may reflect the rapid proliferation rate.

Base Sequence↗
PubMed1996

Expression of classical protein kinase C subspecies in non-neoplastic lymphocytes and non-Hodgkin's lymphomas: an immunohistochemical study.

It is generally accepted that phosphorylation plays a pivotal role in the cellular response of cell differentiation and proliferation. Immunohistochemical expression of classical protein kinase C (cPKC) subspecies (alpha, beta and gamma) in eight reactive lymphoid tissues, three normal spleens and 149 non-Hodgkin's lymphomas was examined. cPKC beta was observed primarily in the mantle zone B cells, but appeared as very faint staining in Ki-67 positive proliferated B cells in the germinal centers of secondary lymph follicles. In contrast to the reactive state, high levels of cPKC subspecies were recognized in the majority of 149 cases of non-Hodgkin's lymphoma, including those thought to have arisen from germinal center cells such as follicular lymphoma. The expression of cPKC alpha was found in higher frequency in T cell lymphomas than B cell lymphomas (P < 0.01) by the Chi-squared test. High levels of cPKC alpha were present only in high grade or highly aggressive lymphomas, showing the highest incidence in the small non-cleaved cell type, according to the International Working Formulation and National Cancer Institute (P < 0.01). cPKC gamma was not detected in normal lymphoid cells and was expressed in only four cases of non-Hodgkin's lymphomas. It is presumed that cPKC alpha and beta have a relationship to cell activation and proliferation of lymphoid cells of reactive and neoplastic states. It might be considered that the expression of cPKC alpha may have a relationship with aggressiveness in non-Hodgkin's lymphomas.

B-Lymphocytes↗
PubMed1996

Establishment and characterization of new human Burkitt's lymphoma cell lines (HBL-7 and HBL-8) that are highly metastatic in SCID mice: a metastatic SCID mouse model of human lymphoma lines.

Two newly established human Burkitt's lymphoma cell lines (HBL-7 and HBL-8) were characterized by immunophenotypic, cytogenetic and molecular studies. Both cell lines were negative for Epstein-Barr virus (EBV) genome and had chromosomal translocation: t(8;14) (q24;q32). Immunoglobulin (Ig) gene rearrangement analyses confirmed that both cell lines were derived from primary lymphoma cells. These cell lines were heterotransplanted subcutaneously into severe combined immunodeficiency (SCID) mice to investigate the metastatic capacity. The most striking feature of both cell lines was to show highly spontaneous metastasis to distant organs, particularly spleen, bone marrow and ovaries in SCID mice. To elucidate the metastatic factors involved in the process of spontaneous metastasis, cell surface adhesion molecules or extracellular matrix receptors were analyzed. However, the results did not allow a significant correlation between expression levels of those molecules or matrix receptors and spontaneous metastasis in the SCID mouse model. The HBL-7 and HBL-8 cell lines, however, may be a useful tool to elucidate the metastatic mechanisms of human lymphomas in an animal model.

Adolescent↗
PubMed1996

Contrast between effects of aminobisphosphonates and non-aminobisphosphonates on collagen-induced arthritis in mice.

1. Bisphosphonates (BPs) are inhibitors of bone resorption, and many derivatives have been developed for the treatment of enhanced bone resorption. Aminobisphosphonates (aminoBPs) are particularly potent in this respect. We have shown previously that aminoBPs, such as 4-amino-1-hydroxybutylidene-1,1-bisphosphonic acid (AHBuBP), induce histidine decarboxylase, the enzyme forming histamine, and increase macrophages, granulocytes and osteoclast numbers. Non-aminoBPs do not show this activity. 2. In the present study, an additional aminoBP, cycloheptyl-aminomethylene bisphosphonate (CHAMBP), was shown to have similar properties to AHBuBP suggesting that these actions are common among aminoBPs. 3. In experiments carried out to determine if aminoBPs affect immune responses, we found that CHAMBP and AHBuBP each exacerbated the arthritis induced in mice by the co-injection of type II collagen and an adjuvant, a model for rheumatoid arthritis. In contrast, dichloromethylene bisphosphonate (C12MBP), a typical non-aminoBP, did suppress the arthritis. 4. On the basis of these results, and those obtained previously, we propose that the exacerbating effects of CHAMBP and AHBuBP may be related to their ability to stimulate the synthesis of histamine and to increase macrophages and granulocytes. Conversely, we propose that the suppressive effect of C12MBP on arthritis is related to its cytotoxic action on macrophages or granulocytes.

Animals↗
PubMed1996

Tissue changes in glutathione metabolism and lipid peroxidation induced by swimming are partially prevented by melatonin.

The present study used male Sprague-Dawley rats to investigate changes in glutathione [reduced (GSH) and oxidized GSH (GSSG)]. lipid peroxidation (as indicated by tissue levels of malonaldehyde and 4-hydroxyalkenals), and the activity of the antioxidant enzyme glutathione peroxidase after a bout of swimming (30 min.) with or without melatonin (N-acetyl-5-methoxytryptamine) treatment. In muscle, the concentration of GSH and the GSH/GSSG ratio were decreased following 30 min. of swimming: these changes are indicative of enhanced oxidative stress. Pretreatment with melatonin prevented these effects. In liver, swimming increased significantly both GSH and GSSG, and decreased the GSH/GSSG ratio. When animals were treated with melatonin, concentrations of GSH and GSSG were also increased after swimming: however, the reduction in the GSH/GSSG ratio was prevented by melatonin. Brain GSH/GSSG ratio was not affected by exercise or by melatonin. Swimming enhanced the levels of lipid peroxidation products is muscle: this was prevented in animals treated with melatonin. Glutathione peroxidase activity was significantly elevated after swimming in both liver and brain with the change not being influenced by concurrent melatonin treatment. It is concluded that swimming imposes an oxidative stress on liver and skeletal muscle and the results show that melatonin confers partial protection against oxidative toxicity, especially in muscle.

Animals↗
PubMed1996

The dsbB gene product is required for protease production by Burkholderia cepacia.

Burkholderia cepacia KF1, isolated from a pneumonia patient, produces a 37-kDa extracellular metalloprotease. A protease-deficient and lipase-proficient mutant, KFT1007, was complemented by a clone having an open reading frame coding for a 170-amino-acid polypeptide which showed significant homology to Escherichia coli DsbB. KFT1007, a presumed dsbB mutant, also failed to show motility, and both protease secretion and motility were restored by the introduction of the cloned dsbB gene of B. cepacia. The mutant KFT1007 excreted a 43-kDa polypeptide that is immunologically related to the 37-kDa mature protease. These results suggested that the dsbB mutant secretes a premature and catalytically inactive form of protease and that disulfide formation is required for the production of extracellular protease by B. cepacia.

Amino Acid Sequence↗
PubMed1996

Raf, but not MEK or ERK, is sufficient for differentiation of hippocampal neuronal cells.

To elucidate signal transduction pathways leading to neuronal differentiation, we have investigated a conditionally immortalized cell line from rat hippocampal neurons (H19-7) that express a temperature sensitive simian virus 40 large T antigen. Treatment of H19-7 cells with the differentiating agent basic fibroblast growth factor at 39 degrees C, the nonpermissive temperature for T function, resulted in the activation of c-Raf-1, MEK, and mitogen-activated protein (MAP) kinases (ERK1 and -2). To evaluate the role of Raf-1 in neuronal cell differentiation, we stably transfected H19-7 cells with v-raf or an oncogenic human Raf-1-estrogen receptor fusion gene (deltaRaf-1:ER). deltaRaf-1:ER transfectants in the presence of estradiol for 1 to 2 days expressed a differentiation phenotype only at the nonpermissive temperature. However, extended exposure of the deltaRaf-1:ER transfectants to estradiol or stable expression of the v-raf construct yielded cells that extended processes at the permissive as well as the nonpermissive temperature, suggesting that cells expressing the large T antigen are capable of responding to the Raf differentiation signal. deltaRaf-1:ER, MEK, and MAP kinase activities in the deltaRaf-1:ER cells were elevated constitutively for up to 36 h of estradiol treatment at the permissive temperature. At the nonpermissive temperature, MEK and ERKs were activated to a significantly lesser extent, suggesting that prolonged MAP kinase activation may not be sufficient for differentiation. To test this possibility, H19-7 cells were transfected or microinjected with constitutively activated MEK. The results indicate that prolonged activation of MEK or MAP kinases (ERK1 and -2) is not sufficient for differentiation of H19-7 neuronal cells and raise the possibility that an alternative signaling pathway is required for differentiation of H19-7 cells by Raf.

Animals↗
PubMed1996

Development of an MR simulator: experimental verification of geometric distortion and clinical application.

PURPOSE: To evaluate the geometric distortion on magnetic resonance (MR) images obtained with a permanent magnet system and determine the usefulness of MR imaging-assisted x-ray simulation in radiation therapy treatment planning (RTTP). MATERIALS AND METHODS: The authors measured the distortion on MR images of grid-pattern phantoms. MR imaging-assisted x-ray simulation was performed with skin markers in 14 patients with bone tumors. Treatment planning had already been performed with a conventional system. RESULTS: On phantom images, most of the positional displacements within a 120-mm radius from the center of the static magnetic field were less than 2 mm; larger displacements were observed in the peripheral region of the images. MR imaging was useful in the RTTP of all patients. The original radiation field was modified after MR examination in six patients. CONCLUSION: The amount of image distortion within the practical area is acceptable for RTTP. MR imaging-assisted x-ray simulation is useful for patients with bone tumors and warrants further investigation.

Aged↗
PubMed1996

Successful erythropoietin treatment for severe anemia in nephrotic syndrome without renal dysfunction.

A 62-year-old woman presented with nephrotic syndrome and severe anemia although the renal function was not impaired. Renal biopsy revealed the histology of membranoproliferative glomerulonephritis, and the proteinuria was resistant to steroid therapy. Iron deficiency, bleeding and other causes of anemia were ruled out, however, her serum erythropoietin level was inappropriately low. The anemia was rapidly corrected by administration of recombinant human erythropoietin. It is suggested that inappropriately low erythropoietin level, in part at least, accounts for the anemia in nephrotic syndrome. It is proposed that erythropoietin therapy should be taken into consideration for severe anemia in nephrotic syndrome even when the renal function is not impaired.

Anemia↗
PubMed1996

Lung cancer cell lines inhibit leukotriene B4 production by human polymorphonuclear leukocytes at the level of phospholipase A2.

We studied cellular interactions between human polymorphonuclear leukocytes (PMN) and lung cancer cell lines by investigating the influence of cancer cells on the production of leukotriene B4 (LTB4) and superoxide anion (O2-) by stimulated PMN. Of the nine cancer cell lines established from human lung cancers that we examined, H23 cells showed the highest LTA4 hydrolase activity. When PMN were stimulated by the calcium ionophore A23187 in the presence of H23 cells, the production of LTB4, 5(S)-hydroxyeicosatetraenoic acid (5-HETE), and 12(S)-hydroxyeicosatetraenoic acid (12-HETE) decreased in a dose-dependent manner. On the contrary, H23 did not inhibit O2- production by PMN. Two other cell lines (N417 and Q9) caused similar inhibition of LTB4 production by PMN. These three cancer cell lines alone did not generate any metabolites of the arachidonic acid (AA) lipoxygenase pathway or any O2- upon stimulation with A23187 alone. The addition of AA dose-dependently reversed the H23-induced inhibition of LTB4, 5-HETE, and 12-HETE production by PMN, suggesting inhibition at the phospholipase A2 (PLA2) level. Furthermore, addition of the cancer cell line Q9 inhibited 14C release from [14C]AA prelabeled PMN in a cell number-dependent manner in the buffer, with and without albumin. The supernatant of H23 cells also inhibited the production of LTB4 by PMN stimulated by A23187, as did the addition of H23 lysate or its 10(4) x g centrifugation supernatant. While neither the 10(5) x g supernatant (cytosol) nor the pellet (microsome) exhibited inhibitory activity, the combination of the separated cytosol and microsomal fractions restored the inhibitory activity. Furthermore, addition of the 10(4) x g supernatant of Q9 lysate to partially purified human cytosolic PLA2 inhibited PLA2 activity in a dose-dependent manner. Our results indicate that the lung cancer cell lines used in our study inhibit LTB4 production by human PMN through inhibition of phospholipase A2 activity, which may contribute to a predisposition to pulmonary infections in patients with lung cancer.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1996

Morphologic and histologic characterization of cardiac myxomas by magnetic resonance imaging.

The purpose of this study was to assess the role of ECG-gated spin-echo (SE) magnetic resonance (MR) images, cine MR images, and gadolinium-diethylenetriaminepentaacetic acid (Gd-DTPA)-enhanced MR images for the morphologic and histologic diagnosis of atrial myxomas. Four patients with left atrial myxoma were imaged with a 1.5-T MR imager. The T1-weighted images and the cine MR images were obtained before injection of Gd-DTPA. After the injection of Gd-DTPA, the T1-weighted images were obtained again. Gd-DTPA-enhanced images of the myxomas were histologically compared with the extracted specimens. The tumors were represented more clearly on the cine MR images as low-intensity areas than on the SE images as high-intensity areas. On post-Gd-DTPA images, the 2 tumors were homogeneously enhanced and the other 2 were inhomogeneously enhanced. The locus of enhancement on post-Gd-DTPA images fitted with histologic myxoma or inflammation, and the unenhanced region reflected the necrosis or cystic changes in the specimens, respectively. The morphologic diagnosis of cardiac myxomas by MRI first should be done with SE images, and when the images are unclear, the cine MR images must be supplemented to depict the tumor clearly. Moreover, Gd-DTPA-enhanced MRI could elucidate histologic characteristics in myxomas.

Adult↗
PubMed1996

Follistatin and activin in bone: expression and localization during endochondral bone development.

The involvement of activin and follistatin, an activin-binding protein, in endochondral bone development was examined by sc implantation of demineralized bone matrix in rats. Immunoreactive follistatin was localized in proliferating chondrocytes and round osteoblasts, whereas it was not detected in hypertrophic chondrocytes and osteoblasts surrounding bone marrow. Western blot analysis also revealed that immunoreactive follistatin was higher during the initial stages of chondrogenesis (day 5) and osteogenesis (days 11 and 14) and lower during the conversion from cartilage to bone (day 9). These results suggest that follistatin is produced by proliferating cells, and the expression decreases with differentiation of the cells. Implants injected with follistatin on days 9 and 10 contained lower calcium levels on day 14 than those injected with rat albumin. Furthermore, the follistatin-injected implants were still mainly composed of cartilage, suggesting that the disappearance of follistatin is necessary for the conversion of cartilage to bone. In contrast, immunoreactive activin beta A (55-60 kDa) was continuously detected in implants on days 7-14. The content of C propeptide of type II procollagen was increased and cartilageous area was enlarged on day 7 by activin A injections on days 5 and 6, suggesting a chondrogenic effect of activin in the initial stage of cartilage formation. These results indicate that proliferating chondrocytes and round osteoblasts produce follistatin, and that the activity of activin is regulated by changes in the expression of follistatin at the stages of chondrogenesis and transition from cartilage to bone.

Activins↗
PubMed1996

Immunoradiometric assay for follistatin: serum immunoreactive follistatin levels in normal adults and pregnant women.

A sensitive and specific immunoradiometric assay for follistatin was developed using antifollistatin mouse monoclonal and rabbit polyclonal antibodies. The sensitivity of the assay was 0.5 micrograms/L, and cross-reactivities with recombinant human activin A and bovine inhibin were less than 0.1%. The intra- and interassay coefficients of variation were less than 10%, and the recovery rate was about 90% in human serum. The addition of activin A to the same sample resulted in a minimal influence on follistatin recovery, indicating that this assay system can measure the total level of activin-bound and unbound follistatin. Gel filtration analysis of human serum showed that the majority of immunoreactivity was eluted in a larger molecular size position than that of free follistatin, suggesting that the large part of follistatin is bound to other proteins, presumably activins, in serum. Using this assay, immunoreactive follistatin levels in various biological fluids and human sera were examined. The dose-response curves of porcine follicular and amniotic fluids were parallel to the standard curve, and porcine follicular fluid contained extremely high follistatin immunoreactivity (5.6 mg/L). The serum follistatin level in normal human volunteers was 13.3 +/- 4.7 micrograms/L (mean +/- SD; n = 60), with a tendency to increase gradually with age. On the other hand, the serum follistatin level was remarkably elevated in pregnant women (62.7 +/- 35.3 micrograms/L; n = 57), with a positive correlation with weeks of pregnancy. These data indicated that circulating immunoreactive follistatin is detectable in human serum, and the levels vary with physiological conditions such as aging and pregnancy.

Activins↗
PubMed1996

Activation of chicken gizzard myosin light chain kinase by Ca2+/calmodulin is inhibited by autophosphorylation.

Myosin light chain kinase (MLCK) is a calmodulin-dependent protein kinase which phosphorylates the 20,000 dalton regulatory light chain of myosin II. Here we show that activation of chicken gizzard MLCK by Ca2+/ calmodulin is inhibited by autophosphorylation at 2 sites in the absence of Ca2+/calmodulin. Two phosphorylation sites are located in the functional domain of the kinase, the threonine site toward the actin binding domain near the N-terminus of MLCK and the serine site in immediate proximity to the calmodulin binding site. The autophosphorylation was significantly inhibited by the binding of calmodulin to MLCK in the presence of Ca2+.

Animals↗
PubMed1996

ME3221, a surmountable angiotensin AT1-receptor antagonist, prevents hypertensive complications in aged stroke-prone spontaneously hypertensive rats.

The protective effects of ME3221, 3-methoxy-2,6-dimethyl-4-[[2'-(1H-tetrazol-5-yl)-1,1'-biphenyl-4-y l]methoxy] pyridine, on aged (32-week-old) stroke-prone spontaneously hypertensive rats (SHRSP) were studied following long-term (for 8 months) oral administration. At a dose of 10 mg/kg/day, ME3221 suppressed the mortality and the hypertensive complications observed in control SHRSP: cerebral apoplexy (hemorrhage, and spongeform and malacia in the cerebral cortex), increased proteinuria, and total N-acetyl-beta-D-glucosaminidase activity, and cardiac hypertrophy and pleural effusion. The protective activity of ME3221, a surmountable angiotensin AT1-receptor antagonist, was comparable to losartan, an insurmountable AT1-antagonist, and also to enalapril, an angiotensin-converting enzyme inhibitor. In addition, ME3221 reduced the systolic blood pressure more effectively than the two reference drugs.

Angiotensin Receptor Antagonists↗
PubMed1996

Structural organization of the gene encoding corn cystatin.

A genomic DNA clone encoding corn cystatin, a cysteine proteinase inhibitor of corn, was isolated from a lambda EMBL3 phage genomic library. The genomic DNA clone spans approximately 2.2 kb and consists of three exons and two introns. The exon number and the intron breakpoints coincide with those of the genes for two types of oryzacystatin.

Amino Acid Sequence↗
PubMed1996

Effects of LHRH, FSH and activin A on follistatin secretion from cultured rat anterior pituitary cells.

We demonstrated the release of follistatin, an activin-binding protein, from cultured rat anterior pituitary cells by measuring immunoreactive (ir-) follistatin in a specific immunoradiometric assay. Ir-follistatin release gradually increased in cultures over 1-18 days and reached its maximal level at 12-15 days of incubation. The basal ir-follistatin levels in the culture media increased about 3- (P < 0.01) and 5-fold (P < 0.001) in 2 and 10% fetal calf serum for 6 days, respectively. LHRH and activin A caused an approximately 2.0- (P < 0.05) and 1.8-fold (P < 0.05) rise in ir-follistatin release, respectively, in contrast to the lack of significant FSH effects. The culture medium condensed on sulfate-cellulofine gel was resolved by polyacrylamide gel electrophoresis and blotted with anti-follistatin polyclonal antibody, resulting in at least three protein bands ranging from 35 to 50 kDa under non-reducing conditions. These results indicated that follistatin is produced in anterior pituitary cells and that its secretion is regulated at least in part by LHRH and activin, implying an autocrine/paracrine role of activin and follistatin in the pituitary.

Activins↗