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Biomedical subjects

M Abe

Publications and source records attributed to M Abe.

At least 523 records · Page 29Linked to original sources
PubMed1996

Evaluation of the effects of steroids on experimental septic lung injury.

To evaluate the clinical usefulness of steroids for septic lung injury, we investigated the effects of methylprednisolone (MP) on this disorder using an experimental rat model of cecal ligation and puncture (CLP). While 92% of the rats that underwent CLP (CLP rats) died within 30 h, those given high-dose MP (30 mg/kg) just after the operation (CLP + MP rats) survived for a significantly longer period (p < 0.01). Concentrations of endotoxin (ET) in arterial blood were significantly higher in the CLP + MP rats than in the CLP rats, while those in the bronchoalveolar lavage fluid (BALF) were significantly lower. Alveolar macrophages (AM) obtained from the CLP rats (CLP-AM) generated more O2-than did AM from sham-operated rats (sham-AM) following stimulation. However, the administration of MP did not reduce the upregulated generation of O2-by CLP-AM. While CLP-AM produced less leukotriene (LT)B4 than did sham-AM following stimulation with A23187, the administration of MP further reduced LTB4 production. When AM were cultured with [3H]arachidonic acid (3H-AA), the uptake of the isotope and the 3H release were significantly less in CLP-AM than in sham-AM. The administration of MP did not cause recoveries in the uptake and release of 3H-AA by CLP-AM. Although the survival time of CLP rats was significantly prolonged and the translocation of ET into BALF was reduced by steroid administration, the steroid effects were not explained by those on altered AM function. The upregulated generation of O2- and reduced LTB4 production from CLP-AM were not reversed by the treatment of this drug.

Animals↗
PubMed1996

Soluble interleukin-6 receptor levels in pleural effusions.

Generation of soluble cytokine receptors is a general phenomenon, and the roles of several such receptors have been investigated in clinical settings. Unlike other soluble cytokine receptors, soluble interleukin-6 receptor (sIL-6R) can act as an agonist and thus is implicated as an important modulator in the acute-phase reaction of prolonged inflammation. The purpose of the present study was to determine the roles of pleural sIL-6R in both differential diagnosis of pleural diseases and in the induction of acute-phase protein. Specific sandwich enzyme-linked immunosorbent assays were used to determine sIL-6R and IL-6 in 19 tuberculous, 48 malignant and 10 transudative effusions. Although IL-6 levels in pleural effusions were strikingly different, no significant differences in pleural sIL-6R levels were found between the groups. Pleural levels of IL-6 were invariably much higher, whereas those of SIL-6R were invariably lower than serum levels. Furthermore, IL-6, but not sIL-6R, levels in effusions correlated significantly with serum C-reactive protein levels. These results suggest that: (1) pleural levels of sIL-6R are not increased even in strong inflammation such as tuberculous pleurisy, nor significantly different among pleural diseases; and (2) the local levels of sIL-6R are not as important as expected for the induction of acute-phase proteins in patients with pleural diseases.

Antigens, CD↗
PubMed1996

Stereoscopic synthesized brain-surface imaging with MR angiography for localization of a peripheral mycotic aneurysm: case report.

A patient with subacute bacterial endocarditis and a peripheral mycotic aneurysm is presented. We used a combined multi-slice surface anatomy scanning (SAS) and contrast-enhanced MR angiography image to determine the exact location of the small lesion by applying a skin marker on the scalp and visualizing the relationship of the marker to the brain surface structures and to the lesion. This technique was useful for the removal of a small peripheral aneurysm using only a limited craniotomy.

Aged↗
PubMed1996

Human T lymphocyte virus type I-induced myeloneuropathy in rats: implication of local activation of the pX and tumor necrosis factor-alpha genes in pathogenesis.

The pathogenetic roles of human T lymphocyte virus type I (HTLV-I) and cytokines were investigated in HTLV-I-induced myeloneuropathy in Wistar-King-Aptekman-Hokudai rats. In the nervous system, pX messenger RNAs of HTLV-I were selectively expressed in the diseased spinal cord and peripheral nerves but not in the unaffected cerebrum and cerebellum, even though proviral DNAs were consistently identified in these tissues. Among several cytokines examined, mRNA expression and production of tumor necrosis factor (TNF)-alpha in the spinal cord and cerebrospinal fluid correlated positively with the development of spinal cord lesions. The collective evidence strongly suggests that selective activation of HTLV-I, in particular Tax expression and production of TNF-alpha induced by HTLV-I infection in target spinal cord and peripheral nerves, is causally related to apoptotic death of oligodendrocytes and Schwann cells, a major pathogenetic pathway of the HTLV-I-induced myeloneuropathy.

Animals↗
PubMed1996

Effects of transgenic mixed-haplotype MHC class II molecules A alpha d A beta z on autoimmune disease in New Zealand mice.

The MHC haplotype heterozygosity (H-2d/H-2z) acts as one major predisposing genetic element for autoimmune disease resembling systemic lupus erythematosus (SLE) in the F1 hybrid of NZB (H-2d) and NZW (H-2z) mice. To determine a possible role of mixed-haplotype A molecules, we introduced a transgene A beta z into H-2d/H-2d homozygous (NZB x NZW.H-2d)F1 mice, in which, compared with the original H-2d/H-2z heterozygotes, the incidence and titer of IgG anti-DNA antibodies, serum levels of nephritogenic retroviral gp70/anti-gp70 immune complexes (ICs) and the associated incidence of IC-type lupus nephritis were reduced. Evidence for the formation of mixed-haplotype A alpha d A beta z molecules in the transgenic mice was obtained by A beta z molecule expression on the cell surface of splenic B cells and macrophages, thymic epithelial cells and mature B cells in the bone marrow. A alpha d A beta z-restricted T cell clones showed good proliferative responses to spleen cells from the transgenic mice, to an extent much larger than seen in cells from the original (NZB x NZW)F1 mice, suggesting that the expression of functional A alpha d A beta z molecules on cells in transgenic mice is considerably high. Compared with findings in transgene-negative littermates and the original (NZB x NZW)F1 mice, the A beta z transgene to a greater extent promoted serum levels of IgM anti-double-stranded (ds) DNA antibodies and IgM anti-gp70/gp70 ICs in the transgenic mice. None the less, the production of IgG anti-dsDNA antibodies and IgG anti-gp70/gp70 ICs as well as the development of renal disease was markedly suppressed. Possible mechanisms of such effects of the transgene are discussed.

Animals↗
PubMed1996

Normal D-JH rearranged products of the IgH gene in SCID mouse bone marrow.

SCID mice are profoundly immunodeficient, resulting from an inability to carry out the V(D)J recombination reaction during both B cell and T cell development. Recently, however, it was revealed that normal rearrangement frequently did occur in the TCR delta and gamma chain loci in the SCID thymus. To evaluate whether the normal rearrangement occurring in SCID is a T-cell-specific phenomenon, we directly cloned using PCR the DQ52-JH2 and DFL16.1-JH2 rearranged segments of the IgH gene from SCID bone marrow. The subsequent analysis revealed that normal V(D)J recombination occurred in a significant number of the analyzed clones. By quantitative Southern hybridization it was shown that the quantity of normal DQ52-JH2 joints existing in the SCID bone marrow is approximately 4-7% that in normal bone marrow. D-JH rearrangement in SCID mice and normal mice differs in the frequency of nucleotide insertion (N insertion). Although most of the normal mouse clones exhibited N insertion in the D-JH rearrangement, in SCID mouse clones N insertion was identified in only a few D-JH rearrangements. Furthermore, in several normal rearranged clones, the recombination occurred at the short homologous sequence. These observations suggest that the V(D)J recombination of IgH normally occurs at the early stage of SCID B cell development, just as TCR gene rearrangement occurs during SCID T cell development. Furthermore, the features of rearranged products isolated from SCID bone marrow cells were remarkably similar to those from leaky SCID mice.

Animals↗
PubMed1996

Bone growth rather than myofibrillar protein turnover is strongly affected by nutritional restriction at early weaning of calves.

Our previous study revealed that weaning of calves aged 5 wk (early weaning) resulted in transient nutritional restriction with subsequent repletion. The present study was conducted to examine age-related changes in nitrogen balance, bone growth and myofibrillar protein degradation after early weaning in calves. At weaning, calves used in Experiment 2 had more severe nutritional restriction than those used in Experiment 1 due to a shorter duration of the suckling period (3 vs. 4 wk), a lesser amount of daily milk replacer (500 vs. 600 g) and a shorter period when given solid feed (for the last week vs. throughout the suckling period). In both experiments, nitrogen and calcium retentions were lower at weaning and transiently increased at 6 wk after weaning. However, detrimental effects on nitrogen and calcium retention immediately after weaning were more evident, and compensatory increases of nitrogen and calcium retention after weaning were more pronounced and continuous in Experiment 2 than in Experiment 1. The changes in plasma intact osteocalcin concentrations and urinary hydroxyproline excretion after weaning were similar to those for nitrogen and calcium retention in Experiment 2, whereas fractional degradation rate of myofibrillar protein was constant throughout the study in both experiments. These results suggest that the extent of nutritional restriction at weaning affects subsequent enhanced utilization of nitrogen and calcium, and that age-related changes in nitrogen retention after early weaning partly reflect changes in bone growth regulated by both forming and resorbing activities, independent of myofibrillar protein degradation.

Aging↗
PubMed1996

Unique recognition of activin and inhibin by polyclonal antibodies to inhibin subunits.

Inhibin-A is a glycoprotein composed of an alpha subunit containing a glycosylation site and a beta A subunit, whereas activin-A is a homodimer of two inhibin beta A subunits. We examined the recognition of activin-A and inhibin-A by several antisera to the alpha or beta A subunit, and factors affecting the recognition. A total of six polyclonal antibodies to inhibin subunits, i.e., two antisera to a peptide fragment of the alpha subunit [alpha (1-19) and alpha (1-26)], and four antisera to the beta A subunit [beta A (1-10), beta A (70-79), beta A (87-99), and beta A (94-105)], was generated. On Western blot analysis, the anti-beta A (87-99) and beta A (94-105) sera recognized recombinant human activin-A but not inhibin-A under non-reducing conditions. When inhibin-A was deglycosylated with N-glycosidase-F, inhibin-A could be recognized by the anti-beta A (87-99) and beta A (94-105) sera. In addition, when activin-A bound to a nitrocellulose membrane was pre-incubated with recombinant human follistatin, the recognition of activin-A by the anti- beta A (87-99) and beta A (94-105) sera was decreased. These results suggested that the lower affinity of follistatin to inhibin-A than to activin-A might be likely explained as reflecting a site associated with the glycosylation of inhibin-A. However, the exposure of amino acids 87-105 of the inhibin beta A subunit on the molecular surface through deglycosylation did not increase the affinity of inhibin-A for follistatin but rather resulted in poor binding with follistatin. The present data suggest that (1) amino acids 87-105 of the inhibin/activin beta A subunit are located on the molecular surface, although this region of inhibin-A is concealed by the carbohydrate chain of the alpha subunit, (2) the region responsible for follistatin binding within the activin beta A subunit is spanned by amino acids 87-105, and (3) the mode of binding of inhibin-A to follistatin is quite different from that of activin-A to follistatin, and the former may be influenced by glycosylation.

Activins↗
PubMed1996

Clinical usefulness of determining the rate of thermal clearance within heated tumors.

Between June 1987 and June 1988, 28 patients (28 tumors) with liver, retroperitoneal, intrapelvic, or superficial tumors were treated with hyperthermia combined with radiotherapy and/or chemotherapy. Hyperthermia was administered once or twice a week for 30-60 min per session, up to a total of 2-11 sessions, with an 8-MHz RF capacitive heating device. Blood flow in the tumors was evaluated from the rate of thermal clearance (TCR) using the bio-heat transfer equation. The TCR was measured in the middle of the first heating session and at the end of the last heating session by turning off the output power of the heating device. For 9 patients, contrast-enhanced CT scans were taken and CT numbers at the centers of tumors were measured before and after the entire course of hyperthermia. Changes in TCR were closely related to average tumor center temperature, changes in CT number, and tumor response. When smaller and more superficial tumors were treated by hyperthermia combined with radiotherapy and/or chemotherapy that consisted of many heating sessions and during which a high average tumor center temperature was achieved, a better tumor response was obtained. The better the tumor response, the higher the local control rate became. The cause-specific survival rate of patients who achieved good tumor responses was higher than that of patients who showed poor tumor responses. Changes in TCR and CT number in heated tumors were useful and important indicators of tumor response to hyperthermia.

Adolescent↗
PubMed1996

Relationship between the angiotensin converting enzyme gene polymorphism and the effects of enalapril on left ventricular hypertrophy and impaired diastolic filling in essential hypertension: M-mode and pulsed Doppler echocardiographic studies.

OBJECTIVE: To investigate the relationship between the angiotensin converting enzyme (ACE) gene polymorphism and the effects of the ACE inhibitor enalapril on left ventricular hypertrophy and impaired diastolic filling. DESIGN AND METHODS: Enalapril (5-10 mg/day) was administered for 12 months to 60 previously untreated patients with essential hypertension. M-mode and pulsed Doppler echocardiography were performed before and after treatment, and changes in various parameters after treatment with enalapril were examined. ACE gene polymorphism was examined by the polymerase chain reaction method and the patients were classified as having the 190 bp deletion homozygous (DD) genotype, the 490 bp insertion homozygous (II) genotype or the 490 bp insertion 190 bp deletion heterozygous (ID) genotype. RESULTS: The DD genotype was observed in 10 patients (17%), the ID genotype in 24 patients (40%) and the II genotype in 26 patients (43%). Plasma ACE activity before treatment with enalapril was significantly higher in seven patients with DD genotype than it was in 18 patients with ID genotype and in 14 patients with II genotype. In all of the 60 patients, the left ventricular mass index, the peak atrial systolic velocity:early diastolic velocity ratio and the deceleration time from the peak of the early diastolic wave to the baseline in transmitral flow velocity were decreased significantly after treatment with enalapril. The changes in left ventricular mass index and atrial systolic velocity:early diastolic velocity ratio after enalapril administration were significantly greater in the DD genotype group than they were in the other two genotype groups. CONCLUSION: Enalapril-induced regression of left ventricular hypertrophy and improvement in left ventricular impaired diastolic filling were significantly greater in the DD genotype group than they were in the ID and II genotype groups, suggesting that the circulating and tissue renin-angiotensin systems, particularly the former system, are most active in hypertensive patients with the DD genotype.

Adult↗
PubMed1996

Interferon-gamma inducible protein (IP-10) expression is mediated by CD8+ T cells and is regulated by CD4+ T cells during the elicitation of contact hypersensitivity.

To investigate the potential roles of CD4+ and CD8+ T cells during contact hypersensitivity, we examined the T-cell-dependent expression of proinflammatory cytokine genes in the responses to dinitrofluorobenzene and oxazolone. Whole cell RNA was isolated from challenged ear tissue and analyzed for level of cytokine gene expression by Northern blot and densitometry analysis. Expression of interleukin 1 beta and the three chemokine genes (IP-10, JE, and KC) examined was dependent on the hapten dose used for sensitization and correlated with the immune response, i.e., ear swelling, elicited. Antibody-mediated depletion of CD8+ T cells before sensitization resulted in the absence of IP-10 expression following hapten challenge, indicating the ability of immune CD8+ T cells to mediate IP-10 expression. Depletion of CD4+ T cells resulted in higher levels of IP-10 and KC expression during elicitation of contact sensitivity, suggesting CD4+ T cells inhibit the expression of these proinflammatory genes. Depletion of CD4+ T cells resulted in contact hypersensitivity responses of higher magnitude and depletion of CD8+ T cells resulted in responses of lower magnitude. Transfer of CD8+ T-cell-depleted immune cells resulted in low, but detectable levels of IP-10 expression, indicating the ability of some oxazolone-immune CD4+ T cells to mediate IP-10 expression. These results indicate the differential induction of proinflammatory cytokine gene expression during elicitation of contact hypersensitivity in which expression of IP-10 is primarily mediated by immune CD8+ T cells and inhibited by immune CD4+ T cells.

Animals↗
PubMed1996

Intradermal dermoid cyst associated with occult spinal dysraphism.

A 2-year-old boy with congenital lumbosacral skin lesions is described. He presented with associated occult spina bifida and a sagittal cleft of the vertebral body deep in the skin lesions. The skin lesions presented as a combination of a lipoma, telangiectasia, mild hypertrichosis, and a dermoid cyst. Magnetic resonance imaging (MRI) revealed that the lipoma extended to the spina bifida region, but that it did not connect to the dura. MRI also demonstrated no other spinal lesions requiring surgical treatment. The intradermal location of the dermoid cyst observed in our patient was unusual. We discuss the location of dermoid cysts in the lumbosacral region associated with spinal dysraphism.

Dermoid Cyst↗
PubMed1996

Comparison of in vivo efficacy of hypoxic cytotoxin tirapazamine and hypoxic cell radiosensitizer KU-2285 in combination with single and fractionated irradiation.

Development of strategies to eradicate radioresistant hypoxic cells would be of great benefit for clinical radiotherapy. In the present study, the in vivo effects of a promising hypoxic cytotoxin, tirapazamine (3-amino-1,2,4-benzotriazine 1,4-di-N-oxide), were examined in comparison with those of KU-2285, one of the best hypoxic cell radiosensitizers, in combination with both single and fractionated irradiation. The tumor response was assessed by the standard in vivo-in vitro clonogenic assay using SCCVII tumors in C3H mice and EMT-6/KU tumors in Balb/c mice with different characteristics of tumor hypoxia. With single-dose irradiation (18 Gy), both tirapazamine and KU-2285 showed significant enhancement of cell killing in a dose-dependent manner, but tirapazamine was more effective for SCCVII tumors with acutely hypoxic cells, while KU-2285 was more effective for EMT-6/KU tumors predominantly with chronically hypoxic cells. In fractionated irradiation regimens (4 fractions of 5 Gy at 12 h intervals), tirapazamine showed more marked combined effects at 10 and 20 mg/kg than KU2285 at 100-200 mg/kg in both SCCVII and EMT-6/KU tumors. We concluded that the effectiveness of KU-2285 and tirapazamine was correlated with the nature of tumor hypoxia with single-dose irradiation, whereas tirapazamine appeared more potent than KU-2285 with fractionated irradiation. These findings suggest the potential usefulness of tirapazamine in clinical fractionated radiotherapy.

Animals↗
PubMed1996

Changes in cell proliferative parameters of SCCVII and EMT6 murine tumors after single-dose irradiation.

To understand better the repopulation kinetics of tumor cells after radiotherapy, we investigated changes in cell proliferative parameters after single-dose irradiation of SCCVII tumors in C3H/He mice and EMT6 tumors in Balb/c mice. The following parameters were determined 0-15 days after single irradiation at 20 or 30 Gy; dividing fraction (DF), potential doubling time (Tpot), number of clonogenic cells per tumor (Ncln), and volume doubling time (Tvol). DF and Tpot were determined by in vivo-in vitro cytokinesis-block assay with cytochalasin B, Ncln was measured by in vivo-in vitro colony-forming assay, and Tvol was determined by growth delay assay. In both tumors, longer Tpot and lower DF and Ncln were obtained for 3-4 days after irradiation, but in SCCVII tumors these values returned to the pretreatment levels 9 days after irradiation. In EMT6 tumors, Tpot, DF, and Ncln did not return to the pretreatment levels even 12 days after irradiation. In the regrowth phase of both tumors following irradiation at 20 Gy, Tvol was longer than the pretreatment level, although Tpot was similar in SCCVII and only slightly longer in EMT6. Therefore, the cell loss factor in the regrowth phase was considered to be higher than the pretreatment level in both tumors. From the results, recruitment of previously quiescent cells into the proliferative pool in these tumors was suggested to contribute to repopulation after radiation.

Animals↗
PubMed1996

Analysis of lectin binding properties on human Burkitt's lymphoma cell lines that show high spontaneous metastasis to distant organs in SCID mice: the binding sites for soybean agglutinin lectin masked by sialylation are closely associated with metastatic lymphoma cells.

Alterations in cell surface carbohydrates on human lymphoma cell lines with different spontaneous metastatic potential in the severe combined immunodeficiency (SCID) mouse model were analyzed. A difference in cell surface carbohydrates between high- (HBL-2, HBL-7 and HBL-8) and no- or low-(HBL-4, HBL-6, Daudi and Raji) spontaneous metastatic human lymphoma cell lines were analyzed on a FACScan using fluorescein-isothiocyanate (FITC)-conjugated lectins. The most consistent difference in lectin binding properties was found with soybean agglutinin (SBA) lectin. High-metastatic lymphoma cells (HBL-7 and HBL-8 cells) in vitro were found to bind the SBA lectin, but the cells in vivo (in primary tumors and metastatic tumors of SCID mice) showed considerably reduced SBA lectin binding. In addition, HBL-2 cells that almost did not bind SBA lectin in vitro and in vivo showed high spontaneous metastasis. Neuraminidase treatment revealed that SBA lectin binding sites were masked by sialic acid. On the other hand, no- or low-metastatic lymphoma cells in vitro and in vivo were found to bind SBA lectin. HBL-8 cell clones without SBA lectin binding showed high spontaneous metastasis to distant organs in SCID mice but HBL-8 cell clones with SBA lectin binding showed very low spontaneous metastasis. Sophora Japonica agglutinin (SJA) lectin is able to recognize the carbohydrates in common with SBA lectin, but it does not appear to be associated with metastatic capacity. These results suggest that the sialylation of particular carbohydrate residues on human lymphoma cells that are recognized by SBA lectin may be associated with the spontaneously metastatic capacity of human lymphoma cell lines in our SCID mouse model.

Animals↗