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Biomedical subjects

K Abe

Publications and source records attributed to K Abe.

At least 703 records · Page 39Linked to original sources
PubMed1998

Effect of prostaglandin E1 on pulmonary hypertension after protamine injection during cardiac surgery.

BACKGROUND: The effects of prostaglandin E1 on pulmonary hypertension were assessed after protamine injection at the end of cardiopulmonary bypass during cardiac surgery. METHODS: Ten patients scheduled for cardiac surgery presented with pulmonary hypertension (mean pulmonary artery pressure greater than 30 mmHg) after protamine injection and were treated by infusion of 0.02 microg x kg(-1) x min(-1) prostaglandin E1. Hemodynamic measurements were made on occasions after cardiopulmonary bypass. Prostaglandin E1 decreased pulmonary artery pressure, pulmonary vascular resistance, right ventricular stroke work index and pulmonary vascular resistance/systemic vascular resistance ratio, but did not change blood pressure, systemic vascular resistance, left ventricular stroke work index or cardiac output. CONCLUSION: Prostaglandin E1 normalized pulmonary hypertension after protamine injection, but did not change arterial blood pressure and cardiac output.

Aged↗
PubMed1998

The fluid-attenuated inversion-recovery pulse sequence in assessment of central nervous system involvement in myotonic dystrophy.

We compared the fluid-attenuated inversion recovery (FLAIR) sequence with conventional spin-echo (SE) imaging for detection of involvement of the central nervous system in five patients with myotonic dystrophy (MD). The diagnosis was made based on clinical features and DNA analysis. All patients showed abnormal high-intensity lesions in the white matter on T2-weighted images, although these were more clearly visible using FLAIR.

Adult↗
PubMed1998

Early-appearing tumor-infiltrating natural killer cells play an important role in the nitric oxide production of tumor-associated macrophages through their interferon production.

Both natural killer (NK) cells and macrophages are thought to be the main effectors responsible for early antitumor defense. In this study, we investigated the role of tumor-infiltrating NK cells in initiating nitric oxide (NO) production by tumor-associated macrophages (TAM). The in vivo depletion of NK cells prior to the i.p. inoculation of melanoma cells resulted in a significant decrease in the NO production of the TAM prepared from the peritoneal exudate cells (PEC). Such prior NK cell depletion also decreased the ability of TAM to show any antitumor activity in vitro. The addition of NG-monomethyl-L-arginine (Me-L-Arg) to the culture partially inhibited the ability of TAM to suppress the proliferation of melanoma cells and also decreased their cytolytic activity against melanoma cells. These results suggest that the TAM exhibited both cytostatic and cytolytic activities through their NO production. In an in vivo assay, the administration of Me-L-Arg permitted the more rapid growth of i.p. inoculated melanoma cells compared with the control. On the other hand, the decreased NO production of TAM, resulting from the prior NK cell depletion, was restored by the i.p. administration of interferon gamma (IFN gamma). In addition, the in vivo administration of anti-IFN gamma mAb into mice inoculated i.p. with melanoma cells also significantly decreased the NO production of TAM in peritoneal exudate cells. Furthermore, the tumor-infiltrating NK cells produced a considerable level of IFN gamma. Overall, these results indicate that early-appearing tumor-infiltrating NK cells play an important role in the NO production of TAM through their IFN gamma production.

Animals↗
PubMed1998

Antitumor vaccination effect of dendritic cells can be augmented by locally utilizing Th1-type cytokines from OK432-reactive CD4+ T cells.

In order to enhance the antitumor vaccination effect of dendritic cells (DC) pulsed with class I tumor peptide, we tried to utilize the local cytokine help of CD4+ T cells reactive to a streptococcal preparation OK432. DC were prepared from murine bone marrow cells by culture with both granulocyte/macrophage-colony-stimulating factor and interleukin(IL)-4. The peritumoral injections of OK432 induced OK432-reactive CD4+ T cells in the draining lymph nodes, and their in vitro production of interferon gamma was thus significantly enhanced by restimulation with OK432-pulsed DC. In addition, anti-P815 mastocytoma cytotoxic T lymphocytes were generated from the in vivo OK432-treated P815-draining lymph node cells only when the lymph node cells were restimulated in vitro with the DC pulsed with both P1A peptide and OK432. Moreover, the peritumoral injections of OK432 and the subsequent vaccination of the DC, pulsed with both OK432 and P1A peptide, significantly suppressed the growth of s.c. inoculated P815. Interestingly, a significant level of IL-12 was detected in the coculture supernatant of both OK432-pulsed DC and OK432-reactive CD4+ T cells. Collectively, our results suggest that the antitumor vaccination effect of DC pulsed with class I tumor peptide could thus be effectively augmented by locally utilizing the Th1-type cytokines from OK432-reactive CD4+ T cells.

Animals↗
PubMed1998

Characterization of B16 melanoma-specific cytotoxic T lymphocytes.

A B16 melanoma-specific CD8+ T cell line (AB1) was established from the spleen cells of C57BL/6 mice cured of B16 melanoma with interleukin (IL)-12 treatment. The AB1 line exclusively used T cell receptor Vbeta11. The AB1 cells exhibited a cytolytic activity against both syngeneic B16 melanoma and allogeneic P815 mastocytoma, whereas a cold inhibition assay revealed specificity of the AB1 cells against B16 melanoma. Their lostability to kill a class I loss variant of B16 melanoma was restored by the transfection of H-2Kb gene. In addition, their interferon (IFN)-gamma production was significantly suppressed by the addition of anti-H-2Kb monoclonal antibody, and RT-PCR analysis showed that the AB1 line expressed the mRNA encoding IFN-gamma, but not IL-4 or IL-10. The experiment using synthetic peptides of tyrosinase-related protein-2 (TRP-2) revealed that the AB1 cells could recognize TRP-2(181-188) peptide. Moreover, the AB1 cells showed an in vivo antitumor effect against established pulmonary metastases of B16 melanoma. Overall, these results indicate that the Tc1-type Vbeta11+ AB1 cells exert an antitumor activity against syngeneic B16 melanoma through recognition of TRP-2(181-188) peptide in an H-2Kb-restricted manner.

Animals↗
PubMed1998

Tctex3, related to Drosophila polycomblike, is expressed in male germ cells and mapped to the mouse t-complex.

Tctex3 showing restricted expression in male germ cells has been isolated during the process of chromosome walking in the mouse t-complex region. The total sequence of Tctex3 cDNA predicts a protein of 580 amino acids with two C4HC3 type PHD fingers. The region containing this conserved motif is shared among members of the Polycomblike proteins that include the mouse M96 and Drosophila Polycomblike. A partial cDNA for a human homolog of Tctex3, HUTEX3, has also been isolated. Mouse Tctex3 gene was mapped adjacent to Tsc2 gene on mouse Chromosome (Chr) 17, and HUTEX3 was located closely to HSET gene in the HLA class II region of chromosome 6.

Amino Acid Sequence↗
PubMed1998

Differences in antigenic sites, recognized by anti-liver-kidney microsome-1 (LKM-1) autoantibody, between HCV-positive and HCV-negative sera in Japanese patients.

Anti-liver-kidney microsome-1 (LKM-1), which reacts with cytochrome P450 IID6 (CYP2D6), is an autoantibody present in autoimmune hepatitis type II, which affects primarily young patients. Recently, it has been shown some adult patients with chronic hepatitis C are also positive for anti-LKM-1. Thus, anti-LKM-1-positive patients can be classified into two subgroups: (1) those with autoimmune hepatitis type II and (2) those with chronic hepatitis C. We investigated the antigenic epitopes of CYP2D6 with which each of these two anti-LKM-1-positive subgroups reacted. Multiple deletion mutants of CYP2D6 were constructed from a human liver cDNA library and five recombinant fusion proteins expressed. Antigenic epitopes were determined by immunoblot analysis using these proteins. Anti-LKM-1 present in HCV-negative sera recognized at least two peptide regions of aa213-280 and aa341-477 of human CYP2D6. In contrast, anti-LKM-1 present in HCV-positive sera recognized only a single region of aa341-477. Thus, the sera of patients with autoimmune hepatitis type II and patients with chronic hepatitis C recognize different antigenic epitopes of the CYP2D6 molecule. To our knowledge, this is the first time LKM-1 autoantigens have been analyzed at the molecular level in Japanese patients.

Asian People↗
PubMed1998

Hypoxic-ischemic tolerance phenomenon observed in neonatal rat brain.

OBJECTIVE: Our purpose was to determine whether hypoxic-ischemic brain damage would be protected against by advance conditioning of the animal with 4 hours of hypoxic exposure. STUDY DESIGN: Neonatal rats were exposed on postnatal day 7 to (1) 4 hours of hypoxia with 8% oxygen (preconditioning hypoxic group) or (2) 4 hours of normoxia (sham-preconditioning group). At 24 hours after the conditioning, rats from both groups were exposed to left carotid artery ligation followed by 2 hours of hypoxia (8% oxygen/92% nitrogen). All the rats were killed 1 week after hypoxia-ischemia, and their brains were extracted for histologic study. RESULTS: Two types of brain damage were histologically observed at 1 week after hypoxia-ischemia in both groups: (1) generalized infarction in the ligated hemisphere and (2) predominant neuronal loss in the hippocampal region. The total incidence of brain damage was significantly decreased in the preconditioning hypoxic group (10/24 rats, 41.7%) compared with the sham-preconditioning hypoxic group (17/22 rats, 77.3%; P < .05). CONCLUSION: Our results show that the hypoxic-ischemic tolerance phenomenon may be induced in the hypoxic-ischemic brain damage model by conditioning the animal before the insult with 4 hours of hypoxic exposure.

Animals↗
PubMed1998

Three-graft technique for ascending aorta and total aortic arch replacement.

We have developed a procedure for total aortic arch replacement using three separate Hemashield grafts and establishing deep hypothermic circulatory arrest and continuous retrograde cerebral perfusion followed by antegrade cerebral perfusion. This method is technically simple and yields secure anastomoses.

Aorta↗
PubMed1998

Apoptosis induction in synovial fibroblasts by ceramide: in vitro and in vivo effects.

Several lipid second messengers are important mediators of extracellular signals. Among them ceramide, which is formed by cell membrane sphingomyelin, influences the apoptotic signal pathway through Fas antigen. We examined the apoptotic effect of cell-permeable C2-ceramide on rheumatoid synovial fibroblasts in vitro and in vivo. Exposure of cultured human rheumatoid synovial fibroblasts to C2-ceramide for 24 hours produced internucleosomal DNA fragmentation and morphologic changes characteristic of apoptosis. This C2-ceramide-mediated apoptosis was dose dependent as confirmed by analysis of cytosolic oligonucleosome-bound DNA of treated synovial fibroblasts. We also demonstrated that intra-articular administration of C2-ceramide into Fas-deficient MRL lpr/lpr mice produced a profound reduction of synovial hyperplasia within 24 hours. In situ nick end labeling analysis confirmed the induction of apoptosis in synovial lining cells. Our results indicate that C2-ceramide may function as a potent inducer of apoptosis in the synovium and suggest that pharmacologically-induced apoptosis may be useful as a new therapeutic modality for rheumatoid arthritis.

Animals↗
PubMed1998

Delayed and selective motor neuron death after transient spinal cord ischemia: a role of apoptosis?

OBJECTIVE: The mechanism of spinal cord injury has been thought to be related to tissue ischemia, and spinal motor neuron cells are suggested to be vulnerable to ischemia. We hypothesized that delayed and selective motor neuron death is apoptosis. METHODS: Thirty-seven Japanese domesticated white rabbits weighing 2 to 3 kg were used in this study and were divided into two subgroups: a 15-minute ischemia group and a sham control group. Animals were allowed to recover at ambient temperature and were killed at 8 hours, and 1, 2, 4, and 7 days after reperfusion (n = 3 at each time point). By means of this model, cell damage was histologically analyzed. Detection of ladders of oligonucleosomal DNA fragment was investigated with gel electrophoresis up to 7 days of the reperfusion. Immunocytochemistry, in situ terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick-end labeling staining was also performed. RESULTS: After 15 minutes of ischemia, most of the motor neurons showed selective cell death at 7 days of reperfusion. Typical ladders of oligonucleosomal DNA fragments were detected at 2 days of reperfusion. Immunocytochemistry showed in situ terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick-end staining was detected at 2 days of reperfusion selectively in the nuclei of motor neurons. CONCLUSION: These results suggest that delayed and selective death of the motor neuron cells after transient ischemia may not be necrotic but rather predominantly apoptotic.

Animals↗
PubMed1998

Amyloid beta protein inhibits cellular MTT reduction not by suppression of mitochondrial succinate dehydrogenase but by acceleration of MTT formazan exocytosis in cultured rat cortical astrocytes.

Alzheimer's disease amyloid beta protein (Abeta) inhibits cellular reduction of the dye 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT). Kaneko et al. have previously hypothesized that Abeta works by suppressing mitochondrial succinate dehydrogenase (SDH), but Liu and Schubert have recently demonstrated that Abeta decreases cellular MTT reduction by accelerating the exocytosis of MTT formazan in neuronal cells. To ask which is the case in astrocytes, we compared the effects of Abeta and 3-nitropropionic acid (3-NP), a specific SDH inhibitor, on MTT reduction in cultured rat cortical astrocytes. Treatment with 3-NP (10 mM) decreased cellular activity of MTT reduction, regardless of the time of incubation with MTT. On the other hand. Abeta-induced inhibition of cellular MTT reduction was dependent on the time of incubation with MTT. The cells treated with Abeta (0.1-1000 nM) exhibited normal capacity for MTT reduction at an early stage of incubation ( < 30 min), but ceased to reduce MTT at the late stage (> 1 h). Microscopic examination revealed that Abeta treatment accelerated the appearance of needle-like MTT formazan crystals at the cell surface. These observations support that Abeta accelerates the exocytosis of MTT formazan in astrocytes. In addition to inhibition of MTT reduction, Abeta is known to induce morphological changes in astrocytes. Following addition of Abeta (20 microM), polygonal astrocytes changed into process-bearing stellate cells. To explore a possible linkage between these two effects of Abeta, we tested if astrocyte stellation is induced by agents that mimic the effect of Abeta on MTT reduction. Cholesterol (5 5000 nM) and lysophosphatidic acid (0.2-20 microg/ml) were found to accelerate the exocytosis of MTT formazan in a similar manner to Abeta, but failed to induce astrocyte stellation. Therefore, Abeta-induced inhibition of MTT reduction is unlikely to be directly linked to its effect on astrocyte morphology.

Amyloid beta-Peptides↗
PubMed1998

Vaccination with activated B cells pulsed with tumor-lysates can induce tumor-specific CD4+ T cells in vivo.

Activated B cells, pulsed with tumor-lysates, were examined for their potential to induce tumor-specific CD4+ T cells in vivo, MH2 cells, which are CD4+ T cells and can also recognize purified protein derivative from mycobacterium tuberculosis (PPD), showed a proliferative response in the presence of both syngeneic activated B cells and PPD in a major histocompatibility complex class II-restricted manner. For B cells to function as efficient antigen presenting cells, they need to be activated. Both irradiation and several inhibitors for antigen-processing were observed to block the antigen-presenting ability of activated B cells. Based in these findings, the possibility of anti-tumor vaccination with activated B cells was thus investigated. The spleen cells from mice, which were immunized with activated B cells pulsed with B16 melanoma-lysates, produced a higher level of interferon (IFN)-gamma than those from mice, which were immunized with either non-pulsed activated B cells or the tumor-lysates alone, after in vitro restimulation. This IFN-gamma production was also dependent on the CD4+ T cells. Moreover, the splenic CD4+ T cells in such mice were suggested to increase their ability to generate B16 melanoma-specific cytotoxic T lymphocytes after in vitro restimulation. Even more importantly, immunization with B16 melanoma lysate-pulsed activated B cells elicited a protective immunity against B16 melanoma at rechallenge. Collectively, these results indicate that an anti-tumor effect could be induced by immunization with activated B cells, pulsed with the tumor-lysates, by eliciting tumor-specific IFN-gamma producing CD4+ T cells in vivo.

Animals↗
PubMed1998

Serotonin inhibits the induction of long-term potentiation in rat primary visual cortex.

1. The effect of serotonin (5-hydroxytryptamine; 5-HT) on the induction of long-term potentiation (LTP) in rat visual cortex was investigated by using slice preparations in vitro. 2. Bath application of 5-HT (0.1-10 microM) did not affect the baseline synaptic potentials evoked by single-pulse test stimulation, but inhibited the induction of LTP in a concentration-dependent manner. 3. The effect of 5-HT was blocked by the 5-HT1 receptor antagonist pindolol or the 5-HT2,7 receptor antagonist ritanserin, but not by the 5-HT3,4 receptor antagonist MDL72222. 4. These results suggest that 5-HT plays a role in suppressing the induction of LTP in the rat visual cortex.

Animals↗
PubMed1998

Type A fibril of the mouse tectorial membrane shows D-periodicity: an atomic force microscopic examination.

This study demonstrated that type A fibrils of the mouse tectorial membrane showed a morphology characteristic of collagen, as demonstrated using an atomic force microscope. In the topographical imaging mode, the surface of the type A fibrils showed a periodic pattern, consisting of alternating grooves and ridges. The periodicity of the type A fibrils was 69.1 +/- 0.6 nm, which is in accordance with characteristic collagen D-periodicity. The difference in height between grooves and ridges was 1.6 +/- 0.3 nm. In the variable deflection imaging mode, the type A fibrils showed a clear banding pattern, which consisted of alternating light and dark zones, with D-periodicity. In addition, the type A fibrils exhibited one minor dark band in the light zone and one minor light band in the dark zone.

Aged↗
PubMed1998

Enhancement of heat shock protein expression after transient ischemia in the preconditioned spinal cord of rabbits.

PURPOSE: This investigation was designed to evaluate the mechanism used to acquire a tolerance to spinal ischemia. We investigated inductions of the heat shock protein (HSP) 70 gene and protein in rabbit spinal cord with or without preconditioning. METHODS: Neurologic function, morphologic changes, and inductions of HSP70 messenger RNA (mRNA) and protein were compared in the cases of a 15-minute ischemia 2 days after sham treatment and a 15-minute ischemia 2 days after 10-minute preconditioning. RESULT: HSP70 mRNA was induced at 8 hours of reperfusion after a 15-minute ischemia 2 days after sham treatment. HSP70 protein was induced slightly in selective motor neuron cells at 8 hours of reperfusion, and about 70% of motor neuron cells showed selective cell death after 7 days of reperfusion (p < 0.01). On the other hand, large populations of the motor neuron cells survived at 7 days after the 15-minute ischemia that was applied at 2 days after preconditioning (p < 0.01). HSP70 mRNA was induced persistently as compared with the case of a 15-minute ischemia 2 days after sham treatment. The motor neuron cells strongly produced immunoreactive HSP70 from 8 hours to 2 days. CONCLUSION: Preconditioning with 10-minute ischemia enhanced and prolonged the HSP70 gene expression at both mRNA and protein levels and saved the motor neuron cells from subsequent lethal ischemia. These changes of HSP70 gene expression may play an important role in the acquisition of ischemic tolerance of motor neuron cells in rabbit spinal cord.

Animals↗
PubMed1998

Decreased blood pressure variability at rest in patients with primary aldosteronism.

Increased blood pressure (BP) variability in essential hypertension (EH) is attributed in part to a reduction in baroreflex sensitivity. We previously showed that baroreflex sensitivity is not reduced in hypertension associated with primary aldosteronism (PA) compared with normotensive (NT) subjects. This study examined whether the preservation of baroreflex function in patients with PA would prevent an increase in BP variability. The beat-to-beat BP (measured with Finapres) and RR interval (from electrocardiograms) were monitored for 10 min in the supine and standing positions in 34 patients with PA, 60 patients with EH, and 45 NT subjects. Recordings were also performed during mild ergometer exercise in 7 PA patients, 8 EH patients, and 9 NT subjects. Blood pressure variability was assessed by both standard deviation (SD) and coefficient of variation (CV). Baroreflex sensitivity (BRS) was assessed by the closed-loop gain between systolic BP and RR interval variability. The SD and the CV of systolic BP (SBP) and the CV of diastolic (DBP) BP were significantly smaller in patients with PA than in patients with EH in both supine and standing positions. The SD of SBP and DBP were similar in patients with PA and NT subjects, although the CV were significantly smaller in patients with PA. The BRS was inversely correlated with both the SD and CV for SBP in the supine (r = -0.397 and -0.440, P < .05, respectively) and standing (r = -0.457 and -0.412, P < .05, respectively) positions in patients with PA. Exercise reduced the BRS in all groups (70%, 26%, and 64% for PA, EH, and NT, respectively, P < .01). Blood pressure variability did not change significantly during exercise, compared with rest, in the PA and NT groups but was decreased (P < .05) in the patients with EH. In conclusion, primary aldosteronism is characterized by decreased supine and standing BP variability, which is due in part to the preservation of baroreflex function. Our data further showed that BP variability is minimized by nonbaroreflex mechanisms during mild exercise.

Adult↗