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Biomedical subjects

A Iguchi

Publications and source records attributed to A Iguchi.

At least 109 records · Page 6Linked to original sources
PubMed1999

Cryopreserved aortic homograft replacement in a patient with Takayasu's arteritis.

A patient with severe long-standing Takayasu's arteritis underwent successful replacement of the aortic root and ascending aorta with a cryopreserved aortic homograft. Her postoperative course was uneventful and echocardiography demonstrated evidence of neither aortic regurgitation nor graft detachment more than 2 years after the operation. Magnetic resonance image demonstrated no signs of graft enlargement.

Adult↗
PubMed1999

Central nervous system-mediated hyperglycemic effects of NIK-247, a cholinesterase inhibitor, and MKC-231, a choline uptake enhancer, in rats.

We investigated the effects of intracerebroventricular administration of NIK-247 (9-amino-2,3,5,6,7,8-hexahydro-1H-cyclo-penta(b)-quinoline monohydrate hydrochloride; a cholinesterase inhibitor) or MKC-231 (2-(2-oxypyrrolidin-1-yl)-N-(2,3-dimethyl-5,6,7,8-tetrahydrofur o[2,3-b]quinolin-4-yl) acetoamide; a choline uptake enhancer) on plasma glucose level in comparison with that of neostigmine administration in rats. The extents of NIK-247- and MKC-231-induced hyperglycemia were considerably less than that by neostigmine, suggesting that the potencies of the drugs to produce the peripheral hyperglycemia may be pharmacologically negligible.

Aminoquinolines↗
PubMed1999

[Gene therapy to treat Parkinson's disease].

One recent strategy of gene therapy is to have cells express the lacking substances. Decline in dopamine D2 receptors (D2R) is observed in late-stage Parkinson's disease. We have constructed a replication-deficient adenovirus vector to transfer rat D2R cDNA (AdCMV.DopD2R) to the brain as a possible therapeutic strategy and a replication-deficient adenovirus vector to express nothing (AdCMV.Null) as a control. Using tissue culture cells infected with this vector, we detected D2 R cDNA by Northern analysis and receptor protein in membrane preparations as specific binding of the D2R ligand, [3H] spiperone. In vivo demonstration involved autoradiographic analysis of [3H] spiperone binding in rat striatum, D2R expression was amplified above normal concentrations in the injection site. We investigated the expression and functionality of the adenoviral vector. Comparative analysis of the autoradiographic images from the striatum injected with AdCMV.DopD2R and the contralateral striatum injected with a control vector, AdCMV. Null, in male rats indicated that D2R binding was increased by 40-60% on days 3 and 5 after injection, but then declined to baseline levels by day 21. When injected with apomorphine on days 3 and 7 after vector injection, experimental groups that had received unilateral striatal injections of AdCMV. DopD2R exhibited a distinct and significant laterality in rotational behavior. These results provide the first demonstration of an adenovirally mediated, intracerebral delivery of a functional neurotransmitter receptor.

Adenoviridae↗
PubMed1999

[Adverse effects of anti-thymocyte globulin/anti-lymphocyte globulin therapy].

This single-centre study evaluated the adverse effects of anti-thymocyte globulin (ATG) and anti-lymphocyte globulin (ALG) as used for the treatment of aplastic anemia and/or for conditioning regimens prior to stem cell transplantation. ATG/ALG was given to 29 patients a total of 37 times. The incidence of adverse effects was 62.1% (23/37), and fever was the most frequent adverse effect. Therapy was discontinued in only 4 patients (10.8%) due to severe adverse effects. Adverse effects occurred more frequently with ATG (rabbit-derived) than with ALG (horse-derived). Seven patients underwent 2 or 3 cycles of ATG/ALG therapy, for a combined total of 8 times; 6 of those patients (75% (6/8)) experienced adverse effects. Shorter intervals between repeated cycles of therapy appeared to heighten the risk of adverse reactions.

Adolescent↗
PubMed1999

Fibrin gel induces the migration of smooth muscle cells from rabbit aortic explants.

A major step in the pathogenesis of atherosclerosis is the vectorial migration of smooth muscle cells (SMCs) from the arterial media into the intima. Although subcultured SMCs usually show synthetic phenotype, the behaviour of contractile SMCs may be crucial for the subsequent migration of the cells. In the present study, we utilized an in vitro assay system to evaluate the effects of fibrin gels on the migration of SMCs from explants taken from rabbit aorta. After cultured for 5-7 days in a serum-free condition, SMCs appeared from explants covered with fibrin gel. The cells were positive on immunostaining for SMC specific alpha-actin. No migration of SMCs from the control explants without fibrin gel was observed. Then the percentage of explants showing cell migration and the number of migrating cells increased with time. The migration of SMCs into fibrin gels was not dependent on the concentration of fibrinogen used for the preparation of fibrin gel in the range of 1.5-3 mg/ml. Variations of thrombin concentration in the range of 0.25-1.25 U/ml had no significant effect. However, there was less migration of SMCs with higher concentrations of thrombin. Thrombin inhibitors, hirudin and PPACK had no significant effect on the migration of SMCs. An RGD-containing peptide, GRGDS inhibited the migration of SMCs although a control peptide GRGES at the same concentration had no significant effect. A monoclonal antibody to alphavbeta3, LM609, completely inhibited the migration of SMCs from the explants, suggesting that alphavbeta3 integrin is involved in the migration of SMCs into fibrin gels. SMCs which migrated from the explants showed the positive staining with the monoclonal antibodies against SMC myosin heavy chain isoforms, SMemb, SM1 and SM2, suggesting that they are in an intermediate state changing from contractile to synthetic state. In conclusion, the present study showed that fibrin gel induces the migration of SMCs from explants into itself and the process may not need other growth factors or cytokines.

Animals↗
PubMed1998

Centrally administered TRH-induced insulin secretion is impaired in the Otsuka-Long-Evans-Tokushima Fatty rats, a model of spontaneous non-insulin-dependent diabetes mellitus.

To investigate whether insulin secretion induced by stimulation of the vagus nerve is preserved or impaired in Otsuka-Long-Evans-Tokushima Fatty (OLETF) rats, we injected 10(-8) mol of thyrotropin-releasing hormone (TRH) into the third cerebral ventricle and determined the serum level of insulin in the unanesthetized, unrestrained rats. Intracerebroventricular (i.c.v.) injection increased the serum levels of glucose and insulin in both OLETF and Long-Evans-Tokushima-Otsuka (LETO) rats, a nondiabetic control strain, at 8-12 weeks of age. At 24-28 weeks of age, the increased level of glucose in OLETF rats was comparable to LETO rats but that of insulin was lower than control after the i.c.v. injection of TRH. Pretreatment with i.v. atropine had no significant effect on such hyperglycemia. However, the increases in the serum levels of insulin were suppressed in both OLETF and LETO rats. The plasma levels of epinephrine, norepinephrine, and glucagon rose significantly after TRH. There was no significant difference in the levels of any hormones between the two groups. In OLETF rats at 24-28 weeks of age, i.v. glucose load induced significantly higher serum levels of glucose and insulin than LETO rats. The results suggest that the vagus nerve-mediated insulin secretion is impaired in OLETF rats, similar to an autonomic diabetic neuropathy in the early stage of diabetes. This impairment may play some role in deteriorating glucose tolerance in this spontaneously developed diabetes model.

Animals↗
PubMed1998

Effect of crosslinking by factor XIIIa on the migration of vascular smooth muscle cells into fibrin gels.

We evaluated the migration of vascular smooth muscle cells into crosslinked fibrin gels, using an in vitro assay system. Vascular smooth muscle cells from bovine fetal aorta migrated into non-crosslinked and crosslinked fibrin gels and showed a characteristic elongated spindle-shaped appearance with long cytoplasmic processes. The cells displayed two-fold increase in migration into crosslinked fibrin gels compared to non-crosslinked gels, suggesting the importance of fibrin crosslinking by factor XIIIa on its three-dimensional structure for the migration of smooth muscle cells.

Animals↗
PubMed1998

Angiogenic stimuli are essential for survival of vascular endothelial cells in three-dimensional collagen lattice.

Cultured vascular endothelial cells derived from bovine aorta (BAECs) can survive and proliferate in the condition of two-dimensional monolayer culture in the presence of serum without any specific growth factors. When BAECs were embedded in collagen lattice, they underwent apoptotic death within 2 days unless the cultures were repeatedly supplied with angiogenic growth factor such as fibroblast growth factor-2 (FGF-2). Supplementation with FGF-2 induced endothelial cell differentiation, resulting in capillary-like tube formation inside collagen lattice. Following tube formation, withdrawal of FGF-2 induced disruption of the tube structures associated with the characteristic apoptotic cell death. These effects of FGF-2 were regulated by tyrosine phosphorylation, but not mediated through protein kinase C pathway. This model of endothelial cell apoptosis inside collagen lattice may represent in vivo endothelial cell-matrix interaction during angiogenesis process, indicating that apoptotic death of endothelial cells may regulate angiogenesis and the regression of vessels.

Animals↗
PubMed1998

Swimming stress that causes hyperglycemia increases in vivo release of noradrenaline, but not acetylcholine, from the hypothalamus of conscious rats.

The effects of acute swimming stress (10 min) on noradrenaline release from the medial basal hypothalamus (MBH; consisting of the ventromedial and dorsomedial hypothalamus) and acetylcholine release from the lateral hypothalamic area (LHA) were investigated in freely moving rats by using in vivo microdialysis techniques. Serum glucose, noradrenaline and adrenaline concentrations were also determined. Acute swimming stress produced significant hyperglycemia, with increases in serum noradrenaline and adrenaline concentrations. The release of noradrenaline from the MBH was significantly stimulated during the swimming stress. On the other hand, the swimming stress has no significant effect on the release of acetylcholine from the LHA. These findings support the idea that hypothalamic noradrenergic neurons play an important role in the sympathoadrenal hyperglycemic response to stressful stimuli. Moreover, it is suggested that hypothalamic cholinergic neurons are not involved in the responses of serum glucose, noradrenaline and adrenaline concentrations to swimming stress.

Acetylcholine↗
PubMed1998

Inhibition of angiogenesis on glycated collagen lattices.

Advanced glycation endproduct (AGE) accumulation in extracellular matrix proteins has been demonstrated in diabetic patients with a significant correlation with the severity of diabetic complications. AGE accumulation induces matrix protein cross-link formation, resulting in an increased stiffness of matrix fibres and the reduction of the susceptibility of matrix proteins to proteolytic degradation. We examined whether glycation-induced collagen cross-linking may affect vascular endothelial cell behaviours such as invasion, proliferation and differentiation, using the in vitro angiogenesis model of capillary-like structure formation in three-dimensional matrices of collagen type I. Endothelial cells cultured on collagen gel with angiogenic factors (the combination of fibroblast growth factor-2 and vascular endothelial growth factor) invaded the underlying collagen matrix, and organized capillary-like cord structures in the gel. We found that endothelial cell invasion into glycated collagen gel was significantly attenuated without any effect on proteinase activity including cell-associated plasminogen activator and matrix metalloproteinase in the conditioned medium. In addition, subsequent capillary-like cord formation was also inhibited in glycated collagen gel. In contrast, endothelial cell proliferation was enhanced on glycated collagen gel with or without angiogenic factors compared with control collagen gel. These results suggest that the structural alterations of extracellular matrix proteins through the glycation-induced cross-link formation affect the interaction between endothelial cell and extracellular matrix, resulting in the impairment of an adequate neovascularization in diabetic patients.

Angiogenesis Inducing Agents↗
PubMed1998

Prophylactic intravesical instillation chemotherapy against recurrence after a transurethral resection of superficial bladder cancer: a randomized controlled trial of doxorubicin plus verapamil versus doxorubicin alone. The Kyushu University Urological Oncology Group.

PURPOSE: We investigated whether verapamil (VR), a known chemosensitizing agent of P-glycoprotein-mediated multidrug resistance, could enhance the preventative effect of doxorubicin (Adriamycin, ADM) on both intravesical recurrence and disease progression after transurethral resection (TUR) of superficial bladder cancer. METHODS: The patients were randomized into two groups: one group received an intravesical instillation of ADM (30 mg) plus VR (15 mg) after TUR of superficial bladder cancer (19 times over 1 year), and the other group received ADM alone on the same treatment schedule. The nonrecurrence rate, the incidence of disease progression at the first recurrence and the side effects were compared over a median follow-up of 38.5 months. RESULTS: Of the 226 patients registered, 157 were evaluable. No significant differences were observed in the patients' characteristics between the two groups. Although the incidence of disease progression at the first recurrence was not significantly different between the two groups, the ADM plus VR instillation group did show a significantly higher nonrecurrence rate than the ADM-only instillation group, and such significance persisted even when any possible bias was allowed for in a multivariate analysis. In terms of side effects, the incidence and severity of bladder irritation symptoms were not significantly different between the two groups. CONCLUSIONS: Intravesical instillation chemotherapy with ADM plus VR was found to have a significantly greater beneficial effect than with ADM alone for preventing recurrence after TUR of superficial bladder cancer.

Administration, Intravesical↗
PubMed1998

Up-regulation of vascular endothelial growth factor in response to glucose deprivation.

Vascular endothelial growth factor (VEGF), also known as a vascular permeability factor (VPF), is an endothelial specific mitogen and is a potent inducer of angiogenesis. Recently it has been reported that hypoxia induces VEGF mRNA expression in various cells. Since both oxygen and glucose are required for efficient production of energy, we examined the effect of glucose deprivation on VEGF mRNA expression and VEGF protein production in U-937 (a human monocytic cell line) cells. Both the mRNA expression and secretion of VEGF increased after exposure to low glucose. Addition of L-glucose, the L-stereoisomer of D-glucose, did not prevent the up-regulation of VEGF expression. The conditioned medium from glucose-deprived cells, followed by supplementation with glucose, did not up-regulate VEGF mRNA expression in U-937 cells. The low glucose-induced VEGF mRNA expression returned to the control level after supplementation with D-glucose. Furthermore, oligomycin, a mitochondrial ATP synthase inhibitor, increased VEGF protein production. The results suggest that the up-regulation of VEGF mRNA in U-937 cells in response to glucose deprivation is not mediated by autocrine factors from the cells nor is the osmotic change of the medium mediated by the deficiency of glucose metabolism in the cells. Our results also suggest that the intracellular ATP depletion due to glucose deprivation may be one of the causes for increased VEGF mRNA expression. We speculate that local hypoglycemia may act as an essential trigger for angiogenesis through the VEGF gene expression.

Adenosine Triphosphate↗
PubMed1998

Electroencephalogram abnormality and high-dose busulfan in conditioning regimens for stem cell transplantation.

High-dose busulfan (BU) is widely used in combined chemotherapy before allogeneic or autologous bone marrow transplantation. Convulsions are reported as a side-effect of high-dose BU. We recorded electroencephalograms (EEGs) before and on the third day of BU administration in 22 patients. Abnormal EEGs were observed on the third day in 13 cases (59%). These patients were older (P < 0.05) and had had larger doses of BU (P < 0.025) than the nine patients with normal EEGs. Convulsions occurred in two of the 22 patients, one of whom was receiving prophylaxis with phenytoin. Gamma aminobutyric acid (GABA), a natural mediator of defense against epileptic activity, concentrations in cerebrospinal fluid measured before and after administration of BU showed no definite changes.

Adolescent↗
PubMed1998

Physiological concentrations of 17beta-estradiol inhibit the synthesis of nitric oxide synthase in macrophages via a receptor-mediated system.

We investigated the effect of estrogen on inducible nitric oxide synthase (iNOS), which is not well understood, in contrast to the known effect of estrogen on endothelial nitric oxide synthase (eNOS). When J774 cells, a murine macrophage cell line, were incubated with interferon-gamma and lipopolysaccharide, iNOS was induced, and a large amount of NO was released. Pre- or coincubation with 17beta-estradiol inhibited this induction of iNOS protein and NO release; however, 17beta-estradiol did not have a direct effect on enzyme activity of iNOS. The analog, 17alpha-estradiol, did not have such an effect. Tamoxifen, an antiestrogen, and ICI182780, an estrogen-receptor antagonist, inhibited the influence of 17beta-estradiol on iNOS. Thus 17beta-estradiol inhibited the induction of iNOS by a classic receptor-mediated pathway. The inhibition of the NO release from iNOS by 17beta-estradiol is in contrast to the reported augmentation of continuous NO release from eNOS. These harmonious effects of estrogen on iNOS and eNOS may have some role in the antiatherosclerotic effects of 17beta-estradiol.

Animals↗
PubMed1998

Induction of macrophage VEGF in response to oxidized LDL and VEGF accumulation in human atherosclerotic lesions.

The interaction between macrophages and oxidatively modified low density lipoprotein (Ox-LDL) appears to play a central role in the development of atherosclerosis, not only through foam cell formation but also via the induction of numerous cytokines and growth factors. The current study demonstrated that Ox-LDL upregulated vascular endothelial growth factor (VEGF) mRNA expression in RAW 264 cells, a monocytic cell line, in a time- and concentration-dependent manner and that Ox-LDL stimulated VEGF protein secretion from the cells. Lysophosphatidylcholine, a component of Ox-LDL, also enhanced VEGF mRNA expression in RAW 264 cells and VEGF secretion from RAW 264 cells, with a maximal effect at a concentration of 10 micromol/L lysophosphatidylcholine. Immunohistochemical studies showed that human early atherosclerotic lesions exhibited intense VEGF immunoreactivity in subendothelial macrophage-rich regions of the thickened intima. In atherosclerotic plaques, VEGF staining was also observed in foam cell-rich regions adjacent to the lipid core or the neovascularized basal regions of plaque consisting predominantly of smooth muscle cells. High-power-field observation revealed that VEGF was localized in the extracellular space as well as at the macrophage cell surface. These observations suggest the possible involvement of Ox-LDL in the development of human atherosclerosis through VEGF induction in macrophages.

3T3 Cells↗
PubMed1998

Outcome of medically treated Stanford type B aortic dissection.

Optimal treatment for patients with uncomplicated type B dissection remains a matter of debate. From January, 1987, through June, 1996, 43 patients with acute type B dissection were treated exclusively by medical therapy according to our management guidelines. After discharge, aortography and enhanced computed tomography were performed every 6 months to evaluate the diameter of the dissected aorta. All 43 patients survived the acute phase and were discharged alive from the hospital. There was no death related to aortic dissection. Three patients underwent surgical treatment in the chronic phase because of aortic enlargement. Aortic enlargement in 3 additional patients was managed medically. The values for freedom from aortic enlargement for 43 patients at 1, 3, and 5 years were 100%, 91%, and 86%, respectively. The long-term survival rates of patients treated medically and discharged from the hospital are acceptable.

Aged↗