Biomedical subjects

M Minami

Publications and source records attributed to M Minami.

At least 361 records · Page 20Linked to original sources

PubMed1995

Transient expression of FGF receptor-4 mRNA in the rat cerebellum during postnatal development.

The fibroblast growth factor (FGF) receptor-4 mRNA in the adult rat brain is expressed preferentially in the medial habenular nucleus. In this paper, we examined the expression of FGFR-4 mRNA in the brain during postnatal development. Interestingly, in addition to the persistent expression of FGFR-4 mRNA in the medial habenular nucleus, FGFR-4 mRNA was transiently expressed in the proliferative zone of the external granule layer of the developing cerebellum. The localization and transient expression of FGFR-4 mRNA in the developing cerebellum suggest that FGFR-4 mRNA was expressed by proliferative granule cells. The present findings indicate that FGFR-4 in the brain has an important role in the postnatal development of the cerebellar cortex.

Animals↗

PubMed1995

A preliminary study on plasma concentrations of bifemelane, indeloxazine and propentofylline in aged patients with organic brain disorders.

1. Plasma concentrations of cerebral metabolic activating drugs (bifemelane, indeloxazine and propentofylline) were studied in 68 patients (male 25, female 43) with dementia or other organic brain diseases. 2. The variations in plasma concentrations of these drugs were much bigger than expected. Measurements of bifemelane level with time course also disclosed that the concentrations were relatively stable for several months, but they varied very much among patients. 3. These findings suggest that drug monitoring are important in terms of evaluation of drug efficacy and prevention of side effects.

Aged↗

PubMed1995

Endothelin-1-like immunoreactivity in cerebral cortex of Alzheimer-type dementia.

1. Endothelin-1-like immunoreactivity (ET-1-LI) in cerebral cortex in postmortem brains obtained from patients with Alzheimer-type dementia (ATD) was measured by enzyme-immunoassay. 2. The ET-1-LI in the ATD brains was significantly increased in frontal and occipital cortex than those in the control brains and a significant correlation was found between frontal and temporal lobe of ATD brains. 3. These findings may explain the clinico-radiological results that the cerebral blood flow is decreased in ATD patients, the mechanism of which is still unknown.

Aged↗

PubMed1995

Effects of piroxicam and esculetin on the MDA-MB-231 human breast cancer cell line.

We investigated the effects of piroxicam, esculetin, prostaglandin E2 (PGE2) and leukotriene B4 (LTB4) on a human breast cancer cell line (MDA-MB-231). Both piroxicam and esculetin suppressed cell growth and thymidine incorporation, though esculetin was more active in inhibiting cell growth in the presence of linoleic acid (LA). Esculetin reduced the secretion of LTB independent of LA. Piroxicam reduced the secretion of PGE in the absence of LA but only at higher concentrations in the presence of LA. When the relationship between cell growth and PGE and LTB concentration was evaluated by multivariate regression analysis, cell growth was associated with the PGE and LTB concentration when the cells were treated with esculetin alone or with esculetin and LA. Cell growth was associated only with the PGE concentration when they were treated with piroxicam alone or with piroxicam and LA. Therefore, it appears that the growth of MDA-MB-231 cells in vitro is affected by both lipoxygenase and cyclooxygenase products, though lipoxygenase inhibition is more active than cyclooxygenase inhibition on suppression of cell growth in the presence of LA.

Breast Neoplasms↗

PubMed1995

Brain natriuretic peptide as a marker for hypertensive left ventricular hypertrophy: changes during 1-year antihypertensive therapy with angiotensin-converting enzyme inhibitor.

PURPOSE: Secretion of brain natriuretic peptide (BNP), a cardiac hormone, is accelerated via hypertrophied ventricles in experimental hypertension. The present study examined whether regression of left ventricular (LV) hypertrophy by long-term treatment with an angiotensin-converting enzyme inhibitor (ACEI) affects plasma BNP concentration in patients with essential hypertension. PATIENTS AND METHODS: Thirty-one hypertensive patients with LV hypertrophy were treated with ACEI (16 with enalapril; 15 with lisinopril) for 1 year. Serial changes were recorded in LV mass index, LV systolic function, and plasma concentrations of BNP and atrial natriuretic peptide (ANP). RESULTS: ACEI therapy significantly reduced LV mass index at 6 months, and more so at 1 year. Septal and posterior wall thicknesses were also reduced. Plasma BNP and ANP were markedly elevated at study entry, but only BNP levels correlated with LV mass index. Both peptide levels declined after 6 months, and this decline was enhanced at 1 year. There was a close relation between BNP decline and LV mass index reduction overall and with enalapril and lisinopril separately. Changes in ANP and in LV mass index were not related. CONCLUSION: Long-term ACEI therapy can reduce elevated plasma BNP. In this study, changes in BNP reflected the magnitude of regression of LVH. Plasma BNP may be a useful marker for LVH during antihypertensive therapy in patients with essential hypertension and LVH.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1995

Magnetic resonance imaging of osteomyelitis in the mandible. Comparative study with other radiologic modalities.

Magnetic resonance imaging of 14 histopathologically confirmed cases of osteomyelitis of the mandible was retrospectively reviewed. The findings of magnetic resonance imaging were compared with conventional radiography, computed tomography, bone scintigraphy, and histopathologic examinations. All lesions in bone marrow were shown as areas of low (64%) or low-to-intermediate (36%) signal intensity on T1-weighted images, and areas of high (29%), mixed (high and low, 21%; high and intermediate, 36%) or low (14%) signal intensity on T2-weighted images. Histopathologically, high T2-weighted signal intensity areas that showed enhancement after contrast injection corresponded to active infection. These were not collections of pus but were predominantly areas of granulation tissue. Magnetic resonance imaging showed larger areas of abnormality than plain radiography or computed tomography. Bone scintigraphy did not accurately reveal the locations of lesions but showed heterogeneous increased uptake in all patients. MRI was an extremely useful technique for assessing osteomyelitis of the mandible.

Acute Disease↗

PubMed1995

Rice balls and bear hunts: Japanese and North American family narrative patterns.

In past research, the form of Japanese children's personal narratives was found to be distinctly different from that of English-speaking children. Despite follow-up questions that encouraged them to talk about one personal narrative at length, Japanese children spoke succinctly about collections of experiences rather than elaborating on any one experience in particular (Minami & McCabe, 1991). Conversations between mothers and children in the two cultures were examined in order partly to account for the way in which cultural narrative style is transmitted to children. Comparison of mothers from the two cultures yielded the following salient contrasts: (1) In comparison to the North American mothers, the Japanese mothers requested proportionately less description from their children. (2) Both in terms of frequency and proportion, the Japanese mothers gave less evaluation and showed more verbal attention to children than did North American mothers. (3) Japanese mothers pay verbal attention more frequently to boys than to girls. In addition, at five years, Japanese children produce 1.22 utterances per turn on average, while North American children produce 2.00 utterances per turn, a significant difference. Thus, by frequently showing verbal attention to their children's narrative contributions, Japanese mothers not only support their children's talk about the past but also make sure that it begins to take the shape of narration valued in their culture. The production of short narratives in Japan is understood and valued differently from such production in North America.

Child Language↗

PubMed1995

Transforming growth factor-alpha in human submandibular gland and saliva.

A sensitive sandwich enzyme immunoassay (EIA) for transforming growth factor-alpha (TGF-alpha) utilizing a polyclonal antibody that recognizes limited epitopes of both human TGF-alpha and rat TGF-alpha in combination with a monoclonal anti-TGF-alpha IgG1 galactosidase conjugate was developed. This assay shows no cross-reactivity with human epidermal growth factor. We can quantify the TGF-alpha level in not only human TGF-alpha (detection limit: 1 pg/ml), but also rat TGF-alpha (detection limit: 10 pg/ml) by virtue of cross-reactivity. Employing this assay system, we demonstrated that TGF-alpha is present in both human submandibular glands and submandibular/sublingual saliva.

Animals↗

PubMed1995

Expression of endogenous retroviruses, ERV3 and lambda 4-1, in synovial tissues from patients with rheumatoid arthritis.

We addressed the question of whether or not expression of human endogenous retroviruses (ERV), ERV3 and lambda 4-1, is related to the pathogenesis of rheumatoid arthritis (RA). In genomic Southern hybridization, there were no significant differences between RA patients and healthy volunteers with regard to frequencies of restriction fragment length polymorphism (RFLP) patterns, for either ERV3 or lambda 4-1. By Northern blot analysis using fresh synovial tissues, cultured synovial cells, and peripheral blood mononuclear cells (PBMC) from patients with RA, we noted two molecular species of ERV3 mRNAs of 3.5 kb and 9.0 kb sizes, and one single molecular species of lambda 4-1 mRNAs of 4.2 kb size. The expression was detected not only in RA patients but also in synovial cells from osteoarthritis (OA) as a non-RA control and PBMC from healthy volunteers, and was not related to RA activities or treatments. Although ERV3 and lambda 4-1 expression may not be directly associated with the pathogenic pathway of RA, the possibility exists that human ERV may have a causative role in autoimmune diseases, including RA. We also examined the effect of cytokines on the transcriptional regulation of ERV3. Although the level of ERV3 expression in cultured synovial cells did not change with IL-1 beta treatment, the level for cultured proximal tubular epithelial cells (hKEC) was up-regulated.

Arthritis, Rheumatoid↗

PubMed1995

Elevated glucose concentration and natriuretic peptides receptor response on vascular smooth muscle of spontaneously hypertensive rats.

1. Hyperglycaemia is believed to be a major cause of diabetic vascular complications such as accelerated atherosclerosis. In order to elucidate the effect of hyperglycaemia on vascular response in spontaneously hypertensive rats (SHR), the natriuretic peptides receptor responses to vascular smooth muscle cells (VSMC) which are thought to suppress atherosclerosis were studied under high glucose (HG:22.2 mmol/L) conditions. 2. The total number of cells in SHR is higher and natriuretic peptides receptor response is smaller than that of cells in the Wistar-Kyoto (WKY) rat. Membrane bound protein kinase C (PKC) activity in HG or SHR is higher compared to that of cells in normal glucose (NG:5.6 mmol/L) or WKY. Cells cultured in HG for at least 2 passages had higher total cell number and receptor mediated cGMP formation were suppressed compared to cells cultured in NG both in SHR and WKY. Specific PKC inhibitor PKC (19-36) 1 mu mol/L prevented HG induced suppression of natriuretic peptides response. 3. These results show that hyperglycaemia may be linked to suppressed natriuretic peptides receptor response which is caused by increased PKC activity both in WKY and SHR. This suppressed response may cause the accelerated atherosclerosis by hyperglycaemia.

Animals↗

PubMed1995

Enhanced phosphoinositide turnover signalling stimulated by endothelin B-type receptor in endothelial cells from spontaneously hypertensive rats.

1. Endothelin (ET) B-type (ETB) receptor-mediated signal transduction was examined after stimulation with ET-3 in cultured aortic endothelial cells (EC) from spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) rats (8 weeks old). 2. The EC from both rat strains expressed only ETB receptor mRNA. The receptor densities and affinities, which were non-selective for ET-1, -2, -3 and Sarafotoxin S6c, and mRNA expression were similar in WKY and SHR. 3. The cytosolic Ca2+ level in the absence of extracellular Ca2+, inositol 1,4,5-trisphosphate levels, protein kinase C and phospholipase C activities in response to ET-3 were greater in SHR EC than in WKY EC. 4. The 45Ca uptake in response to ET-3, which was blocked by Ni2+, was smaller in SHR EC than in WKY EC. 5. The 6-keto-PGF1alpha production was augmented in SHR, though nitric oxide formation after stimulation with ET-3 was similar. 6. These results suggest that ETB receptor-mediated phosphoinositide turnover signalling is augmented in SHR EC through postreceptor mechanism.

6-Ketoprostaglandin F1 alpha↗

PubMed1995

Effect of thrombin and PDGF on endothelin production in cultured mesangial cells derived from spontaneously hypertensive rats.

1. Basal endothelin-1 (ET-1) production in mesangial cells of spontaneously hypertensive rats (SHR) was not different from that of Wistar-Kyoto (WKY) rats, although a trend toward increased ET-1 production was observed in these cells of SHR. 2. Thrombin and platelet-derived growth factor (PDGF) stimulated ET-1 production in a concentration-dependent manner in these cells of both rat strains, but thrombin- and PDGF-induced stimulation of ET-1 production were clearly greater in cells of SHR than WKY rats. 3. The protein kinase C (PKC)-activating phorbol ester, phorbol myristate acetate, stimulated ET-1 production in cells of both rat strains, but this stimulation was significantly greater in cells of SHR than in cells of WKY rats. 4. An inactive enantiomer of phorbol ester, 4alpha-PDD, had no effect on the ET-1 production in these cells of both rat strains. 5. Neither thrombin nor PDGF stimulated ET-1 production in PKC-depleted cells of both rat strains.

Animals↗

PubMed1995

Animal models of vascular dementia with emphasis on stroke-prone spontaneously hypertensive rats.

1. Two experimental models designed to reflect different aspects of vascular dementia (rats with cerebrovascular occlusion and rats with cerebral embolization) and stroke-prone spontaneously hypertensive rats (SHRSP) have been evaluated. The focus was on SHRSP as a model for vascular dementia. 2. Neuropathological data revealed that the cerebrovascular disorder in SHRSP was associated with lesions in their brains similar to those seen in typical human cases of multiple cerebral infarction. 3. SHRSP that died from cerebral infarction exhibited behavioural changes, including increased activity and disrupted circadian rhythms, which might correspond to the state of delirium observed in patients with dementia. 4. SHRSP displayed cognitive impairments in a step-through passive avoidance task. 5. When compared to age-matched Wistar Kyoto (WKY) rats, both conscious and anaesthetized SHRSP had significantly decreased cerebral spinal fluid (CSF) levels of acetylcholine (ACh). 6. These findings suggest that the SHRSP might serve as a suitable animal model for vascular dementia in humans caused by cerebrovascular lesions.

Animals↗

PubMed1995

Dietary docosahexaenoic acid (22: 6n-3) prevents the development of hypertension in SHRSP.

1. We previously reported that hypertension in stroke-prone spontaneously hypertensive rats (SHRSP) caused renal membrane phospholipid degradation. Renal phospholipase A2 activity increased and membranous phospholipids decreased along with age in SHRSP. Membranous abnormalities induced by membrane fluidity and calcium permeability changes may contribute to the elevation of blood pressure in SHRSP. DHA, a major component of fish oil, constitutes a part of membrane phospholipid acylchains. 2. The purpose of this study was to clarify the effect of DHA on the relationship between the renal function and the development of hypertension in SHRSP. 3. Six week old male SHRSP were fed a semi-purified diet supplemented with DHA (0, 1 and 5%) for 14 weeks. 4. The systolic blood pressure of control SHRSP (DHA 0%) significantly increased from 120.2 mmHg to 202.9 mmHg. This increase in systolic blood pressure was significantly inhibited in a dose-dependent manner by 1 and 5% DHA diet to 167.8 to 149.8 mmHg, respectively. 5. Serum creatinine concentration and blood urea nitrogen (BUN) were significantly lower in DHA (5%)-treated SHRSP than in the control SHRSP. 6. These results indicate that DHA prevents the development of hypertension in SHRSP, which is associated with changes in renal function.

Animals↗

PubMed1995

Role of an endogenous monoamine oxidase inhibitor, isatin, in SHRSP brain.

1. The acute effects of isatin, an endogenous monoamine oxidase (MAO) inhibitor, on norepinephrine (NE) and serotonin (5-HT) concentrations in the brain of stroke-prone spontaneously hypertensive rats (SHRSP) and Wistar-Kyoto rats (WKY) were determined in order to elucidate its pathophysiological role. 2. Isatin was identified in purified extracts of SHRSP brain. 3. A single dose of isatin significantly increased NE concentration in the cerebral cortex of WKY. Isatin also significantly increased 5-HT concentration in WKY brains. 4. After isatin administration NE and 5-HT levels in the SHRSP brain did not differ from those in WKY. 5. These data suggest that isatin, an endogenous MAO inhibitor, presents in the SHRSP brain and maintains high blood pressure.

Animals↗

PubMed1995

Suppression of naloxone-precipitated withdrawal jumps in morphine-dependent mice by stimulation of prostaglandin EP3 receptor.

1. We have shown that intracisternal (i.c.) administration of interleukin-1 beta (IL-1 beta) attenuates naloxone-precipitated withdrawal jumps in morphine-dependent mice, and the effect was partly mediated by the corticotropin-releasing factor. To elucidate further other possible mechanisms involved in the inhibitory effect of IL-1 beta on morphine withdrawal jumping behaviour, in this study, we examined the involvement of the prostaglandin-synthesis pathway, because prostaglandins have been shown to mediate the several central effects of IL-1. Furthermore, we examined the effects of subtype-selective prostaglandin receptor agonists on morphine withdrawal jumping behaviour. 2. Mice were rendered morphine-dependent by subcutaneous implantation of a pellet containing 11.5 +/- 0.3 mg morphine hydrochloride for 48 h. Morphine withdrawal syndromes were precipitated by intraperitoneal (i.p.) injection of naloxone (10 mg kg-1). The degree of physical dependence on morphine was estimated by counting the number of jumps, one of the typical withdrawal signs in mice, for 40 min. 3. The inhibitory effect of IL-1 beta (1 ng/mouse) administered intracisternally 30 min before naloxone (10 mg kg-1, i.p.) was significantly blocked by pretreatment with sodium salicylate (a cyclo-oxygenase inhibitor, 10 ng or 30 ng/mouse) administered intracisternally 15 min before IL-1 beta, while i.c. administration of sodium salicylate alone (3 ng, 10 ng or 30 ng/mouse) followed by i.c. administration of vehicle instead of IL-1 beta did not significantly change the number of jumps precipitated by naloxone. 4. Intracisternal administration of M&B28,767 (an EP3-receptor agonist, 1 fg-30 ng/mouse) and sulprostone (an EP1/EP3-receptor agonist, 10 fg-100 ng/mouse) 30 min before naloxone (10 mg kg,-1 i.p.) attenuated withdrawal jumps with a U-shaped dose-response, reaching a peak at 10 pg/mouse and 100 pg/mouse, respectively. On the other hand, i.c. administration of iloprost (an EP1/IP-receptor agonist, 10 fg-100 ng/mouse), butaprost (an EP2-receptor agonist, 10 fg-100 ng/mouse) or prostaglandin F2 alpha (a FP-receptor agonist, 10 fg-100 ng/mouse) 30 min before naloxone (10 mg kg-1, i.p.) did not significantly change the number of jumps precipitated by naloxone. 5. These results indicate that the prostaglandin-synthesis pathway is, at least in part, involved in the inhibitory effect of IL-1 beta on naloxone-precipitated withdrawal jumps in morphine-dependent mice, and that the prostaglandin synthesized in the brain suppresses the morphine withdrawal jumping behaviour via the EP3-receptor, but not via the EP1-, EP2-, IP- or FP-receptor.

Alprostadil↗

PubMed1995

Effects of BMY21190, an inhibitor of cAMP phosphodiesterase, on infarct size and myeloperoxidase activity in the ischemic myocardium of a canine occlusion-reperfusion model.

This study was performed to assess the effect of BMY21190, an inhibitor of cAMP phosphodiesterase, on infarct size using a canine ischemic model that underwent a 90-min occlusion and a 6-hour reperfusion of the left coronary artery. The infarct zone/area at risk of the BMY21190 group was significantly smaller than that of the vehicle group (36.1 +/- 7.8%; 62.4 +/- 4.3%, respectively; p < 0.05). Myeloperoxidase activity, an indicator of neutrophil infiltration, was significantly correlated to infarct size (r = 0.6893, p < 0.02). Myeloperoxidase activity (0.14 +/- 0.07 U/100 mg tissues) measured in the area at risk from hearts of the BMY21190-treated group was significantly lower than that of the vehicle-treated tissue (0.40 +/- 0.08 U/100 mg tissue, p < 0.05). It is suggested that BMY21190 reduces infarct size through the inhibition of neutrophil infiltration in the canine model.

3',5'-Cyclic-AMP Phosphodiesterases↗

PubMed1995

Adrenomedullin as a novel antimigration factor of vascular smooth muscle cells.

The present study investigated the effect of adrenomedullin, a novel vasorelaxant peptide, on the migration of cultured rat vascular smooth muscle cells (SMCs) by using the Boyden-chamber method. Fetal calf serum (FCS) and platelet-derived growth factor (PDGF)-BB strongly stimulated SMC migration. Adrenomedullin clearly inhibited SMC migration stimulated with 5% and 10% FCS in a concentration-dependent manner. The migration induced by 10 and 25 ng/mL PDGF-BB was also inhibited by adrenomedullin in a concentration-dependent manner. Inhibition by adrenomedullin of FCS- and PDGF-induced SMC migration was paralleled by an increase in the cellular level of cAMP. In fact, the percent increase in cAMP level was strongly correlated with the percent decrease in migration activity of SMCs after treatment with adrenomedullin. 8-Bromo cAMP, a cAMP analogue, reproduced the inhibition by adrenomedullin of FCS- and PDGF-induced SMC migration. An activator of adenylate cyclase, forskolin, also reduced FCS- and PDGF-induced SMC migration. These data indicate that adrenomedullin inhibits the migration of SMCs stimulated with FCS and PDGF, probably through a cAMP-dependent process. On the basis of these results and the finding that adrenomedullin is synthesized in and secreted from vascular endothelial cells, adrenomedullin may play a role as a local antimigration factor in some pathophysiological states.

Adrenomedullin↗