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Biomedical subjects

Y Mochizuki

Publications and source records attributed to Y Mochizuki.

At least 91 records · Page 5Linked to original sources
PubMed1999

Pharbin, a novel inositol polyphosphate 5-phosphatase, induces dendritic appearances in fibroblasts.

We have cloned a cDNA encoding a novel protein pharbin with a homology to inositol polyphosphate 5-phosphatases. Pharbin contains relatively well-conserved catalytic motifs for 5-phosphatase, a proline-rich sequence corresponding to the SH3-binding motif, and a sequence consistent with the CaaX motif at the C-terminus. COS-7 cells transfected with pharbin exhibited elevated hydrolytic activity on the 5-phosphate group of inositol 1,4,5-trisphosphate, inositol 1,3,4,5-tetrakisphosphate, and phosphatidylinositol 4, 5-bisphosphate. Thus, pharbin indeed serves as an inositol polyphosphate 5-phosphatase. When pharbin was transfected to C3H/10T1/2 fibroblasts, it was located to the plasma membrane-associated structures including membrane ruffles. The cells were converted to dendritic forms within 24 h. The protein with deleted or point-mutated CaaX motif hardly induced the dendritic forms but remained associated with the membranes. These results imply that the CaaX motif is required for the morphological alteration but that some other structural element is likely to also be responsible for the membrane localization.

Amino Acid Sequence↗
PubMed1999

Cerebrovascular acetazolamide reactivity and platelet function in asymptomatic cerebral thrombosis.

In order to find out the relationship between the cerebrovascular acetazolamide reactivity and platelet function in asymptomatic cerebral thrombosis, 10 cases of asymptomatic cerebral infarction and 10 age-matched control subjects were studied. The cerebrovascular acetazolamide reactivity was measured using xenon computed tomography method. As markers of platelet function, the plasma concentrations of platelet factor 4, beta-thromboglobulin, thromboxane B2, and 11-dehydrothromboxane B2 were determined. The cerebrovascular acetazolamide reactivity was significantly lower in the asymptomatic cerebral infarction group than in the control group. The plasma concentrations of platelet factor 4, beta-thromboglobulin, thromboxane B2, and 11-dehydrothromboxane B2 were higher in the asymptomatic cerebral infarction group than in the control group. There was a significant negative correlation between the cerebrovascular acetazolamide reactivity and the plasma concentrations of platelet factor 4, beta-thromboglobulin, thromboxane B2, and 11-dehydrothromboxane B2. The low cerebrovascular acetazolamide reactivity is considered to be related to platelet activation in asymptomatic cerebral thrombosis.

Acetazolamide↗
PubMed1999

Differences in regional cerebral blood flow in two types of leuko-araiosis.

Cerebral blood flow and cerebrovascular acetazolamide reactivity were investigated in patients with periventricular hyperintensity and in patients with leuko-araiosis in centrum semiovale. Fifteen patients with periventricular hyperintensity, 15 patients with leuko-araiosis in centrum semiovale and 15 age-matched controls without leuko-araiosis were studied. The regional cerebral blood flow was measured using the stable xenon CT method before and 20 min after intravenous injection of 17 mg/kg acetazolamide. The blood flow and the cerebrovascular acetazolamide reactivity in the area of leuko-araiosis were significantly lower in the periventricular hyperintensity group and the leuko-araiosis in centrum semiovale group than the control group. The blood flow in the cerebral cortex was significantly lower in the leuko-araiosis in centrum semiovale group than in the periventricular hyperintensity group and the control group. The cerebrovascular acetazolamide reactivity in the cerebral cortex did not show any significant difference among the three groups. The blood flow in the cerebral cortex was decreased in patients with leuko-araiosis in centrum semiovale but the cerebrovascular acetazolamide reactivity in the cerebral cortex was normal in patients with leuko-araiosis.

Acetazolamide↗
PubMed1999

Corpus callosum atrophy and cerebral blood flow in chronic alcoholics.

The corpus callosum atrophy and cerebral blood flows were investigated in chronic alcoholics without Marchiafava-Bignami disease. Fifteen cases of chronic alcoholics and 15 age-matched healthy controls were studied. The sagittal plane of magnetic resonance imaging of the head was scanned into a computer and the corpus callosum was measured and the callosal index was calculated. Cerebral blood flows were measured using stable xenon computed tomography (CT) method. Regional cerebral blood flows in the frontal, temporal, parietal and occipital cortex, frontal, temporal and occipital white matter, caudate nucleus, putamen and thalamus were measured. The corpus callosum area, the thickness of the genu, the thickness of the trunk, the thickness of the splenium, and the callosal index were significantly smaller in the chronic alcoholic group than in the healthy control group. Blood flows in the cerebral cortex, thalamus and putamen were significantly lower in the chronic alcoholic group than in the healthy control group. Significant positive correlations were present between the corpus callosum atrophy and the cerebral cortex blood flows. Corpus callosum atrophy and decreased cerebral blood flows may be seen in chronic alcoholics without Marchiafava-Bignami disease.

Alcoholism↗
PubMed1999

Reconstruction of hepatic organoid by rat small hepatocytes and hepatic nonparenchymal cells.

Hepatic cells isolated from an adult rat liver, consisting of small hepatocytes (SHs), mature hepatocytes (MHs), liver epithelial cells (LECs), Kupffer cells, sinusoidal endothelial cells, and stellate cells, were cultured in a medium supplemented with 10% fetal bovine serum, 10 mmol/L nicotinamide, 1 mmol/L ascorbic acid 2-phosphate, 10 ng/mL epidermal growth factor, and 1% dimethyl sulfoxide. The SHs rapidly proliferated and formed a colony. About 10% of cytokeratin 8 (CK8)-positive cells formed SH colonies. All SHs at day 10 immunocytochemically showed positivity for albumin, transferrin, CK8, and CK18, which are markers for hepatocytes. In contrast, alpha-fetoprotein (AFP)-, CK14-, OC2-, and glutathione S-transferase placental type (GST-P)-positive cells, which are thought to be markers for hepatic immature cells, were rarely observed. At day 20 some cells in the colonies were positive for AFP, CK7, CK19, and GST-P. LECs and stellate cells proliferated and surrounded the colonies. About 2 weeks after plating, piled up cells were often observed on the SH colonies. In those colonies LECs and stellate cells invaded under the colonies. The invasion of the cells and gradual deposits of extracellular matrix (ECM) such as type I collagen, type IV collagen, and laminin induced alteration of the shape of the SHs from relatively flat to cuboidal or rectangular. With the cellular structural changes, the expression of albumin, connexin 32 (Cx32), and tryptophan 2,3-dioxygenase (TO) messenger RNAs increased. In addition, overlapping nonparenchymal cells (NPCs) on the piled up cells induced the formation of duct- or cyst-like structures consisting of MHs. In the present experiment we showed that SHs could differentiate to MHs by interacting with NPCs and ECM. Thus, SHs may be "committed progenitor cells" that can further differentiate into MHs.

Animals↗
PubMed1999

Beneficial effect of basic fibroblast growth factor on the repair of full-thickness defects in rabbit articular cartilage.

The effects of exogenous basic fibroblast growth factor (bFGF) on the repair of full-thickness cartilage defects were examined. Four-millimeter diameter, cylindrical defects were made in rabbit articular cartilage and were filled with human recombinant bFGF. The addition of bFGF to the defect induced the formation of a thick cartilage layer composed of chondrocytes and a metachromatic-stained matrix after 6 weeks. The score of the bFGF-treated tissue, as evaluated by a semiquantitative histological scale, was significantly higher than that of the untreated tissue. At 24 weeks, the cartilage-like matrix that contained the proteoglycans and type II collagen was thicker in the bFGF-treated tissue than in the untreated tissue. Immunohistochemical analysis of the tissues at 6-12 weeks with an anti-bFGF monoclonal antibody suggested that a single application of bFGF increased the number of differentiating chondrocytes that synthesized bFGF at a high level. In contrast, immunostaining of the tissues at 6-12 weeks with a monoclonal antibody against proliferating cell nuclear antigen showed that the number of proliferating cells in the bFGF-treated tissue was fewer than in the untreated tissue. These findings suggest that administration of bFGF into cartilagenous defects promotes the differentiation of chondrocytes and their matrix synthesis, and that this growth factor is useful for improving cartilage repair.

Animals↗
PubMed1999

Healing of the intimal dissection of the internal thoracic artery graft.

We report healing of the intimal dissection of an internal thoracic artery graft. Triple coronary artery bypass grafting was performed using left internal thoracic artery and saphenous vein grafts. One month after operation, the intimal dissection of the internal thoracic artery graft was clearly visible by coronary angiography; however, after 1 year of only medical treatment consisting of warfarin, ticlopidine, and nitrate, the intimal dissection was undetectable by coronary angiography.

Aged↗
PubMed1999

Iodine-impregnated drapes enable recording of precordial electrocardiogram.

Although we believed that the use of a polyester film drape for primary elective open sternum with delayed sternal closure made it impossible to record precordial electrocardiograms on the drape, we confirmed that it is possible to record electrocardiograms on an iodine-impregnated drape due to the iodine anion electrical conductibility.

Electric Conductivity↗
PubMed1999

Transient myocardial dysfunction associated with angiotensin-converting enzyme inhibitor-induced angioedema: recognition by serial echocardiographic studies.

We report a case of a 58-year-old woman who had angiotensin converting enzyme inhibitor-induced angioedema after she underwent a biopsy of a hypopharyngeal mass. The angioedema was associated with severe transient myocardial dysfunction documented on echocardiography. She did not have anaphylaxis or coronary artery disease. To our knowledge this is the first reported case of transient myocardial dysfunction in the setting of angiotensin converting enzyme inhibitor-induced angioedema without anaphylaxis.

Angioedema↗
PubMed1999

Significant role of neuronal non-N-type calcium channels in the sympathetic neurogenic contraction of rat mesenteric artery.

1. The possible involvement of pre-junctional non-N-type Ca2+ channels in noradrenaline (NA)-mediated neurogenic contraction by electrical field stimulation (EFS) was examined pharmacomechanically in the isolated rat mesenteric artery. 2. EFS-generated contraction of endothelium-denuded mesenteric artery was frequency-dependent (2 - 32 Hz) and was abolished by tetrodotoxin (TTX, 1 microM), guanethidine (5 microM) or prazosin (100 nM), indicating that NA released from sympathetic nerve endings mediates the contractile response. 3. NA-mediated neurogenic contractions to lower frequency stimulations (2 - 8 Hz) were almost abolished by an N-type Ca2+ channel blocker, omega-conotoxin-GVIA (1 microM) whereas the responses to higher frequency stimulations (12 - 32 Hz) were less sensitive to omega-conotoxin-GVIA. The omega-conotoxin-GVIA-resistant component of the contractile response to 32 Hz stimulation was inhibited partly (10 - 20%) by omega-agatoxin-IVA (10 - 100 nM; concentrations which are relatively selective for P-type channels) and to a greater extent by omega-agatoxin-IVA (1 microM) and omega-conotoxin-MVIIC (3 microM), both of which block Q-type channels at the concentrations used. 4. omega-Agatoxin-IVA (10 - 100 nM) alone inhibited 32 Hz EFS-induced contraction by 10 approximately 20% whereas omega-conotoxin-MVIIC (3 microM) alone inhibited the response by approximately 60%. 5. These omega-toxin treatments did not affect the contractions evoked by exogenously applied NA. 6. These findings show that P- and Q-type as well as N-type Ca2+ channels are involved in the sympathetic neurogenic vascular contraction, and suggest the significant role of non-N-type Ca2+ channels in NA release from adrenergic nerve endings when higher frequency stimulations are applied to the nerve.

Animals↗
PubMed1999

Central motor conduction time in Parkinson's disease.

Central motor conduction time (CMCT) was analysed in 11 patients with Parkinson's disease and 10 age matched healthy controls. CMCT was measured during muscle relaxation, muscle contraction and in patients with Parkinson's disease before and 1 h after intravenous infusion of L-dopa (0.25%, 20 ml). Although the CMCT during muscle contraction did not differ significantly between Parkinson's disease and healthy controls, the CMCT during muscle relaxation was significantly shorter in Parkinson's disease than in healthy controls. The CMCT during muscle relaxation in Parkinson's disease was significantly longer after intravenous infusion of L-dopa than before, but the CMCT during muscle contraction did not differ significantly before and after intravenous infusion of L-dopa. The CMCT during muscle contraction was significantly shorter than the CMCT during muscle relaxation in healthy controls. However, in Parkinson's disease, the CMCT did not differ significantly between muscle relaxation and contraction. We consider that the central motor conduction pathway during muscle relaxation in Parkinson's disease is modified to be similar to that during muscle contraction in healthy subjects. Copyright 1999 Harcourt Publishers Ltd.

Journal Article↗
PubMed1999

Regional differences in cerebrovascular reactivity to acetazolamide in Alzheimer's disease.

The cerebral blood flow and cerebrovascular reactivity to acetazolamide were investigated in Alzheimer's disease using stable xenon computed tomography (CT). Ten patients with Alzheimer's disease and 10 healthy controls were studied. The regional cerebral blood flow was measured using the xenon delivery and analysis system (AZ-7000 model, Anzai Sogyo, Tokyo, Japan) and CT (PreSage, Yokogawa Medical Systems, Tokyo, Japan). The subjects inhaled room air followed by a mixture of 30% xenon and 50% oxygen for 3 min. Serial scanning was performed once before xenon inhalation, three times in the wash-in process and five times in the washout process of 5 min. The xenon concentration in the end-tidal expired gas was recorded continuously by the thermoconductivity method. The regional cerebral blood flow was measured before and 20 min after i.v. injection of 17 mg/kg acetazolamide. The blood flows in the frontal lobe, parietal lobe and temporal lobe were reduced but the blood flows in the caudate nucleus, putamen and thalamus were normal in the Alzheimer's disease group. The cerebrovascular reactivity to acetazolamide was reduced in the frontal, parietal and temporal cortex but was normal in the other areas. There is a regional difference in the cerebral blood flow and the cerebrovascular reactivity to acetazolamide in Alzheimer's disease Copyright 1999 Harcourt Publishers Ltd.

Journal Article↗
PubMed1999

Effects of nicotinamide-related agents on the growth of primary rat hepatocytes and formation of small hepatocyte colonies.

AIMS/BACKGROUND: We report in this study that, 10 mM nicotinamide can stimulate the proliferation of primary rat hepatocytes in serum-free Dulbecco's modified Eagle's medium supplemented with 10 ng/ml epidermal growth factor and that small hepatocyte colonies appear from 4 to 5 days after plating. We examined the effects of nicotinamide-related agents on the growth and differentiation of primary rat hepatocytes and on the appearance of small hepatocyte colonies. METHODS: As nicotinamide is an aqueous vitamin named niacin and known to act as an inhibitor of poly (ADP-ribose) polymerase (PARP), we therefore chose to examine the effects on hepatocytes of three nicotinamide-related agents, nicotinic acid (NA) which is also a niacin, 3-aminobenzamide (3-AB) which is a strong inhibitor of PARP but is not a niacin, and 3-acetylpyridine (3-AP) which is a weak inhibitor of PARP and also not a niacin. To examine their effects on the growth of the cells and on the formation of the colony, immunocytochemistry for BrdU was carried out. Expression of albumin, tryptophan 2,3-dioxygenase (TO), and connexin 32 (Cx32) mRNAs were used as marks of hepatic differentiation. Intracellular NAD+ content was also measured. RESULTS: At concentration of 10 mM, NA could not enhance the proliferation of mature hepatocytes but induced the appearance of small hepatocyte colonies. At concentration of 5 mM, 3-AB enhanced the proliferation of the hepatocytes but did not induce small hepatocyte colonies. On the other hand, although 10 mM 3-AP remarkably inhibited the DNA synthesis of the cells, the expression not only of albumin but also of TO and Cx32 mRNAs in the cells was well maintained for more than one week. The intracellular NAD+ concentration was correlated with the proliferation of the hepatocytes. CONCLUSION: These results suggest that the intracellular NAD+ content may be correlated with the proliferation of primary hepatocytes and that the supplementation of niacin in the medium may be important for the appearance of small hepatocyte colonies.

Albumins↗
PubMed1999

Frontal lobe atrophy and central motor conduction time in chronic alcoholics.

The central motor conduction time (CMCT) was investigated in 12 cases of chronic alcoholism with frontal lobe atrophy, 12 cases of chronic alcoholism without frontal lobe atrophy, and 12 age-matched healthy controls. The CMCT was significantly prolonged in the chronic alcoholics with frontal lobe atrophy as compared to the chronic alcoholics without frontal lobe atrophy and the healthy controls. A significant positive correlation was noted between the CMCT and the degree of frontal lobe atrophy. The CMCT may be prolonged in chronic alcoholics with frontal lobe atrophy.

Alcoholism↗
PubMed1999

Disruption of circumferential actin filament causes disappearance of occludin from the cell borders of rat hepatocytes in primary culture without distinct changes of tight junction strands.

We investigated the relationship of actin filament organization to occludin and tight junction strands in primary cultured rat hepatocytes using an actin depolymerizing agent, mycalolide B. In control cultures, well-developed circumferential actin filaments and occludin immunoreactivity were observed on the most subapical plasma membrane of the cells, and tight junction strands formed well-developed networks in freeze-fracture replicas. In hepatocytes treated with 3 microM mycalolide B for 6 h, circumferential actin filaments and occludin immunoreactivity disappeared from the cell borders. However, there were no marked abnormalities of tight junction strands in freeze fracture replicas. Similar results were obtained from cells cultured in medium with 0.05 mM Ca2+ for 6 h. The close association of occludin with actin and the existence of intact tight junction strands that are virtually free of both occludin and actin suggest a physiological role of occludin, but not the other proteins forming the tight junction strands, in the linkage between actin cytoskeleton and tight junction.

Actins↗
PubMed1999

TPA induced expression and function of human connexin 26 by post-translational mechanisms in stably transfected neuroblastoma cells.

Connexin 26 (Cx26) has been proposed to be a tumor suppressor gene and its expression may modulate development, cell growth and differentiation in various tissues, including the brain. 12-O-tetradecanoylphorbol-13-acetate (TPA) may serve as either tumor promoter (in mammary gland amd skin) or as a differentiating agent (in neuroblastoma and leukemic cells) and may also modulate expression, function and phosphorylation of gap junctions. In this study, to determine the effects of TPA on Cx26 expression and its function in neuroblastoma, we transfected N2A mouse neuroblastoma cells (which are gap junction deficient) with the coding region of human Cx26 gene (which lacks TPA response elements) and examined the changes of expression and function of Cx26 following 10 nM TPA treatment. Individual clones of transfectants stably expressed distinct levels of exogenous Cx26 as judged by Northern and Western blots, immunocytochemistry and electrophysiological recordings. Cx26 channels displayed unitary conductances of about 140-155 pS. Increase of Cx26 expression following TPA treatment was markedly observed using immunocytochemistry and Western blots of membrane fractions although it was not detected in Northern or Western blots of whole cells. This increase in Cx26 expression in the plasma membrane was accompanied by an increase of function as evidenced in measurements of junctional conductance. These results suggest that induction of exogenous Cx26 in neuroblastoma cells by TPA treatment is controlled by post-translational mechanisms.

Animals↗