Three-dimensional imaging of the temporal bone using helical CT in cochlear implant patients.
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Cochlear Implants↗
Biomedical subjects
M Sakata
Publications and source records attributed to M Sakata.
Uptake of Cd-metallothionein into LLC-PK1 cells: a comparative study with CdCl2.
The uptake of the Cd-metallothionein complex (CdMT) into LLC-PK1 cells was investigated and compared with that of CdCl2. The cells were incubated at 37 degrees C for up to 45 min with 1 microM Cd, as either CdMT or CdCl2 at pH 5.5, 6.4, or 7.4. Under all the experimental conditions described below, the accumulation of Cd from CdMT was markedly lower than that from CdCl2. Cd accumulation at pH 7.4 from CdMT increased linearly with the time of incubation, whereas Cd accumulation from CdCl2 was saturable. Metabolic inhibitors, 2,4-dinitrophenol (DNP) and carbonylcyanide p-(trifluoromethoxy)-phenylhydrazone (FCCP), and incubation at low temperature significantly decreased Cd accumulation from both Cd compounds. Coincubation with 30 microM ZnCl2, an antagonist of CdCl2 uptake, slightly decreased Cd accumulation from CdMT, but it markedly decreased that from CdCl2. Cd accumulation from CdMT at pH 5.5 was significantly higher than at pH 6.4 or 7.4, whereas Cd accumulation from CdCl2 at pH 5.5 and 6.4 was significantly lower than at pH 7.4. Although Cd accumulation from CdCl2 at pH 7.4 was significantly decreased by coincubation with 100 microM cysteine or glutathione (GSH), this decrease was not observed at pH 5.5 or 6.4. A small amount of Cd was removed, by the chelating agent EGTA, from the cell membranes after incubation with CdMT at pH 6.4 and 7.4, whereas a considerable amount of Cd was removed by EGTA after incubation with CdMT at pH 5.5 and with CdCl2 at three pHs. It appears that the CdMT complex is taken up into LLC-PK1 cells partially via an energy-dependent process, and the increase in Cd accumulation at low pH is due to the liberation of Cd. High stability and molecular size of the CdMT complex explains why it is not taken up readily into LLC-PK1 cells.
Animals↗
[Clomiphene challenge test].
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Clomiphene↗
[Surgical treatment of aortic dissection (Stanford type A) using hypothermic retrograde cerebral perfusion in patients older than 70 years of age].
Since 1991, 27 consecutive patients with aortic dissection (Stanford A) have been operated on using deep hypothermic retrograde cerebral perfusion (RCP). There were no differences in ECC time (247 +/- 15 vs 307 +/- 22 min), and RCP time (47 +/- 2 vs 47 +/- 3 min) between the aged (> or = 70 y.o., n = 11) and non-aged (< 70 y.o., n = 16) group. Although the aged group showed the higher incidences of postoperative neurological complications of prolonged emergence (2 cases) and delirium (3 cases), respiratory disorder (3 cases), and renal dysfunction (3 cases), there was no significant difference in hospital mortality (18% in the aged vs 13% in the non-aged). We concluded that RCP is well acceptable procedure for surgical treatment of the aged patients with aortic dissection.
Age Factors↗
[A case of hemodialysis-associated innominate vein stenosis inducing superior vena cava syndrome].
Twenty years after making an arteriovenous shunt in the left arm, a 45-year-old man on hemodialysis developed progressive swelling in the face to left arm and venous dilatation on the left anterior chest. Venogram disclosed severe stenosis of the left innominate vein at the junction of the superior vena cava, which was considered to be a primary lesion because he had no history of subclavian vein cannulation or mediastinal disease. Surgical resection of the stenotic lesion and direct anastomosis of the innominate vein resulted in a rapid recovery of the symptom of venous hypertension. This is a rare case of hemodialysis-associated large vein complication leading to superior vena cava syndrome.
Arteriovenous Shunt, Surgical↗
Tissue distribution of DDVP after fatal ingestion.
Tissue distribution of dichlorvos (DDVP) was determined in a case of fatal ingestion using a rapid and simple gas chromatographic (GC) assay. Remarkable autopsy findings were congestion of the lung and kidneys and bleeding ulcer extending from the dorsum of the tongue to the upper pharynx. The serum cholinesterase activity was 2 IU/1, however, miosis was not observed. In the stomach, 250 ml of volatile fluid was found. Tissue distribution of DDVP was determined using a newly developed simple and rapid GC method. DDVP was found in the spleen and heart at higher concentrations (3340 and 815 micrograms/g, respectively), and also detected in the urine at the lowest level (4.5 micrograms/ml). The DDVP concentrations in blood, brain, lung, kidney and liver were 29, 9.7, 81, 80 and 20 micrograms/ml or g, respectively.
Administration, Oral↗
Inhibition of catalase activity in vitro by diesel exhaust particles.
The effect of diesel exhaust particles (DEP) on the activity of catalase, an intracellular antioxidant, was investigated because H2O2 is a cytotoxic oxidant, and catalase released from alveolar cells is an important antioxidant in the epithelial lining fluid in the lung. DEP inhibited the activity of bovine liver catalase dose-dependently, to 25-30% of its original value. The inhibition of catalase by DEP was observed only in the presence of anions such as Cl-,Br-, or thiocyanate. Other anions, such as CH3COO- or SO4-, and cations such as K+, Na+, Mg2+, or Fe2+, did not affect the activity of catalase, even in the presence of DEP extract. Catalase from guinea pig alveolar cells and catalase from red blood cells were also inhibited by DEP extracts, as was catalase from bovine liver. These results suggest that DEP taken up in the lung and located on alveolar spaces might cause cell injury by inhibiting the activity of catalase in epithelial lining fluid, enhancing the toxicity of H2O2 generated from cells in addition to that of O2- generated by the chemical reaction of DEP with oxygen.
Animals↗
Chronic treatment with interleukin-1 beta induces coronary intimal lesions and vasospastic responses in pigs in vivo. The role of platelet-derived growth factor.
Studies in vitro have suggested that inflammatory cytokines may play an important role in the pathogenesis of atherosclerosis. However, little is known about their effects in vivo. Thus, the present study was designed to determine in vivo what histological and functional changes may be induced by chronic treatment with IL-1 beta, one of the major inflammatory cytokines, and also to clarify what mechanisms are involved in those changes. Under aseptic conditions, proximal segments of the left porcine coronary arteries were gently wrapped with cotton mesh absorbing Sepharose beads either with or without recombinant human IL-1 beta. From 1 to 4 wk after the operation, coronary vasospastic responses to intracoronary serotonin or histamine were noted at the IL-1 beta-treated site but not at the control site. Histologically, intimal thickening was greater at the IL-1 beta-treated site than at the control site. Those functional and histological changes induced by the chronic treatment with IL-1 beta were significantly inhibited by the simultaneous treatment with a neutralizing antibody to either IL-1 beta or PDGF. These results indicate that chronic treatment with Il-1 beta induces coronary intimal lesions and vasospastic responses in porcine coronary arteries in vivo and also suggest that these changes are substantially mediated by PDGF.
Animals↗
Comparison of cadmium uptakes from apical and basolateral membranes of LLC-PK1 cells.
Cadmium (Cd) uptake from the apical and basolateral membranes was investigated in LLC-PK1 cells grown as a monolayer on a permeable membrane. The cells were incubated at 37 degrees C for 1 hr with 1 microM CdCl2 from either the apical or the basolateral side. The accumulation of Cd from the apical side was 23% higher than that from the basolateral side. However, the translocation of Cd from the apical to the basolateral side and vice versa were similar. Cytotoxicity, as evaluated by transepithelial electrical resistance (TER), was undetectable at 1 microM Cd concentration. The preincubation of cells with carbonylcyanide p-(trifluoromethoxy)-phenylhydrazone (a metabolic inhibitor) and ouabain (a Na+/K+ - ATPase inhibitor) or coincubation with Cd and 2,4-dinitrophenol (a metabolic inhibitor) decreased both the accumulation (16-24%) and the translocation of Cd (22-25%) from the apical side, but not from the basolateral side. Incubation of cells with 50 and 75 microM CdCl2 for 1 hr resulted in 52-112% higher accumulation and translocation of Cd from the basolateral than from the apical side. The TER decreased at high Cd concentrations, suggesting that Cd concentrations of 10 microM and higher were cytotoxic. It is concluded that uptake of Cd from both the apical and the basolateral membranes represents passive diffusion. Additionally, under nontoxic conditions, about 20% of the Cd taken up at the apical membrane reflects carrier-mediated transport involving sodium ion- and energy-dependent processes; this accounts for higher accumulation through the apical membrane.
Animals↗
Gestational changes of glucose transporter gene expression in the mouse placenta and decidua.
Glucose is required for fetal development and energy metabolism. The glucose transfer from maternal circulation to fetus, in which glucose transporter (GLUT) should play an important role, is fundamental in the utero-placental-fetal system. In this study, the gestational changes of GLUT1 and GLUT3 mRNA level in the mouse placenta and decidua were analyzed by Northern blot analysis. The levels of GLUT1 mRNA in the mouse placenta and decidua increased as gestational day proceeded. Although the level of GLUT3 mRNA in the decidua slightly decreased as pregnancy proceeded, there was a switch in size of a major band of GLUT3 from 4.1 kb to 2.7 kb in the mouse placenta detected by Northern blot analysis. These findings suggest the presence of a difference in the gestational modulation of the level of GLUT1 and GLUT3 in the uteroplacental system.
Animals↗
Intraventricular administration of estradiol modulates rat prolactin secretion and synthesis.
The effect of estradiol (E2) on rat tuberoinfundibular dopaminergic (TIDA) neurons was examined in vivo, employing chronic intraventricular (i.c.v.) infusion technique using an osmotic mini-pump. The activity of TIDA neurons was assessed by the release and synthesis of prolactin (PRL) in the rat pituitary gland and by the changes in the 3, 4-dihydroxyphenylacetic acid (DOPAC) and dopamine (DA) levels and in the DOPAC/DA ratio in the rat hypothalamus. We also examined the [3H] E2 binding in the rat hypothalamus. Ovariectomized female Wistar rats with E2 replacement were treated with daily i.c.v. infusion of 1 microM of E2 or saline vehicle for 1, 3, and 7 days using the Alzet osmotic mini-pump and brain infusion kit. At 1 day of i.c.v. infusion of E2, the serum PRL level was significantly decreased compared with that in the vehicle group. Northern blot analysis of the total RNA isolated from the pituitary glands demonstrated a decrease in the PRL gene transcript level in the E2 group. At 3 days of E2 treatment, however, the serum PRL level was significantly increased compared with that of the vehicle-injected group and Northern blot analysis also demonstrated that the PRL gene transcript level was increased in the E2 group. At 7 days of E2 administration, there were no significant differences between the E2 and vehicle groups in either serum PRL or PRL gene transcript levels. There was a significant increase in the DOPAC/DA ratio after 1 day in the E2 group. However, no significant effects of E2 on this ratio were observed at 3 and 7 days of treatment. The DOPAC concentration in the E2 group was significantly increased at day 1 and significantly decreased at day 3, compared with that of the respective time in vehicle group. At day 7 there was no significant change in DOPAC concentration in either groups. The DA concentrations in the hypothalamus was not changed on any day in either group. Specific [3H] E2 binding was observed in the rat hypothalamus. These data suggest that E2 may have a biphasic effect on the accumulation of PRL gene transcripts and on the PRL secretion in the rat pituitary by first stimulating and then inhibiting the TIDA neuronal activity.
3,4-Dihydroxyphenylacetic Acid↗
Transforming growth factor-alpha regulates subpopulation of giant cells which secrete mouse placental lactogen-I (mPL-I) and/or mPL-II at midpregnancy.
The aim of this study was to determine whether transforming growth factor-alpha (TGF-alpha) regulates expression of mouse placental lactogen-I (mPL-I) and mPL-II at midpregnancy in vitro. Treatment of placental cells from day 9 of pregnancy with TGF-alpha resulted in stimulation of mPL-I secretion and inhibition of mPL-II secretion in a time- and dose-dependent manner without changing the amount of newly synthesized trichloroacetic acid precipitable proteins and cell viability. Moreover, TGF-alpha increased the intra-cellular mPL-I concentration and immuno-precipitable newly synthesized mPL-I concentration both in the medium and cells. TGF-alpha increased the number of cells containing only mPL-I and cells containing both mPL-I and mPL-II, but decreased that of the cells containing only mPL-II assessed by double immunocytochemistry. TGF-alpha increased the number of cells releasing only mPL-I but decreased the number of cells releasing only mPL-II, however TGF-alpha did not affect the number of cells releasing both mPL-I and mPL-II assessed by sequential reverse hemolytic plaque assay (RHPA). TGF-alpha decreased the expression of mPL-II mRNA, but did not change the expression of mPL-I mRNA. In situ hybridization for epidermal growth factor receptor (EGF-R) after RHPA for mPL-I indicated that giant cells releasing mPL-I express EGF-R mRNA. These findings suggest that TGF-alpha regulates the subpopulation of giant cells which produces and releases mPL-I and mPL-II and it results in an increase of mPL-I secretion and decrease of mPL-II secretion, and suggests possible post-transcriptional stimulation of mPL-I secretion and transcriptional inhibition of mPL-II secretion by TGF-alpha. Giant cells releasing mPL-I express EGF-R mRNA, suggesting direct regulation of giant cell differentiation by EGF and TGF-alpha at midpregnancy.
Animals↗
Preferential localization of annexin V to the axon terminal.
To examine the participation of annexin V, a member of Ca(2+)-dependent phospholipid-binding proteins, in the process of synaptic vesicle exocytosis, rat central nervous tissue was analysed using biochemical and morphological techniques. By both fluorescence and confocal laser scanning microscopy, immunoreactivity for annexin V was predominantly localized around neuronal somata and dendrites, and the reactivity was mostly co-labeled with that for synaptophysin. The annexin V immunoreactivity was also detectable, but less intensely, in neuronal perikarya, glial cells and endothelial cells. Both immunoblot and immunoelectron microscopic analyses with intact tissues, synaptosomes and purified synaptic vesicles showed that annexin V was expressed in neurons, preferentially concentrated in axon terminals and associated with synaptic vesicles. Purified synaptic vesicles were relatively homogeneously distributed in the medium where Ca2+ was removed and thus the amount of annexin V was reduced drastically. The vesicles tended to be clustered in the fraction where endogenous annexin V is maintained, and the clusters were more conspicuous when purified human annexin V was added. Synaptic vesicles forming the clusters were not directly fused with each other but separated by a 10-15 nm gap that corresponded well with the size of single annexin V molecules. In axon terminals, globular structures 12-13 nm in diameter, similar in dimension to annexin V molecules, were distinctly found to be attached to the cytoplasmic surface of both vesicle membranes when the two vesicles were close to each other. These results suggest that annexin V belongs to the group of synaptic vesicle-associated proteins. Although its localization and significance in non-neuronal cells were not analysed here, at least in the axon terminal annexin V may participate in the cluster formation of synaptic vesicles by linking with the cytoplasmic surface of the vesicles in a Ca(2+)-dependent manner.
Animals↗
Comparative studies of cadmium and mercury accumulation by LLC-PK1 cells: effects of pH on uptake and efflux.
Effects of pH on internalization, membrane-binding and efflux of Cd were investigated in LLC-PK1 cells and these effects were compared with those of inorganic mercury (Hg). The cells cultured on monolayers were incubated for 30 min in phosphate buffer at pH 5.5, 6.4 or 7.4 containing 1 microM Cd or Hg. After the incubation, the cells were washed with phosphate buffered saline (PBS) or PBS containing chelating agent (EGTA or BAL) to remove membrane-bound Cd or Hg. The decrease in pH significantly decreased Cd concentration in the cells washed with PBS and with PBS-EGTA, and apparently increased the efflux of Cd from the cells. Similar changes were found in Hg concentration in the cells washed with PBS-BAL and Hg efflux from the cells, but these changes in Hg were less significant than those in Cd, respectively. The decrease in pH-increased Hg concentration in the cells washed with PBS, unlike that of Cd. These results suggest that a decrease in pH decreases the internalized Cd as a result of the decrease in membrane-bound Cd and the increase in Cd efflux. The decrease in pH also appears to decrease the internalized Hg by increasing Hg efflux and to increase the membrane-bound Hg.
Analysis of Variance↗
Vascular compressive abducens nerve palsy disclosed by magnetic resonance imaging.
PURPOSE: To assess magnetic resonance imaging as a diagnostic tool of neurovascular compression in a patient with abducens nerve palsy. METHODS: We performed magnetic resonance imaging of the brainstem of a 46-year-old patient with left abducens nerve palsy using spoiled gradient recalled acquisition in the steady state (SPGR), which allows high-resolution T1-weighted imaging and detection of the arteries across the plane of slices as a high-signal-intensity area. RESULTS: Computed tomography of the brain was unremarkable except for leftward shifting of the basilar artery. As disclosed by magnetic resonance imaging with the SPGR, the right vertebral artery was shifted to the left and joined with the left vertebral artery, and the left abducens nerve was compressed by the vertebral artery. No other abnormal signals were seen in the brainstem. CONCLUSIONS: These findings suggest that the abducens nerve palsy in this patient was caused by vascular compression at the root exit zone. Magnetic resonance imaging with the SPGR is useful for the diagnosis of vascular compressive neuropathy.
Abducens Nerve↗
Coronary vascular ATP-sensitive potassium channels are activated to a greater extent in spontaneously hypertensive rats than in Wistar-Kyoto rats.
OBJECTIVE: To determine whether opening of coronary vascular adenosine 5'-triphosphate (ATP)-sensitive potassium (KATP) channels is involved in the maintenance of resting coronary flow in hypertrophied hearts. METHODS: We examined the effects of glibenclamide, a selective inhibitor of KATP channels, on basal coronary vascular tone in Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHRs). Using a Langendorff system, the hearts from WKY rats and SHRs were isolated and perfused with oxygenated Krebs-Henseleit solution at a constant perfusion pressure of 60 and 100 mmHg respectively. RESULTS: Basal coronary flow and myocardial oxygen consumption (MV02) were similar in SHRs and WKY rats. The percentage decreases in coronary flow with glibenclamide at graded doses were greater (P < 0.01) in SHRs than in WKY rats (n = 8), whereas the percentage decreases in MV02 with glibenclamide were similar in the two groups. The decreases in coronary flow caused by U46619 (a thromboxane A2-mimetic agent) were similar in SHRs and WKY rats (n = 4). The increase in coronary flow caused by pinacidil (a KATP opener) was greater in SHRs than in WKY rats; glibenclamide prevented the pinacidil-induced increase in coronary flow in both SHRs and WKY rats. There was a significant positive correlation between the glibenclamide-induced decrease in coronary flow and the degree of left ventricular hypertrophy (r = 0.54, P < 0.05). CONCLUSION: Our results suggest that the basal opening state of coronary vascular KATP channels is activated to a greater extent in SHRs than WKY rats, which may contribute to the maintenance of basal myocardial perfusion in hypertrophied hearts.
15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
Induction of MAGE genes in lymphoid cells by the demethylating agent 5-aza-2'-deoxycytidine.
MAGE genes encoding tumor antigens recognized by cytotoxic T lymphocytes are appropriate target molecules for specific immunotherapy of cancer. We have investigated whether the demethylating agent 5-aza-2'-deoxycytidine (DAC) induces MAGE-1, -2, -3, and -6 in normal and malignant lymphoid cells. DAC induced these MAGE genes in both PHA/interleukin-2 (IL-2)-activated T cells from healthy donors and MAGE-negative T and B cell leukemias in most cases. It also induced MAGE-1 in IL-2-dependent T cell clones and all MAGE genes tested in Epstein-Barr virus-transformed B cell lines. Expression of MAGE-1 protein in the cells was confirmed by western blot analysis with anti-MAGE-1 polyclonal antibody. Therefore, demethylation is a potent stimulus to induce MAGE genes in both normal and malignant lymphoid cells.
Amino Acid Sequence↗
Characterisation of mucins in the tear film of ocular prosthesis wearers.
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Adult↗