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T Iida

Publications and source records attributed to T Iida.

At least 343 records · Page 19Linked to original sources
PubMed1991

[A case of the milk-alkali syndrome with a small amount of milk and magnesium oxide ingestion--the contribution of sustained metabolic alkalosis induced by hypertonic dehydration].

We described a patient with the milk-alkali syndrome induced by the ingestion of small amount of milk (200 ml/day) and ice cream (145 g/day) and the administration of small dose of absorbable alkali (magnesium oxide 2.0 g/day) for the treatment of chronic constipation. The present case shows not only triads, i.e., hypercalcemia (s-Ca 14.3 mg/dl), metabolic alkalosis (s-HCO3- 37.4 mEq/L), and renal insufficiency (s-Cre 2.3 mg/dl) but also hypernatremia (s-Na 161 mEq/L) and hypertonic dehydration after the frequent episodes of elevated body temperature. The milk-alkali syndrome has been defined as the hypercalcemia with a metabolic alkalosis from a high amount of calcium intake and long term administration of absorbable alkali in any form, usually as calcium carbonate for the treatment of peptic ulcer. As the present case could be distinguished from any other cases previously reported with regard to the amount of calcium (0.4 g/day) and alkali (36 mEq/day) intake and the clinical situations that induced the syndrome, we compared the present case with the previous reports, calculating the amount of calcium and alkali intake from milk and absorbable alkali. After the introduction of the H2 blockers for peptic ulceration, the most cases with milk-alkali syndrome had provoked by the smaller amount of calcium than previously reported, which were associated with the treatment of relatively large amount of alkali (50-150 mEq/day), suggesting the role of sustained metabolic alkalosis for the development. In the present case the metabolic alkalosis induced by hypertonic dehydration and enhanced by absorbable alkali intake also could cause an increase of renal tubular reabsorption of calcium and a decrease of ionized calcium which might produce increased secretion of parathyroid hormone followed by vitamin D3 activation and increased Ca absorption from the gut. The metabolic alkalosis might be essential to the development of the milk-alkali syndrome without a high calcium and absorbable alkali intake.

Aged↗
PubMed1990

Cloning and expression of two genes encoding highly homologous hemolysins from a Kanagawa phenomenon-positive Vibrio parahaemolyticus T4750 strain.

We have cloned and sequenced the gene encoding thermostable direct hemolysin (TDH), a possible virulence factor in Vibrio parahaemolyticus gastroenteritis, from a Kanagawa-phenomenon-positive strain, T4750. This strain was found to contain two sequences (tdhA and tdhS) homologous to the tdh gene previously reported by Nishibuchi and Kaper [J. Bacteriol 162 (1985) 558-564] and Taniguchi et al. [Microb. Pathog. 1 (1986) 425-432]. Sequence homology of the coding regior between tdhA and tdhS was 97.2%. The deduced amino acid (aa) sequence of TdhA, excluding the putative signal peptide was identical to that of TDH protein purified from V. parahaemolyticus [Tsunasawa et al., J. Biochem. 101 (1987) 111-121] except for Glu118 instead of Gln118. Although the aa sequence deduced from the second gene, tdhS, differed in eight residues from the TDH protein, it agreed with the sequence of Tdh deduced from the previously cloned tdh gene. Both tdhA and tdhS expressed biologically active hemolysins in Escherichia coli. While the apparent molecular size of TDH purified from a culture supernatant of V. parahaemolyticus T4750 was identical to TdhA protein synthesized in E. coli, it was larger than TdhS. Only one band was detected in the culture supernatant of V. parahaemolyticus T4750 by Western blotting; its mobility was indistinguishable from that of purified TDH. These data suggest that tdhA is the structural gene for TDH found in the culture supernatant of V. parahaemolyticus T4750, and that there was only partial, if any, tdhS expression in the strain T4750 under the test conditions employed.

Amino Acid Sequence↗
PubMed1990

Role of voltage-sensitive calcium channels in [Ca2+]i and secretory responses to activators of protein kinase C in pituitary gonadotrophs.

The gonadotropin secretory response of anterior pituitary cells to phorbol esters includes both extracellular Ca2(+)-dependent and -independent components (Stojilković et al, 1988; J. Biol. Chem. 263, 17301-17306, 1988). In cultured pituitary cells, measurements of [Ca2+]i using Fura-2 and of LH release during cell perifusion studies revealed that the initial effects of phorbols and permeant diacylglycerols on these responses are extracellular Ca2(+)-dependent and are mediated through activation of voltage- and dihydropyridine-sensitive calcium channels. On the other hand, pretreatment with phorbol esters for 30 to 60 min inhibited subsequent [Ca2+]i responses to diacylglycerols and phorbols and significantly reduced agonist-induced biphasic [Ca2+]i responses, with no change in the number of GnRH receptors. These findings demonstrate that protein kinase C exerts both positive and negative control of [Ca2+]i, and indicate that the calcium, phospholipid dependent enzyme participates in the activation of voltage-sensitive calcium channels and hormone secretion in pituitary gonadotrophs.

Animals↗
PubMed1990

Endothelin stimulation of cytosolic calcium and gonadotropin secretion in anterior pituitary cells.

The presence of endothelin, a vasoconstrictor peptide, in the hypothalamus and posterior pituitary suggests that it also regulates neural and other nonvascular target cells. In pituitary gonadotrophs, low doses of endothelin evoked oscillations in the intracellular calcium concentration, and high doses induced a biphasic calcium response. Mobilization of intracellular calcium predominated during the spike phase of the calcium response to endothelin, whereas calcium entry through dihydropyridine-sensitive channels contributed to both the spike and plateau phases of the calcium response. Endothelin was a potent as hypothalamic gonadotropin-releasing hormone (GnRH) in stimulation of gonadotropin release in perifused pituitary cells. Endothelin bound specifically to pituitary cells with a dissociation constant of 70 picomolar, and induced rapid formation of inositol trisphosphate and diacyglycerol. Although intracellular calcium concentration and gonadotropin secretory responses to endothelin were independent to the GnRH receptor, endothelin and GnRH appeared to have a common signal transduction mechanism. These observations suggest that endothelin can act as a neuropeptide to regulate anterior pituitary function.

Animals↗
PubMed1990

The reaction product of peptidylglycine alpha-amidating enzyme is a hydroxyl derivative at alpha-carbon of the carboxyl-terminal glycine.

The peptidylglycine alpha-amidating enzyme catalyzes a reaction that transforms a carboxyl-terminal glycine-extended precursor into a carboxyl-terminal alpha-amidated peptide. We purified an alpha-amidating enzyme from equine serum by simplified steps including substrate affinity chromatography. With the purified enzyme, we detected an intermediate of the alpha-amidating reaction by high performance liquid chromatography analysis. The production of the intermediate required copper, oxygen, and ascorbate and increased linearly with incubation time. The structure of the intermediate was determined to be a hydroxyl derivative at the carboxyl-terminal glycine by fast atom bombardment mass spectrometry and by proton NMR. The intermediate was readily converted into an alpha-amidated product in alkaline conditions in a nonenzymic fashion. The nonenzymic conversion required no cofactor but was extremely accelerated by the addition of copper ion or at higher temperature. Our data suggest that the direct product of the alpha-amidating reaction is not an alpha-amidated peptide but a hydroxyl derivative at the alpha-carbon of the carboxyl-terminal glycine.

Amino Acid Sequence↗
PubMed1990

Brain natriuretic peptide is cosecreted with atrial natriuretic peptide from porcine cardiocytes.

Using primary cultures of atrial cardiocytes from neonatal pig, the secretion brain natriuretic peptide (BNP) and atrial natriuretic peptide (ANP)-like immunoreactivities (LI) was studied in vitro. Porcine cardiocytes time-dependently secreted both BNP-LI and ANP-LI into medium under a serum-free condition, although the amount of BNP-LI secreted was about one-third that of ANP-LI. Phorbol ester and Ca2+ ionophore had less stimulatory effects on secretion of BNP-LI than that of ANP-LI. Reverse-phase HPLC of the conditioned medium revealed a single major BNP-LI component corresponding to synthetic porcine BNP(1-26). These data suggest that a small molecular weight form BNP, possibly BNP(1-26), is cosecreted with ANP from porcine cardiocytes.

Animals↗
PubMed1990

A novel beta-adrenergic receptor antagonist MY336-a: structure of the tetraacetylated compound.

(1R*,3S*)-1,2,3,4-Tetrahydro-8-acetoxy-1,3-bis(acetoxymethyl)-2-acetyl-7 - methoxy-6-methyl-isoquinoline, C21H27NO8, Mr = 421.45, monoclinic, P2(1), a = 11.892 (2), b = 11.067 (2), c = 8.4866 (8) A, beta = 92.12 (1) degree, V = 1116.1 (5) A3, Z = 2, Dx = 1.255 g cm-3, Cu K alpha, lambda = 1.54184 A, mu = 7.702 cm-1, F(000) = 448, T = 293 K, R = 0.048, wR = 0.072 for 2178 observed reflections. The tetrahydropyridine ring adopts a half-boat conformation. The bond lengths and angles are within the normal ranges. There are no intermolecular contacts less than the sum of the van der Waals radii.

Adrenergic beta-Antagonists↗
PubMed1990

Potential bile acid metabolites. 16. Synthesis of stereoisomeric 3 alpha,6,7,12 alpha-tetrahydroxy-5 beta-cholanoic acids.

New synthetic routes to the four possible stereoisomeric 3 alpha,6,7,12 alpha-tetrahydroxy-5 beta-cholanoic acids (and their methyl esters), one of which (3 alpha,6 alpha 7 beta,12 alpha) is new, and some related compounds are described. In addition, the 5 alpha-epimer of the new acid was obtained. The final products were obtained in high purity for use as reference compounds in the analysis of bile acids in human biologic samples. The results of analysis of the prepared stereoisomers by proton and carbon 13 nuclear magnetic resonance spectroscopies are briefly discussed along with the thin-layer and gas-liquid chromatographic properties.

Bile Acids and Salts↗
PubMed1990

Long-term effects of peroxisome proliferators on the balance between hydrogen peroxide-generating and scavenging capacities in the liver of Fischer-344 rats.

In order to clarify whether peroxisomal hydrogen peroxide (H2O2) plays an important role in peroxisome proliferator-induced hepatocarcinogenesis, we examined the change in metabolism of peroxisomal H2O2 in vivo and in vitro using male Fischer-344 rats fed clofibrate, bezafibrate and di(2-ethylhexyl)phthalate (DEHP) for up to 78 weeks. Hepatic peroxisomal fatty acyl-CoA oxidase activity increased 12-20-fold after 2 or 4 weeks treatment; later this level gradually decreased toward controls, and at 78 weeks activity was 3-10-times of control. Although hepatic H2O2 levels were increased slightly by clofibrate, bezafibrate and DEHP, the changes did not correlate with the changes in peroxisomal fatty acyl-CoA oxidase activity. In isolated hepatocytes, the rate of leakage of peroxisomal H2O2 from peroxisomes into the cytosol and the hepatocellular H2O2 content was measured. The rate of leakage of peroxisomal H2O2 into cytosol increased 2.5-4-fold when peroxisomal beta-oxidation activity was induced by peroxisome proliferators, and the increases in this rate corresponded with changes in the peroxisomal beta-oxidation activity. In contrast, the hepatocellular H2O2 contents were not affected by induced peroxisomal beta-oxidation. These data show that H2O2 leaking from peroxisome into cytosol would be quickly decomposed, and thus peroxisomal H2O2 does not appear to play an important role in hepatocarcinogenesis by such an oxidative stress mechanism after the long-term treatment with peroxisome proliferators.

Acyl-CoA Oxidase↗
PubMed1990

Dependence of hormone secretion on activation-inactivation kinetics of voltage-sensitive Ca2+ channels in pituitary gonadotrophs.

The relationships between the activation status of voltage-sensitive Ca2+ channels and secretory responses were analyzed in perfused rat gonadotrophs during stimulation by high extracellular K+ concentration ([K+]e) or the physiological agonist, gonadotropin-releasing hormone (GnRH). Increase of [K+]e to 50 mM evokes an on-off secretory response, with a rapid rise in luteinizing hormone (LH) secretion to a peak at 35 sec (on response) followed by an exponential decrease to the steady-state level. Cessation of K+ stimulation elicits a transient (off) response followed by an exponential decrease to the basal level. The LH response to high [K+]e is nifedipine-sensitive and its amplitude depends on membrane potential. There is a close relationship between the LH secretory response to high [K+]e and the amplitude of the inward Ca2+ current measured at 100 msec in whole-cell patch clamp experiments. In addition, the profile of the LH secretory response is similar to that of the response of intracellular Ca2+ concentration ([Ca2+]i) in K(+)-stimulated cells. In Ca2(+)-deficient medium, the effect of high [K+]e is abolished; subsequent elevation of [Ca2+]e during the K+ pulse is followed by restoration of the on response, but with reduced magnitude. Agonist stimulation during the steady-state phase of the [K+]e pulse or after repetitive stimulation by high [K+]e elicited biphasic [Ca2+]i and secretory responses with a significantly reduced plateau phase; conversely, K(+)-induced LH release was reduced in cells treated with desensitizing doses of GnRH. These findings indicate that depolarization-induced changes in the status of voltage-sensitive Ca2+ channels determine the profiles of [Ca2+]i and LH responses to stimulation by high [K+]e; the initial activation of dihydropyridine-sensitive Ca2+ channels is clearly dependent on membrane potential, whereas their subsequent inactivation depends on increased [Ca2+]i. Such inactivation of voltage-sensitive Ca2+ channels also occurs during GnRH action and may represent an additional regulatory mechanism to limit the entry of extracellular Ca2+ during prolonged or frequent agonist stimulation.

Animals↗
PubMed1990

Long-term effects of hypolipidemic peroxisome proliferator administration on hepatic hydrogen peroxide metabolism in rats.

The effects of prolonged dietary administration of peroxisome proliferators, such as clofibrate, bezafibrate and di(2-ethylhexyl)phthalate (DEHP), on hepatic hydrogen peroxide (H2O2) level and on hepatic activities of the enzymes relating to H2O2 metabolism were examined. Male rats were treated for 79 weeks with the above three peroxisome proliferators. The activities of the peroxisomal beta-oxidation and catalase were increased 8- to 20-fold and 2- to 3-fold, respectively, after 2 or 4 weeks of treatment with these peroxisome proliferators. However at 79 weeks the peroxisomal beta-oxidation activity was 3-8 times that of control. The level of catalase activity was kept at approximately 2-fold even after prolonged treatment of peroxisome proliferators. Although the activities of glutathione peroxidase (GSH-Px) and glutathione S-transferase (GST) were decreased 50-60% at 4-12 weeks by the treatment with peroxisome proliferators, from 20 to 79 weeks those activities approached control levels in the case of clofibrate and bezafibrate but not DEHP-fed rats; GSH-Px and GST activities were kept at approximately 40% those of control. However hepatic capacities of H2O2-degrading enzymes, catalase and GSH-Px, apparently exceeded the H2O2-generating levels obtained on the basis of peroxisomal beta-oxidation activities in the livers of control and treated rats throughout the experimental period. The hepatic H2O2 levels increased only slightly but this increase did not correspond to changes in peroxisomal beta-oxidation. Our results suggest that a large part of H2O2 produced by peroxisomal beta-oxidation could be rapidly scavenged by catalase and GSH-Px in the liver of rats treated with peroxisome proliferators.

Animals↗
PubMed1990

Rapid detection and size determination of PuO2 particles using a charged-particle imaging video monitor system.

A charged-particle imaging video monitor system was constructed and applied to video imaging of the position profile of PuO2 particles on filter paper. The imaging video monitor system consists of a detector head, a silicon intensifier target (SIT) camera, a video frame memory, and a personal computer. The system can display the distribution image of PuO2 particles becoming gradually clearer on a video monitor. The integrated image that is transferred to the computer is analyzed quantitatively for the radioactivity of each PuO2 particle deposited on the filter paper. The system can not only rapidly distinguish PuO2 particle contamination from Rn daughter products, but can also determine the size distribution of the PuO2 particles.

Particle Size↗
PubMed1990

Dynamic eye accommodation evoked by apparent distances.

A three-dimensional optometer (TDO), which can measure simultaneously three major ocular functions in a working environment, was used to measure the visual responses of human subjects viewing: (1) actual artworks and (2) corrugation presented by moving random dots on a cathode ray tube (CRT). Measurements were performed in natural viewing conditions on two emmetropic females. Both subjects demonstrated distinct accommodative responses for the stimuli presented at a fixed distance. The results indicate that the accommodation generally shifts in accord with changes of perceived distance. The usefulness of the TDO was demonstrated in these experiments.

Accommodation, Ocular↗
PubMed1990

Cardiac atrial natriuretic peptide concentrations in experimental obese mice.

Obesity is usually associated with expansion of blood volume. Therefore, we studied whether obesity affects cardiac and plasma atrial natriuretic peptide (ANP) levels in experimental animal model. Mice made obese with gold thioglucose developed cardiac hypertrophy associated with increases in ANP in atrial tissue and plasma. There were significant (p less than 0.01) correlations between the cardiac ANP concentration and body weight or cardiac weight. These data suggest that enhanced synthesis of atrial ANP in obese mice can be mainly ascribed to increased blood volume associated with cardiac hypertrophy.

Animals↗
PubMed1990

The role of protein kinase C in LH release.

To investigate the postreceptor mechanism, especially the role of protein kinase C (C-kinase), in luteinizing hormone (LH) release from anterior pituitary cells, dispersed rat anterior pituitary cells were stimulated with luteinizing hormone-releasing hormone (LH-RH), [D-Ser(tBu)]6 des-Gly-NH2(10) ethylamide (Buserelin), 12-0-tetradecanoyl phorbol-13-acetate (TPA) and trifluoperazine (TFP) and the LH released into the medium was determined by radioimmunoassay. LH released by combined stimulation with TPA and either LH-RH or Buserelin was significantly less than that released by LH-RH or Buserelin alone (LH-RH: p less than 0.05; Buserelin: p less than 0.01). It is thought that this paradoxical phenomenon occurred due to desensitization accompanied by down-regulation of LH-RH receptors induced by TPA. This hypothesis was supported by the finding indicating that the binding capacity of LH-RH receptors decreased in a time-course manner during incubation with TPA. The amount of LH released by combined stimulation with TPA and TFP was significantly greater than with TPA alone (P less than 0.01). This suggests that TFP has dual actions, i.e., facilitating and inhibiting LH release.

Animals↗