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Biomedical subjects

N Satake

Publications and source records attributed to N Satake.

140 records · Page 8Linked to original sources
PubMed1980

Protein effect on the antimony microelectrode in application to biological fluid.

In order to examine the effect of protein on the Sb-microelectrode used for the pH measurement of biological fluids, bovine serum albumin (BSA) and plasma protein were used for test samples. It was found that, BSA, probably by binding to components in the electrode system, produced a marked deviation of both the electromotive force and slope constant of the microelectrode, resulting in an alkaline shift of pH of 0.1-0.7. But the shift of the pH reading could be empirically predicated within an error of +/- 0.03 from the cubic function of protein concentration. Use of Tris standard solution as the calibration buffer, together with corrections for the effects of temperature, ionic strength, Po2, etc. on the Sb-microelectrode, would reduce the alkaline shift to approximately less than 0.08 and 0.04 pH units in the pH measurement of blood plasma and whole blood, respectively.

Antimony↗
PubMed1979

Scotophobin A causes several responses in goldfish if the pineal gland is present.

Rat scotophobin A increased dark avoidance in goldfish in dark and light avoidance shuttlebox experiments, controlled for general and light cycling-induced swimming activity. A possible site of action for scotophobin was suggested by the reports that dark avoidance was also increased in goldfish by pinealectomy, a treatment which increased shock sensitivity as well. It was found that scotophobin alone decreased the voltage required to induce tail-flip contractures in goldfish. The pineal gland was further implicated in the mode of action of scotophobin when it was found that this peptide suppressed the norepinephrine-induced aggregation of goldfish chromatophores whose state is in part controlled by pineal melatonin. Pinealectomized goldfish became insensitive to the effects of scotophobin upon both light-dark preference and chromatophore aggregation state. There observations strongly suggest that the pineal gland is required for the action of scotophobin.

Animals↗
PubMed1979

Scotophobin A causes dark avoidance in goldfish by elevating pineal N-acetylserotonin.

We had shown that synthetic rat scotophobin A caused several effects upon goldfish, apparently mediated by the pineal gland. Here we report that norepinephrine decreased goldfish dark avoidance in a manner that was blocked by scotophobin or pinealectomy. Increased dark avoidance was caused by either propranolol or scotophobin alone. Certain components of the pineal melatonin pathway also affected goldfish light-dark preference: serotonin, and especially N-acetylserotonin, increased dark avoidance, as did the hydroxyindole-O-methyl-transferase (HIOMT) product inhibitor, S-adenosyl-homocysteine. Melatonin and S-adenosyl-methionine were without effect in this regard. Pinealectomy prevented the dark avoidance increase caused by serotonin and N-acetylserotonin. These data suggested that increased dark avoidance behavior in goldfish was correlated with N-acetylserotonin buildup in the pineal, and that scotophobin could cause this, if it were to inhibit pineal HIOMT. To test this hypothesis the effect of various agents upon pineal melatonin levels was determined. Scotophobin was found to both reduce pineal melatonin and to block the melatonin-increasing effect of N-acetylserotonin. This led to the discovery that, indeed, scotophobin was an effective inhibitor (KI50, 6 x 10(-7) M) of purified bovine HIOMT.

Acetylserotonin O-Methyltransferase↗
PubMed1979

Pineal hydroxyindole-O-methyltransferase: mechanism, and inhibition by scotophobin A.

We had shown that the behaviorally active peptide, scotophobin A, a synthetic analogue of native scotophobin, acted to increase dark avoidance in goldfish by inhibiting pineal hydroxyindole-O-methyltransferase (HIOMT), the enzyme which converts N-acetylserotonin (NAS) to melatonin (MEL). Here we determine the reaction sequence of bovine pineal HIOMT and the mechanism whereby scotophobin A inhibits this enzyme. Initial rate studies in which the substrates NAS and the methyl donor, S-adenosylmethionine SAM), were independently varied indicated the enzyme reacted by a sequential mechanism. With the product, S-adenosylhomocysteine (SAH), included in the reaction mixtures, data were obtained consistent with the following order of substrate addition and product discharge: (see text). The turnover number was 5.7 moles melatonin formed/mole HIOMT/min. The substrate KMs were 4.2 x 10(-4) M for NAS and 4.9 x 10(-5) M for SAM. Further studies showed that scotophobin A is an inhibitor (KI = 7 x 10(-7) M) competitive with NAS, indicating that this peptide combines with the enzyme-SAM complex. The structural similarity of the tyrosinamide end of scotophobin A to NAS and several other HIOMT inhibitors, including two antischizophrenic drugs, is consistent with these observations.

Acetylserotonin O-Methyltransferase↗
PubMed1979

The measurement of intracellular sodium activities in the bullfrog by means of double-barreled sodium liquid ion-exchanger microelectrodes.

A double-barreled Na+-selective microelectrode was constructed with monensin as a liquid ion exchanger. The HCl-treated monensin was dissolved in a solvent (Corning 477317) at 10% (weight/weight). Internal reference solution of its ionic barrel was mixture of 0.49 M NaCl and 0.01 M KCl, the pH being adjusted to 3 with 0.1 M citrate-HCl buffer, whereas that of the PD barrel was 0.5 M KCl. Average slope and selectivity ratio (Na+/K+) tested on 10 different microelectrodes were -57.5 +/- 1.87 mV/P(Na) (SEM) and 6.7 +/- 0.44, respectively. The electrical resistance was an order of 10(10) ohm and the response time was less than 10 sec. Using this microelectrode, a free flow micropuncture experiment was carried out in the bullfrog kidney and the intracellular Na+ activity as well as the membrane PD was determined on the proximal tubular cell. Average value (+/- SEM, n = 15) for the intracellular Na+ and K+ was 20.7 +/- 1.56 mEq/L and 61.2 +/- 1.16 mEq/L, respectively, and -68.7 +/- 0.88 mV for the peritubular membrane PD. There was a significant negative correlation between Na+ and K+ activities within the cell, i.e., the lower the ionic activity of cellular Na+ was, the higher the cellular K+, and vice versa, the sum of these two being kept nearly constant. The above finding may be somehow related to the isosmosis in the reabsorptive process across the proximal tubular epithelium.

Animals↗
PubMedDate not supplied

Unsteady flow of Casson fluids through the eccentric circular tube.

As a model of the flow through the false lumen of the dissecting aortic aneurysm, the starting and stopping flows of the Casson fluid through the eccentric circular tube are studied numerically. The calculations are performed by using the one-direction fully developed unsteady flow model. The calculation results show that the non-Newtonian property of the Casson fluid has the following two effects. One is the decrease in the flow rate through the false lumen, the other is the effect to strengthen the non-uniformity of the velocity distribution in the false lumen. Moreover, the calculations based on a triphasic waveform measured by McDonald are performed and the development of the dissecting aortic aneurysm is discussed on the basis of the calculated wall shear stress.

Aortic Dissection↗
PubMedDate not supplied

Increased releasability of platelet products and reduced heparin-induced platelet factor 4 release from endothelial cells in bronchial asthma.

To determine whether or not platelet activation is involved in the mechanism of exacerbation of bronchial asthma, we evaluated adenosine triphosphate (ATP) release from thrombin-stimulated washed platelets, plasma levels of beta-thromboglobulin (beta-TG) and platelet factor 4 (PF4), and plasma beta-TG/PF4 ratios during symptomatic and asymptomatic periods in 15 patients with bronchial asthma compared with 16 normal control subjects. We also measured these parameters during allergen provocation tests and acetylcholine inhalation tests in 6 allergic asthmatics. ATP release, plasma levels of beta-TG and PF4 were significantly increased during symptomatic periods and after the allergen provocations but not after acetylcholine inhalations. However, these findings were not accompanied by the elevation of plasma beta-TG/PF4 ratios. The heparin-induced PF4 release, which is reported to reflect release of PF4 attached on endothelial cells, was significantly reduced in 12 asymptomatic asthmatic patients compared with 11 normal subjects, and it was much more reduced in 7 symptomatic asthmatic patients, suggesting the possibility of the reduced PF4 binding on endothelial cell surface. This finding may represent the prolonged half life of PF4 in asthmatics. We concluded that 1) increased releasability of platelet products and in vivo release of the platelet granular contents are involved in the mechanism of the exacerbation of bronchial asthma, 2) some functional alteration in platelet-endothelial cell interaction may be involved in bronchial asthma, and 3) plasma beta-TG/PF4 ratios are not elevated possibly because of both increased platelet releasability and prolonged half-life of PF4 in the blood in asthmatic patients.

Acetylcholine↗
PubMedDate not supplied

A neonatal case of hydranencephaly caused by atheromatous plaque obstruction of aortic arch: possible association with a congenital cytomegalovirus infection?

A neonate was seen with hydranencephaly and aortic arch obstruction possibly caused by congenital cytomegalovirus infection. At autopsy the aortic arch was occluded by atheromatous plaque between the right brachiocephalic artery and left common carotid artery. Congenital cytomegalovirus infection may have caused cardiovascular disease and hydranencephaly in this case.

Aorta, Thoracic↗