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Biomedical subjects

K Saida

Publications and source records attributed to K Saida.

At least 73 records · Page 4Linked to original sources
PubMed1989

Effects of vasoactive intestinal contractor (VIC) and endothelin on intracellular calcium level in neuroblastoma NG108-15 cells.

Effects on [Ca2+]i levels of endothelin-l (ET) and vasoactive intestinal contractor peptide (VIC), which is a novel member of the endothelin family, were examined in fura 2-loaded neuroblastoma NG108-15 cells. VIC was found to be a very effective stimulus for intracellular Ca2+ mobilization and to be more potent than ET. Intracellular calcium response to sequential addition of two stimulants exhibited the homologous desensitization of either ET or VIC, but no heterologous desensitization between ET and VIC. This indicates evidence suggesting that these two peptides act through distinct receptors.

Calcium↗
PubMed1989

A novel peptide, vasoactive intestinal contractor, of a new (endothelin) peptide family. Molecular cloning, expression, and biological activity.

A new peptide family (endothelin (ET] consisting of three members in mammals appears to be present in mice according to genomic Southern blot analysis. Two ET-related genes were identified by cloning and sequence analysis of a mouse genome. One encoded a peptide identical to porcine and human vasoconstrictor peptide ET, and the other encoded a novel peptide differing from ET in 3 amino acid residues, with 4 cysteines in the same positions as in ET. This novel peptide was synthesized and confirmed to have in vivo pressor activity similar to that of ET. Northern blot analysis, however, indicated the gene of this novel peptide to be expressed only in the intestine, and not in other tissues or cell lines, or endothelial cells. Furthermore, the peptide evoked a strong contractile response in the guinea pig ileum. This peptide may thus be reasonably classified as a gastrointestinal peptide, vasoactive intestinal contractor.

Amino Acid Sequence↗
PubMed1989

Differential activities of two distinct endothelin family peptides on ileum and coronary artery.

A synthesized mouse vasoactive intestinal contractor peptide, which belongs to a novel member of the endothelin family, induced a prolonged contraction in mouse ileum as well as porcine coronary artery in vitro. Studies comparing the effects of vasoactive intestinal contractor and endothelin on different tissues revealed that the maximum ileum contraction of vasoactive intestinal contractor was much higher than that of endothelin in both guinea pig and mouse systems, but that the vasoconstriction activity of vasoactive intestinal contractor was weaker than that of endothelin in porcine artery. These results show that vasoactive intestinal contractor might be a novel gastrointestinal hormone.

Animals↗
PubMed1989

In vivo CNS demyelination mediated by anti-galactocerebroside antibody.

The mechanism of antibody-mediated central nervous system (CNS) demyelination in vivo was studied using rabbit eyes. Injection of anti-galactocerebroside (Gal C) antiserum alone into the normal rabbit vitreous body induced demyelination in the epiretinal myelinated fibers. This activity of the antiserum disappeared after heat treatment at 56 degrees C for 30 min and was restored by supplement of normal fresh serum, suggesting the complement dependency of the activity. Heated anti-Gal C antiserum could induce demyelination, however, when macrophages were introduced by injecting lymphocyte supernatants together with antiserum. Electron microscopic study revealed penetration of macrophage process between the myelin lamella. These findings suggest that the cooperation of anti-Gal C antibody and macrophage can result in the antibody-dependent cell-mediated demyelination in the absence of complement. Because oligodendrocyte generally appeared normal, myelin, not oligodendrocyte is suspected to be the primary target by anti-Gal C antiserum. In contrast, neither anti-MBP nor anti-gangliosides antiserum had the in vivo-demyelinating activity. In CNS demyelination by anti-Gal C antibody, complement-mediated and macrophage-mediated mechanisms may cooperate in varying degrees.

Animals↗
PubMed1989

Follow up study of cardiac involvement in Emery-Dreifuss muscular dystrophy.

A patient with Emery-Dreifuss muscular dystrophy was followed up from 9 to 26 years of age. Serial electrocardiographic studies showed changes ranging from early cardiac conduction abnormality as first degree atrioventricular block to sick sinus syndrome. In addition the development of cardiomyopathy was documented by electrocardiographic, echocardiographic and radionuclide studies of the heart.

Bradycardia↗
PubMed1989

Sarcoplasmic reticulum function in skinned fibers of hypertrophied rat ventricle.

This study was designed to examine the Ca2+ sensitivity of the contractile system and the ability of the sarcoplasmic reticulum (SR) to accumulate and release Ca2+ in chemically (saponin) skinned cardiac fibers obtained from normal and pressure-overloaded hypertrophied rat left ventricles. Left ventricular pressure overload was induced by partial ligation of the abdominal aorta 6-8 wk before study. Age- and weight-matched normal rats served as controls. Pressure over-load increased the left ventricular weight-to-body weight ratio by 51%. There were no differences in the Ca2+-tension relationship between normal and hypertrophied preparations at Ca2+ concentrations of 10(-7) to 10(-4) M. Caffeine-induced Ca2+ release from the maximally Ca2+ -loaded SR was also not different between the two groups at caffeine concentrations of 0.5-30 mM. However, when the relative amount of Ca2+ accumulated in the SR with 10(-6), 3 x 10(-6), or 10(-5) M Ca2+ loading solutions for various loading periods was estimated by the area under the 25 mM caffeine-induced contraction, the accumulation of Ca2+ was significantly slower in hypertrophied fibers than in normal fibers. We conclude that depressed Ca2+ accumulation by the SR plays a role in modulation of contractile performance in this model of chronic pressure overload in rats.

Animals↗
PubMed1988

The specific GTP requirement for inositol 1,4,5-trisphosphate-induced Ca2+ release from skinned vascular smooth muscle.

Exogenous GTP was required for the induction of Ca2+ release from smooth muscle SR by IP3 if endogenous GTP was depleted. NaN3 could function as a partial substitute for GTP as a cofactor for the IP3-induced Ca2+ release from the SR. In contrast to the IP3-induced Ca2+ release, caffeine-induced Ca2+ release from the SR did not require GTP. Pertussis toxin inhibited the IP3-induced Ca2+ release from the SR, whereas it had no effect on caffeine-induced Ca2+ release. These results indicate that in smooth muscle two different Ca2+ release-channels exist in the SR: (a) activated by IP3, and (b) activated by caffeine or Ca2+.

Animals↗
PubMed1988

[Clinical symptoms and disability of myotonic dystrophy in Japan].

We performed the first nationwide survey of myotonic dystrophy (MyD) in Japan. This paper reports the result of analysis of clinical pictures and disability of 670 patients found in this survey. 413 cases (61.6%) were males and 257 (38.4%) were females. Male/female ratio was approximately 1.6. The age of onset was most often in the third or fourth decade. Mean age of onset was 27.7 years in the males and 26.8 years in the females. Eight percent of the cases presented their symptoms before the age of 9 years. These cases were considered to belong to congenital or infantile form of MyD. There were also a few patients who started noticing their symptoms after the age of 60 years. Duration of the illness at the time of examination was approximately 13 years in both sexes. Myotonia was observed in 97.3% of the males and 98.1% of the females. Muscular weakness was seen in 99.0% of the males and 96.5% of the females. Atrophy was present in 93.5% of the males and 88.9% of the females. These data showed that almost all cases had these three major symptoms related to the skeletal muscles. There were 16 cases which lacked myotonia, and most of them belonged to congenital or infantile form of MyD. Cataract was present in more than a half of the patients (54.4% in the males and 52.0% in the females). Mental retardation was observed in 42.4% of the males and 35.9% of the females. Frontal baldness was seen much more frequently in the males (74.6%) than in the females (22.7%). Generally, as the duration of the illness was longer, these clinical symptoms were seen in higher frequency.(ABSTRACT TRUNCATED AT 250 WORDS)

Activities of Daily Living↗
PubMed1987

GTP requirement for inositol-1,4,5-trisphosphate-induced Ca2+ release from sarcoplasmic reticulum in smooth muscle.

We have examined inositol-1,4,5-trisphosphate (IP3)-induced Ca2+ release from the sarcoplasmic reticulum (SR) in the skinned vascular smooth muscle. The amount of Ca2+ in the SR was estimated indirectly by caffeine-induced contraction of the skinned preparation. The Ca2+ release from the SR by IP3 required GTP. A non-hydrolyzable analogue of GTP, guanosine 5'-(beta gamma-imido) triphosphate (GppNHp) could substitute for GTP in the IP3-induced Ca2+ release. These results suggest an involvement of GTP-binding protein in the mechanism of Ca2+ release from the SR by IP3 in smooth muscle.

Animals↗
PubMed1987

Modulation of ryanodine-induced Ca2+ release in amphibian skeletal muscle.

We examined effects of ryanodine on tension in intact and skinned amphibian skeletal muscle. 100 microM ryanodine (RY) alone in the frog Ringer's solution (FR) produced tension in the intact muscle reaching its peak by 1 h; 10 min treatment with RY augmented depolarization-induced tension and prevented a subsequent caffeine-induced contraction. In contrast, RY in Ca2+-free FR was unable to produce tension, after which caffeine produced irreversible tension. In skinned fibers, RY at pCa 6.5 produced tension and abolished a subsequent caffeine-induced contraction; while Ry in 2 mM EGTA did not produce tension. These data indicate that RY, in the presence of CA2+, releases CA2+ from the SR resulting in subsequent depletion of CA in the SR.

Alkaloids↗
PubMed1987

Mechanism of calcium activation in vascular smooth muscle.

The primary stimulus for activation of vascular smooth muscle is an increase in the cytosolic free Ca2+ concentration. The level of activating Ca2+ is determined by a variety of Ca2+ homeostatic mechanisms. Ca2+ entry from the extracellular space occurs through the resting Ca2+ leak and the excitable Ca2+ channels: viz. voltage-gated, receptor-operated and stretch-activated channels. Ca2+ release from sarcoplasmic reticulum is induced by inositol triphosphate (IP3) and, possibly, by Ca2+ itself. Activating Ca2+ binds to calmodulin, forming a complex which induces myosin light chain phosphorylation and initiates smooth muscle contraction. The continuous Ca2+ entry together with the higher Ca2+ sensitivity of the contractile apparatus can then maintain smooth muscle tension. Ca2+ buffering by the sarcoplasmic reticulum and Ca2+ extrusion by Ca2+ pumps serve to lower the cytosolic free Ca2+ concentration. These Ca2+-lowering mechanisms are possibly regulated by cyclic nucleotides.

Animals↗
PubMed1987

Congenital myopathy with type II muscle fiber hypoplasia.

We examined a 14-month-old boy with severe muscular hypotonia and weakness. Loss of tendon reflexes were noted at age 2 months. Right-sided heart failure and dyspnea during sleep developed at age 4 months. Muscle biopsy revealed selective hypoplasia of type II fibers and normal type I fibers. Intercostal and diaphragmatic muscles showed similar changes at necropsy and probably accented the respiratory failure.

Humans↗
PubMed1986

Proliferation of Schwann cells in demyelinated rat sciatic nerve.

Experimental demyelination was induced by intraneural injection of anti-galactocerebroside serum into the sciatic nerves of rats. Schwann cells undergoing mitotic division were observed between days 3 to 9 after the injection and demyelinated segments were still associated with macrophages. Dividing Schwann cells were often present in association with both unmyelinated and myelinated fibers. Whether or not, daughter Schwann cells migrate along the same fiber towards neighboring demyelinated segments remains unclear. When Schwann cells attached to axon membranes of demyelinated segments were studied at later time points, they were present in clusters randomly at various regions of the segments. There was no proximo-distal gradient for the wave of Schwann cell proliferation. Mean Schwann cell internuclear distances were around 40-50 microns at the earliest time of remyelination. Schwann cell redistribution and remyelination progressed regardless of the length of demyelinated segments.

Animals↗