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Biomedical subjects

K Saida

Publications and source records attributed to K Saida.

At least 91 records · Page 5Linked to original sources
PubMed1986

Experimental clioquinol intoxication in rats: abnormalities in optic nerves and small nerve cells of dorsal root ganglia.

Pathological abnormalities in the central (CNS) and peripheral nervous system (PNS) were produced in rats by daily administration of 300-400 mg/kg clioquinol for 7-40 days. The changes comprised axonal degeneration of optic nerve fibers and mitochondrial swellings in small nerve cells of dorsal root ganglia. There were occasional myelin splittings in the spinal nerve roots. No apparent changes were observed in the spinal cord or peripheral nerves. Similar changes were occasionally encountered to a lesser extent in control rats by restricting the diet and water to maintain the body weight comparable to the ranges of experimental animals. It seemed that not only clioquinol intoxication but nutritional deficiency also contributed, in part, to the production of these CNS and PNS abnormalities. The possibility of the presence of peripheral neuropathy in subacute myelooptic neuropathy is discussed.

Animals↗
PubMed1986

Electrophoretic identification of calmodulin in rat parotid gland.

A heat-stable extract of rat parotid gland contained a protein the electrophoretic migration of which on SDS-polyacrylamide gel was accelerated by Ca2+. Its apparent molecular weight was about 17 or 20 K in the presence or absence of Ca2+, respectively; it was able to bind Ca2+. These properties are exactly those of purified calmodulin.

Animals↗
PubMed1986

Role of nonspecific myelin destruction by delayed type hypersensitivity in primary demyelination.

To clarify the role of nonspecific myelin destruction mediated by delayed type hypersensitivity (DTH) in primary demyelination, DTH to tuberculin was induced within the endoneurium by intraneural injection of purified protein derivative (PPD) or sonicated Mycobacterium tuberculosis into the sciatic nerves of Lewis rats and guinea pigs which had previously been sensitized to tuberculin. The morphological features of the nerves proximal to the site of needle insertion were assessed 5 days after injection. By changing the PPD concentration of solution for intraneural injection, various degrees of DTH reaction could be produced in the nerve. Infiltration of mononuclear cells including macrophages was observed around the vessels and in the vicinity of the myelin sheaths. Although nonspecific damage of axons, myelin sheaths and Schwann cells was observed in areas heavily infiltrated with inflammatory cells, primary demyelination was hardly recognized. Another group of Lewis rats previously immunized with galactocerebroside (GC), the major glycolipid hapten of myelin, in Freund's complete adjuvant received intraneural injection of PPD or GC liposomes. Neither cellular nor humoral immunity to GC was detected in these rats. The nerves injected with GC liposomes showed no inflammatory cell infiltration except for a few macrophages containing liposomes and those injected with PPD showed infiltration of mononuclear cells without primary demyelination. Our findings reveal that nonspecific myelin destruction induced by DTH does not play an important role in immune-mediated demyelination.

Animals↗
PubMed1986

Clinical and genetic studies of muscular dystrophy in young girls.

During the years 1971-81, we treated 7 girls with clinical features suggestive of Duchenne dystrophy. Muscle weakness developed at 1.5 or at 5-8 years and progressed rapidly. Two girls were in wheel-chairs in their teens. Muscle atrophy began in the proximal parts of the lower extremities and pseudohypertrophy of the calf occurred in all patients. Serum creatine phosphokinase (CPK) activity was moderately to highly elevated in all cases and EMG showed a moderate to marked myopathic pattern. Chromosomal studies showed normal finding in the five examined. Mental retardation (IQ 37-73) was present in four. Consanguinity was present in 3 out of the 7 cases. Two mothers showed elevated levels of CPK and myopathic patterns on EMG. In addition, one mother had slight muscle weakness at the age of 42 and another had prominent pseudohypertrophy of the calf. Sex-linked recessive inheritance might be considered here, because carriers of autosomal recessive type never showed elevated levels of CPK or mild myopathic symptoms. The other five of our seven might be cases of autosomal recessive inheritance, because the mothers had normal serum CPK levels and in 2 families there was a consanguinity.

Adolescent↗
PubMed1986

Superprecipitation is a model for in vitro contraction superior to ATPase activity.

We investigated which activity of myosin B (natural actomyosin), super-precipitation or ATPase, is better suited as a parameter for measuring in vitro contraction with emphasis on the response of myosin B to Sr2+. The Sr2+ concentration giving half-maximum (KSr2+) binding of Sr2+ to cardiac troponin was not different from that to skeletal troponin, whether the troponins were contained in the actomyosin system or in the isolated state. However, KSr2+ for the ATPase activity of cardiac myosin B is slightly smaller than that of skeletal myosin B. This difference in KSr2+ is more marked when superprecipitation was used as the indication for in vitro contraction. If the above results were compared with those of Kitazawa (1976) using glycerinated fibers of cardiac and skeletal muscle, the differences in KSr2+ between cardiac and skeletal muscle increased in the order: Sr-binding to troponin less than ATPase activity less than superprecipitation less than contraction of glycerinated fibers. The increase in the effect of pH on Ca2+-related properties is also in the order: Ca-binding to troponin less than or equal to ATPase activity less than superprecipitation less than contraction of glycerinated fibers. All the results coincide with one another that the results with super-precipitation are invariably more akin to those with glycerinated fibers than to those with the ATPase activity. It is concluded that superprecipitation is a better parameter for representing in vitro contraction than ATPase activity.

Actomyosin↗
PubMed1986

Regulation of cytoplasmic Ca2+ in vascular smooth muscle.

The vascular smooth muscle of conduit arteries can be excited by either depolarization or agonists. The former stimulus opens potential sensitive Ca2+ channels in the plasmalemma and releases bound Ca2+ from its outer surface. Ne interacts with alpha-receptors to open receptor operated Ca2+ channels which are distinct from the PSCs and also liberates surface bound Ca2+. In addition, it releases "trigger" Ca2+ from the inner plasmalemmal surface which in turn induces Ca2+ release from the sarcoplasmic reticulum. The elevated cytoplasmic free Ca2+ then combines with calmodulin to stimulate myosin light-chain kinase.

Animals↗
PubMed1986

Ultrastructural study of central nervous system demyelination in galactocerebroside sensitized rabbits.

The rabbit eye model was used to investigate the role of delayed type hypersensitivity and of circulating antigalactocerebroside antibody in primary demyelination. Delayed type hypersensitivity reaction to tuberculin was induced within the retinal myelinated layers by injecting purified protein derivative into the vitreous of rabbits that were previously immunized with complete Freund's adjuvant (CFA) alone, or galactocerebroside (GC) in CFA. The morphological features of the myelinated zones were assessed 5 days after injection. All rabbits showed infiltration of mononuclear cells within the myelinated fiber bundles. Rabbits previously sensitized with CFA alone showed nonspecific destruction of nerve fibers in severe inflammatory lesions, but primary demyelination was rarely found. This suggests that myelin destruction induced by delayed type hypersensitivity reaction to interstitial antigens (purified protein derivative, so-called "bystander demyelination") by itself does not play a major role in inducing primary demyelination. On the other hand, primary demyelination was recognized in the vicinity of infiltrating mononuclear cells in rabbits previously immunized with GC in CFA and had elevated titers of serum anti-GC antibody. The destruction of the blood-brain barrier was suggested by the presence of fibrin exudates in demyelinative lesions where observation revealed selective myelin breakdown such as vesicular disruption and active stripping of myelin. This study indicates that the anti-GC antibody is an important factor in central nervous system demyelination of GC-sensitized rabbits.

Animals↗
PubMed1985

Rimmed vacuoles in biopsied muscle of nemaline myopathy.

A case of nemaline myopathy with rimmed vacuoles was presented. Muscle biopsy revealed type I fiber predominance with type grouping, thus suggesting that neurogenic factors played a pathologic role in the degenerative change.

Biopsy↗
PubMed1985

Ca2+ sources mobilized by alpha 1-receptor activation in vascular smooth muscle.

We propose the following model of Ca2+ mobilization by noradrenaline in vascular smooth muscle. Upon receptor occupation Ca2+ from a labile small intracellular store on the inner plasmalemma is released. This Ca2+ does not function as activator Ca2+ but triggers Ca2+ release from the sarcoplasmic reticulum (Ca2+-induced Ca2+ release). Simultaneously Ca2+ from an extracellularly bound store (on the external surface of the plasmalemma) is dislodged, which enters the cell through receptor linked channels. These processes are responsible for the early 'phasic' component of the noradrenaline contraction. In addition, Ca2+ from the free extracellular Ca2+ pool enters through receptor operated channels, supporting the maintained tension development.

Adrenergic alpha-Agonists↗
PubMed1985

Norepinephrine-induced intracellular Ca2+ release from vascular smooth muscle.

In rabbit aorta and superior mesenteric artery, application of NE causes release of Ca2+ from an intracellular Ca2+ store, probably SR. The amount of released Ca2+ is sufficient to activate the myofilaments submaximally. It is suggested that NE mediates Ca2+ release by a rapid increase in the free Ca2+ concentration near the SR (Ca2+-induced Ca2+ release). The uptake of Ca2+ into the store and the Ca2+-induced Ca2+ release is modulated by c-AMP.

Animals↗
PubMed1985

Familial neuropathy with dementia, retinitis pigmentosa, and dysautonomia.

We studied a 59-year-old woman with dementia, retinitis pigmentosa, sensorimotor neuropathy, and attacks of vomiting associated with blood pressure lability and loss of consciousness. Abnormalities included CT evidence of cerebral atrophy, low IQ, slow central and peripheral nerve conduction velocities, axonal degeneration in sural nerve biopsy, and elevated levels of catecholamines and slow waves in EEG during attacks. Her sister, two brothers, and daughter also had progressive muscle weakness, visual disturbance, and similar vomiting attacks. The hereditary nervous system disorder does not fit any previously described condition.

Adult↗
PubMed1985

Hydrocortisone-evoked molecular conversion of alkaline phosphatase in suckling rat small intestine.

Suckling rats were injected with hydrocortisone at 12 and 13 days after birth and were sacrificed for the experiment at 15 days. Alkaline phosphatase in the duodenum was detected as three activity bands on SDS-polyacrylamide gel electrophoresis, while in control rats, the enzyme showed a single band. The electrophoretic pattern in hydrocortisone-treated rats was similar to that observed in adult rats. This result supports the view that the maturation of intestinal alkaline phosphatase is primarily regulated by glucocorticoids.

Alkaline Phosphatase↗
PubMed1984

Rapid alterations of the axon membrane in antibody-mediated demyelination.

Alterations of nodal and paranodal axolemma of the rat sciatic nerve were investigated in antigalactocerebroside serum-induced demyelination. A ferric ion-ferrocyanide (FeFCN) stain that appears to stain the regions with a high sodium channel density in nerve fibers was applied. When acute conduction block was initiated 20 to 180 minutes after the antiserum injection, myelin terminal loops began to be detached from the paranodal axolemma and reaction product of FeFCN stain originally localized at the nodes decreased in density and extended to the paranodal axolemma. By the time that complete conduction block was established, 5 hours after the injection, FeFCN stain was barely detectable around the nodal area. The loss of staining was associated with detachment and vesiculovacuolar degeneration of the paranodal myelin. This rapid deterioration and disappearance of normal cytochemical characteristics of the axolemma in the presence of only modest paranodal demyelination could be a morphological correlate of the loss of excitability of the axon membrane.

Animals↗
PubMed1984

Cyclic AMP modulation of adrenoreceptor-mediated arterial smooth muscle contraction.

We examined the effects of cyclic AMP (cAMP) on the intracellular Ca2+ release in both the intact and skinned arterial smooth muscle. The amount of Ca2+ in the sarcoplasmic reticulum (SR) was estimated indirectly by caffeine-induced contraction of the skinned preparation and directly by caffeine-stimulated 45Ca efflux from the previously labeled skinned preparation. The norepinephrine-induced release contraction was markedly enhanced by dibutyryl cAMP (dbcAMP) and reduced by propranolol. The stimulatory effect of dbcAMP was best observed when the muscle was exposed to 10(-5) M dbcAMP and 2 X 10(-6) M norepinephrine was used to induce the release contraction. 10(-5) M cAMP had no effect on the Ca2+-induced contraction or on the pCa-tension relationship in the skinned preparation. This concentration of cAMP increased Ca2+ uptake into the SR of the skinned preparation when the Ca2+ in the SR was first depleted. 10(-5) M cAMP stimulated Ca2+-induced Ca2+ release from the SR after optimal Ca2+ accumulation by the SR. The results indicate that the stimulatory effect of cAMP on the norepinephrine-induced release contraction could be due to enhancement of the Ca2+-induced Ca2+ release from the SR in arterial smooth muscle.

Animals↗
PubMed1984

Amyotrophic lateral sclerosis: a double-blind crossover trial of thyrotropin-releasing hormone.

A double-blind crossover trial was conducted of thyrotropin releasing hormone treatment in six patients with amyotrophic lateral sclerosis. Patients received 4 mg of thyrotropin releasing hormone intramuscularly daily during the two-week treatment period. Although three patients reported subjective improvement, objective evaluation failed to demonstrate therapeutic effectiveness of thyrotropin releasing hormone in this dosage.

Adult↗
PubMed1984

Extracellular Ca2+ dependence and diltiazem inhibition of contraction in rabbit conduit arteries and mesenteric resistance vessels.

The dependence of norepinephrine-(NE-) and high potassium (80 mM K) depolarization-induced contractions on extracellular versus intracellular calcium (Ca2+) pools was studied in strips of rabbit superior mesenteric artery and its branches, and in perfused mesenteric resistance vessels. 80 mM K contractions were abolished in the presence of 0 Ca2+ 2 mM EGTA in all arteries studied, whereas 10(-5) M NE-induced contractions and stimulated 45Ca efflux in 0 Ca2+ 2 mM EGTA decreased in a graded fashion from proximal to distal arteries. These data indicate a decreasing release of intracellular Ca2+ and an increasing dependence on extracellular Ca2+ for NE-induced contractions as one proceeds from proximal to distal arteries. This pattern was paralleled by increasing sensitivity of NE-induced contractions to inhibition by diltiazem (10(-9)-10(-4) M) from proximal to distal arteries, while inhibition of 80 mM K contractions was similar in all vessels. 45Ca influx induced by 10(-5) M NE in the resistance vessels, wherein the NE does not release intracellular Ca2+, is approximately 10,000-fold more sensitive to the action of diltiazem than that in the aorta. However, when the aorta is activated by 10(-8) M NE, it becomes more sensitive to inhibition by diltiazem than when it is activated by 10(-5) M NE. The former NE concentration does not release intracellular Ca2+ in the aorta, whereas the latter does. Thus, it appears that NE-induced 45Ca influx is most susceptible to inhibition by diltiazem when the NE has not also released intracellular Ca2+. We suggest that the release of intracellular Ca2+ by NE may make its stimulated Ca2+ influx less susceptible to inhibition by diltiazem.

Animals↗
PubMed1984

Characteristics of the norepinephrine-sensitive Ca2+ store in vascular smooth muscle.

A comparison was made between the properties of the norepinephrine- and caffeine-sensitive Ca2+ store in both intact and skinned smooth muscle of the rabbit mesenteric artery. After a first application of 10(-5) M norepinephrine, reapplication of norepinephrine did not induce a second contraction in Ca2+-free medium. However, following this sequence 25 mM caffeine still induced a large contraction. The rates of Ca2+ leakage and Ca2+ filling of the norepinephrine-sensitive store were much faster than those of the caffeine-sensitive one. The amplitude of the norepinephrine-induced contraction in Ca2+-free medium also depended on the amount of Ca2+ present in the caffeine-sensitive store. In the saponin-treated skinned muscle caffeine induced a Ca2+ release only after loading with Ca2+, whereas norepinephrine was unable to induce Ca2+ release in the skinned preparation even after loading with Ca2+. The release of Ca2+ from the caffeine-sensitive store could be activated by Ca2+ itself when the skinned muscle was loaded with Ca2+ above 10(-6) M. These results suggest that the norepinephrine-sensitive Ca2+ store is distinct from a large fraction of the caffeine-sensitive one, and that the norepinephrine-sensitive store is close to the cell membrane. In vascular smooth muscle, under physiological conditions, Ca2+ released from the norepinephrine-sensitive store by norepinephrine may induce Ca2+ release from the caffeine-sensitive Ca2+ store which may be comprised of the sarcoplasmic reticulum.

Animals↗