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Biomedical subjects

K Saida

Publications and source records attributed to K Saida.

At least 127 records · Page 7Linked to original sources
PubMed1980

EAE, EAN and galactocerebroside sera bind to oligodendrocytes and Schwann cells.

Sera from rabbits with EAN induced by sensitization with galactocerebroside (GalC-EAN) bound to the surface of Schwann cells and oligodendrocytes in rat nervous system dispersion cultures. Sera from rabbits with bovine femoral nerve-induced EAN (FN-EAN) bound to Schwann cells, oligodendroglia and occasional fibroblasts. Sera from animals with bovine spinal cord-induced EAE (SC-EAE) bound to these cells and to some astrocytes as well. Absorption of the capacity to bind to oligodendroglia and Schwann cells suggests that GalC is the major, if not the only surface antigen on these two cell types to which these sera bind. The capacity of GalC-EAN, SC-EAE, and FN-EAN sera to bind to the surface of the cells responsible for myelin synthesis in both PNS and CNS correlates with the ability of these sera to cause both PNS and CNS demyelination in vitro and PNS demyelination in vivo.

Animals↗
PubMed1979

Experimental allergic neuritis induced by sensitization with galactocerebroside.

Thirteen of 31 rabbits immunized repeatedly with bovine brain galactocerebroside developed experimental allergic neuritis, manifested by flaccid paresis and hypesthesia of four limbs, 2 to 11 months after the initial inoculation. Electrophysiological studies revealed multifocal conduction block of peripheral nerves. Perivenular demyelinative lesions associated with phagocytic mononuclear cells occurred in spinal ganglia, roots, and less frequently in distal nerves.

Animals↗
PubMed1979

Demyelination produced by experimental allergic neuritis serum and anti-galactocerebroside antiserum in CNS cultures. An ultrastructural study.

Cultures of mouse cerebellum were exposed to sera from rabbits with experimental allergic neuritis induced by whole peripheral nerve immunization (WN-EAN) and to rabbit anti-galactocerebroside (GC) antisera, and were studied by electron microscopy. Both antisera produced almost identical demyelinative patterns. These consisted of large intramyelinic splittings, "smudged" changes of myelin, degeneration of oligodendrocytes, and phagocytosis of myelin by astrocytes, changes similar to those described after application of whole spinal cord-induced experimental allergic encephalomyelitis (WM-EAE) sera. In addition, patterns which have been considered more characteristic of in vivo demyelinative lesions have been found, susch as vesicular disruption of myelin lamellae and peeling off and phagocytosis of myelin by phagocytic mononuclear cells with electron dense cytoplasm. The morphologic similarities between demyelinative patterns in central nervous system (CNS) cultures induced by anti-GC antiserum and WN-EAN serum and WM-EAE serum, and the fact that elevated antibody titers to GC are found in sera from rabbits with WN-EAN and WM-EAE (Saida, et al., 1977), support the concept that anti-GC antibody is the major factor in the production of CNS demyelination in vitro by sera from rabbits with WN-EAN and WN-EAE.

Animals↗
PubMed1979

Peripheral nerve demyelination induced by intraneural injection of experimental allergic encephalomyelitis serum.

Intraneural injection of sera from rabbits with experimental allergic encephalomyelitis, induced by sensitization with bovine brain white matter in complete Freund's adjuvant, produced focal primary demyelinative lesions in rat sciatic nerves. Demyelinating activity was removed by prior incubation of antisera with central (CNS) and peripheral nervous system (PNS) myelin but not with liver or kidney, and was heat-labile and complement-dependent. Recipient animals developed a sensorimotor disturbance of their toes and ankles on the side injected with antiserum. Twenty minutes after antiserum injection, Schwann cells showed focal cytoplasmic outpouching and their external mesaxons opened. Between 1 and 8 hours after injection vacuolation, splitting and vesiculation of myelin became increasingly prominent at Schmidt-Lanterman clefts and paranodal regions, with concomitant degenerative changes in Schwann cell cytoplasm. Polymorphonuclear cell infiltration and endoneurial edema were apparent at this time. Substantial demyelination occurred before the appearance of phagocytic cells. Between 8 hours and 3 days many nerve fibers were surrounded and attacked by invading macrophages. Axons became demyelinated progressively over several internodes by macrophage phagocytosis. Early signs of remyelination were observed by 5 days. These findings suggest that antibodies directed against antigens common to both CNS and PNS myelin can produce in vivo peripheral nerve demyelination.

Animals↗
PubMed1979

A case of the syndrome of inappropriate secretion of TSH.

A girl aged 4 years with goiter and accelerated physical and skeletal growth was found to be hyperthyroid on the basis of elevated serum thyroid hormone level, nevertheless both the basal TSH and TSH responsiveness to TRH were maintained within the normal range. Serum TSH was suppressed by exogenous T3 and dexamethasone administration, but not significantly changed after propylthiouracil (PTU) treatment. The diurnal rhythmicity of anterior pituitary hormones was preserved with the high nocturnal peak of TSH and prolactin. Clinically, neither thyrotoxic signs nor evidences of pituitary tumor were observed. Her accelerated growth and elevated thyroid hormone level appeared to be induced by inappropriate secretion of TSH. In view of the literature, this is the first case of the syndrome of inappropriate secretion of TSH excluding the neoplastic origin in Japan.

Adrenocorticotropic Hormone↗
PubMed1979

In vivo demyelination induced by intraneural injection of anti-galactocerebroside serum: a morphologic study.

Intraneural injection of rabbit anti-galactocerebroside (anti-GC) serum produced focaldemyelinative lesions in rat sciatic nerves. Recipient rats developed a sensory motordeficit of the toes and feet on the side injected with anti-GC serum. Schwann cellabnormalities in recipient nerves were apparent by 20 minutes, followed by myelinsplitting and vesiculation over the next 8 hours. Macrophages first appeared in moder-ate numbers by 15 hours, and degraded myelin was completely phagocvtized by 5 days.An acute inflammatory reaction consisting of endoneurial edema, polymorphonuclearcell infiltration, and fibrin extravasation also was prominent. In vivo demyelinativeactivity of rabbit anti-GC serums was removed by pre-incubation with GC or central orperipheral nervous system myelin and was also lost when the serums were heated at 56C for 30 minutes and injected into nerves of rats previously injected with cobra venomfactor. Anti-GC antibodies are present in the serum of rabbits with experimentalallergic neuritis (WNV-EAN) and encephalomyelitis (WM-EAE) produced, respectively,by immunization with whole peripheral nerve or brain white matter and may play arole in the pathogenesis of demyelination in GC-induced EAN, WN-EAN, or WM-EAE.

Animals↗
PubMed1978

Characteristics of Ca2+- and Mg2+-induced tension development in chemically skinned smooth muscle fibers.

Chemically skinned fibers from guinea pig taenia caecum were prepared by saponin treatment to study the smooth muscle contractile system in a state as close to the living state as posible. The skinned fibers showed tension development with an increase of Ca2+ in the solution, the threshold tension occurring as 5 X 10(-7) M Ca2+. The maximal tension induced with 10(-4) M Ca2+ was as large and rapid as the potassium-induced contracture in the intact fibers. The slope of the pCa tension curve was less steep than that of skeletal muscle fibers and shifted in the direction of lower pCa with an increase of MgATP. The presence of greater than 1 mM Mg2+ was required for Ca2+-induced contraction in the skinned fibers as well as for the activation of ATPase and superprecipitation in smooth muscle myosin B. Mg2+ above 2 mM caused a slow tension development by itself in the absence of Ca2+. Such a Mg2+-induced tension showed a linear relation to concentrations up to 8 mM in the presence of MgATP. Increase of MgATP concentration revealed a monophasic response without inhibition of Ca2+-induced tension development, unlike the biphasic response in striated muscle. When MgATP was removed from the relaxing solution, the tension developed slowly and slightly, even though the Mg2+ concentrations was fixed at 2 mM. These results suggest a substantial difference in the mode of actin-myosin interaction between smooth and skeletal muscle.

Adenosine Triphosphatases↗
PubMed1978

Antiserum-mediated demyelination in vivo: a sequential study using intraneural injection of experimental allergic neuritis serum.

Primary segmental demyelination accompanied by mononuclear phagocytes was induced by injection of antiserum into rat peripheral nerve, and the morphologic sequence of events was studied. Antisera were obtained from rabbits with experimental allergic neuritis (EAN) produced by the inoculation of emulsified bovine peripheral nerves in complete Freund's adjuvant. Sera were injected directly into rat sciatic nerve to circumvent the blood-nerve barrier. Recipient rats developed sensorimotor paralysis on the side injected with experimental allergic neuritis sera. Intense focal demyelinative lesions resulted from injection of experimental allergic neuritis sera. Control sera obtained from rabbits inoculated with bovine serum albumin in complete Freund's adjuvant did not produce paralysis or demyelination. The earliest change was damage to Schwann cells, seen 20 minutes after antiserum injection. Within a few hours lamellar splitting and vacuolation of myelin began to paranodal regions and Schmidt-Lanterman clefts and there were infiltrating polymorphonuclear cells. By 8 hours without the detectable presence of monocytes or macrophages, myelin vesiculation became advanced and widespread. By 15 hours, endoneurial edema had reached its maximum. Macrophages were found in association with myelinated nerve fibers. From that time through the next 5 days, demyelination progressed to complete denudation of axons by macrophage phagocytosis of myelin. Activated cytoplasm of Schwann cells reinvested demyelinated axons, often in concert with persisting phagocytic macrophages. Peripheral nerve demyelination thus transferred evolved rapidly, and myelin destruction occurred prior to the appearance of monocytes or macrophages. Demyelinating activity was lost after absorption by purified peripheral nerve myelin but not by liver or kidney and was heat-labile and complement dependent (T. Saida, K. Saida, D. H. Silberberg, and M. J. Brown: Nature 272: 639, 1978).

Animals↗
PubMed1977

Alterations of fast axoplasmic transport in experimental methyl n-butyl ketone neuropathy.

Methyl n-butyl ketone (MBK) is known to produce a giant axonal neuropathy in man and experimental animals characterized pathologically by a gradual increase in the number of neurofilaments which become associated with focal areas of axonal swelling and thinning of the myelin sheath. Fast axoplasmic transport was studied in rats exposed to MBK. In 10 severely paralyzed rats exposed to MBK there was a significant impediment of fast axoplasmic transport following dorsal root ganglion injections (x +/- S.D. = 283.2 +/- 20.34 mm/day) compared to normal controls (417.6 +/- 23.78 mm/day). In rats undergoing injections into the ventral horn of the spinal cord there was a gradual impairment of the mean down flow rate for transport of [3H]leucine which correlated with the severity of the MBK induced neuropathy. Quantitative morphological determinations showed that the total number of neurotubules per unit cross-sectional myelin area and the number of neurotubules associated with mitochondria in swollen axons was unchanged from normal. The total number of mitochondria in randomly sampled axons varied significantly from controls but the absolute number of mitochondria associated with neurotubules was unchanged from normal. The results of these studies suggest that the impediment of fast axoplasmic transport may be related to the increased neurofilaments producing focal areas of axonal blockage.

Animals↗
PubMed1977

Concurrence of Grave's disease and Hashimoto's thyroiditis.

Early histological changes in the thyroid gland were examined in 30 patients with juvenile thyrotoxicosis, by means of needle biopsy. Based on the degree of lymphocytic infiltration and degenerative changes in follicular epithelium, results were classified into four groups. A: hyperplastic changes without cellular infiltration (6 patients, 20%); B: hyperplastic changes with areas of focal thyroiditis less than 30% of specimen (10 patients, 33%); C: those with 30 to 60% areas ot thyroiditis (10 patients, 33%); D: almost diffuse thyroiditis (4 patients, 13%). Moderate to severe lymphocytic thyroiditis was frequently present in the early stage of hyperplastic thyroid glands. The clinical significance of the 4 histological groups was evaluated. Neither clinical signs nor routine laboratory tests could differentiate these groups except group D, in which thyrotoxic signs were mild and transient. However, serum antithyroid antibodies tended to increase in accordance with severity of thyroiditis. The rate of remission was high in groups C and D, whereas relapse was frequent in group A. These results suggest that Grave's disease and chronic lymphocytic thyroiditis are closely related in the early stage of thyrotoxicosis in children, and that the clinical course may be considerably altered by the degree of associated thyroiditis.

Adolescent↗
PubMed1976

Peripheral nerve changes induced by methyl n-butyl ketone and potentiation by methyl ethyl ketone.

A study of the sequential morphological changes in the peripheral nerve induced by experimental inhalation exposure of methyl n-butyl ketone (MBK) revealed that the earliest change was an increase in the number of neurofilaments in the large myelinated nerve fibers. This change occurred prior to axonal swelling or myelin thinning. As the duration of exposure lengthened the number of neurofilaments gradually increased and ultimately produced axonal swelling with secondary thinning of the myelin sheath. This appears to be the pathogenesis of the "giant axonal" neuropathy. Another change observed early in this neuropathy was the presence of inpouchings of the myelin sheath, which also increased in number in parallel to the duration of exposure. A careful study of the sequential changes in the entire motor unit did not show a predilection for early morphological changes at the axon terminal. Abnormalities at the neuromuscular junction occurred only after a full spectrum of changes were seen in the main nerve trunk, nerve roots and intramuscular nerves. An important observation was the marked potentiation of peripheral neurotoxicity observed when animals were exposed to MBK in combination with methyl ethyl ketone (MEK) at a ratio of 1:5, MBK:MEK. The latter solvent showed no neurotoxic effect alone. This might help explain a recent outbreak of a polyneuropathy affecting many workers. One further observation was that the sural nerve of a patient with prolonged exposure to MBK showed changes similar to those induced experimentally.

Adult↗