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Biomedical subjects

K Sahashi

Publications and source records attributed to K Sahashi.

At least 91 records · Page 5Linked to original sources
PubMed1985

Immunohistochemical demonstration of carbonic anhydrase III and muscle-specific enolase in paraffin-embedded human skeletal muscle sections.

We have demonstrated the histochemical fiber types of human skeletal muscle in paraffin sections by the immunohistochemical method, together with compatible observations previously made in frozen sections that carbonic anhydrase III is mainly localized in type 1 fibers (Shima et al. 1983), and muscle-specific enolase in type 2 fibers (Ibi et al. 1983). This method is useful to analyze the fiber types when frozen muscle samples at biopsy or autopsy cannot be obtained.

Animals↗
PubMed1983

A role of renal K+-stimulated phosphatase activity on elevation of urinary sodium excretion in fluoride-treated rats.

Fluoride administered to nonfasted rats caused an elevation of urinary sodium excretion but not an increased urinary potassium excretion as previously observed by one of us in fasted rats. This elevated urinary sodium excretion was associated with decreased renal K+-stimulated phosphatase activity. The decreased phosphatase activity was reversed by treatment with aldosterone, but not by treatment with prednisolone.

Aldosterone↗
PubMed1983

Amyotrophic lateral sclerosis. Lack of central chromatolytic response of motor neurocytons corresponding to active axonal degeneration.

Ventral spinal roots and anterior horn cells in the lateral nuclear group of the fourth lumbar segment from 21 patients with amyotrophic lateral sclerosis (ALS) and 23 control patients were morphometrically analyzed. The number of large myelinated fibers was remarkably decreased, while small myelinated fibers were well preserved. The population of large myelinated fibers significantly correlated with the population of anterior horn cells. Numerous axonal degenerations were observed in the ventral spinal roots of patients with ALS, even in patients with severe loss of neurons and axons. In spite of this high frequency of active axonal degeneration, the incidence of central chromatolysis of anterior horn cells remained at the control level.

Adult↗
PubMed1983

Degenerating compartment and functioning compartment of motor neurons in ALS: possible process of motor neuron loss.

Using a morphometric method, we studied ventral spinal roots and anterior horn neurons of the fourth lumbar segment in 17 patients with ALS. Both populations of large myelinated fibers and anterior horn cells had significantly high correlations to muscle strength in the legs and duration of symptoms. However, active axonal degeneration was consistently present in terms of either large myelinated fibers or anterior horn cells.

Aged↗
PubMed1982

A newly recognized congenital myasthenic syndrome attributed to a prolonged open time of the acetylcholine-induced ion channel.

Five familial cases (in two families) and one sporadic case of a new congenital myasthenic syndrome were investigated. Symptoms arise in infancy or later life. Typically, one finds selective involvement of cervical, scapular, and finger extensor muscles, ophthalmoparesis, and variable involvement of other muscles. There is a repetitive muscle action potential to single nerve stimulus in all muscles and a decremental response at 2 to 3 Hz stimulation in clinical affected muscles. Microelectrode studies reveal markedly prolonged end-plate potential (epp), miniature end-plate potential (mepp), and miniature end-plate current; normal quantum content of the epp; and a smaller than normal or low-normal mepp amplitude. Light microscopy demonstrates predominance of type I fibers, small groups of atrophic fibers, tubular aggregates and vacuoles near end-plates, abnormal end-plate configuration, and nonspecific myopathic changes. Abundant acetylcholinesterase activity is present at all end-plates, and the activity and kinetic properties of this enzyme in muscle are normal. Calcium accumulated at the end-plate in one patient. Quantitative electron microscopy shows decrease in the size of nerve terminals, increase in the density of synaptic vesicles, and reduction in the length of postsynaptic membranes. There is focal degeneration of junctional folds with corresponding loss of acetylcholine receptor, most marked in cases with the lowest mepp amplitude. There are no immune complexes at the end-plate. Fiber regions near end-plates display dilation, proliferation, and degeneration of the sarcoplasmic reticulum; nuclear, mitochondrial, and myofibrillar degeneration; and vacuoles resembling those found in periodic paralysis. A prolonged open time of the acetylcholine-induced ion channel is considered to be the basic abnormality and may account for the physiological, morphological, and clinical alterations.

Acetylcholine↗
PubMed1981

The immunopathology of acquired myasthenia gravis.

Specific probes (alpha-bungarotoxin for acetylcholine receptor (AChR), staphylococcal protein A for IgG, monospecific antibodies against C3 and C9) labelled with peroxidase were applied to study of the ultrastructure of the MG end plate. In each case of MG there was postsynaptic AChR deficiency, usually greatest at end plates with marked degeneration of junctional folds. Morphometric estimates of postsynaptic AChR correlated linearly with the MEPP amplitude. In each case of MG, IgG was localized on the postsynaptic membrane where AChR is known to be located and on debris in the synaptic space. The abundance of antibody was proportionate to the amount of AChR remaining at the end plate. The localization of C3 was essentially identical with that of IgG. For most cases of MG it can be inferred that binding of IgG and C3 to AChR does not interfere with receptor function. C9, the terminal lytic complement component, was localized on debris in the synaptic space and on remnants of junctional folds. This proves that complement mediated destruction of junctional folds occurs in human MG. Studies in experimental auto-immune MG indicate that antibody-dependent internalization of AChR occurs in subclinical, mild and more severe diseases but increased AChR synthesis can compensate for this in subclinical and mild myasthenia. Complement-mediated injury of the postsynaptic membrane appears to be a requirement for induction of more severe MG.

Complement Activation↗
PubMed1980

Ultrastructural localization of the terminal and lytic ninth complement component (C9) at the motor end-plate in myasthenia gravis.

The terminal and lytic complement component (C9) was localized at the motor end-plate in acquired autoimmune myasthenia gravis (MG) by the immunoperoxidase method, with adequate preservation of fine structure and negligible background staining. C9 was localized on short segments of the postsynaptic membrane on degenerated fragments of the junctional folds shed into the synaptic space, and on disintegrating junctional folds. An inverse relationship was noted between the structural integrity of the junctional folds and the abundance of C9 at a given end-plate region. Destruction of junctional folds by complement may induce relocation of the nerve terminal and increased spatial separation of end-plate regions on the muscle fiber. Destruction of junctional folds by the complement membrane attack complex is a cause of the acetylcholine receptor deficiency at the MG end-plate, but antibody-dependent modulation of the receptor may also contribute to deficiency of the receptor. In certain disorders other than autoimmune MG, pathological mechanisms other than complement-mediated lysis may affect the structural integrity of the postsynaptic region.

Adolescent↗
PubMed1979

Passively transferred experimental autoimmune myasthenia gravis. Sequential and quantitative study of the motor end-plate fine structure and ultrastructural localization of immune complexes (IgG and C3), and of the acetylcholine receptor.

Experimental autoimmune myasthenia gravis (EAMG) was passively transferred with immunoglobulin from rats with chronic EAMG to normal recipients. IgG and C3 were localized on terminal expansions of junctional folds of end-plates by 6 hours. Segments of folds rich in acetylcholine receptor (AChR) and coated with IgG and C3 were shed into the synaptic space by 24 hours, resulting in AChR deficiency of the postsynaptic membrane. Many sensitized postsynaptic regions were destroyed by macrophages by day 2, but effective nerve-muscle contacts were reestablished by day 5. On day 10, end-plates were still structurally abnormal and showed AChR deficiency, but the animals were clinically recovered. On day 54, postsynaptic regions were still reduced in size, with slight reduction of postsynaptic AChR. Throughout the study, the miniature end-plate potential amplitude tended to vary directly with morphometric estimates of the abundance of the postsynaptic membrane reacting for AChR. Complement-mediated injury to the junctional folds and opsonization of the postsynaptic region can explain the morphologic changes. It is not yet known why phagocytic invasion of the end-plate occurs in acute EAMG and in passively transferred EAMG induced by chronic EAMG immuglobulin, but not in chronic EAMG and only rarely in the human disease.

Animals↗