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Biomedical subjects

K Saida

Publications and source records attributed to K Saida.

At least 109 records · Page 6Linked to original sources
PubMed1983

P2 protein-induced experimental allergic neuritis. An ultrastructural study.

Experimental allergic neuritis (EAN) was induced in 2 groups of inbred Lewis rats by sensitization with P2 protein and peripheral nervous system (PNS) myelin, both purified from bovine intradural roots. Light- and electronmicroscopic study of P2-induced EAN revealed demyelinative lesions in spinal ganglia and root nerves and less frequently in peripheral nerves and root entry zones. Both small and large myelinated fibers were demyelinated, contradictory to the reported selective binding of anti-P2 antibodies to myelin of large fibers. The early lesions were characterised by perivenular lymphocytic infiltration, and subsequent "dissolution" of myelin sheath was associated with invasive of phagocytic cells. The distribution of demyelinative lesions and patterns of demyelination resembled those of PNS myelin-induced EAN except that the disease was milder and dissolution of myelin and intramyelinic edema were more frequently found in P2-induced EAN. The abundance of demyelination in P2-induced EAN strikes contrast to the scarcity of myelin change in experimental allergic encephalomyelitis (EAE) induced by myelin basic protein immunization.

Animals↗
PubMed1983

Mechanism of Ca++ antagonist-induced vasodilation. Intracellular actions.

We studied the effects of Ca++ antagonists on intact and skinned muscles of rabbit mesenteric artery. Intact muscle contractions were inhibited by 10(-6) M diltiazem, whereas greater levels were required to abolish contractions in skinned muscle fibers. In contrast, nisoldipine had no effect on skinned muscle contractions, although it inhibited, almost completely, the contraction of intact muscle at concentrations below 10(-6) M. In the presence of EGTA, norepinephrine-induced contractions result from a release of Ca++ from an intracellular store. Diltiazem inhibited these contractions at concentrations between 10(-6) and 10(-4) M. Higher doses were required in studies with skinned muscle preparations. Unlike diltiazem, nisoldipine only partially inhibited the Ca++-free norepinephrine-induced contractions in the range of 10(-7) to 10(-5) M. From these results, we assumed that at low concentrations (below 10(-6) M), diltiazem induced relaxation by blocking Ca++ influx, whereas at relatively high concentrations (above 10(-6) M), an inhibition of Ca++ release from an intracellular store also occurred. A similar conclusion was reached regarding the mechanism whereby nisoldipine inhibits force developments.

Animals↗
PubMed1982

In vivo demyelinating activity of sera from patients with Guillain-Barré syndrome.

The in vivo demyelinating capacity of sera from 27 patients with Guillain-Barré syndrome (GBS) and 47 other individuals was studied by intraneural injection into rat sciatic nerves. The morphological features of the nerves in cross section taken just proximal to the site of needle insertion was assessed 48 hours after injection and the extent of demyelination was quantitated. All 27 GBS serum samples were obtained in the first three weeks of clinical disease. Of these, 11 (41%) produced demyelination. Demyelinative activity of GBS sera correlated only with severity of clinical disease (p less than 0.01). The extent of demyelination after intraneural injection of human sera was less intense on average than that produced by sera from animals with experimental allergic neuritis. Three of 40 (7.5%) sera obtained from normal subjects and patients with other neurological diseases also caused in vivo demyelination, although the activity was weaker and occurred less often than with GBS serum.

Adult↗
PubMed1982

Acute conduction block associated with experimental antiserum-mediated demyelination of peripheral nerve.

Intraneural injection of antisera from rabbits with high antigalactocerebroside antibody levels into rat sciatic nerve produced acute nerve conduction block. This was first apparent in some motor axons between 30 and 60 minutes after injection and progressed to completion within 2 to 4 hours. Concurrent morphological evidence of demyelination was present, but structural changes at the time of onset of block were mild and were restricted to the myelin and Schwann cell, particularly at the paranodal areas and Schmidt-Lanterman clefts. It is suggested that paranodal lesions could account for the observed conduction block.

Animals↗
PubMed1982

Intracellular Ca release in skinned smooth muscle.

The release of internal Ca from saponin-treated skinned smooth muscle of guinea pig taenia caecum was studied. The amount of Ca released was estimated by the area under the contraction curve during treatment with 25 mM caffeine in the presence of 0.1 mM EGTA. The magnitude of the caffeine response in skinned muscle, after loading with 10(-6) M Ca for 3 min, was similar to that in the depolarized muscle in the presence of EGTA before treatment with saponin. This suggests that Ca in the skinned muscle was in a physiological range after loading. The release of Ca from the storage site could be facilitated by Ca itself when the skinned muscle was exposed to Ca above 3 x 10(-6) M. An increase in environmental MG concentration suppressed the Ca-induced Ca release mechanism. Sudden replacement of propionate with Cl in the bathing solution made it possible to release Ca from the storage site. This "depolarization"-induced Ca release occurred only immediately after the application of Cl; thereafter, the Ca release mechanism seemed to be inactivated by the prolonged presence of Cl. These results suggest that two mechanisms of Ca release operate in smooth muscle: (a) release induced by Ca itself, and (b) release by "depolarization".

Animals↗
PubMed1982

Correlation of hepatic thyroxine 5'-monodeiodination with hexose monophosphate shunt in young rats.

The role of NADPH and glutathione (GSH) in hepatic thyroxine (T4) 5'-deiodination and possible metabolic linkage between T4 converting system ad hexose monophosphate shunt were studied in young rats during maturation. Low activity of T4 5'-deiodinase in young rats was enhanced 2-4-fold with the addition of 1 mM NADPH and GSH in vitro, the effect of which was more prominent with NADPH than with GSH. The highest enhancement was observed at 2-3 wk of age, whereas basal T4 5'-deiodinase activity was gradually increased until 5-6 wk of age, decreasing to adult level thereafter. This change was associated with a rise in GSH and glycogen content in the live and significantly correlated to the changes in glutathione reductase activity (r = 0.622, P less than 0.001). In contrast, glucose-6-phosphate dehydrogenase (G6PD) activity remained depressed until 5 wk of age and rose sharply thereafter. Between T4 5'-deiodinase and G6PD activities after 6 wk of age, an inverse correlation was noted (r = -0.749, P less than 0.01). A dose-response relationship between triiodothyronine (T3) production and NADPH in vitro showed similar age-related changes, whereas dose-dependency of T3-formation on GSH was decreasing with age, especially under the presence of 1 mM NADPH. These results indicate that: (1) NADPH and GSH are important cofactors of T4 conversion to T3; (2) NADPH appears to be more rate-limiting in the maturational process of the system; and (3) hexose monophosphate shunt plays a significant role in the regulation of T4 5'-monodeiodination through NADPH and GSH formation.

Animals↗
PubMed1982

Effects of Ca antagonists on Ca fluxes in resistance vessels.

We have examined contractions and 45Ca fluxes induced by norepinephrine (NE) and 80 mM potassium (high K) depolarization and their inhibition by diltiazem in rabbit mesenteric resistance vessels. Contraction induced by both NE and high K depended almost completely on extracellular Ca. Dose-response curves for diltiazem inhibition of NE (10(-5) M) and high K contractions showed ED50 values of 1 X 10(-8) and 6 X 10(-7) M, respectively, indicating that the receptor-operated channel (ROC) was more sensitive than the potential-operated channel (POC) to the action of diltiazem. Diltiazem (10(-6) M) was shown to inhibit NE- and 80 mM K-stimulated 45Ca influx effectively by 87 +/- 15 and 85 +/- 10%, respectively. Comparison of these data to those obtained from aorta suggest that although the sensitivity of the POC is approximately the same in aorta and mesenteric resistance vessels, the sensitivity of the ROC is much greater in the latter. This increased sensitivity is paralleled by a greatly decreased role of intracellular Ca release in NE contraction in mesenteric resistance vessels.

Animals↗
PubMed1982

Immune-mediated demyelination--immunopathological basis for electrophysiological changes.

A focal immune-mediated demyelinating lesion of peripheral nerve was produced by intraneural injection of antiserum to galactocerebroside, a major glycosphingolipid hapten common in CNS and PNS myelin. This model provides an excellent system for correlative studies of physiological and pathological alterations in the processes of demyelination, because the time course of such changes is predictable from animal to animal. Twenty minutes after antiserum injection, Schwann cells showed focal cytoplasmic outpouching and their external mesaxons opened. Between 1 and 8 h after injection "melting," splitting, vesiculation and vacuolation of myelin became increasingly prominent at paranodal regions and Schmidt-Lantermann clefts, with concomitant degenerative changes in Schwann cell cytoplasm. Disruption of myelin in the paranodal region with detachment of the outermost paranodal myelin loops from paranodal axon resulted in an increase in nodal surface area. This seems to be the most critical anatomical alteration responsible for the early changes in propagation of nerve impulses in this antibody-mediated demyelinating lesion. Between 8 h and 3 days axons became demyelinated progressively over several internodes by macrophage phagocytosis. The onset of clinical and saltatory conduction recovery from the lesion corresponded to the appearance of 2-8 myelin lamellae around each remyelinating axon.

Animals↗
PubMed1981

Experimental allergic neuritis induced by galactocerebroside.

Experimental allergic neuritis (EAN), an animal model of human demyelinative neuritis, was induced by sensitization with galactocerebroside, a glycolipid hapten common in central and peripheral nervous system myelin. Between two months and one year after the initial sensitization, 11 of 24 rabbits immunized repeatedly with bovine brain galactocerebroside (GC) in complete Freund's adjuvant developed a neurological disorder manifested by flaccid quadriparesis, limb hypesthesia, and respiratory paralysis. Seventeen of 20 autopsied rabbits, including all those with clinical illness, had small multiple perivascular foci of demyelinative lesions in roots, dorsal root ganglia, proximal peripheral nerves adjacent to ganglia, and, less frequently, in distal nerves. No change was found in the central nervous system. Demyelination started around venules, with splitting and vesiculation of the outer myelin sheaths of adjacent fibers, and later progressed to form confluent lesions. The lesions were associated with infiltration of phagocytic mononuclear cells, mostly macrophages, which insinuated themselves between myelin lamellae, phagocytized myelin, and subsequently denuded axons. Perivenular infiltration of small lymphocytes, comparable to that seen in whole nerve- induced EAN, was not encountered. The distribution of demyelinative lesions seems to correspond to areas known to have a defective blood-nerve barrier.

Animals↗
PubMed1981

Polyacrylamide gel electrophoresis of the alkaline phosphatase of rat dental pulp.

Judging from the mobility after the sodium dodecyl sulphate-gel electrophoresis, the mol. wt of the dental pulp enzyme was estimated to be 125,000-130,000. The electrophoretic behaviour of this enzyme was identical with that of calvarial phosphatase but not with those of kidney and intestinal enzymes. These results suggest that the dental pulp enzyme has a similar molecular structure to bone alkaline phosphatase.

Alkaline Phosphatase↗
PubMed1981

Drug resistance and R plasmids of Escherichia coli strains isolated from pigs, slaughterers, and breeders of pigs in Japan.

We isolated 1,120 drug-resistant Escherichia coli strains from pigs, slaughterers, breeders of pigs, and urban residents and examined their drug resistance. With reference to resistance to tetracycline (Tc) chloramphenicol (Cm), streptomycin (Sm), and sulfanilamide (Su), Tcr, Smr, and Sur strains were most frequently isolated from pigs (57.9%), followed by slaughterers (50.2%) and breeders (42.4%). By contrast, the isolation frequencies of Tcr, Smr, and Sur strains from urban residents were low (12.0%). The isolation frequencies of R plasmids from resistant strains were more than 50% in the case of pigs, slaughterers, and breeders, whereas they were only 13.8% in urban residents. Kanamycin-resistant strains were frequently isolated from pigs (40.3%), slaughterers (22.6%), and breeders of pigs (25.4%), but seldom (only 3.4%) from urban residents. With ampicillin resistance, the frequencies of strains from pigs, slaughterers, breeders, and urban residents were 30.0, 21.5, 5.6, and 13.8%, respectively. R plasmids specifying these latter resistances were frequently seen from pigs (24.0%), slaughterers (23.6%), and breeders (21.1%), but they were not isolated from urban residents. The results suggest that the porcine gut can function as a reservoir of antibiotic resistance plasmids which can then be directly transferred to humans, with the highest frequency of such plasmids appearing in people in the most immediate contact with these animals.

Abattoirs↗
PubMed1981

Axonal lesions in acute experimental demyelination: a sequential teased nerve fiber study.

The relationship between axonal degeneration and primary demyelination was studied in isolated rat sciatic nerve fibers previously exposed to antiserum from rabbits with either experimental allergic neuritis or experimental allergic encephalomyelitis, or immunized with antigalactocerebroside antiserum. Continuous demyelination over one to eight or more internodes was seen in association with phagocytic cells or, later, with increased numbers of Schwann cells. Paranodal demyelination was prominent proximal ahd distal to the zone of continuous demyelination. Axonal degeneration affected 5 to 15% of myelinated fibers exposed to antiserum and was not related to the length of demyelination must proximal to the axonal changes. At times, there were seven or eight consecutive demyelinated internodes with no distal axonal degeneration; in contrast, one demyelinated internode was often associated with axonal degeneration beginning just distally. The inflammatory reaction could account for axonal degeneration in antiserum-mediated demyelination.

Animals↗
PubMed1981

Mode of action of prilocaine on sarcoplasmic reticulum in skinned skeletal muscle fibers.

Single fibers were isolated from the semitendinosus muscle of a frog and the skinned fibers were prepared by the removal of the sarcolemma. In the range of several millimolar concentrations, prilocaine caused a contracture of the single fibers in both polarized and depolarized states. It also induced Ca++ release from the sarcoplasmic reticulum and depressed Ca++ uptake by the sarcoplasmic reticulum. Prilocaine increased the release of Ca++ with increasing concentration, but, unlike caffeine, prilocaine could not enhance the Ca++-induced Ca++ release mechanism of the sarcoplasmic reticulum. Like a depolarization-induced Ca++ release, the prilocaine-induced Ca++ release was not inhibited by Mg++, whereas it was inhibited by sucrose. The Ca++ release induced with prilocaine occurred only immediately after the application; thereafter the Ca++ release mechanism seemed to be inactivated by the prolonged presence of the drug. A similar inactivation in the mechanism of prilocaine-induced Ca++ release also occurred when the extent of depolarization of the sarcoplasmic reticulum membrane increased. These results suggest that the mode of action of prilocaine on the sarcoplasmic reticulum could be a depolarization-like action.

Animals↗
PubMed1980

Antiserum-mediated demyelination: relationship between remyelination and functional recovery.

A focal demyelinative lesion of peripheral nerve was produced by intraneural injection of either antiserum from rabbits with experimental allergic neuritis or experimental allergic encephalomyelitis or antiserum to galactocerebroside. We studied the relationship between clinical and electrophysiological recovery from this lesion and the morphological pattern of remyelination. Foot muscles on the the injected side weakened within an hour of injection and remained paralyzed for 7 days; strength gradually returned to normal by 16 days after injection. Electrophysiological conduction block, apparent within a few hours of injection, persisted for about 7 days. At 8 days we detected dispersed, very low amplitude muscle action potentials with long latency. Morphologically, demyelinated axons were surrounded by Schwann cells at 7 days after injection, but compacted myelin was not present. After 8 days, remyelinating axons became surrounded by thickening compacted myelin. The time of onset of remyelination and the rate of remyelination up to 14 days following the injection were independent of axon size. The onset of clinical and electrophysiological recovery from the lesion corresponded to the appearance of 2 to 8 myelin lamellae around each remyelinating axon. At 37 days after injection, when conduction velocities had returned to preinjection values, myelin thickness of remyelinating fibers had increased to approximately one-third that of control nerves.

Animals↗