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Biomedical subjects

K Kajiyama

Publications and source records attributed to K Kajiyama.

At least 73 records · Page 4Linked to original sources

Central terminations of periodontal mechanoreceptive and tooth pulp afferents in the trigeminal principal and oral nuclei of the cat.

Intra-axonal recording and horseradish peroxidase (HRP) injection techniques were employed to define the response properties of low-threshold mechanoreceptive periodontal afferents and of the tooth pulp afferents and the morphological characteristics of their axon arbors in the nucleus principalis (Vp) and rostrodorsomedial (Vo.r) and dorsomedial parts (Vo.dm) of the nucleus oralis (Vo). The central terminals of 3 fast adapting (FA) and 4 slowly adapting (SA) periodontal afferents and 4 tooth pulp (TP) afferents were recovered for detailed analyses. Stained axons in the trigeminal sensory tract ascended and descended (bifurcating fibers), or descended without bifurcation (descending non-bifurcating fibers). The ratio of the bifurcating fibers to the descending non-bifurcating fibers was about three to one for each type of afferents. The main collaterals given off from the ascending branches terminated in the Vp. Most collaterals given off from the descending branches terminated in the Vo with the exception of few instances. In case of the FA afferents, the ascending branches gave off all main collaterals into the Vp with rostrocaudal and dorsoventral continuities in their arbors, whereas the descending branches gave off all main collaterals, except two collaterals, into the Vo with rostrocaudal discontinuities. The projections from the FA afferents to the Vo.dm was predominant in terms of the number of boutons and the length of preterminal and terminal branches. In case of the SA afferents, the collaterals from the ascending and descending branches formed rostrocaudally and dorsoventrally discontinuous terminal arbors. In terms of the density of boutons the SA afferents were divided into two subtypes. One had a preferential projection into the Vp or Vo, whereas others lacked a selective projection. In case of the TP afferents, the main collaterals of the ascending branches formed partially overlapping terminal arbors, but the terminal arbors formed by the collateral of the descending branches did not overlap. The frequency of collaterals of the TP afferents was less than that of the other types of afferents. The terminal arbors including the density of boutons of the pulpal afferents were less extensive than those of the other types of afferents. The average size of varicosities became smaller in the following subdivisions. Vp, Vo.r and Vo.dm for SA and TP afferents. The size of varicosities of the TP afferents was smaller and that of the FA afferents was larger than that of the SA afferents.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗

Improved recombinant LC16m0 or LC16m8 vaccinia virus successfully expressing hepatitis B surface antigen.

An attempt was made to develop a safe, efficacious live recombinant vaccine using low neurovirulent strains of vaccinia virus: LC16m0 (m0) or LC16m8 (m8). Recombinant vaccinia virus (RVV) was constructed by inserting the hepatitis B surface antigen (HBsAg) gene fused to a 7.5 kDa protein promoter (7.5 kDa promoter) within the vaccinia virus thymidine kinase (TK) gene using the m0 or m8 strain as vectors. These RVVs expressed significant amounts of HBsAg (1.1 microgram/2 X 10(5) cells) consisting of 24.5 and 28 kDa (glycosylated) proteins. HBsAg produced by RVV (vaccinia HBsAg) had physical properties very similar to plasma-derived HBsAg. Considering the safety of RVVs from m0 or m8 that have been constructed with HBsAg without the addition of a promoter and the high induction of anti-HBs antibody with RVV from m0 strain in rabbits, the RVVs constructed in the present study are likely to form the basis of a safe live RVV vaccine for hepatitis B virus (HBV).

Animals↗

Glutamate metabolism of leukocytes and skin fibroblasts in spinocerebellar degeneration with lowered glutamate dehydrogenase activity.

From 21 patients with spinocerebellar degeneration 5 had markedly decreased glutamate dehydrogenase (GDH) activities and high values of serum plasma glutamate level after oral glutamate loading tests. Skin fibroblasts from patients with GHD deficiency showed intracellularly higher glutamate and lower glutathione contents than those from controls and showed significantly decreased viability in L-glutamate-containing medium. These data suggest that glutamate toxicity may at least play a part in this degeneration process.

Adolescent↗

[Application of calcium phosphate ceramics to periodontal therapy. 8. Effects of orthodontic force on repaired bone with hydroxyapatite].

It has been unclear whether M.T.M. is acceptable for patients treated with bone grafts using hydroxyapatite (HAP), which is not biodegradable. Therefore we studied histological changes in bone among HAP during orthodontic tooth movement. HAP was implanted into artificial bone defects adjacent to second premolars in beagle dogs, and as a control no material was implanted Three months after implantation, the second premolars were moved with orthodontic force. Then they were observed histopathologically. The results obtained were as follows. The amount of movement of the teeth in implanted sites was less than in the controls. In the pressure zone, resorption of bone by osteoclasts was observed in both the implanted and the control sites, in addition, root resorption occurred adjacent to HAP. Furthermore multinucleated giant cells were closely attached to HAP and were surrounded by bone and connective tissue. In retention period there was ankylosis between the roots and bone around HAP. In the tension zone, additional bone from HAP was observed. Bone defects were filled with bone in the implanted sites, but with connective tissue in the controls. These results suggest that bone among HAP was resolved by osteoclasts. Clinically, HAP implantation for the pressure zone should be avoided because of the occurrence of root resorption and ankylosis. But for the tension zone it seems to be effective because HAP implantation produces more repaired bone.

Animals↗

[Coronary artery bypass grafting in a patient with Sjögren's syndrome and other autoimmune diseases].

Coronary arterial involvement in collagen disease is a very rare complication. Particularly in Sjögren's syndrome is there no report of coronary artery bypass grafting (CABG). We report a 68-year-old woman with various autoimmune diseases who underwent successful CABG for unstable angina pectoris. She had a history of Sjögren's syndrome, hypothyroidism, thrombocytopenia and lupoid hepatitis, and had been on the regimens of prednisolone and levothyroxine sodium during the last 4 years. Two months prior to admission when the doses of these drugs were increased, she began to complain of angina on mild exertion and occasionally even at rest. Selective coronary angiograms revealed 75% stenosis at Seg. 2 and 99% stenosis at Seg. 6. Based on these findings and severity of the angina, saphenous vein CABG to the posterior descending and the left anterior descending branches was performed. Despite the associated autoimmune diseases, the patient's postoperative course was uneventful and she is now doing well with no attack of angina, 12 months following the operation.

Aged↗

Decreased glutamate dehydrogenase protein in spinocerebellar degeneration.

A radioimmunoassay system for determining content of glutamate dehydrogenase (GDH) in human leukocytes was established and studied in 14 patients with spinocerebellar ataxia or atypical Parkinsonism. The protein content of leukocyte GDH was decreased in four patients and the reduction in the protein content was proportional to that in the enzyme activity. The ratio of GDH activity to protein content was invariable in healthy controls, diseased controls and patients with reduced GDH activity. These results suggested that at least a portion of the partial GDH deficiency was due to the decreased level of the enzyme protein.

Adult↗

Protection by verapamil of mitochondrial glutathione equilibrium and phospholipid changes during reperfusion of ischemic canine myocardium.

Pretreatment of the ischemic myocardium with verapamil protects against mitochondrial respiratory depression observed during ischemic arrest as well as during reperfusion. Since ischemic mitochondrial function appears not to be altered further by reperfusion, the purpose of this study is to identify a biochemical event affecting mitochondria that is specifically associated with reperfusion injury. It has been proposed that increased cellular Ca2+ influx and oxygen toxicity may result from reintroduction of coronary flow. Increased cytosolic Ca2+ is transmitted to the mitochondria with subsequent activation of Ca2+-dependent events, including phospholipase A2. Net production of lysophospholipids (and loss of total diacylphospholipids from the mitochondria) will proceed when reacylation mechanisms are inhibited. Since acyl-CoA:lysophospholipid acyltransferase is a sulfhydryl-sensitive enzyme and since increased activity of glutathione peroxidase shifts the levels of the mitochondrial sulfhydryl buffer, glutathione, towards oxidation, levels of glutathione and its oxidation state were measured during reperfusion in the absence or presence of verapamil pretreatment. Ischemia lowers total glutathione and reduces the redox ratio (reduced glutathione: oxidized glutathione) by 85%. Reperfusion partially returns the redox ratio to control by causing oxidized glutathione to disappear from the matrix. Verapamil maintains both the concentration and the redox potential of glutathione at control levels. Concomitant with alterations in reduced glutathione:oxidized glutathione is a decrease in ischemic mitochondrial phospholipid content. During reperfusion, phosphatidylethanolamine and its major constituent fatty acids (C 18:0 and C 20:4) are specifically lost from the mitochondrial membrane. Accompanying the significant loss of arachidonic acid during reperfusion is the decreased content of 11-OH, 12-OH, and 15-OH arachidonate. These lipid peroxidation products are not increased in ischemia. It is proposed that oxidation of matrix glutathione to glutathione disulfide during ischemia results in formation of glutathione-protein mixed disulfides and inhibition of sulfhydryl-sensitive proteins, including acyl-CoA lysophosphatide acyltransferase. Thus, metabolic events occurring within the ischemic period set the stage for prolonged dysfunction during reperfusion.

Acetyl-CoA C-Acyltransferase↗