Search PubMed⌕ Search

Biomedical subjects

S Wakisaka

Publications and source records attributed to S Wakisaka.

233 records · Page 13Linked to original sources
PubMed1980

Effects of manipulation of the sensorimotor system on focal motor seizures in the monkey.

During focal motor seizures induced by injecting penicillin into the face-hand area of the right motor cortex of 24-month-old monkeys, the sensorimotor system was manipulated by three methods. Elimination, by a paralytic agent, of proprioceptive input from contracting muscles and joints did not alter the electrographic expression of the seizure or the pattern of local glucose utilization in cortical or subcortical components of the sensorimotor system. An overall increase in the rate of energy metabolism occurred in the paralyzed monkeys with electrographic seizures. Cryogenic destruction of up to 90% of the ipsilateral ventral caudal globus pallidus had no effect on electrographic or clinical expression of the seizure. Electrical stimulation of the ipsilateral ventral caudal globus pallidus caused reproducible maximum expression of electrographic and clinical seizure phenomena for the 90-second duration of the stimulus.

Animals↗
PubMed1977

Computer assisted tomography of focal cerebral radiation necrosis in the monkey.

The right occipital lobe in a series of pubescent monkeys was exposed to 3500 rads of orthovoltage radiation in a single dose. Sixteen to 38 weeks later the irradiated region broke down, rather abruptly. The visual evoked response, funduscopic photography, cerebral spinal fluid determinations for protein and lactic dehydrogenase, and computer assisted tomography (CAT) were used to anticipate and reflect the breakdown in neural tissue. CAT scanning demonstrated the two main effects of focal delayed radiation necrosis in this model (in a representative monkey): pronounced vasogenic edema from a break in the blood brain barrier, and contralateral hydrocephalus from brain distortion with obstruction of cerebral spinal fluid circulation. These findings were confirmed by postmortem examinations.

Animals↗
PubMedDate not supplied

Influences of bradykinin and substance P on the met-enkephalin-like peptide content in the rat incisor pulp.

The present study was aimed to examine possible influences of bradykinin (BK) and substance P (SP) on met-enkephalin (ME)-like peptide content in the rat incisor pulp. Des-Arg9-[Leu8]-BK, a potent BK-antagonist, significantly reduced the increased content of ME-like peptides induced by noxious stimulation, while the effect of BK-antagonist was reversed in combination with BK. Morphine decreased the increased content of ME-like peptides. Ethylketocyclazocine, a kappa-agonist, also decreased the increased content of the peptides. From these results, it was suggested that BK might be a trigger in the increase of ME-like peptide content induced by noxious stimulation and, in contrast, ME-like peptides in the pulp might inhibit BK release from the pulp in a negative feedback mechanism. On the other hand, [D-Pro2,D-Trp7,9]-SP, a potent SP-antagonist, did not show any significant influence to ME-like peptide content in the pulp. Furthermore, the content was not changed following cutting of inferior alveolar nerve. From these results, it was suggested that ME-like peptides in the pulp cells might be independent on SP-containing nerves in the pulp.

Animals↗
PubMedDate not supplied

Immunocytochemical demonstration of beta 1-subunit of Na+/K(+)-ATPase in the mechanoreceptive Ruffini-like endings of the rat incisor ligament.

The localization of one of the isoforms of Na+/K(+)-ATPase, the beta 1-subunit, was investigated in the periodontal Ruffini endings of rat incisors by light- and electron-microscopic immunocytochemistry. Immunoreactivity for the rat beta 1-subunit followed the pattern of dendritic terminal arborization in the alveolar half of the lingual periodontal ligament. Ultrastructurally, the reaction products were localized in dilatations of axons, possibly the terminals of Ruffini-like endings in the periodontal ligament. No immunoreactivity was seen in Schwann cells. The immunostaining results support the view that the beta 1-subunit of Na+/K(+)-ATPase is the predominant isoform in sensory neurones, and that this protein is a useful marker for periodontal Ruffini-like endings.

Alveolar Process↗
PubMedDate not supplied

Calbindin D28K-like immunoreactive nerve fibres in the predentine of rat molar teeth.

Immunoelectron-microscopy was applied to reveal the existence of nerve fibres and terminals showing calbindin D28k (CB)-like immunoreactivity (IR) in the rat molar tooth pulp. In the root pulp, thick, smooth-surfaced CB-IR nerve fibres were in bundles accompanying the blood vessels. In the coronal pulp, the fibres arborized repeatedly and extensively. CB-IR nerve fibres had a predominantly thick, smooth-surfaced appearance, though parts appeared thin and beaded. Occasionally some thin, varicose CB-IR nerve fibres ran along the odontoblasts, penetrating into the predentine alongside the dentinal tubules. They could be traced for approx. 10-20 microns into the predentine from the pulp-predentine border. Immunoelectron-microscopy revealed that only some of the nerve terminals in the predentine showed CB-IR, and that predentinal CB-IR nerve terminals were located close to the odontoblast processes. No synaptic structures were observed between them. The presence of CB-IR nerve terminals in the predentine suggests that many, if not all, CB-IR nerve fibres could be nociceptors. The CB could be involved in Ca2+ homeostasis during the activation of nociceptors.

Animals↗
PubMedDate not supplied

Involvement of cAMP responsive element binding protein (CREB) in the synovial cell hyperfunction in patients with rheumatoid arthritis.

OBJECTIVE: To elucidate a possible role of cAMP responsive element binding protein (CREB) in rheumatoid arthritis (RA) synovial cell function, we have studied CREB expression of synovial cells and the effects of an inhibitor of the cAMP/CREB signal pathway on synovial cell function in patients with RA. METHODS: We examined CREB expression by immunohistochemical staining, immunocytochemical staining, and gel shift assays. Effects of cAMP/CREB inhibitor on the proliferation of RA synovial cells were assessed by [3H]-TdR incorporation, and those on proinflammatory cytokine and matrix metalloproteinase (MMP) production by reverse transcription PCR and ELISAs. RESULTS: Immunohistochemical staining of synovial tissue revealed that CREB is expressed mainly in the lining and sublining layers of synovium in patients with RA. DNA binding activity of CREB was ascertained by a gel shift assay. We also confirmed nuclear translocation and phosphorylation of CREB in TNF-alpha stimulated RA fibroblast-like synovial cells by immunocytochemical staining. Modulators of cAMP/CREB signaling pathway, such as Rp-cAMP, had an inhibitory potential on RA synovial cell proliferation in vitro. Rp-cAMP also inhibited the proinflammatory cytokine and MMP production. CONCLUSION: CREB is involved in the synovial cell activity in patients with RA. Inhibition of CREB activity by its inhibitor brings about the correction of aberrant synovial cell functions in patients with RA, thus suggesting a possible clinical application of cAMP/CREB inhibitors.

Aged↗
PubMedDate not supplied

Aberrant expression of Fas ligand on anti-DNA autoantibody secreting B lymphocytes in patients with systemic lupus erythematosus: "immune privilege"-like state of the autoreactive B cells.

BACKGROUND: Fas/Fas ligand (FasL) system has been assigned a pivotal role in the development and maintenance of peripheral tolerance, and mice with defects in their Fas/FasL system develop lupus-like symptoms. In this study we examined FasL expression of peripheral blood lymphocytes in patients with systemic lupus erythematosus (SLE). METHODS: We assessed FasL mRNA and protein expression by reverse transcription (RT)-PCR and immunoblotting and immunocytochemical staining, respectively, in patients with SLE. Anti-DNA antibody secreting B cells were purified using biotin labeled DNA and streptavidin-bead. RESULTS: Expression of FasL protein was not or very weakly detected in freshly isolated PBMC in normal individuals. In contrast, freshly isolated SLE PBMC exhibited the enhanced expression of FasL protein without in vitro stimulation. Not only purified T cells but also purified B cells expressed FasL on their cell surface spontaneously. In addition, freshly isolated anti-DNA autoantibody secreting B cells express FasL without in vitro stimulation. CONCLUSION: The results suggest that autoreactive B lymphocytes which aberrantly express FasL may kill Fas+ immunoregulatory T lymphocytes. Thus aberrantly expressed FasL may facilitate escape of the autoreactive B cells from the immune tolerance system, and may contribute to the sustained secretion of autoantibodies in patients with SLE.

Adolescent↗
PubMedDate not supplied

Immunohistochemical study of giant cell in glioblastoma.

The clinical and immunohistochemical features of supratentorial (5 patients) and cerebellar (1 patient) glioblastomas, in which giant cells were conspicuous were examined. Three of the patients died within 26 months after the first treatment, and the follow-up period is presently 1 year or less in the remaining patients. The giant cells either showed large and bizarre nuclei or were multinucleated. Both giant and smaller cells excluding neuronal, endothelial and infiltrative cells were positive for GFAP, vimentin, and alpha-1 anti-chymotrypsin. The strong positivity for PCNA staining indicated that the capacity of the giant cells to synthesis DNA was preserved. DNA fragmentation, measured by the terminal deoxynucleotidyl transferase (TdT)-mediated deoxyuridine-5'-triphosphate (dUTP)-biotin nick end labeling method, was observed in only 1 patient, who had received radiotherapy just before biopsy, and none of the patients showed bcl-2 positivity. Mutant type of p53 tumor suppressor gene was observed in the giant cells of 3 patients. Giant cell in glioblastoma is of glial origin, synthesizes DNA, and its progression may be related to tumor suppressor gene.

Adult↗