Search PubMed⌕ Search

Biomedical subjects

K Mizukawa

Publications and source records attributed to K Mizukawa.

At least 37 records · Page 2Linked to original sources
PubMed1993

Swinglock removable partial denture and biting forces in partially edentulous patients. Comparison of individual biting forces with and without swinglock removable partial denture.

Several studies have shown that swinglock removable partial dentures are effective for stability of the abutment teeth and the surrounding tissues including alveolar bone. This efficacy has been thought to be due to the dynamic structure of the swinglock attachment. Individual biting force was measured to determine the physiological efficacy of teeth splints by use of the attachment. The results showed that individual biting forces with the swinglock removable partial denture were 10-25% higher than those without the denture. Furthermore, statistical analysis showed that the individual biting forces with the swinglock removable partial denture were significantly higher. The swinglock attachment can stabilize partially edentulous dentition by splinting all residual teeth. In addition, when physical forces are applied to the abutment teeth and the artificial teeth, this attachment can deliver and distribute the stress to the other abutment teeth and alveolar mucosa. The present findings suggest that the swinglock attachment augments the ability to withstand physical forces such as those occurring during biting and mastication.

Bite Force↗
PubMed1992

Post-ischemic administration of bifemelane hydrochloride prohibits ischemia-induced depletion of the muscarinic M1-receptor and its mRNA in the gerbil hippocampus.

Parallel determinations of muscarinic cholinergic M1 receptor (M1-R) binding and of M1-R mRNA levels were carried out in the gerbil hippocampus 14 days after 5 min of transient ischemia. Both were reduced in the ischemic tissue to about 50% of the levels found in sham-operated controls, indicating that the late loss of M1-R is probably dependent on decreased synthesis. Three administrations of bifemelane hydrochloride (15 mg/kg, i.p., just after ischemia and 6 and 12 h later) completely prevented neuronal death in the hippocampus and ischemia-induced losses of hippocampal M1-R and its mRNA. Since vascular dementia may depend upon the ischemia-induced losses in cholinergic communication in the hippocampus, these findings suggest that it may be possible to prevent its occurrence by post-ischemic treatment with bifemelane hydrochloride.

Animals↗
PubMed1992

Abnormal expression of embryonic neural cell adhesion molecule (N-CAM) in the developing mouse cerebellum after neonatal administration of cytosine arabinoside.

We have previously found that neonatal administration of cytosine arabinoside (Ara-C) induces cerebellar malformation, including arrest of granule cell migration and destruction of glial palisade. In the present study, the expression of neural cell adhesion molecule (N-CAM) and its distribution were examined in the mouse malformed cerebellum induced by neonatal Ara-C administration. Western blot analysis demonstrated that, in the control group, the embryonic form of N-CAM (E-N-CAM) was expressed in the 7-day-old mouse (P7) cerebellum, but not in the P14 cerebellum which exhibited only the adult form of N-CAM (A-N-CAM). On the other hand, E-N-CAM was expressed in the Ara-C treated cerebellum not only at P7 but also at P14. Immunohistochemical studies revealed that E-N-CAM was observed in the area below the external granular layer (EGL) of the P7 cerebellum in both the control and Ara-C treated mice. In contrast, E-N-CAM immunoreactivity was found in the arrested EGL cells in the Ara-C treated cerebellum of P14 mice but not in the age-matched controls. Therefore, E-N-CAM was aberrantly expressed in the arrested EGL at P14. From the present and previous findings, it was speculated that the aberrant expression of E-N-CAM in the arrested EGL cells is attributed to abnormal cellular interactions, probably arrested EGL cell-to-Bergmann glia.

Animals↗
PubMed1992

Effects of chronic bifemelane hydrochloride administration on receptors for N-methyl-D-aspartate in the aged-rat brain.

We assayed N-methyl-D-aspartate (NMDA) receptors [3H]3-(2-carboxypiperazin-4-yl)propyl-1-phosphonic acid ([3H]CPP) bindings) and evaluated their distribution in the brain by quantitative autoradiography in young adult and aged rats. In the young adult rats, NMDA receptors were present at relatively high concentrations in the cerebral cortex and hippocampus. In the aged rats, NMDA receptors were decreased in the nealy all areas of the brain, especially in the cerebral cortex and hippocampus. Chronic administration of bifemelane hydrochloride, a drug for sequela of cerebrovascular diseased, at a dose of 15 mg/kg/day for 14 days, markedly attenuated these decrease in NMDA receptors. Since NMDA receptors are considered to be involved in memory and learning processes, our results suggest that bifemelane hydrochloride may be applicable to the treatment of disturbed memory and learning.

Aging↗
PubMed1992

Changes of phorbol ester binding sites in rat brain following intracerebroventricular administration of thyrotropin-releasing hormone (TRH): an in vitro macroautoradiographic investigation.

We examined the influence of the intracerebroventricular (icv) administration of thyrotropin-releasing hormone (TRH) on protein kinase C (PKC) activities in various rat forebrain regions in order to cast light on the mechanism of extra-pituitary non-endocrine physiological actions of TRH in the central nervous system. An in vitro macroautoradiographic method, with [3H]phorbol 12, 13-dibutyrate (PDBu) as the radioactive ligand, was used to investigate quantitative alterations of PKC activities. The optical densities for PDBu binding sites in the striatum and hippocampal formation were significantly increased after the icv administration of TRH, while those in the frontal cortex and septum were unchanged. These findings suggest that TRH may exert some of its non-endocrine functions through striatal and hippocampal neurons which used PKC in their second messenger systems.

Animals↗
PubMed1992

Experience of a small PACS in Tottori University Hospital.

Picture archiving and communications systems (PACS) are expected to become feasible as the way of total radiologic image management. As the first step towards computerized image management, we installed an experimental small PACS with a digital optical archive for magnetic resonance and digitized radiographic film images. During the first 10 months of operation, problems were caused by the frequent mechanical troubles on the acquisition devices, impractical schemes for transmission, and troublesome retrieval and display of images. Although some of them have been solved by the improvements of both hardware and software, the mechanical instability of the digitizer and the inadequate operating procedure of the workstation still remain. As to the characteristics of PACS, the capability of access to every achieved radiologic image is the great advantage for us because the image integration has been impossible in the form of radiographic films for the traditional image management system of our hospital. However, the complicated image display procedure with high overheads is far from ideal for radiologists. The efficiency of image display must be increased to the level of a conventional film viewing system. Furthermore, research is needed on the small PACS to get consensus for the acceptance of a more widely implemented system.

Computer Systems↗
PubMed1992

[Chronic administration of lisuride hydrogen maleate increases muscarinic acetylcholine receptor binding in aged rat brain].

Changes in the distribution and densities of muscarinic acetylcholine receptors (mACh-R) in young adult and aged rat brain, and the effects of chronic administration of lisuride hydrogen maleate (lisuride) on these changes were studied by in vitro quantitative autoradiography of [3H] quinuclidinyl benzilate binding. mACh-R was relatively higher in the striatum, hippocampus and cerebral cortex in the young adult rats. In contrast, mACh-R binding was markedly reduced in the striatum, accumbens nucleus, amygdaloid nucleus and frontal cerebral cortex of aged rats compared to young adult rats. However, chronic administration of lisuride significantly increased mACh-R binding in the parietal cerebral cortex as well as in the above-mentioned regions in aged rats. This lisuride-induced increase in mACh-R of aged rat brain is considered to have important implications concerning the mechanism of therapeutic efficacy of lisuride.

Aging↗
PubMed1991

Time course of changes in lipid peroxidation, pre- and postsynaptic cholinergic indices, NMDA receptor binding and neuronal death in the gerbil hippocampus following transient ischemia.

Brief (5 min) bilateral carotid occlusion in the gerbil produces forebrain ischemia resulting, as previously reported, in almost complete neuronal loss in the CA1 region of the hippocampus; this neuronal destruction occurs between the 4th and 7th day post-ischemia. Various hippocampal biochemical indices were measured from just after such ischemia to 21 days of recirculation, and the temporal pattern of changes compared with that of cell loss. The level of thiobarbiturate reacting substances (TBARS), a measure of lipid peroxidation, was greatly elevated at 30 min after ischemia, rapidly returned to normal levels (by 60 min), but was again elevated on days 4-14. The beginning of this second period of elevation correlated closely with the onset of neuronal loss and the very abrupt and large (to about 32%) decrease in specific N-methyl-D-aspartate (NMDA) binding sites, measured with radioactive CPP. The number of muscarinic binding sites, measured with radioactive quinuclidinyl benzilate, showed an even greater decrease (to 13%) at 21 days post-ischemia, but the decrease was delayed (starting at day 7) and much more gradual than the loss in NMDA binding. In neither case was there any change in binding affinity at any time studied. Acetylcholine (ACh) concentrations were initially greatly decreased (to about 15% at 5 min), transiently increased (to about 130% at 30 min), and then decreased again (to about 15% at 60 min), after which gradual recovery occurred and was completed by day 14. Since no inhibition of choline acetyltransferase activity was observed at any time, the reversible depression in ACh must depend upon some factor other than loss of this key synthetic enzyme.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholinesterase↗
PubMed1991

[Self-expandable metallic stent for use in arterial occlusive lesions].

Gianturco expandable metallic stents were successfully placed in 4 patients with arterial occlusive disease: aortic obstruction or stenosis due to aortitis (n = 2), dissecting aneurysm (n = 1) and arteriosclerotic obstruction of the iliac artery (n = 1). The length of lesion was from 2 to 15 cm. In one case of aortitis (case 1), eleven stents (5 and 6 stents in tandem connected by wire struts) were inserted through a 12 F Teflon sheath. In another aortitis case (case 2) 4 stents in tandem were inserted through a 10 F sheath. In the two cases the sheaths were introduced by femoral arteriotomy. In case 3 and 4 two or four stents in tandem were placed through a 8 F long sheath which was introduced via the femoral artery by Seldinger method. Symptoms disappeared after placement of stents in all four cases. Our results showed the usefulness of expandable metallic stents in the treatment of arterial occlusive diseases.

Adult↗
PubMed1991

Distribution of the beta-2 adrenergic receptor messenger RNA in the rat brain by in situ hybridization histochemistry: effects of chronic reserpine treatment.

We studied the distribution of the rat brain beta-2 adrenergic receptor (AR) mRNA, and the effects of monoamine depletions by chronic reserpine treatment using in situ hybridization histochemistry. In the control group, high level signals of beta-2 AR mRNA were observed in the parietal, frontal and piriform cortices, the medial septal nuclei, the olfactory tubercle, and the midbrain. Moderate signals were found in the striatum, the retrosplenial cortex, the hippocampus, and the thalamic nuclei. After chronic reserpine treatment, beta-2 AR mRNA levels were increased in many brain regions. The large increases were seen in the hippocampus, all thalamic nuclei, the amygdaloid nuclei, and the midbrain, followed by the striatum and the occipital cortex. The receptor up-regulation resulting from chronic monoamine depletion may be due to these increases in beta-2 AR mRNA, indicating that this up-regulation may be caused by increased receptor production rather than decreased receptor degradation.

Animals↗
PubMed1991

Loss of N-methyl-D-aspartate (NMDA) receptor binding in rat hippocampal areas at the chronic stage after transient forebrain ischemia: histological and NMDA receptor binding studies.

Although neuronal death following brain ischemia was originally considered to be due to an energy deficiency resulting from an impaired respiratory chain, the observation of "delayed neuronal death" indicated some other factor. It is believed that delayed neuronal death after transient forebrain ischemia appears as a result of release of glutamate, an excitatory amino acid. In the present study, transient ischemia for 20 minutes in a rat four-vessel occlusion model was induced, and serial changes in histology and N-methyl-D-aspartate receptor (NMDA-R) binding were evaluated up to the chronic stage. Destruction of pyramidal cells and extensive astrocytic proliferation in the CA1 area of the hippocampus was completed by 10 days after cerebral ischemia followed by cerebral blood recirculation. However, the glutamate receptor subtype, NMDA-R, showed no change in all brain regions until after 10 days, but decreased in the hippocampus to 50% after 21 days despite no evidence of histological progression of neuronal death. The results show that the time course for appearance of light microscopic damage in the hippocampal region does not parallel that for depletion of NMDA-R binding sites.

Animals↗
PubMed1991

Morphological investigation of iron-induced epileptic rats: with special reference to c-fos immunohistochemistry and iron staining.

We investigated the iron-induced epileptic rats with special reference to c-fos immunohistochemistry and iron histochemistry in order to elucidate the pathogenesis of post-traumatic epilepsy. The c-fos-immunopositive neurons were observed in a hippocampal formation, especially in the dentate gyrus and CA1 and CA2, in the vicinity of the iron injected cerebral cortex and amygdala only at 3 hours after the iron administration. Three days later after administration, several heavily positively iron staining cells and nerve fibers were observed around the injection site. In the cases of 3 weeks after administration, the large cavity and gliosis were characteristically observed.

Amygdala↗
PubMed1991

[Chronic administration of bifemelane hydrochloride increases somatostatin receptor binding in aged rat brain].

Changes in the distribution and densities of somatostatin receptors (SS-R) in young adult and aged rat brain and the effects of chronic administration of bifemelane hydrochloride (bifemelane) on these changes were studied by in vitro quantitative autoradiography of iodinated [Tyr11] SS-14. SS-R was highest in density in the amygdala, followed by the cingulate cortex, temporal cortex, frontal cortex, hippocampus and septal nucleus in the young adult rats. In contrast, SS-R binding was markedly reduced in the frontal cortex, temporal cortex, cingulate cortex, hippocampus, amygdala and septal nucleus of aged rats compared to young adult rats. However chronic administration of bifemelane significantly increased SS-R binding in the frontal cortex, temporal cortex, cingulate cortex, hippocampus and septal nucleus of aged rats without effects on young adult rats. This bifemelane-induced increase in SS-R is considered to have important implications in the mechanism of the therapeutic efficacy of bifemelane.

Aging↗
PubMed1991

Chronic bifemelane hydrochloride administration enhances muscarinic cholinergic receptor binding in the senescent rat brain.

In senescent rats, the binding ability of muscarinic cholinergic receptors (MCR) was markedly decreased in the cerebral cortex, hippocampus, thalamus, and the striatum compared with young adult rats. This decrease was markedly improved by chronic administration of bifemelane hydrochloride (bifemelane). In view of the findings that bifemelane markedly inhibits the decrease in acetylcholine (ACh) associated with cerebral ischemia, and that it improves amnesia induced by scopalamine, it may be inferred that bifemelane acts on the pre- and post-synaptic ACh neuronal systems. It may improve memory disturbance due to aging or cerebral ischemia, decreased conscious level, and decreased motor function.

Aging↗
PubMed1990

Morphological changes of astroglia in the cerebellar cortex of developing mice after neonatal administration of cytosine arabinoside.

Neonatal administration of cytosine arabinoside (Ara-C) induced marked hypoplasia of the mouse cerebellum. In 17-20-day-old mice with neonatal Ara-C injections, the external granular layer was still preserved as an irregular cell laminae in the superficial part of the cerebellum, in contrast to its complete disappearance in normal animals at these stages. Immunohistochemical examination using anti-glial fibrillary acidic protein and monoclonal antibody-1D11 (Ono et al: Dev. Brain Res., 50:154-159, 1989) demonstrated malformation of a palisade-like arrangement of labeled glial fibers in the superficial part of the Ara-C treated mouse cerebellum. Furthermore, the immunoreactive astroglia were observed just beneath the pial membrane and their processes were oriented to the deeper part of the molecular layer.

Animals↗
PubMed1990

Neurotransmitter and receptor alterations in the rat persistent dyskinesia model induced by iminodipropionitrile.

Chronic administration of iminodipropionitrile (IDPN), a neurotoxin, to rats produces a persistent behavioral syndrome characterized by lateral and vertical head twitching, random circling and hyperactivity. Conventionally, this IDPN-induced dyskinesia has been considered to be due to abnormalities in the serotonin neuronal system. However, the present study also demonstrated marked alterations in the dopamine (DA) and acetylcholine (ACh) neuronal systems. These were activation of DA neurons in the nucleus accumbens and thalamus + midbrain, decreased activity in the other brain areas and a decrease in D1 DA receptors. ACh contents were decreased in most brain areas while muscarinic ACh receptors were increased in the striatum, superior colliculus and geniculate nucleus. These alterations in the ACh neuronal system may be secondary to abnormalities in the DA neuronal system. IDPN-induced dyskinesia was enhanced by administration of L-dopa, which increases DA concentration, but was completely inhibited by ceruletide, which inhibits DA release. The dyskinesia was also inhibited by sulpiride, a central antagonist of D2 DA receptors. Interestingly, apomorphine and bromocriptine, which are DA receptor agonists, did not aggravate, but decreased dyskinesia in the IDPN-treated rats. These results strongly suggest that dyskinesia is caused not by abnormality of postsynaptic receptors in the DA neuronal system but by abnormally enhanced function of the presynaptic DA neurons themselves. In addition, ceruletide may be useful in the treatment of dyskinesia, and bromocriptine alone or in combination with L-dopa may be effective in Parkinson's disease without the development of dyskinesia. Thus, the IDPN-treated rat model is useful for clarifying the biochemical pathophysiology of dyskinesia and developing drugs for its treatment.

Animals↗