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Biomedical subjects

C Tanaka

Publications and source records attributed to C Tanaka.

At least 217 records · Page 12Linked to original sources
PubMed1991

[The connectivity between the greater occipital nerve and adjacent structures: anatomo-clinical considerations].

In order to offer anatomical basis that aid for clinical interpretation of headache of cervical origin a macro-mesoscopic study of greater occipital nerve and its subcutaneous rise out site was accomplished. The authors observed that in its course this nerve delineates angles and direction shifts that can stand for critical points in etiology of occipital pain, so that in its subcutaneous rise out region both occipital artery and vein shape the vasculo-nervous bundle wrapped by sheath of fibrous connective tissue which has continuity and contiguity relation with the adjoining epimysium and perimysium. From our results, anatomo-clinical aspects are discussed.

Cranial Nerves↗
PubMed1991

Differential localization of four subspecies of protein kinase C in the rat striatum and substantia nigra.

The distribution of protein kinase C (PKC) subspecies and their colocalization with neurotransmitters were examined in the rat striatum and substantia nigra (SN), using immunocytochemistry. The alpha- and beta I-PKC immunoreactivies were seen predominantly in the perikarya of the neurons in the striatum and SN. In contrast, the beta II- and gamma-PKC immunoreactivities were abundant in both the perikarya and the neuropils in the striatum and only in the neuropils in the SN. From electron microscopic studies, the alpha- and beta I-PKC immunoreactivities were seen adjacent to the plasma membrane, while the beta II-PKC immunoreactivity was observed in the cytoplasm around the Golgi complex. The gamma-PKC immunoreaction was dense throughout the cytoplasm. The double-staining and lesion studies revealed that the alpha-PKC-immunopositive neurons in the striatum were intrinsic cholinergic neurons, and that most of the alpha-PKC-immunoreactive neurons in the SN were dopaminergic neurons. The beta I-PKC-immunoreactive neurons were intrinsic GABAergic neurons in the striatum. Moreover, most of the beta II- and gamma-PKC-immunoreactive neurons were medium-sized neurons projecting to the SN, and over 90% of GABAergic neurons in the caudate-putamen contained beta II-PKC. The beta II-PKC-immunoreactive neurons showed no gamma-PKC immunoreactivity, and the gamma-PKC-immunoreactive neurons were not beta II-PKC immunoreactive. These findings suggest that alpha-PKC is related to the function of the nigral dopaminergic and the striatal cholinergic neurons, and that the beta I-PKC is involved in the function of the striatal intrinsic GABAergic neurons. The beta II- and gamma-PKC may also modulate a specific neuronal function in the striatonigral system.

Amino Acid Sequence↗
PubMed1991

[Circulating immune complexes and complement breakdown products in childhood IgA nephropathy].

Circulating immune complexes (CIC), mainly IgA-CIC have been frequently detected in IgA nephropathy and recently increased levels of C3 fragments which indicate C3 activation have been reported. However, little is known about the relationship between CIC and complement activation. We determined CIC by the solid-phase anti-C3 Facb enzyme immunoassay in 37 children with IgA nephropathy to investigate the relationship between CIC and clinical and/or histological findings, and also determined C3 fragments whether CIC correlate with complement activation. IgA-CIC were detected in 78% (27/37) with a mean level of 11.9 +/- 3.9 micrograms/ml, which was significantly higher than other glomerular diseases (P less than 0.05). IgA-CIC levels were also found significantly higher in 27 cases with proteinuria than in 10 cases without proteinuria (P less than 0.05). IgG-CIC were detected in 67% (12/18) with a mean level of 4.1 +/- 2.6 micrograms/ml, which was not significantly different from other glomerular diseases. No striking correlation was noted to exist between CIC levels at renal biopsy and the histological severity, because CIC are often present intermittently. C3d was quantitated by the rocket immunoelectrophoresis and C3 by the single radial immunodiffusion to determine the C3d/C3 ratio. The mean value of C3d/C3 was 0.63 +/- 0.19 which was significantly higher than a corresponding value for 15 healthy controls of 0.27 +/- 0.06 (P less than 0.05). Levels of IgA-CIC were found to have a significant positive correlation between C3d/C3 determined simultaneously in 33 cases (r = 0.43, P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1991

Expression of the CRE-BP1 transcriptional regulator binding to the cyclic AMP response element in central nervous system, regenerating liver, and human tumors.

CRE-BP1 is a transcriptional regulator binding to the cyclic AMP response element (CRE). To understand the role of CRE-BP1 in vivo, we studied the expression of the CRE-BP1 gene in monkey tissues including the central nervous system, in rat regenerating liver, and in human cancer tissues compared with normal tissues. The CRE-BP1 mRNA was detected in all tissues examined, and was fairly abundant in brain. The CRE-BP1 mRNA was expressed in monkey brain tissues with different region specificities. In the hippocampus, frontal lobe, and parietal lobe, the CRE-BP1 mRNA was abundant and two mRNA species 4.0 kb and 3.7 kb in length were expressed. In rat liver, the expression of the CRE-BP1 gene was increased up to 4- to 5-fold of the normal level within 12-24 h after partial hepatectomy. Furthermore, the levels of CRE-BP1 mRNA in some clinical samples of human tumors were apparently higher than that in normal tissues. These results suggest that CRE-BP1 may be important for both the signal transduction in brain and cellular proliferation.

Animals↗
PubMed1991

Clebopride enhances contractility of the guinea pig stomach by blocking peripheral D2 dopamine receptor and alpha-2 adrenoceptor.

The mechanism of action of clebopride on the motility of guinea pig stomach was examined by the receptor binding assay for bovine brain membrane and by measuring gastric contractility and the release of acetylcholine from the stomach. The receptor binding assay revealed that clebopride bound to the D2 dopamine receptor with a high affinity and to the alpha-2 adrenoceptor and 5-HT2 serotonin receptor with relatively lower affinity, and not to D1 dopamine, alpha-1 adrenergic, muscarinic acetylcholine, H1 histamine, or opioid receptor. In strips of the stomach, clebopride at 10(-8) M to 10(-5) M enhanced the electrical transmural stimulation-evoked contraction and the release of acetylcholine. This enhancement was attributed to the blockade of the D2 dopamine receptor and alpha-2 adrenoceptor because: 1) Maximum responses obtained with specific D2 dopamine receptor antagonist, domperidone, and with specific alpha-2 adrenoceptor antagonist, yohimbine, were smaller than that with clebopride, and the sum of the effects of these two specific receptor antagonists is approximately equal to the effect of clebopride. 2) The facilitatory effect of clebopride was partially eliminated by pretreatment of the sample with domperidone or yohimbine, and the facilitatory effect of clebopride was not observed in preparations treated with the combination of domperidone and yohimbine. Clebopride also antagonized the inhibitory effects of dopamine and clonidine on the electrical transmural stimulation-evoked responses. These results indicate that clebopride acts on post ganglionic cholinergic neurons at D2 and alpha-2 receptors in this preparation to enhance enteric nervous system stimulated motility.

Acetylcholine↗
PubMed1991

Cisapride stimulates motility of the intestine via the 5-hydroxytryptamine receptors.

The effects of cisapride on intestinal contractility and on release of acetylcholine (ACh) were examined using the longitudinal muscle with the myenteric plexus preparation from the guinea pig ileum, as related to the 5-hydoxytryptamine (5-HT) receptor. 5-HT exerted a dual effect, transient increase in ACh release (EC50 = 2 X 10(-6)M) via the 5-HT3 receptor, followed by inhibition (EC50 = 5 X 10(-9)M) via the 5-HT1 receptor. Cisapride at low concentrations (10(-9)M to 10(-8)M) enhanced electrical stimulation -evoked contraction and ACh release. The effect of cisapride was mimicked by methysergide and was not altered by ICS 205-930. Cisapride antagonized the 5-HT (5 X 10(-9) M)-induced inhibitory effect and the IC50 of cisapride was 1.5 X 10(-9) M. These findings indicate that enhancement by low concentrations of cisapride may be due to a block of the inhibitory 5-HT1 receptor. Cisapride at medium concentrations (10(-8) M to 3 X 10(-7) M) induced enhancement of electrical stimulation-evoked twitch contractions and ACh release evoked by electrical stimulation which were antagonized by 10(-6) M ICS 205-930, while this compound antagonized the 5-HT (2 X 10(-6) M)-and 2-methyl-5-HT-induced excitatory effects, and the IC50 of cisapride was 5.2 X 10(-8) M. Thus, cisapride acts on the putative 5-HT4 receptor as an agonist and the 5-HT3 receptor as an antagonist. Cisapride at high concentrations (10(-6) M to 10(-5) M) evoked contraction and the release of ACh, and these effects were antagonized by ICS 205-930 (10(-6) M).(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1991

[The application of in vivo diffusion weighted magnetic resonance imaging to intracranial disorders].

We have developed a magnetic resonance (MR) spin echo method to obtain diffusion weighted imaging using motion-probing gradient (MPG) pulses in one or three orthogonal directions before and after a 180 degree pulse. Phantom models containing water and acetone, normal volunteers and patients with brain tumors, brain edema and infarction were examined. Experimental models of brain edema including triethyltin intoxication and cold injuries were also examined in Wistar rats. MRI was performed at a 1.0-T clinical machine or a 4.7-T experimental machine using spin echo pulse sequences with or without additional MPGs on one or three orthogonal axes. The one direction method was useful to define diffusion anisotropy of myelinated axonal fibers in white matter. Faster diffusion was detected in the white matter parallel to the direction of MPGs. On the other hand, slower diffusion was detected perpendicular to the direction of MPGs because the myelin sheath restricted water diffusion. The three orthogonal gradients method was useful to demonstrate the difference in the diffusion coefficients in various diseases due to its larger total gradient strength. The clear distinction between the cytotoxic edema, which revealed slower diffusion, and the vasogenic edema, which revealed faster diffusion, was demonstrated in the experimental models using diffusion weighted image. In the clinical cases, faster diffusion was demonstrated in the brain tumor and perifocal vasogenic edema, which was in agreement with the results in the experimental models of rats. Brain tumors such as low grade astrocytoma with microcysts and perifocal vasogenic edema have very wide extracellular space.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Immunocytochemical localization of protein kinase C subspecies in the rat spinal cord: light and electron microscopic study.

Distinct expression of protein kinase C (PKC) subspecies in the central nervous system suggested that each subspecies has a distinct neural function in the processing and modulation of a variety of physiological responses to external signals. In this study, the cellular and subcellular distributions of beta I-, beta II- and gamma-subspecies of PKC were demonstrated by using subspecies-specific antibodies in the rat spinal cord. By light microscopy both gamma- and beta II-subspecies immunoreactivities were found only in neurons of the substantia gelatinosa and axons of the dorsal corticospinal tract in the spinal cord. Use of a double staining method, however, revealed that beta II-subspecies immunoreactivity was localized in the outer part of the lamina II, whereas gamma-subspecies immunoreactivity was found in the inner part of lamina II. Immunoreactive neurons containing beta I-subspecies were scattered in the substantia gelatinosa. Beta I-subspecies immunoreactivity varied in neuronal types. Furthermore, electron microscopic analysis clearly showed the subcellular distribution of these subspecies to be different from one another. Dense gamma-subspecies immunoreactivity was found in the cytoplasm except within cell organelles of the perikarya and dendrites. Some nuclei were stained as strongly as the cytoplasm and others were stained less heavily. The nucleoli had faint or no immunoreactivity. Reaction products of beta II-subspecies were located against the inner plasma membrane but not seen in the nuclei or nucleoli. Beta I-subspecies immunoreactivity appeared to be associated with the Golgi complex. No immunoreactive products of any PKC subspecies were detected in the presynaptic terminals. The different patterns of expression described above imply that individual PKC subspecies may have a specific function in modulating the neuronal activity in the different neurons of the spinal cord.

Animals↗
PubMed1990

Electron microscopic localization of gamma- and beta II-subspecies of protein kinase C in rat hippocampus.

The subcellular distributions of the gamma- and beta II-subspecies of protein kinase C (gamma- and beta II-PKC) were studied in the rat hippocampus by light and electron microscopic immunocytochemistry. Both subspecies were abundant in the hippocampus with distinct subcellular distributions. The immunoreactivity of gamma-PKC was observed throughout the Ammon's horn, while intense beta II-PKC immunoreactivity was observed predominantly in the CA1 region. gamma-PKC was distributed diffusely through the cytoplasm of pyramidal cells from the perikarya to the dendritic spines. In contrast, beta II-PKC was concentrated around the Golgi complex and present diffusely in distal dendrites, except for the dendritic spines. Neither PKC subspecies could be detected in the presynaptic terminal. The postsynaptic localization of gamma- and beta II-PKC in CA1 suggests that both PKC subspecies may correlate to long-term potentiation in the CA1 region contributing to the postsynaptic side. gamma-PKC may have a specific function not only in CA1 but also in the mossy fiber-CA3 pathway at the postsynaptic side. beta II-PKC may have another function concerning the Golgi complex in CA1.

Animals↗
PubMed1990

Radiation inactivation target-size analysis of soluble guanylate cyclase.

The soluble form of guanylate cyclase, which is a heterodimer of two subunits with molecular weights of 82,000 and 70,000, was analyzed by radiation inactivation experiments to determine its functional size. Lyophilized crude extract from rat lung or the purified enzyme were irradiated with different doses from 60Co gamma-rays, and the residual activities were measured in the presence or absence of a potent activator, sodium nitroprusside. The target sizes for the basal activity and for the activity in the presence of sodium nitroprusside were calculated from the decay curve was 77 and 192 kDa, respectively, on the crude enzyme, or as 71 and 163 kDa, respectively, on the purified enzyme. The size for the activatable form of the enzyme was more than twice that of the basal activity and close to the size of the holoenzyme, implying that the enzyme activity must reside on one of the subunits and the activation by sodium nitroprusside requires interaction of both subunits.

Animals↗
PubMed1990

Effects of atrial natriuretic peptide on brain oedema: the change of water, sodium, and potassium contents in the brain.

We examined the effect of atrial natriuretic peptide (ANP) administration on cerebral oedema in rats. Intravenous ANP infusion with total dose of 120 micrograms/kg and 100 micrograms/kg suppressed the elevation of water and Na contents in left middle cerebral artery (MCA) occluded and cold injured brain tissue, indicating that ANP has a suppressive effect on cerebral oedema. Similar ANP infusion at a low dose of 1 microgram/kg/h for 6 h also resulted in observation of the anti-oedematous effect in both models, with no observable occurrence of the known systemic effects of ANP on systolic blood pressure (SBP), heart rate (HR), hematocrit, or serum electrolyte ion (Na+, K+, Cl-) concentrations. The results thus suggest that the anti-oedematous effect of ANP is attributable to water and Na content control by ANP specific to the damaged tissue, possibly through inhibition of sodium transport. Taken together with a recent study in which it was shown that ANP might inhibit sodium transport in cerebral microvessel, our results suggest that ANP suppresses the development of brain oedema by inhibiting sodium transport and the coupled water influx.

Animals↗
PubMed1990

Effects of atrial natriuretic peptide on ischaemic brain oedema evaluated by the proton magnetic resonance method.

The effect of atrial natriuretic peptide (ANP) on cerebral oedema in rats was examined by magnetic resonance (MR). After occlusion of the left middle cerebral artery (MCA) to induce cerebral ischaemia, rats received continuous infusion of ANP for 24 h at a total dose of 120 micrograms/kg or 150 micrograms/kg. Proton relaxation times (T1 and T2) of excised oedematous tissue were measured in vitro and the area of the oedematous region was determined in vivo by the use of magnetic resonance imaging (MRI). The administration of ANP was found to decrease the lengthening of both T1 and T2 in the oedematous tissues and shown by MRI to decrease the area of the oedematous region, compared with group receiving saline. The topographic observations in vivo suggest that ANP suppress the development of the oedematous region.

Animals↗
PubMed1990

Immunocytochemical localization of the alpha subspecies of protein kinase C in rat brain.

The distribution of the alpha subspecies of protein kinase C (PKC) in rat brain was demonstrated immunocytochemically by using polyclonal antibodies raised against a synthetic oligopeptide corresponding to the carboxyl-terminal sequence of alpha-PKC. The alpha-PKC-specific immunoreactivity was widely but discretely distributed in both gray and white matter. The immunoreactivity was associated predominantly with neurons, particularly with perikaryon, dendrite, or axon, but little was seen in the nucleus. Glial cells expressed this PKC subspecies poorly, if at all. The highest density of immunoreactivity was seen in the olfactory bulb, septohippocampal nucleus, indusium griseum, islands of Calleja, intermediate part of the lateral septal nucleus, and Ammon's horn. A moderately high density of the immunoreactivity was seen in the anterior olfactory nucleus, anterior commissure, cingulate cortex, dentate gyrus, compact part of the substantia nigra, interpeduncular nucleus, inferior olive, and olivocerebellar tract. This distribution pattern was consistent with that obtained by in situ hybridization histochemistry. The distribution of alpha-PKC immunoreactivity was different from that of beta I-, beta II-, and gamma-PKC immunoreactivity. These findings suggest that alpha-PKC is involved heavily in the control of specific functions of some restricted neurons.

Amino Acid Sequence↗
PubMed1990

Light and electron microscopic localization of beta I-, beta II-, and gamma-subspecies of protein kinase C in rat cerebral neocortex.

We have localized the beta I-, beta II-, and gamma-subspecies of protein kinase C in cerebral neocortex with light and electron microscopic immunocytochemistry using a monoclonal antibody against gamma-PKC and polyclonal antisera to beta I- or beta II-PKC-specific oligopeptides. The gamma-PKC-immunopositive cell bodies were seen mostly in layers II, V, and VI, and the vast majority of them were pyramidal cells. The beta II-PKC immunoreactive cell bodies were observed in layers II, III, V, and VI, and most of them seemed to be pyramidal cells. Both gamma- and beta II-PKC were colocalized in some pyramidal cells in layers II, V, and VI. The small number of beta I-PKC immunoreactive cell bodies were observed in the neocortex, and many of them were nonpyramidal cells. About 80% of the beta I-PKC-immunoreactive cells were shown to be GABAergic neurons. The gamma-PKC-immunopositive neuropils were observed in layers I, II, V, and VI, while beta II-PKC-immunoreactive neuropils were seen in layers I-III, V, and VI. The distribution of each subspecies is much the same throughout all regions of the neocortex, although with different intensities of immunoreactivity. electron microscopic studies revealed that, in the perikarya, gamma-PKC was distributed throughout the cytoplasm, beta I-PKC was just adjacent to the plasma membrane, and beta II-PKC was located around the Golgi complex. The immunoreactivity of these 3 subspecies was also seen in dendrites and axons, but no immunoreactivity of these subspecies was found in the presynaptic terminals in the present study. The discrete cellular and intracellular distributions of protein kinase C subspecies imply that each subspecies has a specific role in neuronal activity in the cerebral neocortex.

Animals↗