Biomedical subjects

K Terai

Publications and source records attributed to K Terai.

At least 37 records · Page 2Linked to original sources

PubMed1998

Immunohistochemical analyses of fibroblast growth factor receptor-1 in the human substantia nigra. Comparison between normal and Parkinson's disease cases.

The use of neurotrophic growth factors as a means of preventing loss of the dopaminergic (DA) neurons in the substantia nigra (SN) is becoming an accepted treatment strategy for Parkinson's disease (PD). In earlier studies, we showed that there was a selective loss of basic fibroblast growth factor (bFGF) immunoreactivity in DA neurons of the SN in PD suggesting that a deficiency of bFGF might contribute to cell death. As a preliminary step to assessing the potential for using bFGF or its analogs as therapeutic agents, the expression of fibroblast growth factor receptor-1 (FGFR-1) in the SN of normal and PD cases was investigated immunohistochemically. FGFR-1 immunoreactivity could be detected in DA neurons of the SN in young and old neurologically normal cases with an apparent decline with age. FGFR-1 immunoreactivity was also detected in many of the residual SN neurons in most of the idiopathic PD cases. These results indicate that FGFR-1 immunoreactivity, and possibly FGF binding activity, is retained in DA neurons in PD.

Adult↗

PubMed1998

Immunohistochemical localization of GABAA receptors in comparison with GABA-immunoreactive structures in the nucleus tractus solitarii of the rat.

The localization of GABAA receptors was studied by immunohistochemistry in the nucleus tractus solitarii of the rat using a monoclonal antibody (bd17) against the beta-subunit. The pattern of distribution was compared with that of GABA-immunoreactive axons and nerve terminals. Positive staining for GABAA receptors was confined to regions near the surface of neuronal somata and their processes. The highest density of positive staining for GABAA receptors was seen in the central part of the rostral nucleus tractus solitarii where GABA-positive terminals were also rather dense. At both intermediate and caudal levels of the nucleus tractus solitarii, a moderate density of positive staining for GABAA receptors was located in the ventrolateral part, including the ventrolateral subnucleus. In these regions, the density of GABA-positive terminals was low. In the medial nucleus tractus solitarii, including the medial subnucleus, very little or no positive staining for GABAA receptors was detected, although many GABA-positive terminals were observed. The results suggest that the central part of the rostral nucleus tractus solitarii is controlled by the GABAergic system via GABAA receptors, but in the medial subnucleus of the nucleus tractus solitarii the GABA neurons appear to act via receptors that are not detectable by the antibody used.

Animals↗

PubMed1998

Production of monoclonal antibody against histamine and its application to immunohistochemical study in the stomach.

A monoclonal antibody against histamine has been produced. A histamine-haemocyanin conjugate prepared using 1-ethyl-3-(3-dimethylaminopropyl) carbodiimide as a coupling agent was used for immunizing mice. Immunized mice were sacrificed to prepare monoclonal antibody using a hybridoma technique. On immunospot assay, the hybridoma culture supernatant containing a monoclonal antibody was capable of detecting 50 pmol of histamine. Using this antibody, we examined the cellular localization of histamine-like immunoreactivity in the stomach of normal or alpha-fluoromethylhistidine-treated rats and mice. Immunoreactive cells were abundant in the gastric mucosal layer. These positive cells were often located in the basal half of the fundic gland but were rare in the pyloric gland. The cells, small or medium in size, spindle or cone in shape, were intermingled with immunonegative epithelial cells. In the cytoplasm of the positive cells, granular reaction products were densely deposited. In addition, a few positive cells, identified as mast cells by Toluidine Blue staining, were distributed mainly in the submucosal and muscular layer. The antibody preabsorbed with 10 mM histamine gave no positive immunostaining. For pharmacological study, some rats were injected six times with c-fluoromethylhistidine every 8 h. In these rats, positive cells except mast cells were no longer detected. In conclusion, the monoclonal antibody produced appears to be highly specific for histamine. Its application in immunohistochemistry should provide a powerful tool for analysing the roles of histamine in enterochromaffin-like or mast cells in the stomach.

Animals↗

PubMed1997

Encephalitogenic peptide (EP) in human cerebrovascular white matter lesions.

The expression of encephalitogenic peptide (EP), a 68-86 amino acid sequence of guinea pig myelin basic protein (MBP), was investigated in autopsied brains with focal cerebral damage or with diffuse white matter (WM) lesions. EP immunoreactive fibers were distributed in parallel with fibers immunoreactive for amyloid protein precursor (APP), an indicator of WM damages. EP was expressed in the periphery of cerebral infarctions and hematoma in the acute and subacute stages, but was also distributed in diffuse WM lesions due to heterogeneous causes. These data indicate that EP epitopes are exposed specifically in ongoing WM damages, and that the destruction of myelin occurs sporadically in diffuse WM lesions of varying intensity.

Aged↗

PubMed1997

Neurons express proteins of the classical complement pathway in Alzheimer disease.

Occurrence of the classical pathway complement proteins C1q, C1r, C1s, C2, C3, C4, C5, C6, C7, C8 and C9 was studied in human hippocampus and temporal cortex by immunohistochemistry and Western blotting. In Alzheimer disease (AD) cases, positive staining for all of these proteins was observed in pyramidal neurons and senile plaques. In control cases, weaker pyramidal neuron staining was observed except for C1q and C1s which were not detected. On Western blots of AD hippocampal extracts, bands corresponding to those detected in normal serum were found for each of the complement proteins. Comparable bands were also detected in normal hippocampal extracts with the exception of C1s which was not observed. The intensity of the bands was generally stronger in AD than in normal extracts, but, in the latter, there was considerable variability between cases and between bands in a single case. These data suggest that pyramidal neurons may be a source of the complement components known to be associated with Alzheimer lesions.

Aged↗

PubMed1997

Expression of presenilin-1 and -2 mRNAs in rat and Alzheimer's disease brains.

Recently, new genetic linkages have been identified for early-onset familial Alzheimer's disease (AD). Mutations have been found in the presenilin (PS)-1 (S182) gene on chromosome 14 and the PS-2 (STM2/E5-a) gene on chromosome 1. We have investigated the distribution of gene expression of both presenilins in normal rat brain, and in human control and AD cases using in situ hybridization histochemistry. In normal rat brain, intense PS-1 mRNA expression was observed predominantly in neurons, particularly hippocampal pyramidal and dentate granular neurons and cerebellar Purkinje and granular neurons. The distribution of intensely expressing PS-2 mRNA cells was similar to that of PS-1, but additional groups in the brain stem and cortex were identified. Faint but significant mRNA expression of both PS genes was detected in white matter. In control human cases, the same neuronal cell types as seen in rat brain expressed both PS mRNAs in the hippocampus and cerebellum. In AD cases, the expression of both mRNAs was markedly decreased in the hippocampus but not in the cerebellum. In addition, PS-2 hybridization showed increased mRNA expression in astrocyte-like cells in affected areas of AD cases. The present data indicate that the PS genes may play important roles in specific neurons in normal brain, and that the decreased expression in neurons in sporadic AD brain may bear some relationship to the pathogenesis.

Alzheimer Disease↗

PubMed1997

Expression of interleukin-1 receptor antagonist protein in post-mortem human brain tissues of Alzheimer's disease and control cases.

The immunohistochemical localization of interleukin-1 receptor antagonist protein (Il-1ra) was examined in brain tissues of neurologically normal controls as well as in cases of Alzheimer's disease (AD) and Pick's disease. In all control cases, immunoreactivity was observed in some normal-appearing neurons in the neocortex and hippocampus. In AD, there appeared to be increased numbers of positively staining neurons, and the staining of individual neurons was somewhat more intense. Il-1ra was additionally expressed in globular deposits in senile plaques and, weakly, in some extracellular neurofibrillary tangles. In Pick's disease, there was similar staining of normal-appearing neurons and intense staining in some degenerating neurons. Using reverse transcriptase-polymerase chain reaction techniques, the mRNA for IL-1ra was detected in cultured IMR-32 human neuroblastoma cells following differentiation with dibutyryl cAMP and bromodeoxyuridine. Taken together, these data suggest that IL-1ra is a product of normal neurons which may be upregulated in some pathological circumstances.

Aged↗

PubMed1997

Unmasking of an unusual myelin basic protein epitope during the process of myelin degeneration in humans: a potential mechanism for the generation of autoantigens.

A rabbit antiserum (anti-EP), induced against a synthetic peptide corresponding to residues 68 to 86 of guinea pig myelin basic protein, powerfully immunostained abnormal-appearing oligodendrocytic processes and cell bodies in demyelinating areas associated with multiple sclerosis plaques. However, it failed to recognize any structures in normal human, rat, or guinea pig brain. The antiserum recognized the synthetic peptide QDENPVV, which corresponds to human myelin basic protein residues 82 to 88. Immunoabsorption with this peptide eliminated immunohistochemical staining. By contrast, several commercial antibodies recognizing nearby sequences of human myelin basic protein intensely stained all myelinated structures in both normal and multiple sclerosis tissue. The unusual epitope recognized by anti-EP appears to be accessible only in areas of myelin degeneration. If insults occur that repeatedly expose a region of MBP normally sheltered from immunosurveillance, a self-sustaining immune reaction might result.

Adult↗

PubMed1997

[Two cases of infantile autism with intermittent water intoxication due to compulsive water drinking and episodic release of antidiuretic hormone (SIADH)].

The syndrome of water intoxication, resulting from dilutional hyponatremia and characterized by lethalgy, confusion, seizures, and coma was seen in two autistic boys living in the institution for mentally retarded children. Patient 1, a 19 year-old autistic boy showed loss of attention, inactiveness, sleepiness and delirium and then followed by overbreathing, severe vomiting and finally convulsive seizures several times, or coma, since October 1985. In August 1988, he was admitted with generalized tonic clonic convulsion associated with frequent vomiting EEG showed diffuse spike and wave complex with slow background activity. Laboratory data showed inappropriately high serum ADH level (8.5 pg/ml), low sodium concentration (121 mOsm/m/l), serum osmolality (237 mOsm/l) which was lower than urine osmolality (334 mOsm/l), and remarkable body weight gain (8.5 kg). He was diagnosed as water intoxication due to compulsive water drinking and SIADH. Diminished GH secretion to insulin-induced hypoglycemia and exaggerated prolactin response to LHRH stimulation suggested a hypothalamic lesion. Patient 2, a 17-year-old autistic boy, showed essentially the same symptoms and laboratory data as Patient 1, except that he had no epileptic discharge in EEG, and curious GH response to insulin-induced hypoglycemia. A remarkable daily body weight change suggested excessive water drinking and a possible episodic release of ADH. With mild water restriction, this became smaller. Since Patient 1 had epileptic attacks several times without hyponatremia and his EEG showed epileptic discharges, he was diagnosed as having epilepsy. Patient 2 has been seizure-free until now. Abnormality of hypothalamic or pituitary defects and polydipsia and possibility of water intoxication should always be considered when an autistic patients shows recurrent epileptic attacks or episodic strange behaviors with hyponatremia.

Adolescent↗

PubMed1996

Enhancement of immunoreactivity for NF-kappa B in human cerebral infarctions.

The distribution of the nuclear factor-kappa B (NF-kappa B) was investigated immunohistochemically in recently infarcted areas of postmortem human brain. Previously we reported that immunoreactivity for NF-kappa B was enhanced in neurons of Alzheimer disease brain in comparison with control cases. In the present study, a similar enhancement of immunoreactivity was observed in glial cells of infarcted areas, but not in the unaffected surround. Prominent staining for NF-kappa B was seen in some astrocytes, particularly in the penumbra or border zone between ischemic and non-ischemic areas. In some cases, positively stained macrophages were also observed in affected areas. Capillary staining for NF-kappa B was weak and did not differ significantly between affected and unaffected areas. These results suggest that enhanced expression of astrocytic NF-kappa B occurs in cerebral infarcted areas.

Aged↗

PubMed1996

Enhancement of immunoreactivity for NF-kappa B in the hippocampal formation and cerebral cortex of Alzheimer's disease.

The distribution of nuclear factor-kappa B (NF-kappa B) was investigated immunohistochemically in the hippocampal formation, entorhinal cortex, middle temporal gyrus and visual cortex of Alzheimer's disease (AD) and control postmortem cases using a polyclonal antibody against the NF-kappa B p65 subunit. In AD cases, prominent staining for NF-kappa B was seen in neurons and their processes, neurofibrillary tangles and dystrophic neurites. In control cases, only weak staining of some neurons was obtained. The neuronal staining observed in AD was strongest in the hippocampal formation and entorhinal cortex, less in the middle temporal gyrus and least in the visual cortex. There was no difference between AD and control cases in the staining of glial cells and vascular walls. These results suggest that enhanced expression of neuronal NF-kappa B occurs in areas affected by AD pathology.

Aged↗

PubMed1996

Expression of CD43 in human microglia and its downregulation in Alzheimer's disease.

CD43 (leukosialin, sialophorin) expression in brain tissue of neurologically normal and Alzheimer disease (AD) cases was studied immunohistochemically. Abundant CD43-like immunoreactivity was detected in ramified microglia of normal brain. It was also seen in residual leukocytes in capillaries and was faintly detectable on the surface of some normal appearing neurons. In AD brains, the overall expression of CD43 by microglia was markedly lower than in control brains. This was in contrast to HLA-DR which was sharply upregulated due to the activated state of the microglia. This is the first report of a microglial marker which is more highly expressed in the resting or ramified state. Such expression is consistent with theories that CD43 plays an anti-adhesional role, and that cleavage occurs during cellular activation.

Alzheimer Disease↗

PubMed1996

Identification of the cell type origin of odontoma-like cell masses in microphthalmic (mi/mi) mice by in situ hybridization.

Tooth abnormalities occur in microphthalmic (mi/mi) mice. The elongated odontogenic epithelium is interrupted by unresorbed bone at the basal end of the mi/mi incisor, with the epithelium gathered into cell clusters. These clusters develop to odontoma-like masses. To identify the origin of the cell types of these odontoma-like masses, the localization of osteonectin (Osn), osteocalcin (Osc), osteopontin (Osp), matrix Gla protein (MGP) and amelogenin (Am) mRNA in the process of tooth development in mi/mi and +/+ mice was investigated by means of in situ hybridization. Decalcified mandibles of neonatal, 5-, 10-, 14-day-old mice were examined. Osn and Osc mRNA, which localized in osteoblasts and odontoblasts, were also detected in the cells of odontoma-like masses in mi/mi mice. The cells expressing these mRNA were short, columnar and odontoblast-like. Am mRNA was detected in ameloblasts. In mi/mi mice, Am mRNA was also detected in ameloblastic cell clusters, which were formed by the tall columnar cells in the odontoma-like masses. No apparent Osp mRNA expression was detected in the masses. These results indicated that even in odontogenic abnormal cells resulting from physical obstruction in mi/mi mice, the genes that are involved in normal tooth development were still expressed.

Animals↗

PubMed1995

Neuroprotective effects of NBQX on hypoxia-induced neuronal damage in rat hippocampus.

Models of cerebral ischaemia were used for analysis of mechanism of neuronal cell death and/or damage. Ischaemia is caused dominantly by severe hypoxia and hypoglycaemia: in the present study, we examined the influence of severe in vivo hypoxia (5% O2/95% N2 for 30 min at 22 degrees C). After hypoxia, neuronal damage was observed in the CA3 and dentate gyrus (DG) after 3 and 21 days of survival, but not in the CA1.2,3-Dihydroxy-6-nitro-7-sulphamoyl-benzo(F)quinoxaline (NBQX), an antagonist for AMPA/kainate receptors, showed neuroprotective effects in the CA3 and DG. These results suggest that hypoxia may induce neuronal damage in the CA3 and DG through activation of AMPA/kainate receptors.

Analysis of Variance↗

PubMed1995

Extracellular calcium causes the release of calcium from intracellular stores in chick osteocytes.

We have recently demonstrated that a rise in the extracellular divalent cation concentration induces a rapid elevation of cytosolic calcium in chick osteocytes. Here, we demonstrate that cytosolic calcium elevation that occurs in osteocytes on exposure to elevated extracellular calcium is independent of membrane voltage and is insensitive to modulation by organic calcium channel modulators, namely, BAY K 8644, nicardipine, and nifedipine. However, the calcium elevation was sensitive to modulation by an intracellular calcium antagonist, TMB-8, suggesting that the cytosolic calcium elevation was due to mobilization of this cation from an intracellular store.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗

PubMed1994

Divalent cations elevate cytosolic calcium of chick osteocytes.

Though it is proposed that osteocytes have several functions in bone metabolism, only limited definite information including results of calcium regulation has been forthcoming. We demonstrate here for the first time that the concentration of divalent cations, such as calcium, nickel and cadmium, directly regulates the cytosolic calcium concentration in osteocytes.

Animals↗

PubMed1994

Delayed expression of c-fos protein in rat hippocampus and cerebral cortex following transient in vivo exposure to hypoxia.

The time course of c-fos protein expression after hypoxia was examined in rat hippocampus and cerebral cortex using an immunohistochemical method. The rats were exposed to in vivo hypoxia for 30 min in a chamber containing 5% O2 and 95% N2. Immediately after the treatment, c-fos protein-like immunoreactivity was observed in the granule cell layer of the dentate gyrus. The change was transient, and the density of immunoreactive cells returned quickly to a control level 3 h after the exposure. However, the density of positive cells was again increased 1 day after hypoxia and reached the maximum 7 days after. In the cerebral cortex, on the other hand, no change was detected in the pattern of staining at any time, with an exception on 21 days after hypoxia. At this period, positively stained neurons were significantly increased in both density and intensity throughout the entire extent of the cerebral cortex including the cingulate gyrus. These results clearly indicate that hypoxia induces different patterns of c-fos protein expression among various regions of the brain. The biphasic pattern seen in the dentate gyrus as well as the delayed expression in the cerebral cortex may be related to delayed neuronal damages induced by hypoxia.

Animals↗

PubMed1991

Time course of in vitro expression of NADPH-diaphorase in cultured rat brain neurons: comparison with in vivo expression.

The time course of NADPH-diaphorase expression was examined in primary cultures of rat central nervous system and in embryonic or neonatal rat brains using a histochemical method. In cerebral and brainstem cultures from 17-day-old embryonic rats, neuronal cells moderately expressing NADPH-diaphorase were first detected on about the 5th to 7th day of culturing. Both the density of positive cells and the staining intensity increased with age of cultures. The density of positive cells, calculated as a percent of the total number of cells, increased up to day 21 in cultures from both the cerebrum and the brainstem, indicating that NADPH-diaphorase is preferentially expressed in neurons with longer viability. On the other hand, virtually no intensely positive cells were detectable in cerebellar cultures at any period examined up to 21 days. In the in vivo study, moderately stained NADPH-diaphorase-positive neurons were first detected, mainly in the laterodorsal-pedunculopontine tegmental nuclei complex and partly in the striatum, in 16-day-old embryonic rat brain. At 2 days postnatal, intensely stained neurons were detectable in the cerebral cortex as well as in the tegmental nuclei complex and the striatum, indicating some delay in the in vitro, as compared to the in vivo, expression of neuronal NADPH-diaphorase.

Animals↗