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Biomedical subjects

Y Kitamura

Publications and source records attributed to Y Kitamura.

At least 379 records · Page 21Linked to original sources
PubMed1995

Topography of somatosensory evoked magnetic fields following posterior tibial nerve stimulation.

The topography of somatosensory evoked magnetic fields (SEFs) following stimulation of the right and left posterior tibial nerves was investigated in 5 normal subjects (10 nerves). The main deflections N37m-P45m-N60m-P75m and their counterparts P37m-N45m-P60m-N75m were identified in the hemisphere contralateral to the stimulated nerve. Their equivalent current dipoles (ECDs) were located in the foot area of the primary sensory cortex (SI), probably in area 3b. Restricted minor deflections, P40m-N40m and N50m-P50m, were considered to be generated in area 1 in SI. As the generator sources of P37m-N37m, P40m-N40m and N45m-P45m were temporarily changed and interfered with each other, the direction of ECDs appeared to be rotated with the passage of time. Small middle-latency deflections, N100m-P100m, were clearly identified in 2 subjects. ECDs of these deflections were found in the second sensory cortex (SII), in both hemispheres, although they were clearer in the hemisphere contralateral to the stimulated nerve. In conclusion, short- and middle-latency SEFs are mainly generated in area 3b in SI contralateral to the stimulated nerve, and responses generated in area 1 of SI and SII affect the SEFs to some degree, but interindividual differences are large compared with SEFs evoked by upper limb stimulation.

Adult↗
PubMed1995

Pain-related somatosensory evoked magnetic fields.

Somatosensory evoked magnetic fields (SEFs) following painful electrical stimulation of the finger were investigated in 5 normal subjects. Equivalent current dipoles (ECDs) of deflections shorter than 100 msec in latency were located in the primary sensory cortex (SI) in the hemisphere contralateral to the stimulated finger following either non-painful or painful stimulation. Two main deflections, N100m-P100m and N250m-P250m, were independently identified following painful stimulation, although they were not found in SEFs following non-painful weak stimulation. ECDs of the N100m-P100m were considered to be located in the bilateral second sensory cortices (SII). ECDs of the N250m-P250m were identified in the bilateral cingulate cortices and SII, but the intersubject difference was large. Therefore, we considered that contralateral SI and bilateral SII were initially activated by painful noxious stimulation, and then multiple areas including bilateral SII and cingulate cortices were activated. In EEG recordings (evoked potentials), no potential corresponding to N100m-P100m was found, probably because it was difficult to record activation in SII by EEG recordings. The P250 potential which corresponded to the N250m-P250m was clearly identified, probably because activation of multiple areas generated large long-duration EEG potentials which were maximal around the vertex, unlike MEG recordings.

Adult↗
PubMed1995

Disturbed intestinal movement, bile reflux to the stomach, and deficiency of c-kit-expressing cells in Ws/Ws mutant rats.

BACKGROUND & AIMS: Interstitial cells of Cajal (ICCs) are believed to initiate the basic contractile activity of the gastrointestinal tract. Because ICCs in the intestine of mice express c-kit receptor tyrosine kinase and because rats are more commonly used than mice for pathophysiological investigations of the gastrointestinal tract, the number of the c-kit messenger RNA-expressing cells was compared with gastrointestinal movement in rats. METHODS: The c-kit messenger RNA-expressing cells were detected by in situ hybridization. The autonomous contraction of excised segments of the ileum was recorded. The function of the pyloric sphincter was evaluated by measuring the content of bile acids in the stomach. RESULTS: The c-kit messenger RNA-expressing cells were not detectable in the stomach of Ws/Ws mutant rats with a small deletion at the tyrosine kinase domain of c-kit, and the number of c-kit messenger RNA-expressing cells decreased to 7% that of normal control rats in the ileum of Ws/Ws rats. The contractile activity of the ileum was apparently impaired, and the content of bile acids in the stomach was significantly increased in Ws/Ws rats. CONCLUSIONS: The abnormalities in the ileal movement and pyloric sphincter function in Ws/Ws rats were attributable to the deficiency of c-kit messenger RNA-expressing cells.

Animals↗
PubMed1995

Gating of somatosensory evoked responses during active finger movements magnetoencephalographic studies.

The "gating" effects caused by active finger movements on somatosensory evoked magnetic fields (SEFs) following stimulation of the median nerve were examined in normal subjects. The effects of the interfering stimulus were best demonstrated by subtracting the "interference" wave forms from the "control" wave forms to derive the "difference" wave form. The short-latency cortical deflections, N20m-P20m, P30m-N30m and P25m-N35m were significantly attenuated with no latency changes. In contrast, the following middle-latency deflections, the N40m-P40m and the P60m-N60m were clearly changed in terms of latency and duration by the interference. The D30m-U30m and the U60m-D60m in the "difference" wave form were derived from these interference changes. It is considered that the gating effects on all deflections took place in the hemisphere contralateral to the stimulated median nerve, because all of the equivalent current dipoles (ECDs) of the short- and the middle-latency deflections in the "control", "interference" and "difference" wave forms were located there. The gating effects on the short-latency deflections were suggested to be due to the interactions between the neurons in areas 1 and 3b, which were activated by sensory inputs from cutaneous mechanoreceptors, and the neurons in area 3a which were activated by sensory inputs from the muscle spindles. The gating effects on the middle-latency deflections may mainly be due to the excitations of neurons in area 4 caused by either continuous movement-related activities or by sensory inputs spreading from the sensory cortex.

Adult↗
PubMed1995

Germanium intoxication with sensory ataxia.

Sensory ataxia in inorganic germanium intoxication is rare. A 63-year-old housewife had taken inorganic germanium preparations at a dosage of 36 mg a day for about 6 years (total dose about 80 g). She subsequently developed difficulty in writing and gait disturbance with peripheral neuropathy and renal involvement. Germanium, which is not usually detected in the non-germanium user, was accumulated in her hair and nails, permitting a diagnosis of inorganic germanium intoxication. The peripheral neuropathy and renal injury were not reversible after discontinuing the preparation. Pneumonia and sepsis then supervened and the patient died. Autopsy findings showed degeneration and loss of the dorsal root ganglion cells and degeneration of the dorsal column of the spinal cord. Two previously reported cases presented with ataxia. These patients took germanium for long periods and/or large quantities like our case. It was supposed that sensory ataxia was induced by chronic and dose dependent toxicity of inorganic germanium.

Aged↗
PubMed1995

Biphasic effects of MPP+, a possible parkinsonism inducer, on dopamine content and tyrosine hydroxylase mRNA expression in PC12 cells.

When PC12 cells were treated with 1-methyl-4-phenylpyridinium ion (MPP+) at various concentrations for 1 week, the dopamine (DA) content was increased compared to the control at 1-30 microM but was decreased to less than the control at concentrations above 100 microM. Cell death was caused by 300 microM MPP+, indicating that decrease in DA content proceeds cell death. When the cells were treated with 100 microM MPP+ for various periods, DA content was transiently increased (6 h-2 days) and then gradually decreased below the control (4-7 days). These results suggest that MPP+ possesses biphasic effects on DA content, being dependent on both concentrations and treatment periods. Moreover, by treatment with 100 microM MPP+, tyrosine hydroxylase (TH) mRNA expression was also transiently increased and then gradually decreased below the control, suggesting that MPP+ also possesses biphasic effects on TH mRNA expression.

1-Methyl-4-phenylpyridinium↗
PubMed1995

Brain histaminergic system in mast cell-deficient (Ws/Ws) rats: histamine content, histidine decarboxylase activity, and effects of (S) alpha-fluoromethylhistidine.

The mast cell-deficient [Ws/Ws (White spotting in the skin)] rat was investigated with regard to the origin of histamine in the brain. No mast cells were detected in the pia mater and the perivascular region of the thalamus of Ws/Ws rats by Alcian Blue staining. The histamine contents and histidine decarboxylase (HDC) activities of various brain regions of Ws/Ws rats were similar to those of +/+ rats except the histamine contents of the cerebral cortex and cerebellum. As the cerebral cortex and cerebellum have meninges that are difficult to remove completely, the histamine contents of these two regions may be different between Ws/Ws and +/+ rats. We assume that the histamine content of whole brain with meninges in Ws/Ws rats is < 60% of that in +/+ rats. So we conclude that approximately half of the histamine content of rat brain is derived from mast cells. Next, the effects of (S) alpha-fluoromethylhistidine (FMH), a specific inhibitor of HDC, on the histamine contents and HDC activities of various regions of the brain were examined in Ws/Ws rats. In the whole brain of Ws/Ws rats, 51 and 37% of the histamine content of the control group remained 2 and 6 h, respectively, after FMH administration (100 mg/kg of body weight). Therefore, we suggest that there might be other histamine pools including histaminergic neurons in rat brain.

Alcian Blue↗
PubMed1995

Histamine actions in dog retinal central arteries as compared to those in middle cerebral and temporal arteries.

PURPOSE: Mechanisms underlying the relaxant response to histamine were compared in isolated dog retinal arteries (branch of internal and external carotid arteries), middle cerebral arteries (branch of internal carotid artery) and superficial temporal arteries (branch of external carotid artery). METHODS: Changes in the isometric tension of helical strips of the arteries with and without the endothelium were recorded. RESULTS: Histamine produced concentration-related biphasic (phasic and sustained) relaxations in retinal arterial strips contracted partially with prostaglandin (PG)F2 alpha. Relaxations induced by histamine were not dependent on the endothelium. Treatment with cimetidine attenuated the sustained relaxation, whereas chlorpheniramine or indomethacin depressed the phasic relaxation. In addition, the phasic relaxant response to histamine was attenuated by tranylcypromine, a PGI2 synthesis inhibitor. In contrast, the amine-induced relaxant responses in dog middle cerebral arterial branch and temporal arteries were markedly suppressed by cimetidine alone. CONCLUSIONS: In dog retinal arteries, the phasic relaxation caused by histamine is mediated by PGI2 in association with activation of the H1 receptor subtype in subendothelial tissues, possibly smooth muscle, and the sustained relaxation is evoked by direct stimulation of the H2 receptor subtype in smooth muscle. The histamine-induced relaxation in temporal and distal middle cerebral arteries is associated solely with a stimulation of H2 receptors in smooth muscle.

Animals↗
PubMed1995

Expression of bone-related protein messenger RNA in human meningiomas: possible involvement of osteopontin in development of psammoma bodies.

Meningiomas often contain concentric calcified foci, referred to as psammoma bodies. Since calcium phosphate deposits in both psammoma bodies and bone tissues, we examined whether messenger (m) RNA of bone-related extracellular matrix proteins and bone morphogenetic proteins (BMP) were expressed in human meningioma tissues. Northern blotting demonstrated the expression of osteopontin (OPN), matrix Gla protein (MGP), osteonectin (ON) and BMP-4 mRNA but not bone sialoprotein, osteocalcin and BMP-2 mRNA. In situ hybridization revealed that most OPN mRNA-expressing cells were located around the psammoma bodies in meningothelial whorls. Moreover, combination of in situ hybridization and immunohistochemistry on serial sections showed that the OPN mRNA-expressing cells were CD68-positive, suggesting they were macrophages. Immunohistochemistry with anti-OPN antibody and von Kossa staining on the adjacent section showed that the deposition site of OPN protein was consistent with that of calcium phosphate. Neither MGP nor ON mRNA expression appeared to correlate with the calcification. The present result suggests that OPN produced by CD68-positive macrophages may play a significant role for development of psammoma bodies in meningiomas.

Antibodies, Monoclonal↗
PubMed1995

Possible role of osteopontin in deposition of calcium phosphate in human pilomatricomas.

Human pilomatricomas are benign epidermal appendage tumors composed of hair matrix-like basaloid cells and keratinized remnant cells referred to as shadow cells. Deposition of calcium phosphate usually occurs in the shadow cell nests. Because osteopontin is believed to be involved in the deposition of calcium phosphate in bones, we asked whether osteopontin messenger RNA also is expressed in pilomatricomas. Using Northern blotting and in situ hybridization we detected osteopontin messenger RNA in pilomatricoma tissues but not in normal skin tissue. By the combination of in situ hybridization and immunohistochemistry, osteopontin messenger RNA-expressing cells were identified as CD68-positive macrophages surrounding the shadow cell nests. Immunohistochemistry of anti-human osteopontin antibodies revealed that the localization of osteopontin protein was consistent with that of calcium phosphate. The present results suggest that osteopontin produced by macrophages may play a significant role in the deposition of calcium phosphate in the shadow cell nests of pilomatricomas.

Amino Acid Sequence↗
PubMed1995

Expression of vascular permeability factor (VPF/VEGF) messenger RNA by plasma cells: possible involvement in the development of edema in chronic inflammation.

Edema occurs in some types of chronic inflammation such as nasal polyps, uterine cervical polyps and gastric hyperplastic polyps. However, the factors or cellular components involved in the development of edema in chronic inflammation remain to be clarified. Recently, the gene encoding vascular permeability factor (VPF) or vascular endothelial growth factor (VEGF) and the genes encoding its receptors (kinase insert domain-containing receptor (KDR) and fms-like tyrosine kinase-1 [fit-1]) have been cloned. VPF/VEGF induces vascular hyperpermeability and vascular endothelial proliferation through KDR or fit-1 receptors. As there is a possibility that VPF/VEGF may play a role in the development of edema in chronic inflammation, we examined the messenger (m) RNA expression of VPF/VEGF and its receptors in nasal polyp tissues, which is an example of chronic inflammation with remarkable edema. Using northern blotting, all nasal polyp tissues examined expressed mRNA of VPF/VEGF and KDR. In situ hybridization revealed that VPF/VEGF mRNA-expressing cells were scattered in the edematous stroma of nasal polyps. In the adjacent sections, these cells showed the morphological features of plasma cells and expressed mRNA of immunoglobulin light chains. Human B cell leukemia and plasmacytoma cell lines expressed VPF/VEGF mRNA but human mast-cell leukemia and T cell leukemia cell lines did not. The alternatively spliced pattern of VPF/VEGF transcripts observed in nasal polyp tissues was consistent with that in plasmacytoma cell lines. Taken together, the VPF/VEGF mRNA-expressing cells in nasal polyps appeared to be plasma cells, suggesting that plasma cells may play an important role in the development of edema in chronic inflammation through the production of VPF/VEGF.

Base Sequence↗
PubMed1995

Expression of the Runt domain-encoding PEBP2 alpha genes in T cells during thymic development.

The PEBP2 alpha A and PEBP2 alpha B genes encode the DNA-binding subunit of a murine transcription factor, PEBP2, which is implicated as a T-cell-specific transcriptional regulator. These two related genes share the evolutionarily conserved region encoding the Runt domain. PEBP2 alpha B is the murine counterpart of human AML1, which is located at the breakpoints of the 8;21 and 3;21 chromosome translocations associated with acute myeloid leukemia. Northern (RNA) blots of various adult mouse tissues revealed that the levels of expression of both genes were most prominent in the thymus. Furthermore, transcripts of PEBP2 alpha A and mouse AML1/PEBP2 alpha B were detected in T lymphocytes in the thymuses from day 16 embryos and newborns, as well as 4-week-old adult mice, by in situ hybridization. The expression of the genes persisted in peripheral lymph nodes of adult mice. The transcripts were detected in all the CD4- CD8-, CD4+ CD8+, CD4+ CD8-, and CD4- CD8+ cell populations. The results indicated that both genes are expressed in T cells throughout their development, supporting the notion that PEBP2 is a T-cell-specific transcription factor. Transcripts of mouse AML1/PEBP2 alpha B were also detected in day 12 fetal hematopoietic liver and in the bone marrow cells of newborn mice. The implication of mouse AML1/PEBP2 alpha B expression in hematopoietic cells other than those of T-cell lineage is discussed in relation to myeloid leukemogenesis.

Acute Disease↗
PubMed1995

Substitution of an aspartic acid results in constitutive activation of c-kit receptor tyrosine kinase in a rat tumor mast cell line RBL-2H3.

The c-kit protooncogene encodes a receptor tyrosine kinase that mediates signals required for differentiation, proliferation and survival of mast cells. We have already shown the constitutive activation of c-kit receptor tyrosine kinase (KIT) in a human mast cell leukemia line (HMC-1) and a murine mastocytoma cell line (P-815). We here examined whether such constitutive activation of KIT occurred in the rat tumor mast cell line RBL-2H3 as well, which is frequently used as a tool for studying functions of mast cells. In RBL-2H3 cells, KIT was constitutively phosphorylated on tyrosine and activated in the absence of autocrine production of its ligand, stem cell factor (SCF). Sequencing analysis revealed that one of c-kit genes of RBL-2H3 cells had a point mutation, resulting in amino acid substitution of Tyr for Asp in codon 817. When rat wild-type c-kit cDNA and mutant-type c-kit cDNA encoding KITTyr817 were transfected into cells of a human embryonic kidney cell line (293T), only mutant form KITTyr817 was constitutively phosphorylated on tyrosine and activated in the absence of SCF. Since mutations at the same Asp codon constitutively activated KIT in all the human HMC-1, murine P-815, and rat RBL-2H3 cell lines, and since the incorporation of antisense oligonucleotides of c-kit messenger RNA significantly suppressed the proliferation of RBL-2H3 cells, the activating mutations in the Asp codon of the c-kit gene appeared to be involved in neoplastic growth of mast cells.

Amino Acid Sequence↗
PubMed1995

Regulation of neuronal nitric oxide synthase in rat adrenal medulla.

Neuronal nitric oxide synthase (nNOS) has been suggested to be involved in cardiovascular homeostasis. We studied the regulation of nNOS expression, determining nNOS mRNA expression levels in various tissues in spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). We also investigated the effects of antihypertensive treatment with the angiotensin II antagonist hydralazine or reserpine on nNOS mRNA expression. The expression levels of nNOS mRNA and nNOS protein were determined by Northern and Western blot analysis, respectively. NADPH-diaphorase histochemistry was used to identify cells in the adrenal medulla that expressed nNOS. No significant differences in expression levels in SHR and WKY were observed in the cerebellum and brain stem. nNOS mRNA expression levels in the decapsular portion of the adrenal gland were developmentally modulated and in a 24-week-old WKY were 2.5 times higher than in an age-matched SHR. This reduced expression of nNOS mRNA in the decapsular portion of the adrenal gland of SHR seemed to be a result of hypertension in the SHR, because administration of either an angiotensin II antagonist (TCV-116) or hydralazine upregulated nNOS mRNA expression in both SHR and WKY. Marked augmentation of nNOS mRNA expression in the decapsular portion of the adrenal gland by reserpine treatment suggested an intimate relation between nNOS in the decapsular portion of the adrenal gland and the sympathoadrenal system. Reserpine treatment also increased the expression of nNOS protein; however, reserpine treatment did not affect the distribution pattern of nNOS-positive cells (NADPH-diaphorase-positive cells) in the adrenal medulla.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Medulla↗
PubMed1995

Identification of the cells expressing cot proto-oncogene mRNA.

The cell types expressing cot proto-oncogene mRNA were identified by in situ hybridization (ISH) histochemistry. Among a variety of adult mouse tissues examined, four types of glandular cells expressing cot gene were identified: (1) granular duct cells in the submandibular and sublingual glands; (2) serous cells in the parotid gland; (3) peptic (chief) cells in gastric glands; and (4) goblet cells in colonic glands. Investigation of the developmentally regulated expression of cot mRNA using tissues of 14-day and 18-day embryos, newborn and weanling mice showed that cot gene is expressed only in morphologically differentiated and functionally activated cells of these four types. No other types of cells showing ISH signals were observed. Based on these results, cot gene expressions in cultured cells of colonic adenocarcinomas and gastric adenocarcinomas were examined. SW 480 and WiDr cells showed high expression of this gene and so should be useful for functional analysis of Cot kinase. The expression patterns of cot gene in tumor tissues of the parotid gland, and gastric and colonic glands were investigated. Two of the tissues overexpressed this gene markedly, suggesting that overproduction of Cot kinase may be one cause of their transformation.

Adenocarcinoma↗
PubMed1995

Inhibitory effects of pentamidine on N-methyl-D-aspartate (NMDA) receptor/channels in the rat brain.

Effects of pentamidine, a therapeutic drug for Pneumocystis carinii pneumonia (PCP) in acquired immunodeficiency syndrome (AIDS), on specific bindings of [3H](+)-5-methyl-10,11-dihydro-5H- dibenzo[a,d]cyclohepten-5,11-imine maleate (MK-801) and [3H]nitrendipine were investigated in crude synaptic membranes (CSM) of rat brain. Pentamidine inhibited [3H]MK-801 binding but did not change [3H]nitrendipine binding, although neither binding was inhibited by 3'-azido-2',3'-dideoxythymidine or 2',3'-dideoxycytidine (inhibitors for reverse transcriptase of HIV-1), or FK-506 or cyclosporin A (immunosuppressants). In Triton X-100-treated CSM (post-synaptic density-rich fractions), the inhibitory effect of pentamidine on [3H]MK-801 binding was partially prevented by addition of spermine and NMDA plus glycine (Gly). Electrophysiological experiments showed that pentamidine also inhibited Ca(2+)-current evoked by NMDA plus Gly in Xenopus oocytes injected with rat brain mRNA. These results suggest that pentamidine is a potent inhibitor for NMDA receptor/channels.

Animals↗