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Biomedical subjects

N Inoue

Publications and source records attributed to N Inoue.

At least 343 records · Page 19Linked to original sources
PubMed1995

[Psychiatric symptoms following accidental exposure to sarin--a case report].

A middle aged man who inhaled sarin in a train in a subway station in Tokyo in 1995 and showed a variety of symptoms including psychiatric symptoms was reported. He experienced muscle weakness, dyspnea and unconsciousness of sudden onset immediately after exposure to sarin. Marked miosis was observed on admission. Plasma cholinesterase activity was remarkably decreased at that time. He also experienced delirium consisting of visual hallucination, insomnia and irritability at mid-night for more than seven days. These psychiatric symptoms gradually improved without any medication. To date there is no detailed description of such psychiatric symptoms in sarin poisoning.

Humans↗
PubMed1995

Immunosuppressive agents in the treatment of Crohn's disease and ulcerative colitis.

Low doses of 6-mercaptopurine (6MP) were used for the treatment of inflammatory bowel disease, and 20-30 mg/day was found to be effective for patients with ulcerative colitis who were corticosteroid-dependent or corticosteroid-resistant. Corticosteroid was tapered in 20 of 21 patients with ulcerative colitis. Of 15 patients who were refractory to conventional therapy, 11 responded to 6MP treatment. The same doses of 6MP were given to patients with Crohn's disease who were corticosteroid-dependent or who had associated fistula. Treatment with 6MP did not influence the changes in colonic or ileac lesions in Crohn's disease. However, the fistulas were closed or improved in 70% of 10 patients by 6MP treatment. The adverse effects of small doses of 6MP were minimal. These results confirm that immunosuppressive agents are effective for patients with inflammatory bowel disease. In a rat colitis model induced by immunization with trinitrobenzene (TNB), we used anti-CD4 monoclonal antibodies to prevent colonic inflammation; these antibodies were effective for this colitis model, suggesting that a novel therapy targeting CD4 intestinal lymphocytes may be feasible in the treatment of Crohn's disease.

Animals↗
PubMed1995

CD4+ intestinal mucosal lymphocytes in the pathogenesis of Crohn's disease.

To analyze the nature of intestinal mucosal lymphocytes in Crohn's disease, we established T cell lines of patients' intraepithelial lymphocytes. T cell lines from the affected terminal ileum of the patients showed an increased proportion of CD4+V beta 5.2/5.3+ T cells. These cells were increased in number after stimulation with staphylococcal enterotoxins C1 and D, showed an increase in cytolytic activity, and produced a large amount of interferon-gamma. To clarify the role of CD4+ mucosal lymphocytes in the intestinal inflammation, we then developed a novel colitis model by immunizing a rat with trinitrobenzenesulfonic acid (TNB) emulsion with adjuvant. Deep ulceration and granuloma formation in this colitis model resembled the histopathological findings of human Crohn's disease. Immunohistochemical and flow cytometric analysis demonstrated that the number of CD45RC(high)CD4+ mucosal lymphocytes was increased. Interestingly, the administration of anti-CD4 Abs prevented severe inflammation in the model. After treatment with anti-CD4 Abs, the anti-TNB Ab titer, the number of CD45RC(high)CD4+ cells, and interferon-gamma mRNA expression were significantly decreased in the mucosa of the model. These results suggest that some subsets of CD4+ mucosal lymphocytes play an important role in the triggering and progression of inflammation in Crohn's disease.

Animals↗
PubMed1994

Developmental expression of GLUT3 glucose transporter in the rat brain.

The ontogeny of the GLUT3 glucose transporter gene and protein expression was studied in rat brain. Northern blot analysis using total RNA from rat brains at different developmental stages revealed that the levels of GLUT3 mRNA were very low during the embryonic stage and increased towards the postnatal stage. Immunohistochemistry using a specific antibody showed that the expression of GLUT3 protein was barely detectable in the embryonic stage, but was clearly detected on the plasma membrane of neuronal cells from 10 days after birth to the adult. Expression of GLUT3 mRNA and protein in the cerebral neuronal cell cultures was also examined during the maturation of neurons. GLUT3 glucose transporter of primary neuronal cultured cerebral cortical neurons was only detected in mature neurons after they were cultured for 14 days. These results indicate that GLUT3 plays an important role in glucose homeostasis postnatally in neurons of the rat brain.

Amino Acid Sequence↗
PubMed1994

Increased expression of growth-associated protein GAP-43/B-50 following cerebral hemitransection or striatal ischemic injury in the substantia nigra of adult rats.

The substantia nigra receives massive inhibitory gamma-aminobutyric acid (GABA)-ergic inputs, deafferentation of which is supposed to lead to anterograde transsynaptic regression of the nigral neurons. An immunohistochemical technique was used to examine growth-associated protein GAP-43 expression following cerebral hemitransection or transient middle cerebral artery occlusion (MCAO) in the substantia nigra of adult rats. GAP-43 expression was transiently elevated in the substantia nigra pars reticulata (SNr) neurons, but not in the pars compacta neurons at 3 and 4 days post-hemitransection. Massive striatal ischemic injury produced by transient MCAO also caused an increase in GAP-43 synthesis in the SNr neurons at 3 and 4 days after operation. The present findings raise the possibility that deafferentation of the GABAergic inputs leading to transneuronal regression of the SNr neurons is responsible for the elevated expression of GAP-43 in the substantia nigra of adult rats.

Animals↗
PubMed1994

Characterization of genomic PIG-A gene: a gene for glycosylphosphatidylinositol-anchor biosynthesis and paroxysmal nocturnal hemoglobinuria.

Paroxysmal nocturnal hemoglobinuria (PNH) is an acquired hemolytic anemia characterized by the presence of abnormal subpopulations of blood cells that are deficient in surface expression of glycosylphosphatidylinositol (GPI)-anchored proteins. Recent studies showed that the gene termed PIG-A, which participates in the first step of GPI-anchor biosynthesis, is mutated in the abnormal blood cells from patients with PNH. In this study the genomic PIG-A gene was cloned and characterized to obtain nucleotide sequence information for analyzing somatic mutations of PIG-A in patients with PNH. The PIG-A gene is at least 17 kb long and has six exons. The exon-intron boundaries and 583 bp of the 5' flanking region were sequenced. The 5' flanking region has no TATA-like sequence, but includes four CAAT boxes, two AP-2 sequences, and a CRE sequence, some of which are present in regions necessary for the promoter activity. We report pairs of oligonucleotide primers for polymerase chain reaction that should be useful to amplify and analyze various regions of the PIG-A gene in patients with PNH.

Base Sequence↗
PubMed1994

Gene expression of GLUT3 glucose transporter regulated by glucose in vivo in mouse brain and in vitro in neuronal cell cultures from rat embryos.

This study was designed to determine whether glucose regulates the gene expression of glucose transporter GLUT3 in neurons. We examined the regulation of GLUT3 mRNA by glucose in vivo in mouse brain and in vitro by using neuronal cultures from rat embryos. Hypoglycaemia (< 30 mg/dl), produced by 72 h of starvation, increased GLUT3 mRNA in mouse brain by 2-fold. Hybridization studies in situ demonstrated that hypoglycaemia-induced increases in GLUT3 mRNA expression were observed selectively in brain regions including the hippocampus, dentate gyrus, cerebral cortex and piriform cortex, but not the cerebellum. Primary neuronal cultures from rat embryos deprived of glucose for 48 h also showed an increase (4-fold over control) in GLUT3 mRNA, indicating that glucose can directly regulate expression of GLUT3 mRNA. In contrast with hypoglycaemia, hyperglycaemia produced by streptozotocin did not alter the expression of GLUT3 mRNA. We also confirmed previous findings that hypoglycaemia increases GLUT1 mRNA expression in brain. The increase in GLUT1 expression was probably limited to the blood-brain barrier in vivo, since GLUT1 mRNA could not be detected in neurons of the mouse cerebrum. Thus we conclude that up-regulation of neuronal GLUT3 in response to glucose starvation represents a protective mechanism against energy depletion in neurons.

Animals↗
PubMed1994

Cerebellar stroke due to vertebral artery occlusion after cervical spine trauma. Two case reports.

The authors report two cases of cerebellar infarction due to vertebral artery (VA) occlusion resulting from cervical spine trauma. In one patient with dens and C2 body fracture, the left VA was occluded, resulting in a left cerebellar infarction. The second patient, with a subluxation of C4 on C5, presented with cerebellar swelling and infarction along with acute hydrocephalus secondary to bilateral vertebral artery occlusion. Because vertebral artery injuries with cervical trauma are rarely symptomatic, they can be easily overlooked. Bilateral or dominant vertebral artery occlusion, however, may cause rapid and fatal ischemic damage to the cerebellum and brain stem. Rapid recognition and optimal treatment for this injury depends on early vertebral artery angiography.

Angiography↗
PubMed1994

Elevated immunoreactivity for glutamic acid decarboxylase in the rat cerebral cortex following transient middle cerebral artery occlusion.

We investigated the expression of glutamic acid decarboxylase (molecular weight 67,000; GAD67) immunohistochemically in the rat cerebral cortex following transient middle cerebral artery occlusion (MCAO) capable of producing slowly progressive neuronal damage. An increase in GAD67 immunoreactivity was observed in the cerebral cortex ipsilateral to the ischemic insult, most prominent in lamina IV, 3 to 14 days after MCAO. At this stage, light microscopy showed GAD67-positive puncta to be larger and more strongly immunoreactive in the ipsilateral cortex than those in the contralateral side. The elevated expression of GAD67 in the insulted cortex may reflect part of the adaptive functional changes in GABA transmission with slowly progressive cortical ischemic damage.

Animals↗
PubMed1994

In vivo induction of the growth associated protein GAP43/B-50 in rat astrocytes following transient middle cerebral artery occlusion.

Immunohistochemistry was used to investigate the induction of growth-associated protein GAP43/B-50 in the astrocytes of rat cerebrum in vivo following ischemic injury produced by 30 min of transient middle cerebral artery occlusion. Three days after operation, GAP43 immunoreactivity first appeared in some astrocytic populations surrounding the infarcted lesion. Induction of GAP43 in those astrocytes persisted for up to 14 days and disappeared at 30 days postoperation. Double-immunofluorescence staining confirmed that the GAP43-immunoreactive astrocytes examined were all positive for glial fibrillary acidic protein. Our present data suggest that certain astrocytes could be induced to synthesize GAP43 in vivo in response to an ischemic insult in adult rats.

Animals↗
PubMed1994

Principle of the bark of Phellodendron amurense to suppress the cellular immune response.

We previously reported that Wen-Qing-Yin (Unsei-in), a traditional Chinese blended medicine, inhibited the induction phase of various kinds of delayed type hypersensitivity (DTH) and local graft-versus-host (GvH) reactions, but did not affect humoral immune responses or the effector phase of DTH in experimental animals. In another report, we demonstrated that Phellodendri Cortex (bark of Phellodendron amurense Rupr. Rutaceae) was a component having the most potent suppressive effect on the cellular immune response among the 8 medical plants composing Unsei-in. In the present study, we isolated OB-1 and OB-5 from Phellodendri Cortex as the biologically active principles to suppress local GvH reactions in mice. OB-1 and OB-5 are quaternary base alkaloids known as magnoflorine and phellodendrine, respectively. They suppressed the local GvH reaction, when given i.p. to the host mice at 5-20 mg/kg for 8 consecutive days from the day of spleen cell transfer to cause the reaction. Both OB-1 and OB-5 suppressed picryl chloride-induced delayed type hypersensitivity (PC-DTH) when given i.p. to mice at 10 and 20 mg/kg for 5 consecutive days from the day of the sensitization, but did not suppress it when given at the time of the challenge. These results suggest that OB-1 and OB-5 suppress the induction phase but not the effector phase of the cellular immune response. They are expected to have a value as a new type of immunosuppressor.

Analysis of Variance↗
PubMed1994

Palmitoyl-L-carnitine modifies the function of vascular endothelium.

OBJECTIVE: Palmitoyl-L-carnitine, which accumulates in ischaemic myocardium, may influence the function of vascular endothelium in the ischaemic area. The aim of the study was therefore to examine the effect of palmitoyl-L-carnitine on endothelium dependent relaxations of rabbit thoracic aortas and its effects on the intracellular calcium regulation in cultured bovine aortic endothelial cells (BAEC). METHODS: Isometric contraction experiments on rabbit thoracic aorta were performed to evaluate the effect of palmitoyl-L-carnitine on endothelium dependent relaxation. BAEC were isolated by scraping the internal surface of the aorta from slaughtered cow, and were cultured in Dulbecco's modified Eagle's medium supplemented with fetal calf serum (15% v/v). Cultures used in the present study were from the third to the 12th passage. The cytosolic Ca2+ level in BAEC was monitored by the fura-2 method. RESULTS: Palmitoyl-L-carnitine (1-20 microM) inhibited endothelium dependent relaxation induced by acetylcholine and substance P in a dose dependent manner, while having no effect on resting tension and glyceryl trinitrate induced relaxations. Bradykinin, another endothelium dependent relaxant, induced a biphasic Ca2+ transient in BAEC. Pretreatment of BAEC with palmitoyl-L-carnitine (5-10 microM) inhibited bradykinin induced Ca2+ transients. CONCLUSIONS: The inhibitory effect of palmitoyl-L-carnitine on endothelium dependent relaxation results from the suppression of the intracellular calcium signal transduction in endothelial cells. We speculate that palmitoyl-L-carnitine may be an important mediator of the impaired vascular endothelial function in myocardial ischaemia.

Acetylcholine↗
PubMed1994

Alphaherpesvirus origin-binding protein homolog encoded by human herpesvirus 6B, a betaherpesvirus, binds to nucleotide sequences that are similar to ori regions of alphaherpesviruses.

We previously identified a human herpesvirus 6B (HHV-6B) homolog of the alphaherpesvirus origin-binding protein (OBP), exemplified by the herpes simplex virus type 1 UL9 gene product. This finding is of particular interest because HHV-6B is otherwise more closely related to members of the betaherpesvirus subfamily. The prototypic betaherpesvirus, human cytomegalovirus, does not encode an obvious OBP homolog and contains a more complex origin of replication than do alphaherpesviruses. Thus, analysis of the function of the HHV-6B OBP homolog is essential for understanding the mechanism of HHV-6B DNA replication initiation. The HHV-6B OBP homolog, OBPH6B, was expressed in vitro by coupled transcription and translation and in insect cells by infection with recombinant baculoviruses. The expressed protein bound to two DNA sequences located upstream of the HHV-6B major DNA-binding protein gene homolog, within a region that was predicted to serve as an origin of replication on the basis of its sequence properties. The binding sites lie within 23-bp segments and are similar to OBP-binding sites of herpes simplex virus type 1. The two OBPH6B-binding sequences are separated by an AT-rich region and have an imperfect dyad symmetry as do the alphaherpesvirus origin regions. We identified OBPH6B transcripts by reverse transcription PCR in HHV-6B-infected Molt-3 cells. These results suggest that OBPH6B functions in a manner analogous to the alphaherpesvirus OBP and that initiation of HHV-6B DNA replication may resemble that of alphaherpesviruses.

Amino Acid Sequence↗
PubMed1994

An improved method for the purification of human erythropoietin with high in vivo activity from the urine of anemic patients.

An improved method for the purification of human erythropoietin with high in vivo activity from urine was developed. This method involved ion-exchange, gel permeation, affinity chromatography, and reverse-phase chromatography but did not involve any stabilizing procedures. The purified human urinary erythropoietin showed a single broad band with a molecular weight between 37000 and 39000 Da on sodium dodecyl sulfate polyacrylamide gel electrophoresis, and had an in vivo specific activity of 160000 IU/mg comparable to that of human erythropoietin produced in recombinant Chinese hamster ovary cells. We found that omission of the phenol treatment and ethanol precipitation which are usually used in the purification of human urinary erythropoietin greatly improved the biological activity of the final product. Phenol treatment followed by ethanol precipitation did not affect the amino acid composition but decreased the apparent molecular weight and N-acetylglucosamine content of human urinary erythropoietin. These findings suggest that phenol treatment followed by ethanol precipitation does not restore erythropoietin with high branched sugar chains which would have high in vivo specific activity as reported previously (M. Takeuchi, et al. (1989) Proc. Natl. Acad. Sci. U.S.A., 86, 7819-7822).

Anemia↗
PubMed1994

[Antioxidative effect of mammalian liver hydrolyzate on lipid peroxidation].

The antioxidative effect of the mammalian liver hydrolyzate preparation (LH) was investigated mainly in the mouse liver homogenates. At lower concentrations, LH stimulated lipid peroxidation induced by Fe2+ and ascorbic acid in the homogenates, but inhibited completely the oxidation at higher concentrations. LH also inhibited the peroxidation of linolenic acid and linoleic acid. LH reduced 1,1-diphenyl-2-picrylhydrazyl, a free radical model, in a concentration-dependent manner, suggesting that the radical scavenging property of LH is involved in its antioxidative action. Fe2+ and glutathione, contained in LH, seem to act as a stimulator and an inhibitor of peroxidation, respectively.

Animals↗