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Biomedical subjects

A Chiba

Publications and source records attributed to A Chiba.

At least 91 records · Page 5Linked to original sources
PubMed1996

Magnesium-mediated conversion of an inactive form of a hammerhead ribozyme to an active complex with its substrate. An investigation by NMR spectroscopy.

The effects of magnesium ions on a 32-mer ribozyme (R32) were examined by high resolution NMR spectroscopy. In solution, R32 (without its substrate) consisted of a GAAA loop, stem II, a non-Watson-Crick 3-base pair duplex and a 4-base pair duplex that included a wobble G:U base pair. When an uncleavable substrate RNA (RdC11) was added to R32 without Mg2+ ions, a complex did not form between R32 and RdC11 because the substrate recognition regions of R32 formed intramolecular base pairs (the recognition arms were closed). By contrast, in the presence of Mg2+ ions, the R32-RdC11 complex was formed. Moreover, titration of mixtures of R32 and RdC11 with Mg2+ ions also induced the ribozyme-substrate interaction. Elevated concentrations (1.0 M) of monovalent Na+ ions could not induce the formation of the R32-RdC11 complex. These data suggest that Mg2+ ions are not only important as the true catalysts in the function of ribozyme-type metalloenzymes, but they also induce the structural change in the R32 hammerhead ribozyme that is necessary for establishment of the active form of the ribozyme-substrate complex.

Base Composition↗
PubMed1996

Immunohistochemical and Ultrastructural characterization of the terminal nerve ganglion cells of the ayu, Plecoglossus altivelis (Salmoniformes, Teleostei).

BACKGROUND: Little is known on the cytological properties of the terminal nerve ganglion (TNG) cells in teleosts (Demski, 1993. Acta Anat., 148:81-95). MATERIALS AND METHODS: To characterize the TNG cells of a salmonoid fish, Plecoglossus altivelis, we adopted immunohistochemistry and transmission electron microscopy (TEM). RESULTS: The majority of the TNG cells formed a compact mass halfway between the olfactory sac and the olfactory bulb, whereas a few cells were scattered in the ventromedial region of the olfactory bulb. The cell had a voluminous perikaryon that was positive to antisera against gonadotropin-releasing hormone (GnRH), molluscan cardioexcitatory tetrapeptide (FM-RFamide), and neuropeptide Y (NPY). Immunostaining of consecutive sections with each antiserum showed the coexistence of these antigens in the same cells and their processes. Most of the processes originating from the cells projected centrally to the basal forebrain, including the optic nerve. With TEM, the cells revealed a peptidergic nature, i.e., the presence of abundant granular endoplasmic reticula and well-developed Golgi bodies in association with vesicles that were 70-100 nm in diameter. Occasionally, the cells adjoined one another directly without the intervention of glial sheets. Synaptic contacts were frequent in the proximal region of the processes, where thin lateral processes of the cells and axon terminals of unknown origin were intermingled with each other. Terminal buttons being engulfed by the soma were commonly seen. CONCLUSIONS: The TNG cells of the salmonoid fish share many cytological characteristics with the cells of the nucleus olfactoretinalis of advanced teleosts such as acanthopterygians.

Animals↗
PubMed1996

Experimental sensory neuropathy induced by sensitization with ganglioside GD1b.

Three of six rabbits immunized with purified GD1b developed ataxic sensory neuropathy. They laid on the floor with their limbs splayed out, and their movements were awkward; but muscle power, tonus, and superficial sensation appeared to be intact. Sciatic nerve motor conduction studies were normal. Axonal degeneration was present in the dorsal column of the spinal cord, in the dorsal roots, and in the sciatic nerve. Some of the nerve cell bodies in the dorsal root ganglia had degenerated and disappeared. No demyelinative lesions or mononuclear cell infiltrations were seen in those regions. No pathological changes were present in the other three immunized rabbits that showed no clinical symptoms. Control rabbits inoculated only with adjuvants showed neither clinical symptoms nor pathological changes. Anti-GD1b antibody was raised in the sera from all six rabbits immunized with GD1b. The monoclonal anti-GD1b antibody GGR12 immunostained about one-half the rabbit primary sensory neurons. Sensitization with GD1b, therefore, may cause ataxic sensory neuropathy in rabbits due to antibody-mediated damage to the primary sensory neurons.

Animals↗
PubMed1996

A novel ganglioside, 9-O-acetyl GD1b, is recognized by serum antibodies in Guillain-Barré syndrome.

A hitherto undescribed ganglioside was detected in a crude ganglioside fraction of bovine brain using an IgM M-protein binding to Gal beta 1, 3GalNAc residue. We purified and identified it as 9-O-acetyl GD1b based on results of alkali treatment that yielded GD1b and results of fast atom bombardment-mass and gas chromatography-mass spectrometries. 9-O-acetyl GD1b was also found to be present in human peripheral nerve tissue. The reactivities of the serum antibodies from patients with Guillain-Barré syndrome to 9-O-acetyl GD1b, GD1b, and GM1 were determined by ELISA and TLC immunostaining. Nineteen of 85 serum samples from Guillain-Barré syndrome patients had antibodies that bound to 9-O-acetyl GD1b: 14 of the positive samples also reacted with GM1 and GD1b, three reacted with GM1 but not with GD1b, one with GD1b but not with GM1, and one with neither GM1 nor GD1b. These results show that a subset of patients with Guillain-Barré syndrome had antibodies that react with 9-O-acetyl GD1b; therefore, this ganglioside can serve as a target antigen against the antibodies present in Guillain-Barré syndrome.

Animals↗
PubMed1996

Characterization of dp6troglycan-laminin interaction in peripheral nerve.

Dystoroglycan is encoded by a single gene and cleaved into two proteins, alpha and beta-dystroglycan, by posttranslational processing. The 120kDa peripheral nerve isoform of alpha-dystroglycan binds laminin-2 comprised of the alpha 2, beta 1, and gamma 1 chains. In congenital muscular dystrophy and dy mice deficient in laminin alpha 2 chain, peripheral myelination is disturbed, suggesting a role for the dystroglycan- laminin interaction in peripheral myelinogenesis. To begin to test this hypothesis, we have characterized the dystroglycan-laminin interaction in peripheral nerve. We demonstrate that (1) alpha-dystroglycan is an extracellular peripheral membrane glycoprotein that links beta-dystroglycan in the Schwann cell outer membrane with laminin-2 in the endoneurial basal lamina, and (2) dystrophin homologues Dp116 and utrophin are cytoskeletal proteins of the Schwann cell cytoplasm. We also present data that suggest a role for glycosylation of alpha-dystroglycan in the interaction with laminin.

Animals↗
PubMed1996

The drosophila neuromuscular junction: a model system for studying synaptic development and function.

The Drosophila neuromuscular junction has attracted widespread attention as an excellent model system for studying the cellular and molecular mechanisms of synaptic development and neurotransmission. In Drosophila the advantages of invertebrate small systems, where individual cells can be examined with single-cell resolution, are combined with the powerful techniques of patch-clamp analysis and molecular genetics. In this review we examine myogenesis and motoneuron development, the problems of axon outgrowth and target selection, the differentiation of the synapse, and the mechanisms of both synaptic function and plasticity in this model genetic system.

Animals↗
PubMed1996

GM1b is a new member of antigen for serum antibody in Guillain-Barré syndrome.

Serum antibody from some patients with Guillain-Barré syndrome recognized an antigen of a minor component in human brain monosialoganglioside fraction. We purified that antigen, which migrated at a position slightly lower than that of GM1 on a thin-layer chromatogram (TLC), by using Iatrobeads column chromatography and preparative TLC. Structural analyses, including fast atom bombardment mass spectrometry, showed it to be GM1b. An enzyme-linked immunosorbent assay (ELISA) using purified GM1b showed that anti-GM1b antibody was present in 22 of 104 cases tested. No anti-GM1b antibody was present in the sera from control patients with other diseases or from the normal controls. Four sera recognized only GM1b among the 11 ganglioside antigens tested. The other 18 sera had antibodies to other antigens, most of which shared no terminal epitope with GM1b. Eight of nine sera samples with anti-GalNAc-GD1a antibody also had anti-GM1b antibody. Antibody to a minor monosialoganglioside, GM1b, was found to be a useful diagnostic marker for Guillain-Barré syndrome. Further study is needed to determine whether this antibody plays a role in the pathogenetic mechanism of the syndrome.

Carbohydrate Sequence↗
PubMed1996

Distribution of neuropeptide Y and gonadotropin-releasing hormone immunoreactivities in the brain and hypophysis of the ayu, Plecoglossus altivelis (Teleostei).

This paper reports on the distribution, relationship and seasonal variations of neuropeptide Y (NPY)-like and gonadotropin-releasing hormone (GnRH)-like immunoreactants in the brain and hypophysis of the bony fish, the ayu Plecoglossus altivelis. NPY-like immunoreactivity was widely distributed in the brain: labeled cells were found in the nervus terminalis, the nucleus entopeduncularis, the habenula, the nucleus preopticus periventricularis, the nucleus tuberis lateralis, the mediodorsal hypothalamus, the dorsal tegmentum, and other sites. NPY fibers were considerably dense in the telencephalon and hypothalamus, and innervated the hypophysis. GnRH-positive cells occurred in the nervus terminalis and were sparsely distributed in the preoptic and tuberal areas of the hypothalamus. GnRH fibers were found in various regions of the brain. They were relatively dense in the hypothalamus, showing a local concentration in the middle region of the neurohypophysis. The GnRH-positive cells and fibers in the hypothalamo-hypophyseal complex increased in density around the spawning season. In tandem with gonadal maturation, NPY labeling in the cells of the nucleus tuberis lateralis became intense concomitantly with an increase in the labeled varicosities in the middle region of the neurohypophysis. Double immunostaining showed that NPY fibers were closely apposed to GnRH cells in the preoptic area. These results suggest a correlative involvement of NPY and GnRH in the control of the hypophyseal gonadotropic function of the ayu.

Animals↗
PubMed1996

Acute immobilization stress and intraventricular injection of CRF suppress naloxone-induced LH release in ovariectomized estrogen-primed rats.

The present study was undertaken to evaluate the role and possible interaction of the endogenous opioid peptide (EOP) and corticotropin-releasing factor (CRF) in the acute stress-induced suppression of gonadotropin secretion in ovariectomized estrogen-primed rats. An intravenous (i.v.) injection of naloxone (10 or 20 mg/kg), an EOP antagonist, significantly elevated serum luteinizing hormone (LH) levels within 10 min in non-stressed animals. The naloxone-induced LH release was completely eliminated when tested 30 min after the onset of acute immobilization. In a subsequent study, it was found that suppression of the naloxone-induced LH release occurred as early as 5 min after the stress onset, and was still evident 60 min after the end of a 30-min period of immobilization. The effect of naloxone was restored 3 h after liberation of the animal from the 30-min immobilization. An intraventricular (i.c.v.) injection of CRF (1 or 5 micrograms) also significantly suppressed, in a dose-related manner, the effect of a subsequent i.v. injection of naloxone. However, an i.c.v. injection of alpha-helical CRF(9-41) (25 or 50 micrograms), a CRF antagonist, prior to immobilization, could not interfere with the suppressive effect of stress on naloxone-induced LH release. These results suggest that both acute immobilization stress and CRF can inhibit the LH secretory activity without mediation by EOP neurons. However, the stress-related suppression may involve non-CRF mechanism(s).

Analysis of Variance↗
PubMed1995

Permissive role of corticotropin-releasing factor in the acute stress-induced prolactin release in female rats.

The present study examined the role of corticotropin-releasing factor (CRF) in the acute stress-induced release of prolactin (PRL) in ovariectomized estrogen-primed female rats. Acute immobilization stress induced a marked increase in serum PRL levels in animals treated with saline intraventricularly (i.c.v.). However, a prior icv injection of alpha-helical CRF(9-41), a CRF antagonist, completely eliminated the immobilization-induced PRL release in the majority of animals, providing evidence for involvement of CRF in the acute stress-induced PRL release. On the other hand, an i.c.v. injection of CRF did not affect basal PRL release at any dose in non-stressed animals, suggesting that the peptide plays a permissive role which enables other undefined stress mediator(s) to stimulate PRL release.

Acute Disease↗
PubMed1995

Fasciclin III as a synaptic target recognition molecule in Drosophila.

Fasciclin III, a cell adhesion molecule of the immunoglobulin superfamily, is expressed by motor neuron RP3 and its synaptic targets (muscle cells 6 and 7) during embryonic neuromuscular development of Drosophila. We report here that RP3 often incorrectly innervates neighbouring non-target muscle cells when these cells misexpress fasciclin III, but still innervates normal targets in the fasciclin III null mutant. Fasciclin III manipulations do not influence target selections by other motor neurons, including fasciclin III-expressing RP1. We propose that fasciclin III acts as a synaptic target recognition molecule for motor neuron RP3, and also that its absence can be compensated for by other molecule(s).

Animals↗
PubMed1995

Macrophage-lymphocyte cell clusters in the hypothalamic ventricle of some elasmobranch fish: ultrastructural analysis and possible functional significance.

BACKGROUND: Previous studies have demonstrated the existence of lympho-haemopoietic tissue in the meninges and choroid plexuses of various primitive vertebrates, including the stingray Dasyatis akajei and in early human embryos. In the present study, we extend these results analyzing macrophage-lymphocyte cell clusters found in the floor of the hypothalamic ventricle of several specimens of elasmobranchs. METHODS: After aseptical isolation of the brain from several specimens of smooth dogfish Triakis scyllia, cloudy dogfish Scyliorhinus torazame, gummy shark Mustelus manazo, and stingray Dasyatis akajei their hypothalamic regions were processed routinely by light, scanning, and transmission electron microscopy. RESULTS: The study of serial histological sections demonstrated that the macrophage-lymphocyte cell clusters proceeded from the meningeal lymphohaemopoietic tissue, reaching the ventricular lumen along large blood vessels. In this tissue, macrophages, different sized lymphocytes, lymphoblasts, granulocytes, monocytes, and developing and mature plasma cells were closely packed among a meshwork of fibroblastic reticular cell processes. It never invaded the brain parenchyma. A cell layer of glial elements and a continuous basement membrane interposed between the lymphoid tissue and the neural elements although some macrophages had migrated across the ependymal cell layer. In the ventricular lumen very irregular macrophages with long cell processes and containing abundant engulfed material of unknown origin formed big cell clusters with neighboring lymphocytes, lymphoblasts, and plasma cells, similar to those described during the immune response. Moreover, electron lucent cells which resembled the antigen-presenting cells of higher vertebrates established intimate surface cell contacts with the surrounding lymphocytes. In the third ventricle of several specimens of gummy shark, Mustelus manazo, morphologically similar cell clusters appeared but these were not connected to the meningeal lympho-haemopoietic tissue. No intraventricular cell aggregates were found in the stingray brain. CONCLUSIONS: Although we cannot rule out that these macrophage-lymphocyte cell clusters represent a permanent structure in the elasmobranch brain they rather seem to be only established after specific stimulation for preventing the entrance of noxious, foreign materials into the elasmobranch brain parenchyma.

Animals↗
PubMed1995

Anti-Gal-C antibody in autoimmune neuropathies subsequent to mycoplasma infection.

Four of 82 patients with Guillain-Barré syndrome (GBS) and 1 of 12 with multifocal motor neuropathy (MMN), who previously had had Mycoplasma pneumoniae infections, had serum antibody to galactocerebroside (Gal-C). Two patients with GBS without mycoplasma infection also had anti-Gal-C antibody, whereas none of the normal or the disease controls had it. As Gal-C is a major glycolipid antigen in myelin, anti-Gal-C antibody may function in the pathogenesis of autoimmune demyelinative neuropathies. Mycoplasma pneumoniae appears to be an important preceding infectious agent in autoimmune neuropathies with anti-Gal-C antibody.

Antibodies↗
PubMed1995

Ontogenetic development of neuropeptide Y-like-immunoreactive cells in the gastroenteropancreatic endocrine system of the dogfish.

This immunocytochemical study was carried out to elucidate the ontogenetic development of neuropeptide Y-like-immunoreactive cells in the gastroenteropancreatic endocrine system of the cloudy dogfish, Scyliorhinus torazame. Immunostained cells first appeared in the pancreas of the embryo at the 15-mm stage, and were also detected in the vitello-intestinal duct of the yolk stalk at the 20-mm stage. These cells were polymorphic, with occasional processes that were sometimes directed toward the vascular wall or into the cavity of the vitello-intestinal duct. At the 34-mm stage, immunostained cells could also be found in the proximal part of the spiral intestine and, by the 74-mm stage, immunopositive cells were present in the gastric mucosa. In the gut and pancreas, the cells gradually increased in number with development, whereas in the vitello-intestinal duct and internal yolk sac, they decreased and seemed to disappear following hatching. Thus, in juveniles, the distribution of the neuropeptide Y-like-immunoreactive cells in the gastroenteropancreatic endocrine system had attained that of adults. Electron-microscopic immunocytochemistry demonstrated that, in the labeled cells of the vitellointestinal duct, the neuropeptide Y-like antigen was located in cytoplasmic granules, as in the cells of the gut and pancreas.

Animals↗
PubMed1995

HLA and anti-GQ1b IgG antibody in Miller Fisher syndrome and Guillain-Barré syndrome.

We investigated serological human leukocyte antigen (HLA) types in patients with histories of Miller Fisher syndrome (MFS) and Guillain-Barré syndrome (GBS) with ophthalmoplegia, in whom serum anti-GQ1b IgG antibody was present during the acute phase. We examined class I antigens (A, B and C) in 32 patients and class II antigens (DR and DQ) in 30, but found no association. We conclude that particular serologically defined HLA types are not preferred for the immunoresponse of anti-GQ1b IgG antibody in MFS and GBS.

Autoantibodies↗
PubMed1995

Acute stress suppresses the N-methyl-D-aspartate-induced luteinizing hormone release in the ovariectomized estrogen-primed rat.

The effects of N-methyl-D-aspartate (NMDA) and luteinizing hormone releasing hormone (LH-RH) on luteinizing hormone (LH) secretion were examined in ovariectomized estrogen-primed rats under nonstressed and acutely stressed conditions. The basal LH levels were significantly elevated 15 min after the onset of acute immobilization stress, but were not altered in emotionally stressed or nonstressed rats. Intravenous injections of 10 and 40 mg/kg NMDA significantly elevated serum LH levels by 161 and 212%, respectively, from baseline within 10 min in nonstressed animals. However, the NMDA-induced LH release was significantly reduced when tested 30 min after the onset of acute immobilization stress. Acute emotional stress, which did not affect the baseline LH, also suppressed the LH release response to NMDA, suggesting that the reduced LH responses to NMDA in stressed animals was not due to the elevated baseline level. Pituitary LH release responses to LH-RH were not affected by acute immobilization. We conclude from these results: (1) acute immobilization stress exerts both stimulatory and inhibitory effects on LH release, while acute emotional stress has only an inhibitory effect in estrogen-primed ovariectomized rats; (2) this inhibition occurs at the suprapituitary level, and (3) it involves a suppression of the responsiveness of the hypothalamic LH-RH neuronal system to the excitatory amino acid input.

Animals↗
PubMed1995

In vitro selection analysis of trans-acting HDV ribozyme.

In order to identify the functional structure as well as new active variants of the trans-acting genomic ribozyme of human hepatitis delta virus (HDV), we applied an in vitro selection procedure. After 10 generations, a randomized pool of trans-acting ribozymes accumulated in which the secondary structure of each ribozyme confirmed to the pseudoknot model and important bases in single-stranded regions were all conserved. We were surprised that mutated ribozymes derived from genomic sequence were changed to anti-genomic-like sequences. Further investigations of the most active variant confirmed that each mutated base was the most appropriate nucleotide at every position of HDV ribozyme.

Base Sequence↗