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Biomedical subjects

H Shiomi

Publications and source records attributed to H Shiomi.

At least 55 records · Page 3Linked to original sources
PubMed1985

Induction of the intermediate pituitary by stress: synthesis and release of a nonopioid form of beta-endorphin.

beta-Endorphin in the intermediate lobe of the pituitary gland is posttranslationally modified to produce opioid inactive peptides. Whether these are metabolites or biologically relevant products has not been known. It was found that repeated stress induces increased biosynthesis and release of beta-endorphin-like substances from the intermediate lobe of rats and that opioid-inactive N-acetylated beta-endorphin-(1-31) is selectively made and liberated. The possible role of this nonopioid product and the selective release of peptide forms are discussed.

Animals↗
PubMed1985

How is kyotorphin (Tyr-Arg) generated in the brain?

Kyotorphin (Tyr-Arg) was rapidly degraded in the brain homogenates and purified membrane-bound aminopeptidase from monkey brains. The degradation of kyotorphin by these preparations was effectively inhibited by bestatin. When brain homogenates or slices were incubated with bestatin, kyotorphin was accumulated time-dependently in a rate of 1.0 or 2.1 pmol/mg protein/hr, respectively. The bestatin-induced kyotorphin accumulation was inhibited by leupeptin, p-chloromercuribenzoate, but not phenylmethylsulfonylfluoride or diisopropylphosphate. The kyotorphin accumulation was concentrated in the P2 (crude mitochondrial) fraction, particularly in the particulate or synaptosomal fraction. These findings suggest that kyotorphin may be generated in vitro from precursor proteins by membrane-bound, leupeptin-sensitive "kyotorphin converting enzymes" in close vicinity to membrane-bound aminopeptidase which rapidly degrades kyotorphin generated.

Animals↗
PubMed1983

Isolation from bovine brain of a novel analgesic pentapeptide, neo-kyotorphin, containing the Tyr-Arg (kyotorphin) unit.

A novel analgesic peptide, isolated from the bovine brain, was found to contain the Tyr-Arg (kyotorphin) unit at the C-terminal portion. This peptide, in the methanol-soluble fraction, was isolated by gel filtration and cation exchange chromatography. This peptide was termed "neo-kyotorphin" and the amino acid sequence is Thr-Ser-Lys-Tyr-Arg. The synthetically prepared neo-kyotorphin proved to have a dose-dependent analgesic effect in mice. The median analgesic dose, ED50 of neo-kyotorphin was 195 nmol/mouse (intracisternal injection), with the tail pinch test, and the potency was approximately equal that of Leu-enkephalin.

Amino Acids↗
PubMed1982

Analgesic dipeptide, kyotorphin (Tyr-Arg), is highly concentrated in the synaptosomal fraction of the rat brain.

To examine the physiological role of the analgesic dipeptide, kyotorphin (Tyr-Arg), which was isolated from the mammalian brain, its subcellular localization was studied. Kyotorphin was determined using high-performance liquid chromatography (HPLC) with an electrochemical detector. This dipeptide was found to be concentrated in the crude mitochondrial (P2) fraction. Further subfractionation of the P2 fraction revealed that kyotorphin was exclusively localized in the synaptosomal fraction.This finding suggests the possibility that kyotorphin has a neurotransmitter/neuromodulator role in the brain.

Animals↗
PubMed1981

Mechanism of kyotorphin-induced release of Met-enkephalin from guinea pig striatum and spinal cord.

The characteristics of kyotorphin (Tyr-Arg)-induced release of Met-enkephalin from the striatum and the spinal cord of guinea pig were determined by superfusing the slices in vitro and then carrying out radioimmunoassays. Depolarization by 50 mM K+ induced a marked release of Met-enkephalin-like immunoreactivity. The potassium-induced release of Met-enkephalin was calcium-dependent. In preparations from a striatum, the addition of kyotorphin to the superfusion medium produced a concentration-dependent increase in Met-enkephalin. The kyotorphin-induced release of Met-enkephalin was calcium-dependent and was abolished by tetrodotoxin. Similar effects of kyotorphin were seen in the spinal cord preparations. Electrical field stimulation of the striatal slices at a frequency of 10 Hz also evoked significant and calcium-dependent increases in the release of Met-enkephalin and markedly enhanced the kyotorphin-induced release of Met-enkephalin, as compared to the controls not given field stimulation. These results suggest that kyotorphin depolarizes the so-called enkephalinergic neurons and releases Met-enkephalin from nerve terminals. This effect of kyotorphin may be a possible mechanism related to the manifestation of analgesia.

Animals↗
PubMed1980

Regional distribution of a novel analgesic dipeptide kyotorphin (Tyr-Arg) in the rat brain and spinal cord.

Using high performance liquid chromatography, we measured kyotorphin content in discrete regions of the rat brain and spinal cord in an attempt to clarify its physiological significance. Higher concentrations of the dipeptide were found in the midbrain, pons plus medulla oblongata and dorsal cord, which are the most sensitive sites for the microinjection of morphine and/or electrical stimulation-induced analgesia. Kyotorphin may play a physiological role in pain control in the central nervous system.

Animals↗
PubMed1979

A novel analgesic dipeptide from bovine brain is a possible Met-enkephalin releaser.

It is generally accepted that morphine exerts its analgesic effect by binding to specific opiate receptors in the brain and spinal cord. Since Hughes et al. isolated and identified two endogenous pentapeptides, Met- and Leu-enkephalin, from the brain and found that they acted as agonists at opiate receptors, alpha-, beta- and gamma-endorphins, larger peptides than enkephalins and having morphine-like activity, have been identified in either the brain or pituitary of various species. Several studies have demonstrated that enkephalins possess analgesic properties and that they are distributed in the pain-mediated pathways in the central nervous system. These findings suggest that enkephalins are important neurotransmitters or neuromodulators regulating pain transmission. We now report the isolation of a novel substance which has a Met-enkephalin releasing action. Our findings suggest the possibility of a regulating mechanism for the release of endogenous opioid peptides, especially Met-enkephalin.

Analgesia↗
PubMed1979

Comparison of the analgesic effects of various opioid peptides by a newly devised intracisternal injection technique in conscious mice.

To determine accurately the central analgesic effects of opioid peptides, we devised a special technique for intracisternal administration of drugs to conscious mice. When this method was utilized we found that a series of endogenous opioid peptides and enkephalin analogues, (D-Ala2,Met5)-enkephalinamide and (D-Met2,Pro5)-enkephalinamide produced dose-related analgesic effects, as determined by the tail pinch test. These effects were antagonized by pretreatment with naloxone 0.5 mg/kg s.c. This technique should be a most accurate one for the determination of central analgesic effects of various drugs in conscious mice.

Animals↗
PubMed1979

Pain and the bulbospinal noradrenergic system: pain-induced increase in normetanephrine content in the spinal cord and its modification by morphine.

Experiments were carried out to determine whether noxious stimulation produced biochemical changes in noradrenergic neurons in the spinal cord of rats and whether morphine induced different biochemical effects in the presence and the absence of noxious stimuli. Noxious stimuli, but not stress, significantly increased the normetanephrine (NM) concentration only in the dorsal half of the spinal cord without affecting the noradrenaline concentration. The NM increase induced by noxious stimuli remained after transection at the inter-collicular level. The NM increase induced by noxious stimuli remained after transection at the inter-collicular level. When the noxious stimulation was blocked by lidocaine at the peripheral level, the NM increase disappeared. THe NM concentration elevated by pain, was further increased by morphine. The data suggest that the bulbospinal noradrenergic system works as a pain control system: pain itself slightly activates this system, but not to the extent of producing analgesia and the addition of morphine further activates this system to a level sufficient to produce analgesia.

Animals↗
PubMed1979

Macroglobulinemia Waldenström complicated by autoimmune hemolytic anemia, meningeal sign and femoral lysis.

A necropsied case of macroglobulinemia Waldenström with unusual complications was presented; the patient was found to have autoimmune hemolytic anemia, first. During the course of its treatment, he developed monoclonal immunoglobulin M in serum together with lytic osseous lesion in both femurs, and died of meningeal involvement by tumor cells. Clinically, he had hepatosplenomegaly and generalized lymphadenopathy. The macroglobulin was kappa type of light chain, ultracentrifugation showed sharp spike of 21S in 18.6%, and myelogram revealed increased lymphocytoid series of 29.6%. It was proved that autoantibody causing autoimmune hemolytic anemia was composed of IgG and macroglobulin itself had no activity as an anti-red cell antibody. An emphasis was made that autoimmune hemolytic anemia followed by macroglobulinemia is based on the state of immunodeficiency of this patient.

Anemia, Hemolytic, Autoimmune↗
PubMed1978

Morphine analgesia and the bulbospinal serotonergic system: increase in concentration of 5-hydroxyindoleacetic acid in the rat spinal cord with analgesics.

Administration of an analgesic dose of morphine increased the concentration of the metabolite of 5-hydroxytryptamine (5HT), 5-hydroxyindoleacetic acid (5HIAA), in the spinal cord of rats. The time course of the change in 5HIAA concentration in the dorsal half of the spinal cord corresponded to that of the morphine analgesia, while such was not the case in the ventral half. When the spinal cord was transected at C1, the effect of morphine on 5HIAA concentration disappeared. After transection at the inter-collicular level, this effect remained. The possible relationship between morphine analgesia and descending serotonergic neurons in the spinal cord is discussed.

Analgesics↗