Inhibition of immune responses by calcitonin gene-related peptide.
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Animals↗
Biomedical subjects
Y Umeda
Publications and source records attributed to Y Umeda.
Analysis of oligosaccharides by on-line high-performance liquid chromatography and ion-spray mass spectrometry.
Oligosaccharides were analyzed by a combination of high-performance liquid chromatography (HPLC) and mass spectrometry (MS). First, oligosaccharides labeled with 2-aminopyridine were studied to see if they could be analyzed by MS under the conditions used for separation by HPLC. Pyridylamino (PA)-oligosaccharides could be analyzed under these conditions, although the mass spectra were affected. Then, liquid chromatography-mass spectrometry was used to analyze a PA-oligosaccharide mixture derived from human immunoglobulin G. The PA-oligosaccharides were separated on a reversed-phase column and mass-analyzed directly. The observed molecular weights were close to or identical to those expected from the structures, which were estimated from the elution position on HPLC. This method is rapid and simple, as the mass spectrometer can give the accurate molecular weight of each PA-oligosaccharide in one chromatography run, even if the HPLC separation is incomplete. This method can be used to extend the so-called two-dimensional mapping of PA-oligosaccharides. The structure can be studied in greater detail by tandem MS.
Carbohydrate Conformation↗
Ion spray mass spectra of native and recombinant streptococcal antitumor proteins.
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Antibiotics, Antineoplastic↗
A change in the spontaneous release of endogenous acetylcholine from rat striatal slices after repeated injection of haloperidol.
The spontaneous and 50 mM K(+)-stimulated release of endogenous acetylcholine (ACh) from rat striatal slices was measured to investigate an adaptive change of striatal ACh after a withdrawal period for 24 h from chronic treatment of the rat with haloperidol. The haloperidol injections (2.5 mg/kg/day) for a period of 3, 7 or 14 days all reduced the spontaneous release of ACh significantly by 20-50% without changing tissue levels of ACh. On the contrary, these treatments produced a very small (by about 10%) but significant increase in K(+)-stimulated release except for the treatment of 7 days. These results suggest that the spontaneous ACh release is under the control of a dopaminergic mechanism, which might be different from the mechanism controlling the evoked release of ACh and emerges following withdrawal from chronic haloperidol treatment.
Acetylcholine↗
Intrapulmonary bronchial circulation during hemorrhage.
Experiments were conducted on 119 anesthetized and artificially ventilated rats to evaluate effects of a physiological stimulus (hemorrhage) to the sympothoadrenal system on the bronchial circulation. In the presence of a sufficient dose of a vasopressin V1-receptor antagonist, moderate (81 mmHg on average, 33 rats) or severe hypotension (69 mmHg, 28 rats) was produced by controlled hemorrhage (11 or 9 rats, respectively), or by treatment with phenoxybenzamine (0.1 mg/kg, i.v., 12 rats, or 1.0 mg/kg, 10 rats), or the highly selective alpha 1-adrenoceptor antagonist, bunazosin (0.01 mg/kg i.v., 10 rats, or 0.1 mg/kg, 9 rats). During hypotension, the intrapulmonary bronchial blood flow (microsphere method) was decreased in a dose-dependent manner in the two antagonist-treated groups. However, these decreases were only of a moderate degree compared to the severe decrease in the hemorrhage group. Although the bronchovascular resistance was not significantly changed after treatment with either antagonist, this variable was greatly elevated during severe hemorrhagic hypotension, reaching 240 +/- 51% (P less than 0.001 with either antagonist study) of its baseline level. Changes in the pulmonary arterial and left atrial pressures, plasma vasopressin concentration, and renin activity were found to be less influential on these responses in 58 rats. Overall, we concluded that the sympathoadrenal mechanism powerfully increased the resistance and decreased the blood flow of the intrapulmonary bronchial circulation.
Animals↗
Physical treatment of benign paroxysmal positional vertigo.
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Adult↗
Structure of aureobasidin A.
Aureobasidin A, a new antifungal antibiotic, was isolated from the culture medium of Aureobasidium pullulans R106. Aureobasidin A was a cyclic depsipeptide consisting of eight alpha-amino acid units and one hydroxy acid unit. The structures of the units were found by acid hydrolysis of the antibiotic to be 2(R)-hydroxy-3(R)-methylpentanoic acid, beta-hydroxy-N-methyl-L-valine, N-methyl-L-valine, L-proline, allo-L-isoleucine, N-methyl-L-phenylalanine, L-leucine, and L-phenyl-alanine. The sequence of the units was identified by NMR and FAB-MS of the products from the alkaline hydrolysis of aureobasidin A.
Amino Acid Sequence↗
Analysis of nucleic acids by ion-spray mass spectrometry.
We analyzed various synthetic oligonucleotides with the use of ion-spray mass spectrometer. The most suitable conditions were investigated for analyzing oligonucleotides with molecular weights ranging from 3000 to 15000. We have found that the pH of the solvent was critical to reduce the formation of adduct ions in the mass spectra. Tandem mass spectrometry was also used to study the sequences.
Base Sequence↗
[Ion spray mass spectrometry for biopolymers].
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Algorithms↗
Decrease in the evoked release of endogenous dopamine and dihydroxyphenylacetic acid from rat striatal slices after withdrawal from repeated haloperidol.
The release of endogenous DA (dopamine) and DOPAC (3,4-dihydroxyphenylacetic acid) from rat striatal slices was measured after withdrawal from a prior long-term treatment of the rat with haloperidol to investigate adaptive changes in striatal DA and DOPAC release induced by chronic haloperidol treatment. Striatal slices prepared 24 h after the last injection of daily treatment with haloperidol for up to 14 days (2.5 mg/kg per day) were superfused and stimulated for 5 min with K+ (50 mM). Haloperidol treatment for 3 or 7 days decreased K(+)-stimulated DA release by maximally 35%, but a 14-day treatment was not effective. The K(+)-stimulated release of DOPAC, which occurred after the change in DA release, was reduced significantly by the treatment for 7 or 14 days. A higher daily dose of haloperidol (10 mg/kg per day) produced a more pronounced decrease in stimulated DA release after a 14-day treatment without having an effect after 3 days. However, the stimulated release of DOPAC decreased markedly after both 3 and 14 days of haloperidol treatment. The slight reduction in the DA content of the slices after K+ stimulation was seen in some haloperidol-treated tissues, although this change did not always parallel the simultaneous decrease in DA release. These results indicate that the K(+)-induced stimulation of endogenous DA release and the synthesis of DA are impaired after withdrawal from repeated haloperidol treatment.
3,4-Dihydroxyphenylacetic Acid↗
Release of endogenous acetylcholine from rat brain slices with or without cholinesterase inhibition and its potentiation by hemicholinium-3.
The direct measurement of basal and high K(+)-stimulated release of endogenous acetylcholine from striatum and hippocampus slices was achieved without as well as with a cholinesterase inhibitor, physostigmine. Hemicholinium-3, opposite to its well-known activity as an inhibitor of endogenous acetylcholine release, significantly potentiated both the basal and stimulated release, in particular in the absence of physostigmine, suggesting an involvement of some unknown activity stimulating ACh release in hemicholinium-3.
Acetylcholine↗
High-level expression of P-glycoprotein and 85 kD protein as assessed by flow cytometry and immunocytochemistry in leukemias and malignant lymphomas.
Acquired resistance developed after chemotherapy is characterized by lower sensitivity to anticancer agents. We utilized two monoclonal antibodies (MABs): MRK16 which recognized 170 to 180 kD P-glycoprotein and MRK20 which recognized 85 kD protein, to investigate the frequency of multidrug-resistant cancer cells appearing during treatment of 23 cases of leukemias and 27 cases of malignant lymphomas. The reactivities of these MABs with lymphocytes and blastic cells were examined by flow cytometry and immunocytochemistry. The following findings were obtained. First, among 50 cases, increases in MRK16-reactive cells and MRK20-reactive cells were noted in 17 cases (34%) and 28 cases (56%), respectively. Second, the increase of MRK16-positive cells in three cases and the increase of MRK20-positive cells in two cases were correlated with dosages of the corresponding anticancer drugs used. Although we investigated the total amounts of anti-cancer drugs used, we were not able to detect exactly when P-glycoprotein recognized by MRK16 and the 85 kDa protein recognized by MRK20 appeared in these resistant cells during treatment. More cases will be required to investigate the significance between treatment and reactivity of MRK16 or MRK20 with leukemia or lymphomas cells.
ATP Binding Cassette Transporter, Subfamily B, Mem↗
[Double filtration plasmapheresis in case of Goodpasture's syndrome].
This article describes a case of Goodpasture's syndrome controlled by double filtration plasmapheresis (DFPP) combined with steroid and immunosuppressant therapy. A 48-year-old male, clerk, complaining of fever, dry cough and macroscopic hematuria, was admitted to our hospital. Microscopic hematuria was first pointed out at age 40 on an annual check up. His laboratory data on admission revealed severe anemia, azothemia, macroscopic hematuria and proteinuria. His chest radiograph and CT revealed diffuse nodular densities in bilateral lung fields. Specimens obtained by transbronchial lung biopsy and open renal biopsy revealed linear deposition of IgG by direct immunofluorescent antibody methods. Circulating antiglomerular basement membrane antibody level determined with radioimmunoassay was 1.8% on admission, but one week later it elevated to 5.6% with progression of dyspnea, hypoxemia, and renal failure. Steroid pulse therapy and a total of 6 double filtration plasmaphereses were performed in the first month. Subsequently hypoxemia and dyspnea disappeared, and the chest radiograph of the 40th hospital day showed no abnormal shadows. Two months later recurrence of pulmonary hemorrhage was noticed. Immunosuppressant administration (Cyclophosphamide 100 mg/day) and a total of 10 DFPP procedures were performed with success. By DFPP, circulating anti-GBM antibody fell rapidly to within normal ranges, and anti-GBM antibody level elevated in removed plasma. We think DFPP is effective to remove circulating anti-GBM antibody in Goodpasture's syndrome.
Anti-Glomerular Basement Membrane Disease↗
Evoked release of endogenous amino acids from rat striatal slices and its modulation.
The release of endogenous gamma-aminobutyric acid (GABA), glutamate and aspartate stimulated by high K+ was studied by superfusing rat striatal slices. Stimulation with 5 min of 30 mM K+ was applied twice (S1 and S2) at a 20 min interval. The maximum release of GABA following stimulation was 40 (at S1) and 26 (at S2) times greater than the basal release. S1 and S2 each produced a maximum release of almost same magnitude for both glutamate and aspartate (about 2.5 times basal release). The removal of Ca2+ from the perfusion medium reduced the maximum release of these amino acids by more than 80% without affecting basal release significantly. Striatal slices were next stimulated in the same way after the addition of apomorphine or haloperidol to the perfusion medium. Apomorphine, 10 or 100 microM, reduced the K+-evoked release of GABA (by 24% at S1 and 35% at S2 with 10 microM; by 37% at S1 and 47% at S2 with 100 microM) but failed to affect the simultaneous release of glutamate and aspartate. Haloperidol (1 microM) reduced the S1-induced release of GABA but had no significant effect on the subsequent S2-induced release. The evoked release of aspartate or glutamate did not respond significantly to haloperidol, but there was a tendency to a decrease in aspartate release similar to the decrease seen for GABA release, particularly with S1. Based on these results, we discuss the property of GABA, aspartate and glutamate as neurotransmitters and the possible dopaminergic regulation of the release of these amino acids.
Amino Acids↗
Role of atrial natriuretic peptide in the diuresis of a newborn infant with the syndrome of inappropriate antidiuretic hormone secretion.
A fullterm infant had fetal distress and stained amnion. He underwent an exchange blood transfusion at 12 hours after birth because of hyperbilirubinemia. He developed oliguria combined with high urine osmolality during the first 27 hours of life despite normal creatinine clearance. The diagnosis of the syndrome of inappropriate antidiuretic hormone secretion (SIADH) was made on the basis of high urine osmolality, low plasma osmolality and elevated plasma arginine vasopressin (AVP) concentration. We determined the plasma atrial natriuretic peptide (ANP) concentration for the first 4 days of life. After 27 hours after birth, urine volume increased while plasma AVP concentration remained high. On the other hand, plasma ANP concentration gradually increased after 27 hours of life. We speculate that ANP may play an important role in producing the spontaneous diuresis in the newborn infant with SIADH.
Atrial Natriuretic Factor↗
Absent effect of plasma vasopressin on rat brain blood flow during hemorrhage.
We investigated whether a reflex increase in plasma vasopressin level due to hemorrhagic hypotension affects brain blood flow. In 60 lightly anesthetized, artificially ventilated rats, the flow was determined with radiolabeled microspheres. We found excellent maintenance of blood flow throughout all brain regions during the hypotensive state (71 mmHg on average), and such maintenance of flow was not modulated at all by a supramaximal intravenous dose of the selective vasopressin V1-receptor antagonist [d(CH2)5 Tyr-(Me)]AVP. The latter finding also implies that the V1 antagonist failed to unmask the vasodilator type actions of V2 receptors on the maintenance of flow during hemorrhagic hypotension. These were true also when the cervical sympathetic bundles were severed bilaterally. The plasma level of endogenous vasopressin was increased during hypotension, ranging from 118 to 973 pg/ml. Despite this increase, the brain blood flow was entirely independent of the plasma vasopressin level in all the brain regions studied. We conclude that the brain circulation of rats can maintain its blood flow during hemorrhagic hypotension without any apparent contribution from a concomitant reflex increase in plasma vasopressin. Despite our negative results for the brain blood flow, the possible segmental effects of circulating vasopressin on the brain arterial caliber remain to be clarified under conditions of hemorrhagic hypotension.
Animals↗
Characterization of calcitonin gene-related peptide (CGRP) receptors in guinea pig lung.
Receptors for calcitonin gene-related peptide (CGRP) in the lung membranes of guinea pig were characterized by using a millititer plate precoated with polyethylenimine. Specific binding of 125I-CGRP was time-dependent, rapid, and reversible, and the binding increased linearly with increasing concentrations of membrane protein. Scatchard analysis revealed two classes of CGRP binding sites: high affinity sites with a KD value of 7.17 x 10(-11) M and a Bmax of 364 fmol/mg protein and low affinity sites with a KD value of 1.7 x 10(-8) M and a Bmax of 39594 fmol/mg protein. Furthermore, the specific binding of 125I-CGRP was dissociated in the presence of GTP or Gpp(NH)p, suggesting that CGRP receptors in guinea pig lung membranes were coupled to the guanine nucleotide regulatory protein. Scatchard analysis of CGRP binding in the presence of GTP revealed selective inhibition of the binding to high affinity binding sites. Unlabeled CGRP displaced the binding of 125I-CGRP to guinea pig lung membranes with an IC50 value of 3.1 x 10(-10) M. In contrast, salmon calcitonin and human calcitonin displaced the binding at 600-fold higher concentrations. We suggest that both low and high affinity binding sites for CGRP exist in the lung membranes of the guinea pig, and the high affinity binding sites for CGRP may be coupled to GTP binding regulatory protein.
Animals↗
Surfer's ear in Japan.
Fifty-one Japanese professional surfers were examined in order to analyze surfer's ear. Forty-one cases (80%), 71 ears, were diagnosed as surfer's ear. In 19 cases (37%), 30 ears, the external auditory canals had stenosed by more than 50%. In general, surfer's ear begins to appear after 5 years and is further aggravated by continued surfing. The age at which surfing is taken up has no influence on the appearance of surfer's ear. Surfers who surf on northern (colder) coasts have severer surfer's ear than those who frequent the southern (warmer) coasts.
Adolescent↗