[Guillain-Barré syndrome and infection].
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Autoantibodies↗
Biomedical subjects
Q Hao
Publications and source records attributed to Q Hao.
An adrenomedullin (ADM) fragment retains the systemic vasodilator activity of human ADM.
The present study was undertaken to investigate the effects of human ADM, a newly discovered peptide present in normal human plasma, as well as a fragment of human ADM, human ADM13-52, on systemic hemodynamics in the anesthetized cat. Intravenous (i.v.) bolus injections of human ADM and human ADM13-52 decreased systemic arterial pressure (SAP) in a dose-dependent manner. Since neither peptide altered cardiac output, the decreases in SAP reflect reductions in systemic vascular resistance. The systemic vasodilator responses to the same doses of human ADM and human ADM13-52 in the cat were similar. The present study demonstrates the systemic vasodilator activity of ADM is conserved across species. The present data suggest that human ADM13-52 or a peptide structurally similar to it may mediate the hemodynamic properties of ADM in vivo in man. Since cardiac output and heart rate were not altered during the marked systemic vasodepressor response to ADM, activation of the ADM vasodilator mechanism may represent a therapeutic alternative in the clinical management of hypertensive diseases.
Adrenomedullin↗
Differential effects of pinacidil and cromakalim on vascular relaxation and sympathetic neurotransmission.
We tested the hypothesis that pinacidil and cromakalim acted at different sites to relax vascular smooth muscle, in vitro. We compared the effects of pinacidil and cromakalim on tension development in isolated canine and bovine pulmonary artery and vein and canine mesenteric artery and dorsal metatarsal vein, and on the pre- and post-synaptic responses of the canine blood vessels to transmural nerve stimulation. Both pinacidil and cromakalim relaxed bovine and canine blood vessels precontracted to 50% of maximal tension with U46619, prostaglandin F2 alpha, or norepinephrine. Pinacidil- and cromaklim-mediated relaxations of the blood vessels were not mediated by endothelium-derived factors, prostanoids, muscarinic receptors, beta-adrenoceptors, or Ca(2+)-activated or voltage-dependent K+ channels, since they were unaffected by endothelium-rubbing, indomethacin, L-NG-monomethyl-L-arginine, atropine, propranolol, and charybdotoxin. Glibenchlamide, an inhibitor of ATP-activated K+ channels (K+ATP), and KCl (25-60 mM) sufficient to minimize the role of K+ channels almost abolished cromakalim- but not pinacidil-induced relaxation of the blood vessels. Pinacidil inhibited the contractions of the dorsal metatarsal vein and mesenteric artery to norepinephrine and transmural nerve stimulation and the efflux of 2-[14C]norepinephrine during transmural nerve stimulation. In contrast, 1 and 10 nM cromakalim enhanced while 0.1 and 1 microM cromakalim inhibited the contractions of, and 2-[14C]norepinephrine efflux from, the mesenteric artery and dorsal metatarsal vein during transmural nerve stimulation. Thus, pinacidil and cromakalim relax smooth muscle by stimulation of K+ATP channels. Pinacidil also relaxes the blood vessels by a K+ channel independent mechanism. Pinacidil-induced relaxation may also result from presynaptic inhibition of norepinephrine release from the sympathetic neuron.
Animals↗
Adrenomedullin dilates the pulmonary vascular bed in vivo.
The present study was undertaken to investigate the effects of adrenomedullin (ADM), a newly discovered peptide in normal human plasma, in the pulmonary and systemic vascular bed of the intact cat. Because pulmonary blood flow and left atrial pressure were held constant, changes in lobar arterial pressure directly reflected changes in pulmonary vascular resistance. Under conditions of resting (low) pulmonary vasomotor tone, intralobar arterial bolus injections of ADM-(1-52) and two truncated ADM sequences, ADM-(13-52) and ADM-(1-12), had little effect on baseline lobar arterial pressure. In contrast, when pulmonary vasomotor tone was actively increased by intralobar arterial infusion of U-46619, intralobar arterial bolus injections of ADM-(1-52) (10-3,000 ng) and ADM-(13-52) (10-3,000 ng) decreased lobar arterial pressure in a dose-dependent manner, whereas only the highest doses of ADM-(1-52) and ADM-(13-52) (1,000-3,000 ng) mildly decreased systemic arterial pressure. Under the same experimental conditions, injections of ADM-(1-12) had no effect on lobar arterial and systemic arterial pressures. The present data suggest that ADM-(13-52) or a similar ADM fragment is responsible for the marked pulmonary vasodilator activity of ADM-(1-52) in vivo.
15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
Failure to transfer multiple sclerosis into severe combined immunodeficiency mice by mononuclear cells from CSF of patients.
To confirm the reported transfer of multiple sclerosis (MS) by CSF cells, we injected CSF cells from six MS patients in the exacerbation stage into the cisterna magna of 18 severe combined immunodeficiency mice. No clinical neurologic abnormalities or light- or electron-microscopic pathologic changes were present in any transferred mice, and the reported results could not be reproduced.
Adult↗
Tb(III) and Eu(III) as fluorescent probes to investigate the metal-binding sites of trichosanthin.
Tb(III) and Eu(III) ions were used as fluorescent probes in the study of the trichosanthin (TCS). The fluorescence of Tb(III) was increased considerably when bound to TCS to replace the Ca(II) ions. The nonradiative energy transfer from fluorescent tryptophan (Trp) residues to the bound Tb(III) or Eu(III) took place. From a Foster d-d nonradiative energy transfer mechanism, it was obtained that the average distance between the bound Tb(III) and the Trp residue is 1.27nm. The results indicate that the major groups in TCS bound to Ca(II) ions should be the carboxylic side groups of the glutamic acid and/or aspartic acid. The fluorescent quenching of Ca(II)-free TCS by adding Tb(III) or Eu(III) into TCS from which the Ca(II) ions had been removed was discussed as well.
Binding Sites↗
HLAs and genes in Japanese patients with multiple sclerosis: evidence for increased frequencies of HLA-Cw3, HLA-DR2, and HLA-DQB1*0602.
The distribution of HLA-A, B, C, DR and DRB1, DQB1, DPB1 alleles was studied in 60 Japanese patients with clinically definite multiple sclerosis (MS) using serologic and genomic analysis. We found significant associations with HLA-Cw3 (p = 0.002, pc = 0.012, RR = 3.2), DR2 (p = 0.007, RR = 2.6), and DQB1*0602 (p = 0.04, RR = 4.0) in Japanese patients for the first time. The combined presence of Cw3 and DR2 gave a higher risk than each antigen alone. The reported increase in the frequency of DPw4 in Japanese MS patients [12] could not be confirmed by our genomic study. The frequencies of all of the residues in each variable region of the amino acid sequences of DQ beta and DP beta chains were not different between the MS patients and the controls. These results suggest that MS susceptibility may result from polygenic influences and from the presence of environmental factors.
Alleles↗
Mechanisms of signal transduction for adenosine and ATP in pulmonary vascular bed.
The purpose of the present study was to investigate the contribution of pertussis toxin (PTX)-sensitive guanine nucleotide (G) proteins in the pulmonary vascular response to adenosine and ATP in the intact cat under conditions of controlled pulmonary blood flow and left atrial pressure. Adenosine, ATP, and beta-tau-ATP increased lobar arterial pressure in a dose-dependent manner. The pulmonary vasoconstrictor response to adenosine was abolished by BW 1433U, a specific purinergic receptor (P1) inhibitor, PTX pretreatment, indomethacin, and ONO 3708, a thromboxane A2 (TxA2) receptor antagonist. These data suggest that the pulmonary vasoconstrictor response to adenosine depends on activation of P1 purinergic receptors coupled to PTX-sensitive G proteins and subsequent metabolism of liberated arachidonic acid to form TxA2. Because each blocking agent studied produced similar reductions in the pulmonary vasoconstrictor response to ATP without altering the pulmonary vasoconstrictor response to beta-tau-ATP, the present data suggest that ATP constricts the pulmonary vascular bed, in part, by hydrolysis to adenosine. Moreover, the present study suggests that both A1 purinoceptors that are linked to PTX-sensitive G proteins as well as P2x purinoceptors receptors that are independent of PTX-insensitive G proteins mediate the pulmonary vasoconstrictor response to ATP in vivo.
15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
L-NAME enhances pulmonary vasoconstriction without inhibiting EDRF-dependent vasodilation.
The purpose of the present study was to determine the influence of NG-nitro-L-arginine methyl ester (L-NAME) on pulmonary vascular responses to endothelium-dependent relaxing factor- (EDRF) dependent and EDRF-independent substances in the pulmonary vascular bed of the anesthetized cat. Because pulmonary blood flow and left atrial pressure were kept constant, changes in lobar arterial pressure directly reflect changes in pulmonary vascular resistance. When pulmonary vasomotor tone was actively increased by intralobar infusion of U-46619, intralobar bolus injections of acetylcholine, bradykinin, serotonin, and 5-carboxyamidotryptamine (a serotonin1A receptor agonist) decreased lobar arterial pressure in a dose-related manner. The pulmonary vasodilator response to serotonin, but not to 5-carboxyamidotryptamine, acetylcholine, and bradykinin, was significantly decreased by L-NAME (100 mg/kg i.v.). Administration of ritanserin (0.5 mg/kg i.v.), but not L-arginine (1 g/kg i.v. with 60 mg.kg-1 x min-1 i.v. infusion), reversed the inhibitory effects of L-NAME on the pulmonary vasodilator response to serotonin and abolished the enhanced pulmonary vasoconstrictor response to (+-)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminoproprane hydrochloride (a serotonin2 receptor agonist) after L-NAME administration. In conclusion, the present experiments suggest that L-NAME inhibits the pulmonary vasodilator response to serotonin by increasing the sensitivity of serotonin2 receptor-mediated vasoconstriction and not by inhibiting EDRF formation. Because the pulmonary vasodilator responses to bolus administration of acetylcholine and bradykinin were not inhibited by L-NAME, these data suggest that L-NAME does not appear to be an adequate probe to study the role of endogenous EDRF in the adult feline pulmonary vascular bed in vivo.
15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
Vaccination of cyclophosphamide-treated chickens against Newcastle disease virus infection.
Newly-hatched chickens were treated with 3 mg of cyclophosphamide (CY) per day for 4 consecutive days. At 2 weeks of age, these chickens, together with a group of untreated controls, were vaccinated intranasally or subcutaneously with the La Sota strain of Newcastle disease virus (NDV). All chickens were challenged intranasally with the GB strain of NDV 2 weeks later. CY-treated, intranasally vaccinated chickens were highly resistant to NDV challenge, yet none of the chickens produced any detectable humoral antibodies to NDV; antibodies to NDV were detectable in the tracheal washings, however.
Animals↗
Induction of lymphocyte agglutination and lysis by Newcastle disease virus.
Five strains of Newcastle disease virus (NDV) were tested for their ability to agglutinate and lyse chicken lymphocytes. All 5 strains agglutinated lymphocytes, and the agglutination was inhibited by anti-NDV sera. All 5 strains also caused a different degree of direct virus-induced lysis of 51Cr-labeled chicken lymphocytes. This direct lymphocyte cytotoxicity was lost after heating at 56 degrees C for 30 min, or after treatment with a high concentration of formalin (1:100 dilution). Neither a low concentration of formalin (1:5000) nor trypsin treatment had any effect on cytotoxicity.
Agglutination↗
Fluorescence spectroscopic study of the interaction of saporin with phospholipid vesicles.
Saporin-S6 (SO-6) is a type-1 ribosome-inactivating protein purified from the seeds of Saponaria officinalis. The fluorescence characteristics of SO-6 were studied in the presence and absence of phospholipids. The interaction of SO-6 with DMPG or DMPC vesicles results in a decrease in the fluorescence emission intensity of tryptophan without any shift in the emission maximal wavelength. The results of fluorescence titration indicate that DMPG/SO-6 saturation molar ratio is 100: 1, but the binding of DMPC with SO-6 does not reach a saturating plot. A shielding of the tryptophan fluorescence from quenching by acrylamide on interaction with the phospholipids was observed, and this shielding was more pronounced in the presence of DMPG. The interaction of SO-6 with DMPG vesicles is stronger in the liquid-crystalline phase than in the gel phase. Extrinsic fluorescence studies indicated that the interaction of the protein with DMPG vesicles does not modify the phase transition temperature of the lipid, but decreases the amplitude of the change of fluorescence anisotropy associated with the co-operative melting of 1,6-diphenyl-1,3,5-hexatriene (DPH)-labelled vesicles. These results indicate that both electrostatic and hydrophobic components are involved in the SO-6-lipid vesicle interaction.
Acrylamide↗
Interaction between chicken lymphocytes and Newcastle disease virus.
Different strains of Newcastle disease virus (NDV) were added to chicken lymphocytes and JMV-1 and MSB-1 Marek's-disease-derived tumor cell lines to determine the virus-cell interaction. NDV caused fusion and lysis of the cells, and cells supported the growth and multiplication of NDV.
Animals↗
Influence of nifedipine, verapamil and diltiazem on pulmonary vascular resistance and vasoconstrictors in cats.
In the present study, the effects of three classes of L-type calcium channel-blocking agents, nifedipine, verapamil and diltiazem, on the lobar arterial pressure and the vasoconstrictor responses in the pulmonary vascular bed were compared to those of cromakalim, a KATP channel activator, in the anaesthetized cat under controlled pulmonary blood flow and constant left atrial pressure. These drugs were infused intralobarly in doses selected which did not raise left atrial pressure, change cardiac output or alter systemic arterial pressure. Intralobar bolus injections of calcium channel-blocking agents and of the K+ channel activator decreased the lobar arterial pressure in a dose-related manner when pulmonary vasomotor tone was actively elevated by intralobar arterial infusion of U46619. The pulmonary vasodilator response to these agents was accompanied by a dose-related decrease of systemic arterial pressure. In decreasing lobar arterial pressure at elevated pulmonary vasomotor tone, the order of potency was nifedipine > verapamil > diltiazem, whereas in reducing systemic arterial pressure, the order of potency was nifedipine > diltiazem > verapamil. The calcium channel-blocking agents were less active than the reference drug, cromakalim, in both vascular beds. Intralobar arterial infusions of nifedipine, verapamil and diltiazem, at the rates of 0.03 mumol/min, 0.2 mumol/min and 0.1 mumol/min, respectively, caused no changes in cardiac output and in systemic and pulmonary arterial pressure. Infusion of all three calcium-channel-blocking agents blocked the pulmonary vasoconstrictor responses to BAY K 8644 (calcium entry promoter) and U46619 (thromboxane A2 mimic). Nifedipine infusion also reduced the pulmonary vasoconstrictor responses to methoxamine and BHT933 (alpha 1- and alpha 2-adrenoceptor agonists, respectively), whereas verapamil infusion reduced the responses only to methoxamine. Infusion of diltiazem caused no significant decrease of responses to either alpha-adrenoceptor agonist. The results of the present study suggest that the dihydropyridine, nifedipine, is more potent than the non-dihydropyridines, verapamil and diltiazem, in reducing the pulmonary vascular resistance and more effective in inhibiting the vasoconstrictor responses to the alpha-adrenoceptor agonists, to U46619 and to BAY K 8644 in the feline pulmonary circulation at the infusion rates which cause no or little hemodynamic changes.
15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗