Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0043167 (
pertussis
)
19,595
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Changes in serum immunoglobulin levels of IgG1, IgG2 and IgM were studied in cows immunised with a butanol extract of bovine erythrocytes. Donor and recipients were matched to differ at only one known red cell antigen, the V antigen, and after the first course of injections a weak antibody response to V antigen was associated with elevated levels of IgG2 immunoglobulins. A second course of injections of V antigens together with Bordetella
pertussis
led to a stronger and more longlasting antibody response to V and this was associated with elevated levels of IgG1 and correspondingly decreased levels of IgG2. One cow calved during the period of investigation and it was found that even though serum antibody levels disappeared three weeks before calving there was a high antibody titre in the colostrum which was passed on to the calf. The loss of serum antibodies before calving was associated with a fourfold drop in serum IgG1 and an increase in serum IgG2 levels.
Res Vet Sci 1976
Sep
PMID:Changes in bovine immunoglobulin levels during a response to homologous erythrocyte membrane antigen. 82 19
Studies were conducted in rats to determine whether pre-feeding antigen can prevent the development of Bordetella
pertussis
-induced homocytotropic antibody (HCA) formation and anaphylactic sensitization to the fed antigen. DA rats fed ragweed for a minimum of 2 wk and Sprague-Dawley rats fed horse serum for at least 4 wk demonstrated specific unresponsiveness to anaphylactic sensitization as measured by their inability to form HCA and their normotensive response to intravenous challenge with antigen. This state was more easily attained when feeding of antigen was started at the age of 30 days than at 90 or 150 days, and resistance to anaphylactic sensitization could be maintained by continued feeding of antigen. However, if anaphylactically sensitized to the fed antigen. The results suggest that induction of anaphylactic sensitization can be prevented by pre-feeding antigen.
J Allergy Clin Immunol 1977
Sep
PMID:Prevention of homocytotropic antibody formation and anaphylactic sensitization by prefeeding antigen. 89 76
In this work we demonstrate a suppressive activity on the induction of experimental allergic encephalomyelitis (EAE) in Lewis rats, transferable to syngeneic animals, challenged with encephalitogenic mixture (myelin basic protein, complete Freud's adjuvant plus Bordetella
pertussis
organisms) 24 h later. This activity is probably effected by T cells and not by (an) inhibitory serum factor(s). The induction of this specific protection could be due to the penetration of the myelin basic protein antigen into the thymus where we first found suppressive cells. From the thymus, suppressor cells could then emigrate to spleen (on day 15) and to nondraining lymph nodes (on day 17). In the course of normal EAE in Lewis rats and especially at the time of self cure, this suppression is not demonstrated, but possible.
Eur J Immunol 1977
Sep
PMID:Evidence for suppressor cells in Lewis rats' experimental allergic encephalomyelitis. 92 33
A delayed hypersensitivity response was induced in the rat paw using
pertussis
vaccine. Oedema was measured after the challenging injection. D-penicillamine and levamisole enhanced the response, while indomethacin suppressed it. This model is useful to distinguish the effects of anti-inflammatory drugs from those like D-Penicillamine which have a specific activity in rheumatoid arthritis.
Agents Actions 1976
Sep
PMID:Pertussis vaccine oedema: an experimental model for the action of penicillamine-like drugs. 97 Feb 90
Male Wistar rats have been sensitized to Bordetella
pertussis
using a mixture of Freund's incomplete adjuvant and
pertussis
organisms. Intrapleural challenge 12 days later with
pertussis
produced a marked delayed inflammatory response, maximal at 48 hours and dominated by influx of mononuclear cells. Dosing with D-penicillamine (25 mg/kg) and levamisole (5 mg/kg) at the time of challenge produced a significant enhancement of the reaction. A long period of dosing with either drug, or treatment with indomethacin (3 mg/kg), suppressed the response. The relevance of this to the testing and mode of action of antirheumatic drugs is discussed.
Agents Actions 1976
Sep
PMID:Pertussis vaccine pleurisy: a model of delayed hypersensitivity. 97 Feb 91
The authors present the results of study of humoral immunity in rabbits after oral and subcutaneous immunization with
pertussis
vaccine. There was an increase in agglutinin titre and of the protective properties of the serum both after the oral administration of the vaccine according to two different schemes and after the subcutaneous immunization. However, rabbits immunized orally displayed a more prolonged (150-day) persistence of agglutinin titres, as well as of preventive and protective activity of the sera than rabbits immunized subcutaneoulsy.
Zh Mikrobiol Epidemiol Immunobiol 1976
Sep
PMID:[Comparative study of the immunologic effectiveness of the oral and subcutaneous methods of administering pertussis vaccine]. 101 77
In 1974 it was recommended that
pertussis
vaccine should continue to be offered in a triple vaccine together with diphtheria and tetanus vaccines. Further data on the prevalence of whooping cough and the incidence of adverse reactions have shown no reason to change this policy; the hazard of whooping cough remains greater than that of immunization.
Br Med J 1975
Sep
20
PMID:Whooping-cough vaccine. Statement by Joint Committee on Vaccination and Immunization of the Central Health Services Council and the Scottish Health Service Planning Council. 117 53
TRH stimulates a biphasic increase in intracellular free calcium ion, [Ca2+]i. Cells stably transfected with TRH receptor cDNA were used to compare the response in lines with and without L type voltage-gated calcium channels. Rat pituitary GH-Y cells that do not normally express TRH receptors, rat glial C6 cells, and human epithelial Hela cells were transfected with mouse TRH receptor cDNA. All lines bound similar amounts of [3H][N3-Me-His2]TRH with identical affinities (dissociation constant = 1.5 nM). Both pituitary lines expressed L type voltage-gated calcium channels; depolarization with high K+ increased 45Ca2+ uptake 20- to 25-fold and [Ca2+]i 12- to 14-fold. C6 and Hela cells, in contrast, appeared to have no L channel activity. GH4C1 cells responded to TRH with a calcium spike (6-fold) followed by a sustained second phase. When TRH was added after 100 nM nimodipine, an L channel blocker, the initial calcium burst was unaffected but the second phase was abolished. GH-Y cells transfected with TRH receptor cDNA responded to TRH with a 6-fold [Ca2+]i spike followed by a plateau phase (>8 min) in which [Ca2+]i remained elevated or increased. Nimodipine did not alter the peak TRH response or resting [Ca2+]i but reduced the sustained phase, which was eliminated by chelation of extracellular Ca2+. In the transfected glial C6 and Hela cells without calcium channels, TRH evoked transient, monophasic 7- to 9-fold increases in [Ca2+]i, and [Ca2+]i returned to resting levels within 3 min. Thapsigargin stimulated a gradual, large increase in [Ca2+]i in transfected C6 cells, and subsequent addition of TRH caused no further rise. Removal of extracellular Ca2+ from transfected C6 cells shortened the [Ca2+]i responses to TRH, to endothelin 1, and to thapsigargin. The TRH responses were
pertussis
toxin-insensitive. In summary, TRH can generate a calcium spike in pituitary, C6, and Hela cells transfected with TRH receptor cDNA, but the plateau phase of the [Ca2+]i response is not observed when the receptor is expressed in a cell line without L channel activity.
Mol Endocrinol 1992
Sep
PMID:Characterization of the calcium response to thyrotropin-releasing hormone (TRH) in cells transfected with TRH receptor complementary DNA: importance of voltage-sensitive calcium channels. 127 82
The regulation of Cl- channels in human myoballs by G proteins was studied using whole-cell and inside-out patch recordings. After perfusion of the cell with 0.1 mM GTP[gamma S], the specific Cl- conductance, GCl, at standard resting potential (-85 mV) was increased from 5.9 microS/cm2 to 103 microS/cm2, and the kinetics upon stepping the potential to positive values was changed from an activating current with very slow inactivation to a fast inactivating current with no potential-dependent activation. These effects were not affected by the simultaneous blockade of several signal cascades involving G proteins. Addition of the protein kinase blockers PKI (25 microM), H8 (10 microM), or of the phospholipase-A2-blocking agent quinacrine (10 microM), had not much influence on these GTP[gamma S] effects. Buffering of the intracellular Ca2+ concentration (0.1 microM) or addition of the Ca2+/calmodulin antagonist trifluoperazine (50 microM) was also without effect. Pre-incubation of the cells with
pertussis
toxin or with cholera toxin did not change GCl. In excised inside-out patches voltage-clamped at -85 mV, application of GTP[gamma S] influenced the "intermediate" Cl- channel, the Cl- channel type having the highest density in these cells, by increasing the number of transitions in a half-conductance state. The probability of the channel being in one of the two conducting states rose from 0.015 to 0.67, and the kinetics of the single-channel currents was changed so that, on average, it was similar to the whole-cell current kinetics seen after application of GTP[gamma S]. It is concluded that a G protein is directly interacting with these channels.
Pflugers Arch 1992
Sep
PMID:Chloride channels in cultured human skeletal muscle are regulated by G proteins. 127 15
A number of neuropeptides were shown to produce potent mitogenic effects on Swiss 3T3 fibroblasts by activating the phospholipase C pathway. Here we provide evidence for the activation by PACAP of the adenylate cyclase pathway in 3T3, as well as in non-tumoral pituitary fibroblasts, similarly to what was seen in pituitary endocrine cells. In these cells, PACAP triggered elevation of both intracellular and extracellular contents of cAMP and the effect was time- and dose-dependent, with half-maximal stimulations being induced with about 0.1 nM. Following activation of protein kinase C (PKC) by the phorbol ester phorbol 12-myristate 13-acetate (PMA), PACAP-induced cAMP production was amplified in pituitary endocrine cells, but was either unchanged or dampened in 3T3 and pituitary fibroblasts, respectively. Pretreatment of cells with
pertussis
toxin (PT) failed to change the effect of PMA on PACAP-stimulated adenylate cyclase activity, irrespective of the cell type being used. However, PT dramatically reduced the potentiation by PMA of cAMP production enhanced by forskolin in 3T3 cells. These results provide new evidence pointing to the presence in fibroblasts of receptors for PACAP, coupled to cAMP production, which may play a role in the modulation of the mitogenic signal. They also indicate that, compared with pituitary endocrine cells, PKC activation in fibroblasts differentially affected PACAP-induced cAMP formation and that these effects were unaltered upon inhibition by PT of Gi-like proteins.
Mol Cell Endocrinol 1992
Sep
PMID:Pituitary adenylate cyclase polypeptide (PACAP) stimulates cyclic AMP formation in pituitary fibroblasts and 3T3 tumor fibroblasts: lack of enhancement by protein kinase C activation. 128 Feb 35
<< Previous
1
2
3
4
5
6
7
8
9
10
Next >>