Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0043167 (pertussis)
 19,595 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

During development, motion of nerve growth cones ceases on contact with particular targets. The signaling mechanism is unknown. In culture, growth cone collapse can be caused by solubilized embryonic brain membranes, central nervous system myelin, a 35-kilodalton protein isolated from myelin, and mastoparan. Collapse induced by each of these is blocked by pertussis toxin. Thus, collapse of growth cones is mediated by G protein-coupled receptors, which may be activated by proteins associated with the cell surface as well as by soluble ligands.
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PMID:Mediation by G proteins of signals that cause collapse of growth cones. 841 98

The interactions between cultured neonatal rat oligodendrocytes from the optic nerve were examined. Spontaneous contact between oligodendrocytes in vitro resulted in collapse of the fine structure of the oligodendrocytes at the points of contact. To increase the frequency of oligodendrocyte-oligodendrocyte interactions, one oligodendrocyte was removed from the substrate and placed into contact with the end of a process of another oligodendrocyte. Within 15-30 minutes, the fine structure of the second oligodendrocyte had collapsed at the point of contact with the manipulated oligodendrocyte. Manipulated contact induced an approximately three-fold increase in intracellular free calcium concentration that preceded the inhibition of motility. To demonstrate that a release of calcium from internal stores was involved, the experiment was repeated with calcium removed from the medium by chelation with EGTA. Calcium elevation and contact-induced collapse still occurred in the absence of extracellular calcium. The contact-induced calcium increase was blocked by the combination of EGTA and thapsigargin (to deplete calcium from IP3 sensitive intracellular storage sites). Pertussis toxin sensitive G-proteins have been implicated in modulating calcium channels and in mediating a release of calcium from internal stores in certain cells. Pertussis toxin prevented the contact-induced calcium increase and the coincident morphological change in oligodendrocytes. These results suggest that oligodendrocytes are able to recognize and react to specific molecules on the surface of other oligodendrocytes. Moreover, the similarity of this response to the previously characterized response of oligodendrocytes to purified myelin supports the idea that molecules present in myelin and exposed on the surfaces of oligodendrocytes might be used in intercellular communication between oligodendrocytes.
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PMID:The inhibition of motility that results from contact between two oligodendrocytes in vitro can be blocked by pertussis toxin. 883 96

Axons in the adult mammalian CNS normally do not regenerate following axotomy even though they retain the capacity for growth under certain experimental conditions. Although this implies that the regeneration of adult axons is under regulative control, very little is known about the signaling pathways "responsible" for this regulation. This study examines the possibility that a G protein signaling system exists in adult mouse optic fibers and that it functions to regulate axonal outgrowth. To induce the growth of optic fibers, retinas from adult mouse were placed in organotypic culture under serum free conditions and allowed to regenerate onto a laminin substrate. Heterotrimeric G proteins were stimulated by adding mastoparan (MST) to the medium while monitoring growing fibers with time lapse microscopy. Mastoparan treatment produced rapid growth cone collapse and axonal retraction which persisted while MST was present. Prior addition of pertussis toxin (PTX), which irreversibly inactivates the G proteins, G(o) and G (i),completely blocked the effect of MST, confirming that MST was acting through the PTX sensitive G proteins. Selective activation of G proteins in the growth cone by local application of MST with a micropipet was equally effective. For comparison, equivalent experiments were performed on embryonic day 15 retinal explants and on retinal explants from adult goldfish, which normally regenerate in vivo. MST similarly inhibited these axons and this effect was blocked by PTX. However, embryonic fibers were less reliably affected compared to goldfish or adult mouse, suggesting a developmentally regulated sensitivity. The presence of G-proteins in the mouse axons was further tested immunohistochemically using antibodies against G(o)/G(i). Positive staining was detected in the growth cones and shaft of adult and embryonic mouse optic fibers. These findings demonstrate that G protein activation inhibits axonal outgrowth and suggest that there may be a G protein signaling pathway that normally regulates this outgrowth. However, since this pathway appears to exist in both axons that can regenerate and those that normally do not, the presence of PTX-sensitive G proteins alone cannot account for regenerative failure. Regenerative failure may instead be explained as the selective or increased activation of this pathway in the adult mammalian CNS.
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PMID:Heterotrimeric G protein activation rapidly inhibits outgrowth of optic axons from adult and embryonic mouse, and goldfish retinal explants. 886 10

Chick collapsin-1, a member of the semaphorin family, has been implicated in axonal pathfinding as a repulsive guidance cue. Collapsin-1 induces growth cone collapse via a pathway which may include CRMP-62 and heterotrimeric G proteins. CRMP-62 protein is related to UNC-33, a nematode neuronal protein required for appropriately directed axonal extension. Mutations in unc-33 affect neural microtubules, the basic cytoskeletal elements for axoplasmic transport. Using computer-assisted video-enhanced differential interference contrast microscopy, we now demonstrate that collapsin-1 potently promotes axoplasmic transport. Collapsin-1 doubles the number of antero- and retrograde-transported organelles but not their velocity. Collapsin-1 decreases the number of stationary organelles, suggesting that the fraction of time during which a particle is moving is increased. Collapsin-1-stimulated transport occurs by a mechanism distinct from that causing growth cone collapse. Pertussis toxin (PTX) but not its B oligomer blocks collapsin-induced growth cone collapse. The holotoxin does not affect collapsin-stimulated axoplasmic transport. Mastoparan and a myelin protein NI-35 induce PTX-sensitive growth cone collapse but do not stimulate axoplasmic transport. These results provide evidence that collapsin has a unique property to activate axonal vesicular transport systems. There are at least two distinct pathways through which collapsin exerts its actions in developing neurons.
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PMID:A novel action of collapsin: collapsin-1 increases antero- and retrograde axoplasmic transport independently of growth cone collapse. 929 68

During axonal growth, repulsive guidance cues cause growth cone collapse and retraction. In the chick embryo, membranes from the posterior part of the optic tectum containing ephrins are original collapsing factors for axons growing from the temporal retina. We investigated signal transduction pathways in retinal axons underlying this membrane-evoked collapse. Perturbation experiments using pertussis toxin (PTX) showed that membrane-induced collapse is mediated via G(o/i) proteins, as is the case for semaphorin/collapsin-1-induced collapse. Studies with Indo-1 revealed that growth cone collapse by direct activation of G(o/i) proteins with mastoparan did not cause elevation of the intracellular Ca(2+) level, and thus this signal transduction pathway is Ca(2+) independent. Application of the protein phosphatase inhibitor okadaic acid alone induced growth cone collapse in retinal culture, suggesting signals involving protein dephosphorylation. In addition, pretreatment of retinal axons with olomoucine, a specific inhibitor of cdk5 (tau kinase II), prevented mastoparan-evoked collapse. Olomoucine also blocks caudal tectal membrane-mediated collapse. These results suggest that rearrangement of the cytoskeleton is mediated by tau phosphorylation. Immunostaining visualized complementary distributions of tau phospho- and dephosphoisoforms within the growth cone, which also supports the involvement of tau. Taking these findings together, we conclude that cdk5 and tau phosphorylation probably lie downstream of growth cone collapse signaling mediated by PTX-sensitive G proteins.
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PMID:Role of cdk5 and tau phosphorylation in heterotrimeric G protein-mediated retinal growth cone collapse. 1052 12

In most nonneural systems, platelet-activating factor (PAF) receptor effects are mediated by G-proteins that are often pertussis toxin-sensitive. The activation of pertussis toxin-sensitive G-proteins linked to PAF receptors results in the mobilization of intracellular calcium, at least in part, through the second messenger inositol triphosphate. We have sought to determine if a pertussis toxin-sensitive G-protein is involved in the PAF receptor-mediated phenomena of growth cone collapse and of synaptic enhancement in primary neuronal culture. Using infrared differential interference contrast microscopy and patch-clamp recording techniques, pertussis toxin, but not the inactive B oligomer of the toxin, was found to block both the growth cone collapse and the enhanced synaptic release of excitatory transmitter induced by a nonhydrolyzable PAF receptor agonist, making it likely that Go, Gq, or Gi is the G-protein transducer of PAF receptors in primary neurons. We believe that PAF acts directly on neuronal receptors, which are linked to pertussis toxin-sensitive G-proteins, on the tips of developing neurites, and on presynaptic nerve terminals, leading to growth cone collapse and enhanced synaptic release of transmitter.
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PMID:Neuronal platelet-activating factor receptor signal transduction involves a pertussis toxin-sensitive G-protein. 1090 21

A medical officer for the Expanded Program on Immunization (EPI) of the World Health Organization (WHO) calls for staff at all health facilities to screen and, if appropriate, immunize every infant, child, and woman of reproductive age attending health facilities. Routine immunization services tend to miss many women and children who should be immunized. Three important components comprise the health team approach needed to avoid missed opportunities: awareness to screen, a well-organized referral system within each health facility, and regular availability of vaccines. In the health facility, the nonimmunized child is at risk of contracting measles, so all such children should be immunized before they leave the health facility. The WHO/EPI medical officer presents five ways to avoid missed opportunities: screen and immunize at every opportunity, administer all required vaccines, stress real and avoid false contraindications, train staff, and open new vials of vaccine when needed. Contraindications to immunization include severe adverse reactions after a dose of vaccine (collapse or shock, convulsions without fever, anaphylaxis, or encephalitis/encephalopathy), neurological disease (for vaccines containing whole cell pertussis), immune deficiency diseases or immunosuppression due to drugs (generally for live vaccines), and symptomatic HIV infections (for BCG or yellow fever vaccines). The following conditions do not preclude immunization: minor illnesses (e.g., upper respiratory infections); allergy, asthma, hay fever, or "snuffles"; prematurity, small-for-date infants; malnutrition; breast feeding; family history of convulsions; treatment with antibiotics, low-dose corticosteroids, or locally acting steroids; eczema or localized skin infection; chronic diseases of the heart, lung, kidney, or liver; stable neurological conditions (e.g., Down syndrome), and history of jaundice after birth. WHO/EPI has an exit survey for use at district-level clinics or hospitals available so program managers can learn if they are missing chances to immunize children.
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PMID:Opportunities to immunise. 1229 31

Pertussis, also known as whooping cough, is a highly contagious disease, which is most dangerous to infants less than one year old. About half of the babies reported nationally to the Centers for Disease Control and Prevention (CDC) as having the disease are hospitalized. As many as 16/100 babies reported with pertussis get pneumonia, and about 2/100 have convulsions. For those babies reported to have pertussis, about 1/500 has brain problems, some of which can become permanent, and about 1/250 will die because of complications from the disease. Serious illness is less likely in older children and adults. Pertussis vaccine is generally administered in combination with diphtheria and tetanus vaccines, known as DTP vaccine. A primary series of DTP keeps 70-90/100 children from getting pertussis, usually through the elementary school years at least. About half of the children who receive DTP vaccine will not experience any discomfort at all. Some will have minor problems such as soreness, swelling and redness where the shot was given; fever; fussiness; drowsiness; and loss of appetite lasting 1-2 days. Once per 100 to 1000 shots, moderate problems can occur: crying non-stop for 3 hours or more, fever of 105 degrees (F) or higher. For 1 shot in 1750, a child may experience a seizure (convulsions, fits, spasms, twitching, jerking, or staring spells) usually caused by fever, or collapse or fainting (becoming blue, pale, limp, and non-responsive). Very rarely, DTP causes long seizures, decreased consciousness, or coma that usually does not last. Permanent brain damage can very infrequently follow such acute brain problems. There are no tests that can tell in advance if a child will be adversely affected by the DTP vaccine. Definitely the benefits from the DTP vaccine far outweigh the risks for almost all children.
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PMID:Facts about pertussis and DTP vaccine. 1234 38

The effects of histamine in the normal and H. pertussis vaccinated rat have been investigated. In the normal animal small doses of histamine (from 1 to 30 mg./kg., i.v.) produced significant, reversible alterations in the blood pressure, electrocardiogram and electroencephalogram. Doses of 100 mg./kg. or more caused bronchoconstriction and doses of 200 mg./kg. or more an effect on the muscular contractions after electrical stimulation of the nerve. Acute histamine intoxication resulted on rapid injection of 500 mg./kg. intravenously; death was probably due to cardiovascular collapse. In the vaccinated rat, a distinction could be made between the immediate and delayed effects of histamine. With a sublethal dose of histamine (5 mg./kg.) alterations in the blood pressure, electrocardiogram and electroencephalogram were noted. The neuromuscular system, which in the normal animal was the least reactive to histamine, showed the most marked increase in sensitivity in the vaccinated rat. The delayed effects of histamine observed after an interval of 5 to 30 min. were characteristic and irreversible, leading to death of the animal. The mechanism of death in the vaccinated rat after histamine appears to differ from that of the normal animal and has been discussed in the light of present knowledge.
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PMID:Some effects of histamine in the normal and Haemophilus pertussis vaccinated rat. 1352 39

We have reviewed evidence of adverse events after exposure to aluminium-containing vaccines against diphtheria, tetanus, and pertussis (DTP), alone or in combination, compared with identical vaccines, either without aluminium or containing aluminium in different concentrations. The study is a systematic review with meta-analysis. We searched the Cochrane Vaccines Field Register, the Cochrane Library, Medline, Embase, Biological Abstracts, Science Citation Index, and the Vaccine Adverse Event Reporting System website for relevant studies. Reference lists of retrieved articles were scanned for further studies. We included randomised and semi-randomised trials and comparative cohort studies if the report gave sufficient information for us to extract aluminium concentration, vaccine composition, and safety outcomes. Two reviewers extracted data in a standard way from all included studies and assessed the methodological quality of the studies. We identified 35 reports of studies and included three randomised trials, four semi-randomised trials, and one cohort study. We did a meta-analysis of data from five studies around two main comparisons (vaccines containing aluminium hydroxide vs no adjuvant in children aged up to 18 months and vaccines containing different types of aluminium vs no adjuvants in children aged 10-16 years). In young children, vaccines with aluminium hydroxide caused significantly more erythema and induration than plain vaccines (odds ratio 1.87 [95% CI 1.57-2.24]) and significantly fewer reactions of all types (0.21 [0.15-0.28]). The frequencies of local reactions of all types, collapse or convulsions, and persistent crying or screaming did not differ between the two cohorts of the trials. In older children, there was no association between exposure to aluminium-containing vaccines and onset of (local) induration, swelling, or a raised temperature, but there was an association with local pain lasting up to 14 days (2.05 [1.25-3.38]). We found no evidence that aluminium salts in vaccines cause any serious or long-lasting adverse events. Despite a lack of good-quality evidence we do not recommend that any further research on this topic is undertaken.
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PMID:Adverse events after immunisation with aluminium-containing DTP vaccines: systematic review of the evidence. 1517 37


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