ASSOCIATIVE SYMMETRY BY PIGEONS AFTER FEW-EXEMPLAR TRAINING

The present experiment investigated whether pigeons can show associative symmetry on a two-alternative matching to-sample procedure The procedure consisted of a within subject sequence of training and testing with reinforcement and It provided (a) exemplars of symmetrical responding and (b) all prerequisite discriminations among test samples and comparisons After pigeons had learned two arbitrary matching tasks (A B and C D) they were given a reinforced symmetry test for half of the baseline relations (B1-A1 and D1-C1) To control for the effects of reinforcement during testing two novel nonsymmetrical responses were concurrently reinforced using the other baseline stimuli (D2-A2 and B2-C2) Pigeons matched at chance on both types of relations thus indicating no evidence for symmetry These symmetrical and nonsymmetrical relations were then directly trained in order to provide exemplars of symmetry and all prerequisite discriminations for a second test The symmetrical test relations were now B2-A2 and D2-C2 and the nonsymmetrical relations were D1-A1 and B1-C1 On this test 1 pigeon showed clear evidence of symmetry 2 pigeons showed weak evidence and 1 pigeon showed no evidence The previous training of all prerequisite discriminations among stimuli and the within subject control for testing with reinforcement seem to have set favorable conditions for the emergence of symmetry in nonhumans However the variability across subjects shows that methodological variables still remain to be controlled

Homology and errors

A recent review of the homology concept in cladistics is critiqued in light of the historical literature. Homology as a notion relevant to the recognition of clades remains equivalent to synapomorphy. Some symplesiomorphies are homologies inasmuch as they represent synapomorphies of more inclusive taxa; others are complementary character states that do not imply any shared evolutionary history among the taxa that exhibit the state. Undirected character-state change (as characters optimized on an unrooted tree) is a necessary but not sufficient test of homology, because the addition of a root may alter parsimonious reconstructions. Primary and secondary homology are defended as realistic representations of discovery procedures in comparative biology, recognizable even in Direct Optimization. The epistemological relationship between homology as evidence and common ancestry as explanation is again emphasized. An alternative definition of homology is proposed. (c) The Willi Hennig Society 2012.

Endotoxin exposure during sensitization to Blomia tropicalis allergens shifts TH2 immunity towards a TH17-mediated airway neutrophilic inflammation: role of TLR4 and TLR2

Experimental evidence and epidemiological studies indicate that exposure to endotoxin lipopolysaccharide (eLPS) or other TLR agonists prevent asthma. We have previously shown in the OVA-model of asthma that eLPS administration during alum-based allergen sensitization blocked the development of lung TH2 immune responses via MyD88 pathway and IL-12/IFN-γ axis. In the present work we determined the effect of eLPS exposure during sensitization to a natural airborne allergen extract derived from the house dust mite Blomia tropicalis (Bt). Mice were subcutaneously sensitized with Bt allergens co-adsorbed onto alum with or without eLPS and challenged twice intranasally with Bt. Cellular and molecular parameters of allergic lung inflammation were evaluated 24 h after the last Bt challenge. Exposure to eLPS but not to ultrapure LPS (upLPS) preparation during sensitization to Bt allergens decreased the influx of eosinophils and increased the influx of neutrophils to the airways. Inhibition of airway eosinophilia was not observed in IFN-γdeficient mice while airway neutrophilia was not observed in IL-17RA-deficient mice as well in mice lacking MyD88, CD14, TLR4 and, surprisingly, TLR2 molecules. Notably, exposure to a synthetic TLR2 agonist (PamCSK4) also induced airway neutrophilia that was dependent on TLR2 and TLR4 molecules. In the OVA model, exposure to eLPS or PamCSK4 suppressed OVA-induced airway inflammation. Our results suggest that B. tropicalis allergens engage TLR4 that potentiates TLR2 signaling. This dual TLR activation during sensitization results in airway neutrophilic inflammation associated with increased frequency of lung TH17 cells. Our work highlight the complex interplay between bacterial products, house dust mite allergens and TLR signaling in the induction of different phenotypes of airway inflammation.