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Inhaled vapours may stimulate both olfactory receptor cells and endings of the trigeminal nerve1. The trigeminal nerve often contributes a pungent, irritating attribute to odours. Many odorants exhibit some pungency when dilute and most become pungent when concentrated2 Because the trigeminal system commonly shares the chemosensory burden with olfaction, it is relevant to ask whether these anatomically distinct systems interact3–6. Two obscure psychophysical observations argue for an inhibitory influence of trigeminal over olfactory activity. Katz and Talbert observed that a vapour with both odour and pungency might lose odour at high concentrations, irritation masking odour7. The nineteenth century philosopher Alexander Bain, noting that concentrated carbon dioxide (carbonic acid) evokes pungency, remarked “if a current of carbonic acid accompanies an odour, the effect (odour) is arrested” (ref. 8). We have taken up Bain's forgotten observation and used carbon dioxide to endow otherwise benign concentrations of odorant with varying degrees of pungency. The experiments reported here reveal a strong mutual interaction between pungency and odour, occurring without attenuation even when irritant enters one nostril and odorant the other.

THERE has been much interest in perceptual interactions between the ears and between the eyes, but much less in those between the nostrils, or more precisely, the two sides of the olfactory system1–4. This report reveals that, for a wide range of supraliminal stimulation, there is considerable interaction between the two sides. The facets considered here are bilateral additivity of odour intensity, and bilateral influence of an adapting stimulus presented unilaterally.

DEVELOPMENT of the immunoglobulin producing system of cells is controlled by the avian bursa of Fabricius1,2. Elucidation of the role of the bursa in developing immunological potential began with the discovery that surgical removal of this hindgut lymphoid organ in the newly hatched chicken prevents later development of normal antibody response3. Depression of antibody response is greatest when the bursa is removed immediately after hatching. After 8–10 weeks, bursectomy alone no longer has a demonstrable effect on antibody response4. It was discovered later that normal embryonic development of the bursa could be inhibited by testosterone or other androgens5. Chickens which are given testosterone during embryonic life are often even more immunologically deficient than chickens which are subjected to bursal removal at hatching. Chickens which are surgically or hormonally bursectomized have reduced numbers of plasma cells and decreased levels of circulating gamma globulin. Near lethal whole body irradiation of newly hatched chicks in addition to bursectomy completely prevents later development of germinal centres and plasma cells and such chickens are agammaglobulinaemic6,7. Germinal centres, plasma cells and immunoglobulin synthesis can be restored in bursectomized-irradiated chicks by injection of their unirradiated bursal lymphocytes8. These observations suggest that the bursa could be the only source of the germinal centre and plasma cell line but that some radiosensitive bursal cells leave the bursa before hatching.

IN the chicken there are two central lymphoid organs, the thymus and the bursa of Fabricius. Recognition of the roles of these two organs in the ontogeny of immunological responsiveness permits definition of two functionally and morphologically distinct lymphoid cell lines1–4. The avian thymus, like the mammalian thymus, is essential to the normal development of a population of small lymphocytes and cellular immunity, while the bursa of Fabricius plays a similar part in the ontogeny of the plasma cell line and humoral immunity4. In addition, the thymus may contribute towards full development of humoral immune responsiveness4–6. A bursa equivalent has not been identified in all species, but evidence indicates that lymphoid tissues associated with organized gut exercise these functions in rabbits. These lymphoid tissues include Peyer's patches, sacculus rotundus and appendix3,7.

TASTE thresholds for the bitter substance PTC (phenylthiourea or phenylthiocarbamide) and related compounds containing the grouping (HNCS)showa bimodal distribution, leading to the designation ‘tasters’ for the more sensitive individuals and ‘non-tasters’ or ‘taste blind’ for the less sensitive. Genetic and population studies have generally attributed this to a simple Mendelian dominance system in humans, non-human primates and some rodent species. All other bitter and non-bitter compounds tested so far have produced Gaussian distributions of thresholds1,2. We have found now, however, that sensitivity to the taste of PTC predicts sensitivity to caffeine, a common bitter substance that lacks the HNCS grouping. This was shown by threshold measurements and magnitude estimation of supra-threshold concentrations.

RECENT discoveries1–7 seem to indicate that humoral immune responses to some antigens require the interaction of thymus-dependent and thymus-independent cells. An antigen sensitive cell of thymic origin would exist, which is responsible for recognizing antigen, and which differs from the antigen insensitive cells from bone marrow capable of synthesizing antibody. Support for this view comes from experiments involving transplantation of thymus or thoracic duct lymphoid cells into animals which were rendered incapable of forming antibody to sheep cells (SRBC) by irradiation or neonatal thymectomy. An interaction between thymus cells and precursors of antibody forming cells was first demonstrated by injecting irradiated mice with SRBC mixed with thymus cells, marrow cells, or both1. The antibody response in mice given both cell types exceeded the sum of responses to the individual cell types. Thymus or thoracic duct lymphocytes mixed with SRBC and injected into neonatally thymectomized mice elicited antibody responses comparable with those in normal mice2–5. From these experiments and others in which adult mice were thymectomized and irradiated but protected from death by the presence of bone marrow, and injected with SRBC mixed with thoracic duct lymphocytes, it seems clear that antibody synthesizing cells were derived from thymus-independent cells by way of precursors in the marrow. Thus responses to SRBC, like those to other antigens, rely on a thymus-independent population for antibody production. We conclude that the lymphoid system is organized into thymus-dependent and thymus-independent lymphoid populations and that the latter are involved in synthesizing and secreting antibody.