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Objective Fragrances and strong odors have been characterized as putative triggers that may exacerbate asthma symptoms and many asthmatics readily avoid odors and fragranced products. However, the mechanism by which exposure to pure, non-irritating odorants can elicit an adverse reaction in asthmatic patients is still unclear and may involve both physiological and psychological processes. The aim of this study was to investigate how beliefs about an odors relationship to asthmatic symptoms could affect the physiological and psychological ‘ responses of asthmatics. Methods Asthmatics classified as ‘moderate-persistent’, according to NIH criteria, were exposed for 15 mi to a fragrance which was described either as eliciting or alleviating asthma symptoms. During exposure, participants were asked to rate odor intensity, perceived irritation and subjective annoyance while physiological parameters such as electrocardiogram, respiratory rate, and end tidal carbon dioxide (etCO2) were recorded. Before, immediately after, and at 2 and 24 h post-exposure, participants were required to subjectively assess their asthma symptom status using a standardized questionnaire. We also measured asthma status at each of those time points using objective parameters of broncho-constriction (spirometry) and measures of airway inflammation (exhaled nitric oxide, FeNO). Results Predictably, manipulations of perceived risk altered both the quality ratings of the fragrance as well as the reported levels of asthma symptoms. Perceived risk also modulated the inflammatory airway response. Conclusions Expectations elicited by smelling a perceived harmful odor may affect airway physiology and impact asthma exacerbations.

Age-related decreases in olfactory sensitivity are often accompanied by a decrease in the quality of life. However, the molecular mechanisms underlying these changes are not well described. Inhaled substances including odorants are detected by sensory neurons in the olfactory cleft covered with a layer of mucus. This olfactory mucus is the first molecular machinery responsible for tissue protection and for detection of environmental odorants. Yet, little is known about the molecular identities of the actors because of the lack of information on the mucus proteome and its age-related changes. Here, we sampled human mucus from different nasal locations and from young and elderly subjects. The composition of the mucus was extensively analyzed by shotgun proteomic analysis for a vast array of proteins. We also explored correlations between the levels of each mucus proteins with the olfactory sensitivity of subjects. This analysis revealed previously unrecognized proteins with potentially important functions in olfaction. Taken together, this report describes the most comprehensive catalogue of the nasal mucus proteins to date, their positional and age-related differences, and candidate proteins associated with olfaction. This catalogue will provide fundamental information useful for future studies, such as identification of olfactory auxiliary proteins, causes of age-related declines in olfaction, and biomarkers for neurodegenerative disorders.

RGS3 and RGS4 are GTPase-activating proteins expressed in the brain and heart that accelerate the termination of G i/o -and G q -mediated signaling. We report here the determinants mediating selective association of RGS4 with several G protein-coupled receptors (GPCRs) that form macromolecular complexes with neuronal G protein-gated inwardly rectifying potassium (Kir3 or GIRK) channels. Kir3 channels are instrumental in regulating neuronal firing in the central and peripheral nervous system and pacemaker activity in the heart. By using an epitopetagged degradation-resistant RGS4 mutant, RGS4(C2V), immunoprecipitation of several hemagglutinin-tagged G i/o -coupled and G q -coupled receptors expressed in Chinese hamster ovary (CHO-K1) cells readily co-precipitated both Kir3.1/Kir3.2a channels and RGS4(C2V). In contrast to RGS4(C2V), the closely related and functionally active RGS3 "short" isoform (RGS3s) did not interact with any of the GPCR-Kir3 channel complexes examined. Deletion and chimeric RGS constructs indicate both the N-terminal domain and the RGS domain of RGS4(C2V) are necessary for association with m2 receptor-Kir3.1/Kir3.2a channel complexes, where the GPCR was found to be the major target for RGS4(C2V) interaction. The functional impact of RGS4(C2V) "precoupling" to the GPCR-Kir3 channel complex versus RGS3s "collision coupling" was a 100-fold greater potency in the acceleration of G protein-dependent Kir3 channel-gating kinetics with no attenuation in current amplitude. These findings demonstrate that RGS4, a highly regulated modulator and susceptibility gene for schizophrenia, can directly associate with multiple GPCR-Kir3 channel complexes and may affect a wide range of neurotransmitter-mediated inhibitory and excitatory events in the nervous and cardiovascular systems.

Microtubule-organizing centers recruit α- and β-tubulin polypeptides for microtubule nucleation. Tubulin synthesis is complex, requiring five specific cofactors, designated tubulin cofactors (TBCs) A–E, which contribute to various aspects of microtubule dynamics in vivo. Here, we show that tubulin cofactor D (TBCD) is concentrated at the centrosome and midbody, where it participates in centriologenesis, spindle organization, and cell abscission. TBCD exhibits a cell-cycle-specific pattern, localizing on the daughter centriole at G1 and on procentrioles by S, and disappearing from older centrioles at telophase as the protein is recruited to the midbody. Our data show that TBCD overexpression results in microtubule release from the centrosome and G1 arrest, whereas its depletion produces mitotic aberrations and incomplete microtubule retraction at the midbody during cytokinesis. TBCD is recruited to the centriole replication site at the onset of the centrosome duplication cycle. A role in centriologenesis is further supported in differentiating ciliated cells, where TBCD is organized into “centriolar rosettes”. These data suggest that TBCD participates in both canonical and de novo centriolar assembly pathways.

Human body odors have important communicative functions regarding genetic identity, immune fitness and general health, but an expanding body of research suggests they can also communicate information about an individual’s emotional state. In the current study, we tested whether axillary odors obtained from women experiencing psychosocial stress could negatively influence personality judgments of warmth and competence made about other women depicted in video scenarios. 44 female donors provided three types of sweat samples: untreated exercise sweat, untreated stress sweat and treated stress sweat. After a ‘washout’ period, a commercial unscented anti-perspirant product was applied to the left axilla only to evaluate whether ‘blocking’ the stress signal would improve the social evaluations. A separate group of male and female evaluators (n = 120) rated the women in the videos while smelling one of the three types of sweat samples. Women in the video scenes were rated as being more stressed by both men and women when smelling the untreated vs. treated stress sweat. For men only, the women in the videos were rated as less confident, trustworthy and competent when smelling both the untreated stress and exercise sweat in contrast to the treated stress sweat. Women’s social judgments were unaffected by sniffing the pads. The results have implications for influencing multiple types of professional and personal social interactions and impression management and extend our understanding of the social communicative function of body odors.

Managing the response to odors and irritants in the workplace is critical to maintaining the health and well being of workers. There is a critical need for regulatory organizations in the United States and elsewhere to harmonize guidelines for occupational exposure limits. In addition, management must engage in risk communication and education of workers in order to ensure that misperception of risk from odors does not lead to illness and loss of well being.

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