Kentucky assay: artificial cigarette smoke odor
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ABSTRACT:
PROVIDER: PRJNA626543 | ENA |
REPOSITORIES: ENA
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Project description:Mice have 1,100 odorant receptors. Nearly all are orphan receptors. The pattern of receptor responses to odors is the input that allows the brain to detect and discriminate odors The Kentucky assay measures the function of each of the 1,100 odorant receptors and 14 TAARs in vivo.
2020-04-20 | GSE148915 | GEO
Project description:Kentucky assay: cigarette smoke
| PRJNA626542 | ENA
Project description:Mice have 1,100 odorant receptors. Nearly all are orphan receptors. The pattern of receptor responses to odors is the input that allows the brain to detect and discriminate odors The Kentucky assay measures the function of each of the 1,100 odorant receptors and 14 TAARs in vivo.
2020-04-20 | GSE148916 | GEO
Project description:Gene expression patterns were assessed in normal human bronchial epithelial (NHBE) cells exposed to cigarette smoke from a reference cigarette (2R4F, University of Kentucky) and a typical American brand of "light" cigarettes ("Lights") in order to develop a better understanding of the genomic impact of tobacco exposure, which can ultimately define biomarkers that discriminate tobacco-related effects and outcomes in a clinical setting. NHBE cells were treated with whole cigarette smoke for 15 minutes and alterations to the transcriptome assessed at 2, 4, 8 and 24 hours post-exposure using high-density oligonucleotide microarrays. Keywords: time course, cigarette smoke exposure
2008-03-04 | GSE10700 | GEO
Project description:normal human bronchial epithelial cultures from two cultures in parallel exposed to cigarette smoke (CS) or air (mock) at timepoints 4 hours and 24 hours. Keywords = cigarette smoke Keywords = microarray Keywords = bronchial cell Keywords = tobacco Keywords: time-course
2005-02-23 | GSE2302 | GEO
Project description:Mammalian females are born with a finite number of non-renewing primordial follicles, the majority of which remain in a quiescent state for many years. Due to their non-renewing nature, these M-bM-^@M-^\restingM-bM-^@M-^] oocytes are particularly vulnerable to xenobiotic insult, resulting in premature ovarian senescence and the formation of dysfunctional oocytes. In this study we characterised the mechanisms behind cigarette smoke induced ovotoxicity, which is characterised by primordial follicle depletion. C57BL/6 5 week old female mice were exposed to cigarette smoke five times per week, for 12-18 weeks using a custom-designed and purpose-built nose-only, directed flow inhalation and smoke-exposure system. This was done in the hopes of gaining a better understanding of the mechanisms underpinning cigarette smoke induced ovotoxicity. C57BL/6 5 week old female mice were exposed to cigarette smoke (twelve 3R4F reference cigarettes (University of Kentucky, USA) twice/day, 2.7 mg particulate matter) five times per week, for 12-18 weeks using a custom-designed and purpose-built nose-only, directed flow inhalation and smoke-exposure system. Their ovaries were then collected for RNA extraction and hybridization on an Illumina Sentrix Mouse ref-8 v2 Beadchip
2012-12-13 | E-GEOD-42889 | biostudies-arrayexpress
Project description:To investigate the impact of cigarette smoke on lung gene expression, female BALB/c mice were obtained from Charles River at 6-8 weeks of age. Using a whole body exposure system (SIU48, PROMECH LAB AB, Vintrie, Sweden), mice (5 per group) were exposed to room air or the mainstream cigarette smoke of twelve 3R4F reference cigarettes (University of Kentucky, Lexington, USA) with filters removed 5 days per week, twice daily for 50 minutes/exposure for 8 weeks, as previously described. Control animals were exposed to room air only. Lungs were collected and stored in RNALater at -80°C prior to RNA extraction.
2014-04-01 | GSE55127 | GEO
Project description:These studies tested the hypotheses that smoke induces changes in mRNA profiles that are dependent on sex and the health status of the lung, and that the effects of smoke are different after 1 day compared to 5 days of smoke exposure. The ways in which the lungs modulate their response to cigarette smoke after repeated exposures are important for understanding the toxicology of smoke, for developing biomarkers of chronic smoke exposure, and for understanding the therapeutic potential in regulatory signaling pathways that are beneficial or detrimental to lung health. Sex-matched 5-7-week old wildtype (WT) and Scnn1b-overexpressing (BENaC) littermates were exposed to cigarette smoke or sham (room air) exposure. Exposure occurred in a plexiglass chamber attached to a smoke delivery device using an exposure chamber and smoking machine (inExpose Exposure System, SCIREQ, Chandler, AZ). Mice were exposed to mainstream + sidestream smoke from 6 reference cigarettes with filters removed per day (3R4F research cigarettes, University of Kentucky). Each cigarette was puffed for 2 sec every 25 sec, using the standard Federal Trade Commission smoking machine protocol. The sham-exposed control mice were exposed to room air in the exposure chamber for a time equivalent to that needed for active smoke exposure. Mice were exposed to cigarette or sham smoke for 1 day or 5 consecutive days. Samples were harvested 4 hours after the completion of the final smoke exposure. The right lung was used for gene expression analysis.
2019-03-18 | GSE109776 | GEO
Project description:To investigate the impact of cigarette smoke on lung gene expression, female BALB/c mice were obtained from Charles River at 6-8 weeks of age. Using a whole body exposure system (SIU48, PROMECH LAB AB, Vintrie, Sweden), mice (5 per group) were exposed to room air or the mainstream cigarette smoke of twelve 3R4F reference cigarettes (University of Kentucky, Lexington, USA) with filters removed 5 days per week, twice daily for 50 minutes/exposure for 8 weeks, as previously described. Control animals were exposed to room air only. Lungs were collected and stored in RNALater at -80M-BM-0C prior to RNA extraction. Impact of an 8 week cigarette smoke exposure on BALB/c mouse lung gene expression was assessed.
2014-04-01 | E-GEOD-55127 | biostudies-arrayexpress
Project description:In the context of male reproductive health, epidemiological studies have observed reduced testis size and abnormal sperm counts and morphology in adult men exposed in utero, although these findings are not always repeated. The ambiguity of these reports is confounded by a lack of controlled animal studies investigating the effects of maternal cigarette smoke exposure on male offspring reproductive health. In this study we examined the effects of cigarette induced reproductive toxicity on male offspring exposed during the gestational and weaning period using our novel direct nasal exposure mouse model of cigarette smoke-induced chronic obstructive pulmonary disease and female subfertility. This was done too gain a better understanding of the adverse effects of gestational maternal smoking on male offspring fertility. C57BL/6 5 week-old female mice were exposed via the nose-only to cigarette smoke [twelve 3R4F reference cigarettes (University of Kentucky, USA) twice/day, five times per week, for 12-18 weeks]. Each exposure lasted 60 minutes. Control mice received room air. In total, 27 mice underwent cigarette smoke exposure. Eleven week-old female mice exposed to cigarette smoke for 6 weeks were separated into groups of three and housed with a single control stud male aged 7-8 weeks with proven fertility for a maximum of 12 weeks. Females were monitored every second day for post-coital plugs and pregnancy. Pregnant females were separated into single cages and litter sizes/pup weights recorded. Smoke exposure via dams continued throughout mating/pregnancy/lactation until weaning of pups at 21days post birth. The testis of exposed offspring were then collected for RNA extraction and hybridization on an Illumina Sentrix Mouse ref-8 v2 Beadchip
2013-10-23 | E-GEOD-51530 | biostudies-arrayexpress