Disease relevance of Nasal Cavity

• A case of squamous cell carcinoma of the nasal cavity occurred in a 57-year-old man who had 25 years of occupational exposure to low concentrations of formaldehyde in the textile-finishing industry [1].
• N-Nitrosomethyl(2-hydroxypropyl)amine also mainly induced esophageal carcinomas (100% incidence) and lung tumors, whereas N-nitrosomethyl(2,3-dihydroxypropyl)amine mainly induced nasal cavity tumors and gave rise to a high incidence of esophageal tumors; however, it appeared to be less potent than the monohydroxy compound [2].
• Olfactory neuroblastoma (OLF NB) is an uncommon neurogenic tumor arising in the nasal cavity [3].
• In order to induce a non-lethal infection restricted to central aminergic neurons projecting to the olfactory bulbs a series of temperature sensitive (ts) and G-protein monoclonal antibody escape mutants of vesicular stomatitis virus (VSV) were instilled into the nasal cavity of mice [4].
• TP53, p14ARF, p16INK4a and H-ras gene molecular analysis in intestinal-type adenocarcinoma of the nasal cavity and paranasal sinuses [5].

High impact information on Nasal Cavity

• Mouse embryos, homozygous for the small eye (Sey) mutation die soon after birth with severe facial abnormalities that result from the failure of the eyes and nasal cavities to develop [6].
• These segments line the boundary between organism and external environment inside the olfactory part of the nasal cavity [7].
• Exposure to propylene oxide for up to 2 years induced inflammatory and proliferative responses in nasal cavity of both species [8].
• Microautoradiographic localization of bound metabolites in the nasal cavities of F344 rats treated with the tobacco-specific carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone [9].
• Single and multiple intragastric doses of diallylnitrosamine [(DAN) CAS: 16338-97-9] administered to Syrian golden hamsters induced tumors, primarily of the respiratory tract, in which the nasal cavity epithelium was the preferred site [10].

Chemical compound and disease context of Nasal Cavity

• Squamous cell carcinomas associated with the nasal cavity have been the most frequently observed neoplasms in the 91YCl3 study and one of the most frequent in the 144CeCl3 study, whereas few squamous cell carcainomas have been seen in the 90SrCl2 study [11].
• Anosmia induced by pretreatment of the nasal cavity by application of ZnSO4 eliminated the effects of both SLVO and scent of linalool on RSNA, GVNA and BP [12].
• The nasal cavities of 3 dogs were infused with zinc sulfate to produce a more complete and longer-lasting anosmia [13].
• However, when administered intraperitoneally to galagos (a prosimian), DENA induced primarily mucoepidermoid carcinoma of the nasal cavity [14].
• CONCLUSIONS: A malignant triton tumor in the nasal cavity is a rare disease [15].

Biological context of Nasal Cavity

• However, the results of published studies can be interpreted that pneumococci may enter the brain directly from the nasal cavity by axonal transport through olfactory nerves [16].
• Analysis of mutants indicates that although initial NP formation is grossly normal, cells in the Fgf8-expressing domain undergo high levels of apoptosis, resulting in cessation of nasal cavity invagination and loss of virtually all OE neuronal cell types [17].
• The data suggest a model in which Fgf8 expression defines an anterior morphogenetic center, which is required not only for the sustenance and continued production of primary olfactory (OE and VNO) neural stem and progenitor cells, but also for proper morphogenesis of the entire nasal cavity [17].
• Because NGF binds to trkA tyrosine-kinase receptors, the NGF released during TDI exposure may mediate SP upregulation in airway sensory neurons, innervating the nasal cavity [18].
• We demonstrated that exposure of the behaving mouse to odorant for a few minutes led to induction of the immediate early gene c-fos for several hours in a fraction of the olfactory sensory neurones in the nasal cavity [19].

Anatomical context of Nasal Cavity

• Compared to related compounds, N-nitrosobis(2-hydroxypropyl)amine and N-nitrosobis(2-acetoxy-propyl)amine which are also pancreatic carcinogens, BOP induced only a few neoplasms of the lung, liver, and kidney and none in the nasal cavity, larynx, and trachea [20].
• Most of these animals died with tumors of the tongue, pharynx, esophagus, and nonglandular stomach and with squamous cell tumors and olfactory carcinomas of the nasal cavity, but there were no tumors of the respiratory tree [21].
• Air enters the nose through two external nares and passes back through the nasal cavity, which is divided down the midline by a cartilaginous nasal septum [22].
• Additional defects are observed in the FKO nasal bones and sutures, the nasal cavity cartilage and bony projections, and the olfactory epithelium [23].
• Primary sensory olfactory neurons reside in a neuroepithelium lining the nasal cavity and project topographically onto the surface of the olfactory bulb, a rostral extension of the telencephalon [24].

Associations of Nasal Cavity with chemical compounds

• Prevention of N-nitrosobis(2-oxopropyl)amine-induced nasal cavity tumors in rats by orchiectomy [25].
• Nitroso-3-piperidinol resembled nitrosopiperidine in inducing a high incidence of tumors of the nasal cavity and upper alimentary tract, and a few liver tumors [26].
• Nitroso-4-piperidinol and nitroso-4-piperidone caused a high incidence of tumors of the nasal cavity but very few tumors of the upper alimentary tract [26].
• Pathogenesis of tumors induced with N-nitrosomethylpiperazine in the olfactory region of the rat nasal cavity [27].
• 4-(N-Methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone (NNK), a major nitrosamine formed in tobacco smoke, induces a high incidence of lung, liver, and nasal cavity tumors in rats [28].

Gene context of Nasal Cavity

• These findings demonstrate that Fgf8 is crucial for proper development of the OE, nasal cavity and VNO, as well as maintenance of OE neurogenesis during prenatal development [17].
• Little to no immunoreactivity with CYP1A1 antibody was observed in fixed nasal sections of control rats, yet intense immunoreactivity was seen in epithelia throughout the nasal cavity of MCS-exposed rats [29].
• Phosphacan, unlike neurocan, was present within the mesenchyme surrounding the E11.5 and E12.5 nasal cavity [30].
• In the present study, the regional distribution and cell-specific expression of CYP2A in the rat nasal cavity were examined using an antibody to rabbit CYP2A10/11 [31].
• Despite a normal spatial pattern of DBA-stained neurons within the nasal cavity, there was a distorted axonal projection of these neurons onto the surface of the olfactory bulb in N-CAM-180 null mutants [32].

Analytical, diagnostic and therapeutic context of Nasal Cavity

• BACKGROUND: Acoustic rhinometry (AR) uses sonar principles to map the anatomy of the nasal cavity and has been used in other studies to assess acute airway responses to allergen exposure [33].
• The nasal cavity of Fisher-344 rats was instilled with rhodamine-labeled latex microspheres [34].
• Denervation was achieved by destroying the olfactory mucosa with ZnSO(4) (0.17 M) irrigation of the nasal cavities [35].
• Nasal lavage was performed, before and after intranasal application of PACAP (200 microL of a 1 microm PACAP solution in each nasal cavity), with and without the addition of histamine [36].
• Western blotting analysis of Ym1/2 confirmed the accumulation of this protein in the regenerating olfactory mucosa consecutively to olfactory axotomy or bulbectomy but also after ZnSO4 irrigation of the nasal cavity [37].

References