Journal articles on the topic 'Nasal olfactory tissues'
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1
Muluk, Nuray Bayar. "Olfactory functions in Behçet’s disease: A review." Romanian Journal of Rhinology 8, no. 32 (October 1, 2018): 213–17. http://dx.doi.org/10.2478/rjr-2018-0023.
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Abstract OBJECTIVES. We reviewed the relationship between olfactory functions and Behçet’s disease (BD). MATERIAL AND METHODS. We searched Pubmed, Google, Google Scholar and Proquest Cebtral Database with the key words of “olfactory”, “functions”, “smell”, “nasal” and “Behçet’s disease”. RESULTS. Behçet’s disease influences the nasal mucosa. Nasal mucosal inclusion causes mucosal ulcers, pain, burning, nasal obstruction, epistaxis, nasal itching and dysosmia. Nasal cartilage deformity is also reported. The higher rate of comorbid chronic rhinosinusitis (CRS) in BD patients may likewise be because of the complex mechanism of the disease inclining the host tissues to bacterial infections. Olfactory functions may decrease in BD. Odor identification may be lower in patients BD. CONCLUSION. An olfactory dysfunction may be seen in patients with BD. BD patients should be evaluated for the involvement of the olfactory function and may require treatment because of a malfunction of the olfactory system that influences the quality of life. Neurological involvement associated with BD might play a more important role in causing olfactory dysfunction than mucosal involvement.
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Olson, M. J., J. L. Martin, A. C. LaRosa, A. N. Brady, and L. R. Pohl. "Immunohistochemical localization of carboxylesterase in the nasal mucosa of rats." Journal of Histochemistry & Cytochemistry 41, no. 2 (February 1993): 307–11. http://dx.doi.org/10.1177/41.2.8419465.
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The enzymatic esterase activity of carboxylesterases is integral to the nasal toxicity of many esters used as industrial solvents or in polymer manufacture, including propylene glycol monomethyl ether acetate, dimethyl glutarate, dimethyl succinate, dimethyl adipate, and ethyl acrylate. Inhalation of these chemicals specifically damages the olfactory mucosa of rodents. We report the localization and differential distribution of a 59 KD carboxylesterase in nasal tissues of the rat by immunohistochemistry. Rabbit antiserum against the 59 KD rat liver microsomal carboxylesterase bound most prominently to the olfactory mucosa when applied to decalcified, paraffin-embedded sections of rat nasal turbinates. Within the olfactory mucosa, anti-carboxylesterase did not bind to sensory neurons, the target cell for ester-initiated toxicity; these cells apparently lack carboxylesterase. Instead, the antibody was preferentially bound by cells of Bowman's glands and sustentacular epithelial cells which are immediately adjacent to the olfactory nerve cells. In contrast, non-olfactory tissues (respiratory mucosa and squamous epithelium), which are more resistant to the toxicity of esters, had less carboxylesterase content. The distribution of immunoreactivity correlated well with the distribution of carboxylesterase catalytic activity described elsewhere. These findings help to link the metabolic fate of inhaled esters to the site-specific pathological findings that follow exposure to such chemicals.
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Jung, Su Young, Dong Choon Park, Sung Su Kim, and Seung Geun Yeo. "Expression, Distribution and Role of Aquaporins in Various Rhinologic Conditions." International Journal of Molecular Sciences 21, no. 16 (August 14, 2020): 5853. http://dx.doi.org/10.3390/ijms21165853.
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Aquaporins (AQPs) are water-specific membrane channel proteins that regulate cellular and organismal water homeostasis. The nose, an organ with important respiratory and olfactory functions, is the first organ exposed to external stimuli. Nose-related topics such as allergic rhinitis (AR) and chronic rhinosinusitis (CRS) have been the subject of extensive research. These studies have reported that mechanisms that drive the development of multiple inflammatory diseases that occur in the nose and contribute to the process of olfactory recognition of compounds entering the nasal cavity involve the action of water channels such as AQPs. In this review, we provide a comprehensive overview of the relationship between AQPs and rhinologic conditions, focusing on the current state of knowledge and mechanisms that link AQPs and rhinologic conditions. Key conclusions include the following: (1) Various AQPs are expressed in both nasal mucosa and olfactory mucosa; (2) the expression of AQPs in these tissues is different in inflammatory diseases such as AR or CRS, as compared with that in normal tissues; (3) the expression of AQPs in CRS differs depending on the presence or absence of nasal polyps; and (4) the expression of AQPs in tissues associated with olfaction is different from that in the respiratory epithelium.
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Grubb, B. R., T. D. Rogers, R. C. Boucher, and L. E. Ostrowski. "Ion transport across CF and normal murine olfactory and ciliated epithelium." American Journal of Physiology-Cell Physiology 296, no. 6 (June 2009): C1301—C1309. http://dx.doi.org/10.1152/ajpcell.00578.2008.
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The nasal epithelium of the cystic fibrosis (CF) mouse has been used extensively in CF research because it exhibits ion transport defects similar to those of human CF airways. This tissue is composed of ∼50% olfactory (OE) and ∼50% ciliated epithelium (CE), and on the basis of previous observations, we hypothesized that a significant fraction of the bioelectric signals from murine nasal tissue may arise from OE rather than CE, while CE is the target tissue for CF gene therapy. We compared the bioelectric properties of isolated OE from the nasal cavity and CE from the nasopharynx in Ussing chamber studies. Hyperabsorption of Na+ [amiloride response; CF vs. wild type (WT)] was ∼7.5-fold greater in the OE compared with the CE. The forskolin response in native tissues did not reliably distinguish genotypes, likely due to a cyclic nucleotide-gated cation conductance in OE and a calcium-mediated Cl− conductance in CE. By potential difference assay, hyperabsorption of Na+ (CF vs. WT) and the difference in response to apical 0 Cl− buffer (CF vs. WT) were ∼2-fold greater in the nasal cavity compared with the nasopharynx. Our studies demonstrate that in the CF mouse, both the hyperabsorption of Na+ and the Cl− transport defect are of larger magnitude in the OE than in the CE. Thus, while the murine CF nasal epithelium is a valuable model for CF studies, the bioelectrics are likely dominated by the signals from the OE, and assays of the nasopharynx may be more specific for studying the ciliated epithelium.
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Kincaid, Anthony E., and Jason C. Bartz. "The Nasal Cavity Is a Route for Prion Infection in Hamsters." Journal of Virology 81, no. 9 (February 14, 2007): 4482–91. http://dx.doi.org/10.1128/jvi.02649-06.
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ABSTRACT Animals that naturally acquire the prion diseases have a well-developed olfactory sense that they utilize for a variety of basic behaviors. To assess the potential for the nasal cavity to serve as a point of entry for prion diseases, a small amount of prion-infected brain homogenate was placed inferior to the nostrils of hamsters, where it was immediately sniffed into the nasal cavity. Hamsters extranasally inoculated with the HY strain of transmissible mink encephalopathy (TME) agent had an incubation period that was not significantly different from per os inoculation of the same dose of the HY TME agent. However, the efficiency of the nasal route of inoculation was determined to be 10 to 100 times greater based on endpoint dilution analysis. Immunohistochemistry on tissues from hamsters killed at 2-week intervals after inoculation was used to identify the disease-associated form of the prion protein (PrPd) to determine the route of prion neuroinvasion. Nasal mucosa-associated lymphoid tissue and submandibular lymph nodes initially accumulated PrPd as early as 4 weeks postinfection. PrPd was first identified in cervical lymph nodes at 8 weeks, in the mesenteric lymph nodes, spleen, and Peyer's patches at 14 weeks, and in the tongue 20 weeks after inoculation. Surprisingly, there was no evidence of PrPd in olfactory epithelium or olfactory nerve fascicles at any time after inoculation. Therefore, the HY TME agent did not enter the central nervous system via the olfactory nerve; instead, PrPd accumulated in elements of the cranial lymphoreticular system prior to neuroinvasion.
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Pahrudin Arrozi, Aslina, Daijiro Yanagisawa, Tomoko Kato, Hiroyasu Akatsu, Yoshio Hashizume, Daita Kaneda, and Ikuo Tooyama. "Nasal Extracts from Patients with Alzheimer’s Disease Induce Tau Aggregates in a Cellular Model of Tau Propagation." Journal of Alzheimer's Disease Reports 5, no. 1 (April 6, 2021): 263–74. http://dx.doi.org/10.3233/adr-210298.
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Background: Emerging evidence indicates that the misfolded tau protein can propagate aggregates between cells in a prion-like manner. This prion activity has been typically studied in brain extracts of patients with Alzheimer’s disease (AD), but not in the olfactory region that can be a potential biomarker in AD. Objective: To investigate the prion seeding activity of tau in nasal mucosa tissues using a cell culture model of tau propagation. Methods: Brain and nasal mucosa homogenates were added to HEK293T cells expressing three repeat or four-repeat domains of tau with the L266V, V337M (3RD*VM) and P301L and V377M mutations (4RD*LM) fused to the enhanced green fluorescence protein (EGFP) respectively. We also measured the level of phosphorylated tau (p-tau), total tau (t-tau), and p-tau/t-tau ratio and performed correlation analysis between tau prion activity and the level of tau. Results: We found that brain and nasal tissue homogenates from patients with AD significantly induced tau aggregation in HEK293T cells either expressing tau 3RD*VM-EGFP or 4RD*LM-EGFP compared with control brain and nasal tissue homogenates. The levels of p-tau and p-tau/t-tau ratio were significantly increased in the brain of patients with AD; however, no significant difference was found in nasal tissue compared with their respective control tissue homogenates. Conclusion: These results suggest that the nasal tissues contain tau seeds, similar to the brain, albeit without changes in the levels of p-tau and t-tau. Therefore, a cellular bioassay using nasal tissues would have great potential as an AD biomarker because of the usefulness of nasal tissue biopsy.
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DeJoia, Crista, Brian Moreaux, Kimberly O'Connell, and Richard A. Bessen. "Prion Infection of Oral and Nasal Mucosa." Journal of Virology 80, no. 9 (May 1, 2006): 4546–56. http://dx.doi.org/10.1128/jvi.80.9.4546-4556.2006.
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ABSTRACT Centrifugal spread of the prion agent to peripheral tissues is postulated to occur by axonal transport along nerve fibers. This study investigated the distribution of the pathological isoform of the protein (PrPSc) in the tongues and nasal cavities of hamsters following intracerebral inoculation of the HY strain of the transmissible mink encephalopathy (TME) agent. We report that PrPSc deposition was found in the lamina propria, taste buds, and stratified squamous epithelium of fungiform papillae in the tongue, as well as in skeletal muscle cells. Using laser scanning confocal microscopy, PrPSc was localized to nerve fibers in each of these structures in the tongue, neuroepithelial taste cells of the taste bud, and, possibly, epithelial cells. This PrPSc distribution was consistent with a spread of HY TME agent along both somatosensory and gustatory cranial nerves to the tongue and suggests subsequent synaptic spread to taste cells and epithelial cells via peripheral synapses. In the nasal cavity, PrPSc accumulation was found in the olfactory and vomeronasal epithelium, where its location was consistent with a distribution in cell bodies and apical dendrites of the sensory neurons. Prion spread to these sites is consistent with transport via the olfactory nerve fibers that descend from the olfactory bulb. Our data suggest that epithelial cells, neuroepithelial taste cells, or olfactory sensory neurons at chemosensory mucosal surfaces, which undergo normal turnover, infected with the prion agent could be shed and play a role in the horizontal transmission of animal prion diseases.
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TAMURA, Hiro-omi, Yuki HARADA, Atsushi MIYAWAKI, Katsuhiko MIKOSHIBA, and Michio MATSUI. "Molecular cloning and expression of a cDNA encoding an olfactory-specific mouse phenol sulphotransferase." Biochemical Journal 331, no. 3 (May 1, 1998): 953–58. http://dx.doi.org/10.1042/bj3310953.
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Previously we demonstrated the presence of phenol sulphotransferase (P-ST) in mouse nasal cytosols and identified its zonal location in mouse nasal cavity by staining with an antiserum raised against a rat liver P-ST isoenzyme, PSTg. In the present study a cDNA was isolated from a mouse olfactory cDNA library by immunological screening with the antiserum. The isolated cDNA consisted of 1347 bp with a 912 bp open reading frame encoding a 304-residue polypeptide. Both the nucleotide and deduced amino acid sequences of the cDNA were 94% identical with those of a rat liver P-ST isoenzyme, ST1C1. The expressed enzyme in Escherichia coli displayed high P-ST activity towards phenolic odorants such as eugenol and guaiacol, and it showed a high N-hydroxy-2-acetylaminofluorene sulphation activity in comparison with the rat ST1C1 enzyme. These results indicate that the olfactory P-ST encoded by the cDNA is a mouse orthologue of rat ST1C1; however, expression of the olfactory P-ST mRNA is specific for nasal tissues as revealed by reverse transcriptase-mediated PCR (RT–PCR).
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Calderon-Garciduenas, Lilian, Robert R. Maronpot, Ricardo Torres-Jardon, Carlos Henriquez-Roldan, Robert Schoonhoven, Hilda Acuna-Ayala, Anna Villarreal-Calderon, et al. "DNA Damage in Nasal and Brain Tissues of Canines Exposed to Air Pollutants Is Associated with Evidence of Chronic Brain Inflammation and Neurodegeneration." Toxicologic Pathology 31, no. 5 (August 2003): 524–38. http://dx.doi.org/10.1080/01926230390226645.
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Acute, subchronic, or chronic exposures to particulate matter (PM) and pollutant gases affect people in urban areas and those exposed to fires, disasters, and wars. Respiratory tract inflammation, production of mediators of inflammation capable of reaching the brain, systemic circulation of PM, and disruption of the nasal respiratory and olfactory barriers are likely in these populations. DNA damage is crucial in aging and in age-associated diseases such as Alzheimer's disease. We evaluated apurinic/apyrimidinic (AP) sites in nasal and brain genomic DNA, and explored by immunohistochemistry the expression of nuclear factor NF κB p65, inducible nitric oxide synthase (iNOS), cyclo-oxygenase 2 (COX2), metallothionein I and II, apolipoprotein E, amyloid precursor protein (APP), and beta-amyloid1-42 in healthy dogs naturally exposed to urban pollution in Mexico City. Nickel (Ni) and vanadium (V) were measured by inductively coupled plasma mass spectrometry (ICP-MS). Forty mongrel dogs, ages 7 days—10 years were studied (14 controls from Tlaxcala and 26 exposed to urban pollution in South West Metropolitan Mexico City (SWMMC)). Nasal respiratory and olfactory epithelium were found to be early pollutant targets. Olfactory bulb and hippocampal AP sites were significantly higher in exposed than in control age matched animals. Ni and V were present in a gradient from olfactory mucosa > olfactory bulb > frontal cortex. Exposed dogs had (a) nuclear neuronal NF κB p65, (b) endothelial, glial and neuronal iNOS, (c) endothelial and glial COX2, (d) ApoE in neuronal, glial and vascular cells, and (e) APP and β amyloid1-42 in neurons, diffuse plaques (the earliest at age 11 months), and in subarachnoid blood vessels. Increased AP sites and the inflammatory and stress protein brain responses were early and significant in dogs exposed to urban pollution. Oil combustion PM-associated metals Ni and V were detected in the brain. There was an acceleration of Alzheimer's-type pathology in dogs chronically exposed to air pollutants. Respiratory tract inflammation and deteriorating olfactory and respiratory barriers may play a role in the observed neuropathology. These data suggest that Alzheimer's disease may be the sequela of air pollutant exposures and the resulting systemic inflammation.
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Carboni, Anthony A., Kay J. Cullen, and William G. Lavelle. "The Effects of Zinc on the Olfactory Neuroepithelium and Olfactory Bulbs of the Sprague-Dawley Rat after oral Administration of Zinc-Gluconate Trihydrate." American Journal of Rhinology 20, no. 3 (May 2006): 262–68. http://dx.doi.org/10.2500/ajr.2006.20.2854.
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Background The most frequent causes of upper respiratory infections are human rhinoviruses. The nasopharyngeal area, which includes the respiratory epithelium, mucosa, and the olfactory neuroepithelium (ONe), is a first-line of defense against airborne viruses and allergens, some of which manage to penetrate the nasal mucosa and invade the tissues of the nasal respiratory epithelium. Biochemical evidence from several studies suggests that zinc is an effective cold treatment and that over-the-counter (OTC) zinc-gluconate compounds may provide the high pharmacologic doses of zinc needed to act as an effective means of treating and reducing the duration and severity of symptoms of the common cold. Methods A series of male Sprague-Dawley rats were fed an oral preparation of zinc-gluconate trihydrate or received the equivalent through drinking water to investigate the potential cytotoxic and/or neurotoxic insult to the olfactory receptor cells and other tissue in the ONe and afferent neuronal pathways. Results Coronal sections of the rat ONe and corresponding olfactory bulbs showed consistent cellular and tissue damage of increasing severity that correlated with the duration of treatment with the zinc compound when compared with the control group animals. Conclusion The results of this analysis indicate that the repeated oral administration of such zinc-containing compounds have neurotoxic effects on the ONe and to the mitral cells in the olfactory bulbs of treated rats. These findings point toward the need for increased investigation into the potential deleterious effects of zinc-containing compounds to humans as well.
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Genter, Mary Beth, Paul P. Van Veldhoven, Anil G. Jegga, Bhuvana Sakthivel, Sue Kong, Kristin Stanley, David P. Witte, Catherine L. Ebert, and Bruce J. Aronow. "Microarray-based discovery of highly expressed olfactory mucosal genes: potential roles in the various functions of the olfactory system." Physiological Genomics 16, no. 1 (December 16, 2003): 67–81. http://dx.doi.org/10.1152/physiolgenomics.00117.2003.
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We sought to gain a global view of tissue-specific gene expression in the olfactory mucosa (OM), the major site of neurogenesis and neuroregeneration in adult vertebrates, by examination of its overexpressed genes relative to that in 81 other developing and adult mouse tissues. We used a combination of statistical and fold-difference criteria to identify the top 269 cloned cDNAs from an array of 8,734 mouse cDNA elements on the Incyte Mouse GEM1 array. These clones, representing known and poorly characterized gene transcripts, were grouped according to their relative expression patterns across the other tissues and then further examined with respect to gene ontology categories. Approximately one-third of the 269 genes were also highly expressed in developing and/or adult central nervous system tissues. Several of these have been suggested or demonstrated to play roles in neurogenesis, neuronal differentiation, and/or neuronal migration, further suggesting that many of the unknown genes that share this expression pattern may play similar roles. Highly OM-specific genes included a palate, lung, and nasal epithelium carcinoma-associated gene ( Plunc); sphingosine phosphate lyase ( Sgpl1), and paraoxonase 1 ( Pon1). Cell-type-specific expression within OM was established using in situ hybridization for several representative expression pattern clusters. Using the ENSEMBL-assembled mouse genome and comparative genomics analyses to the human genome, we assigned many of the unknown expressed sequence tags (ESTs) and poorly characterized genes to either novel or known gene products and provided predictive classification. Further exploration of this database will provide additional insights into genes and pathways critical for olfactory neurogenesis, neuronal differentiation, olfaction, and mucosal defense.
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Guzzo, Adam C., Robert G. Berger, and Denys deCatanzaro. "Excretion and binding of tritium-labelled oestradiol in mice (Mus musculus): implications for the Bruce effect." REPRODUCTION 139, no. 1 (January 2010): 255–63. http://dx.doi.org/10.1530/rep-09-0382.
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Male mouse urine contains 17β-oestradiol (E2) and other steroids. Given that males actively direct urine at proximate females and intrauterine implantation of blastocysts is vulnerable to minute amounts of exogenous oestrogens, males' capacity to disrupt early pregnancy could be mediated by steroids in their urine. When male mice were implanted with osmotic pumps containing tritium-labelled E2 (3H-E2) or injected i.p. with 3H-E2, radioactivity was reliably detected in their urine. Following intranasal administration of 3H-E2 to inseminated females, radioactivity was detected in diverse tissue samples, with there being significantly more in reproductive tissues than in brain tissues. When urine was taken from males injected with 3H-E2, and then intranasally administered to inseminated females, radioactivity was detected in the uterus, olfactory bulbs, and mesencephalon and diencephalon (MC+DC). When inseminated and ovariectomised females were perfused at the point of killing to remove blood from tissues, more radioactivity was detected in the uterus than in muscle, olfactory bulbs, MC+DC and cerebral cortex. Pre-treatment with unlabelled E2 significantly reduced the uptake of 3H-E2 in the uterus. Taken with evidence that males deliver their urine to the nasal area of females, these results indicate that male urinary E2 arrives in tissues, including the uterus, where it could lead to the disruption of blastocyst implantation.
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Chemuturi, Nagendra V., and Maureen D. Donovan. "Role of Organic Cation Transporters in Dopamine Uptake across Olfactory and Nasal Respiratory Tissues." Molecular Pharmaceutics 4, no. 6 (September 25, 2007): 936–42. http://dx.doi.org/10.1021/mp070032u.
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Kociánová, I., A. Gorošová, F. Tichý, P. Čížek, and M. Machálka. "Structure of Masera's Septal Olfactory Organ in Cat (Felis silvestris f. catus) - Light Microscopy in Selected Stages of Ontogeny." Acta Veterinaria Brno 75, no. 4 (2006): 471–75. http://dx.doi.org/10.2754/avb200675040471.
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The septal organ /SO/ (Masera's organ /MO/) is a chemoreceptor presently considered one of three types of olfactory organs (along with the principal olfactory region and vomeronasal organ). Notwithstanding the septal organ having been first described by Rodolfo Masera in 1943, little is known of the properties of sensory neurons or of its functional significance in chemoreception. Until now the septal organ has been described only in laboratory rodents and some marsupials. This work refers to its existence in the domestic cat (Felis silvestris f. catus). The septal organ can be identified at the end of embryonic period - 27 or 28 days of ontogenesis in cats (the 6th developmental stage of Štěrba) - coincident with formation of the principal olfactory region in nasal cavity. At 45 days of ontogenesis (the 9th developmental stage of Štěrba), this septal olfactory organ is of circular or oval shape, 120 μm in diameter, in ventral part of septum nasi, lying caudally to the opening of ductus incisivus. The structure of the epithelium of septal olfactory organ is clearly distinct from the respiratory epithelium of the nasal cavity. It varies in thickness, cellular composition, as well as free surface appearance, and even lack the typical structure of sensory epithelium, in this developmental period. Nerve bundles and glandular acini are lacking in the lamina propria mucosae of the septal organ and in the adjacent tissues. Glands appear as the single non-luminized cords of epithelia extending from the surface. The adjacent respiratory epithelium contains numerous goblet cells.
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Al Khafaji, Ammar S., and Maureen D. Donovan. "Endocytic Uptake of Solid Lipid Nanoparticles by the Nasal Mucosa." Pharmaceutics 13, no. 5 (May 20, 2021): 761. http://dx.doi.org/10.3390/pharmaceutics13050761.
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Nanoparticles may provide unique therapeutic opportunities when administered via the nasal cavity, yet the primary uptake and transfer pathways for these particles within the nasal mucosa are not well understood. The endocytic pathways involved in the uptake of fluorescently labeled, (Nile Red) solid lipid nanoparticles (SLNs) of different sizes (~30, 60, and 150 nm) were studied using excised bovine olfactory and nasal respiratory tissues. Endocytic activity contributing to nanoparticle uptake was investigated using a variety of pharmacological inhibitors, but none of the inhibitors were able to completely eliminate the uptake of the SLNs. The continued uptake of nanoparticles following exposure to individual inhibitors suggests that a number of endocytic pathways work in combination to transfer nanoparticles into the nasal mucosa. Following exposure to the general metabolic inhibitors, 2,4-DNP and sodium azide, additional, non-energy-dependent pathways for nanoparticle uptake were also observed. While the smallest nanoparticles (30 nm) were the most resistant to the effects of pharmacologic inhibitors, the largest (150 nm) were still able to transfer significant amounts of the particles into the tissues. The rapid nanoparticle uptake observed demonstrates that these lipid particles are promising vehicles to accomplish both local and systemic drug delivery following nasal administration.
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Michel, D., E. Moyse, A. Trembleau, F. Jourdan, and G. Brun. "Clusterin/ApoJ expression is associated with neuronal apoptosis in the olfactory mucosa of the adult mouse." Journal of Cell Science 110, no. 14 (July 15, 1997): 1635–45. http://dx.doi.org/10.1242/jcs.110.14.1635.
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The molecular events orchestrating neuronal degeneration and regeneration remain poorly understood. Attempts at identifying genes specifically expressed during these processes, have constantly led to the (re)isolation of the clusterin/ApoJ gene, whose expression is highly reactive to injury in a wide variety of tissues. To get insight into the function of clusterin in neuron loss, we have assessed in detail the clusterin gene expression in an experimental model of neurodegeneration, using the peripheral olfactory system of adult mouse. The sensory neurons of olfactory nasal mucosa can be massively induced to degenerate in vivo, by surgical removal of their only synaptic target: the olfactory bulb. We have previously shown that this neuron loss results from a near-synchronized induction of apoptosis genetic programs. We present here evidence that clusterin gene expression is tightly correlated to the onset of neuronal apoptoses in lesioned olfactory mucosae. The simultaneous preparation of DNA and RNA from the same tissue samples reveals that a strong clusterin mRNA accumulation coincides with the wave of nucleosome-sized DNA fragmentation. However, double detection of apoptotic nuclei by the TUNEL method and of clusterin messengers by in situ hybridization revealed that the clusterin gene expression is not induced in dying neurons, but in the glial sheath surrounding the axon bundles of degenerating olfactory neurons. Clusterin immunocytochemistry reveals that the clusterin protein accumulates not only in these producing cells, but also in the olfactory epithelium, suggesting the possibility of clusterin internalization by cells located at a distance from the synthesis loci. In view of this localization and of the activities of the clusterin protein reported so far, possible functions of clusterin in nervous plasticity are discussed.
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Reed, C. J., and F. De Matteis. "Cumene hydroperoxide-dependent oxidation of NNN'N'-tetramethyl-p-phenylenediamine and 7-ethoxycoumarin by cytochrome P-450. Comparison between the haemoproteins from liver and olfactory tissue." Biochemical Journal 261, no. 3 (August 1, 1989): 793–800. http://dx.doi.org/10.1042/bj2610793.
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The interaction of cytochromes P-450 of the liver and olfactory epithelium of male hamsters with cumene hydroperoxide (CHP) has been characterized with regard to the ability of CHP to (1) support 7-ethoxycoumarin-O-de-ethylase (ECOD) activity, (2) support the oxidation of NNN'N'-tetramethyl-p-phenylenediamme (peroxidase activity) and (3) cause inactivation of cytochrome P-450. In the liver, CHP was found to support both ECOD and peroxidase activities while causing only minimal inactivation of cytochrome P-450. In contrast, in the olfactory epithelium CHP was virtually unable to support ECOD activity, peroxidase activity was 4-fold greater than in the liver, and extensive inactivation of cytochrome P-450 occurred. The reasons for these differences have been investigated with particular reference to the mode of cytochrome P-450-catalysed decomposition of CHP, that is, via homolytic or heterolytic cleavage of the hydroperoxide dioxygen bond. In both tissues, cumenol (2-phenylpropan-2-ol) was the major product of CHP decomposition detected. The radical scavenger nitrosobenzene inhibited cumenol formation by 84% in the olfactory epithelium, but by only 38% in the liver. This may indicate that dioxygen-bond scission occurs predominantly homolytically in the nasal tissue, whereas there is a balance between homolysis and heterolysis in the liver. It is suggested that the inability of CHP to support ECOD activity in the olfactory epithelium and the extensive inactivation of cytochrome P-450 that it causes both stem from decomposition of the hydroperoxide occurring homolytically rather than heterolytically in this tissue.
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Martinez, Quentin, Julien Clavel, Jacob A. Esselstyn, Anang S. Achmadi, Camille Grohé, Nelly Pirot, and Pierre-Henri Fabre. "Convergent evolution of olfactory and thermoregulatory capacities in small amphibious mammals." Proceedings of the National Academy of Sciences 117, no. 16 (April 6, 2020): 8958–65. http://dx.doi.org/10.1073/pnas.1917836117.
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Olfaction and thermoregulation are key functions for mammals. The former is critical to feeding, mating, and predator avoidance behaviors, while the latter is essential for homeothermy. Aquatic and amphibious mammals face olfactory and thermoregulatory challenges not generally encountered by terrestrial species. In mammals, the nasal cavity houses a bony system supporting soft tissues and sensory organs implicated in either olfactory or thermoregulatory functions. It is hypothesized that to cope with aquatic environments, amphibious mammals have expanded their thermoregulatory capacity at the expense of their olfactory system. We investigated the evolutionary history of this potential trade-off using a comparative dataset of three-dimensional (3D) CT scans of 189 skulls, capturing 17 independent transitions from a strictly terrestrial to an amphibious lifestyle across small mammals (Afrosoricida, Eulipotyphla, and Rodentia). We identified rapid and repeated loss of olfactory capacities synchronously associated with gains in thermoregulatory capacity in amphibious taxa sampled from across mammalian phylogenetic diversity. Evolutionary models further reveal that these convergences result from faster rates of turbinal bone evolution and release of selective constraints on the thermoregulatory-olfaction trade-off in amphibious species. Lastly, we demonstrated that traits related to vital functions evolved faster to the optimum compared to traits that are not related to vital functions.
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Li, Mao, Markus Schweiger, Ichiro Nakano, Daniel Ryan, Litia Carvalho, and Bakhos Tannous. "BSCI-16. Olfactory receptor 5B21 drives breast cancer metastasis." Neuro-Oncology Advances 3, Supplement_3 (August 1, 2021): iii4. http://dx.doi.org/10.1093/noajnl/vdab071.015.
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Abstract Olfactory receptors (ORs), responsible for the sense of smell, play an essential role in physiological processes (even outside the nasal epithelium) and cancer. In breast cancer, however, the expression and role of ORs remain understudied. We examined the significance of ORs transcript abundance in breast cancer metastasis to different tissues including the brain, bone, and lung. While we found 20 OR genes to be differentially expressed in different metastasis versus primary tumor, OR5B21 displayed high relation with all metastases. Knockdown of OR5B21 significantly decreased the invasion and migration of breast cancer cells in culture as well as metastasis to different organs including the brain, in vivo. On the other hand, overexpression of OR5B21 in the primary cells had the opposite effect. Mechanistically, OR5B21 was associated with epithelial to mesenchymal transition through STAT3/NFkB/CEBPβ signaling pathway. We propose OR5B21 (and potentially other ORs) as a novel oncogene contributing to breast cancer metastasis, and as a potential target for therapy.
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BOUDJELAL, Mohamed, Asipu SIVAPRASADARAO, and John B. C. FINDLAY. "Membrane receptor for odour-binding proteins." Biochemical Journal 317, no. 1 (July 1, 1996): 23–27. http://dx.doi.org/10.1042/bj3170023.
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Specific binding of 125I-labelled bovine odour-binding protein (OBP) to isolated membranes from nasal mucosa was demonstrated. The interaction reached equilibrium within 30 min at 37 °C and was reversible. A Scatchard analysis of the equilibrium binding revealed a single population of binding sites, with the calculated equilibrium dissociation constant and maximum number of binding sites being 2.25±0.5 μM and 18.5±2 pmol/mg of membrane protein respectively (n = 2). Receptor activity was decreased on digestion by trypsin, proteinase K or endoglycosidase H, was heat labile and was sensitive to thiol-group-specific reagents. With the exception of rat and mouse major urinary proteins, which exhibit a high degree of structural similarity with OBP and bind similar ligands, other members of the lipocalin family, such as retinol-binding protein and β-lactoglobulin, failed to inhibit the binding of 125I-labelled OBP to its receptor. The receptor seems not to be restricted to olfactory tissues, as it was detected in a variety of other tissues. This suggests that OBP is unlikely to play a role only in olfactory signal transduction. It might have a much broader role within the body; possibilities include a role in detoxification or signalling.
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Cole, Philip, and Renato Roithmann. "The Nasal Valve and Current Technology." American Journal of Rhinology 10, no. 1 (January 1996): 23–38. http://dx.doi.org/10.2500/105065896781795111.
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The principal features and the respiratory role of the nasal valve are surveyed briefly and contributions of current computer-aided techniques of imaging, rhinomanometry, and acoustic rhinometry to an understanding of its structure and function are presented. The nasal valve is a dynamic segment of the anterior nasal airway, where the major portion of nasal resistance is localized and nasal resistance to respiratory airflow approximates half the airflow resistance of the entire respiratory system. This functioning valvular segment of the airway extends several mm beyond its triangular entrance in the compliant vestibule to the hemi-piriform entrance of the rigid cavum. Alar muscles assist in stabilizing the compliant lateral wall of the valve by resisting transmural pressures generated by inspiratory airflow and, by adjustment of alar positioning, these muscles can also direct the inspiratory air stream (e.g., olfactory sniffs). Abundant erectile tissues of both medial and lateral nasal walls are prominent in the valve region, and they play the governing role in regulation of valve lumen and consequent nasal airflow resistance. Pathological mucosal swelling is the commonest cause of obstructive nasal disease, and the narrowed site of the valve is so vulnerable to obstruction that recurring physiological mucovascular swellings frequently impede airflow in the presence of small anterior structural deviations. Assessment of obstructive nasal disease by symptomatology is unreliable, and rhinoscopy has substantial limitations; however, current technology provides minimally invasive, objective, and reliable methods for the study of nasal patency and for the acquisition of useful and dependable clinical information.
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Kataoka, Kosuke, Kohtaro Fujihashi, Keita Oma, Yoshiko Fukuyama, Susan K. Hollingshead, Shinichi Sekine, Shigetada Kawabata, Hiro-O. Ito, David E. Briles, and Kazunori Oishi. "The Nasal Dendritic Cell-Targeting Flt3 Ligand as a Safe Adjuvant Elicits Effective Protection against Fatal Pneumococcal Pneumonia." Infection and Immunity 79, no. 7 (May 2, 2011): 2819–28. http://dx.doi.org/10.1128/iai.01360-10.
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ABSTRACTWe have previously shown that a pneumococcal surface protein A (PspA)-based vaccine containing DNA plasmid encoding the Flt3 ligand (FL) gene (pFL) as a nasal adjuvant prevented nasal carriage ofStreptococcus pneumoniae. In this study, we further investigated the safety and efficacy of this nasal vaccine for the induction of PspA-specific antibody (Ab) responses against lung infection withS. pneumoniae.C57BL/6 mice were nasally immunized with recombinant PspA/Rx1 (rPspA) plus pFL three times at weekly intervals. When dynamic translocation of pFL was initially examined, nasal pFL was taken up by nasal dendritic cells (DCs) and epithelial cells (nECs) but not in the central nervous systems, including olfactory nerve and epithelium. Of importance, nasal pFL induced FL protein synthesis with minimum levels of inflammatory cytokines in the nasal washes (NWs) and bronchoalveolar lavage fluid (BALF). NWs and BALF as well as plasma of mice given nasal rPspA plus pFL contained increased levels of rPspA-specific secretory IgA and IgG Ab responses that were correlated with elevated numbers of CD8+and CD11b+DCs and interleukin 2 (IL-2)- and IL-4-producing CD4+T cells in the nasal mucosa-associated lymphoid tissues (NALT) and cervical lymph nodes (CLNs). Thein vivoprotection by rPspA-specific Abs was evident in markedly reduced numbers of CFU in the lungs, airway secretions, and blood when mice were nasally challenged withStreptococcus pneumoniaeWU2. Our findings show that nasal pFL is a safe and effective mucosal adjuvant for the enhancement of bacterial antigen (Ag) (rPspA)-specific protective immunity through DC-induced Th2-type and IL-2 cytokine responses.
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Stefani, Ambra, Alex Iranzo, Evi Holzknecht, Daniela Perra, Matilde Bongianni, Carles Gaig, Beatrice Heim, et al. "Alpha-synuclein seeds in olfactory mucosa of patients with isolated REM sleep behaviour disorder." Brain 144, no. 4 (April 1, 2021): 1118–26. http://dx.doi.org/10.1093/brain/awab005.
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Abstract Isolated REM sleep behaviour disorder (RBD) is an early-stage α-synucleinopathy in most, if not all, affected subjects. Detection of pathological α-synuclein in peripheral tissues of patients with isolated RBD may identify those progressing to Parkinson’s disease, dementia with Lewy bodies or multiple system atrophy, with the ultimate goal of testing preventive therapies. Real-time quaking-induced conversion (RT-QuIC) provided evidence of α-synuclein seeding activity in CSF and olfactory mucosa of patients with α-synucleinopathies. The aim of this study was to explore RT-QuIC detection of α-synuclein aggregates in olfactory mucosa of a large cohort of subjects with isolated RBD compared to patients with Parkinson’s disease and control subjects. This cross-sectional case-control study was performed at the Medical University of Innsbruck, Austria, the Hospital Clinic de Barcelona, Spain, and the University of Verona, Italy. Olfactory mucosa samples obtained by nasal swab in 63 patients with isolated RBD, 41 matched Parkinson’s disease patients and 59 matched control subjects were analysed by α-synuclein RT-QuIC in a blinded fashion at the University of Verona, Italy. Median age of patients with isolated RBD was 70 years, 85.7% were male. All participants were tested for smell, autonomic, cognitive and motor functions. Olfactory mucosa was α-synuclein RT-QuIC positive in 44.4% isolated RBD patients, 46.3% Parkinson’s disease patients and 10.2% control subjects. While the sensitivity for isolated RBD plus Parkinson’s disease versus controls was 45.2%, specificity was high (89.8%). Among isolated RBD patients with positive α-synuclein RT-QuIC, 78.6% had olfactory dysfunction compared to 21.4% with negative α-synuclein RT-QuIC (P < 0.001). The extent of olfactory dysfunction was more severe in isolated RBD patients positive than negative for olfactory mucosa a-synuclein RT-QuIC (P < 0.001). We provide evidence that the α-synuclein RT-QuIC assay enables the molecular detection of neuronal α-synuclein aggregates in olfactory mucosa of patients with isolated RBD and Parkinson’s disease. Although the overall sensitivity was moderate in this study, nasal swabbing is attractive as a simple, non-invasive test and might be useful as part of a screening battery to identify subjects in the prodromal stages of α-synucleinopathies. Further studies are needed to enhance sensitivity, and better understand the temporal dynamics of α-synuclein seeding in the olfactory mucosa and spreading to other brain areas during the progression from isolated RBD to overt α-synucleinopathy, as well the impact of timing, disease subgroups and sampling technique on the overall sensitivity.
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Jacobs, Sophie, Caroline Zeippen, Fanny Wavreil, Laurent Gillet, and Thomas Michiels. "IFN-λ Decreases Murid Herpesvirus-4 Infection of the Olfactory Epithelium but Fails to Prevent Virus Reactivation in the Vaginal Mucosa." Viruses 11, no. 8 (August 16, 2019): 757. http://dx.doi.org/10.3390/v11080757.
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Murid herpesvirus-4 (MuHV-4), a natural gammaherpesvirus of rodents, can infect the mouse through the nasal mucosa, where it targets sustentacular cells and olfactory neurons in the olfactory epithelium before it propagates to myeloid cells and then to B cells in lymphoid tissues. After establishment of latency in B cells, viral reactivation occurs in the genital tract in 80% of female mice, which can lead to spontaneous sexual transmission to co-housed males. Interferon-lambda (IFN-λ) is a key player of the innate immune response at mucosal surfaces and is believed to limit the transmission of numerous viruses by acting on epithelial cells. We used in vivo plasmid-mediated IFN-λ expression to assess whether IFN-λ could prophylactically limit MuHV-4 infection in the olfactory and vaginal mucosae. In vitro, IFN-λ decreased MuHV-4 infection in cells that overexpressed IFN-λ receptor 1 (IFNLR1). In vivo, prophylactic IFN-λ expression decreased infection of the olfactory epithelium but did not prevent virus propagation to downstream organs, such as the spleen where the virus establishes latency. In the olfactory epithelium, sustentacular cells readily responded to IFN-λ. In contrast, olfactory neurons did not respond to IFN-λ, thus, likely allowing viral entry. In the female genital tract, columnar epithelial cells strongly responded to IFN-λ, as did most vaginal epithelial cells, although with some variation from mouse to mouse. IFN-λ expression, however, failed to prevent virus reactivation in the vaginal mucosa. In conclusion, IFN-λ decreased MuHV-4 replication in the upper respiratory epithelium, likely by protecting the sustentacular epithelial cells, but it did not protect olfactory neurons and failed to block virus reactivation in the genital mucosa.
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Schwartz, Mathieu, Franck Menetrier, Jean-Marie Heydel, Evelyne Chavanne, Philippe Faure, Marc Labrousse, Frédéric Lirussi, et al. "Interactions Between Odorants and Glutathione Transferases in the Human Olfactory Cleft." Chemical Senses 45, no. 8 (August 21, 2020): 645–54. http://dx.doi.org/10.1093/chemse/bjaa055.
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Abstract Xenobiotic metabolizing enzymes and other proteins, including odorant-binding proteins located in the nasal epithelium and mucus, participate in a series of processes modulating the concentration of odorants in the environment of olfactory receptors (ORs) and finely impact odor perception. These enzymes and transporters are thought to participate in odorant degradation or transport. Odorant biotransformation results in 1) changes in the odorant quantity up to their clearance and the termination of signaling and 2) the formation of new odorant stimuli (metabolites). Enzymes, such as cytochrome P450 and glutathione transferases (GSTs), have been proposed to participate in odorant clearance in insects and mammals as odorant metabolizing enzymes. This study aims to explore the function of GSTs in human olfaction. Using immunohistochemical methods, GSTs were found to be localized in human tissues surrounding the olfactory epithelium. Then, the activity of 2 members of the GST family toward odorants was measured using heterologously expressed enzymes. The interactions/reactions with odorants were further characterized using a combination of enzymatic techniques. Furthermore, the structure of the complex between human GSTA1 and the glutathione conjugate of an odorant was determined by X-ray crystallography. Our results strongly suggest the role of human GSTs in the modulation of odorant availability to ORs in the peripheral olfactory process.
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Morgan, Kevin T. "Approaches to the Identification and Recording of Nasal Lesions in Toxicology Studies." Toxicologic Pathology 19, no. 4_part_1 (November 1991): 337–51. http://dx.doi.org/10.1177/0192623391019004-103.
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The identification, recording, and interpretation of nasal lesions can be a difficult task in toxicology studies. The objective of this article is to provide some guidelines for approaches to nasal toxicologic pathology, based on the author's experience and information available in the published literature. Identification of treatment-induced nasal lesions requires adequate in-life and post-mortem observation, and thorough histopathology. Histopathologic assessment is dependent upon high quality and consistent histologic preparations, adequate knowledge of nasal anatomy and histology, and experience with the range of aging, background, and treatment-induced lesions that may be encountered. In recent years there has been a marked increase in the number of articles reporting nasal pathology in studies for which materials were delivered by inhalation and by non-inhalation routes. Because of the increasing size of this database, it is recommended that standardized and systematic nomenclature be developed for these changes. The following points are considered to be particularly important: 1) alert animal care staff to clinical changes that may indicate nasal lesions; 2) screen animals for nasal disease, such as nasal nematodes in non-human primates; 3) record gross lesions during trimming of decalcified nasal tissues; 4) save spare tissue in fixative; 5) remember that the normal bilateral symmetry of the nose can be a valuable diagnostic aid; 6) avoid excessive lumping or splitting of diagnoses; 7) develop a logical order for recording of lesions (the approach preferred by the author is degenerative, inflammatory, regenerative, proliferative, for each of the epithelial types in a logical anatomical order, such as squamous, transitional, respiratory, and olfactory); 8) accurately determine the site of toxic responses; 9) keep a notebook of interesting or important observations and ideas if you are using a computerized data acquisition system; 10) consider the role of factors that may account for lesion distribution (regional dose and tissue susceptibility) during interpretation of tissue responses; and 11) during preparation of the descriptive narrative, clearly define what occurred, where and when it occurred, and consider the use of simple anatomical diagrams as an adjunct to the text. Adequate lesion detection and characterization by the toxicologic pathologist is often a critical feature of toxicology studies, and can play an important role in determination of human risks associated with exposure to xenobiotics. A systematic but flexible approach is recommended.
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Perrott, Matthew R., Christina J. Sigurdson, Gary L. Mason, and Edward A. Hoover. "Mucosal transmission and pathogenesis of chronic wasting disease in ferrets." Journal of General Virology 94, no. 2 (February 1, 2013): 432–42. http://dx.doi.org/10.1099/vir.0.046110-0.
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Chronic wasting disease (CWD) of cervids is almost certainly transmitted by mucosal contact with the causative prion, whether by direct (animal-to-animal) or indirect (environmental) means. Yet the sites and mechanisms of prion entry remain to be further understood. This study sought to extend this understanding by demonstrating that ferrets exposed to CWD via several mucosal routes developed infection, CWD prion protein (PrPCWD) amplification in lymphoid tissues, neural invasion and florid transmissible spongiform encephalopathy lesions resembling those in native cervid hosts. The ferrets developed extensive PrPCWD accumulation in the nervous system, retina and olfactory epithelium, with lesser deposition in tongue, muscle, salivary gland and the vomeronasal organ. PrPCWD accumulation in mucosal sites, including upper respiratory tract epithelium, olfactory epithelium and intestinal Peyer’s patches, make the shedding of prions by infected ferrets plausible. It was also observed that regionally targeted exposure of the nasopharyngeal mucosa resulted in an increased attack rate when compared with oral exposure. The latter finding suggests that nasal exposure enhances permissiveness to CWD infection. The ferret model has further potential for investigation of portals for initiation of CWD infection.
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Everett, Helen E., Fabian Z. X. Lean, Alexander M. P. Byrne, Pauline M. van Diemen, Shelley Rhodes, Joe James, Benjamin Mollett, et al. "Intranasal Infection of Ferrets with SARS-CoV-2 as a Model for Asymptomatic Human Infection." Viruses 13, no. 1 (January 15, 2021): 113. http://dx.doi.org/10.3390/v13010113.
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Ferrets were experimentally inoculated with SARS-CoV-2 (severe acute respiratory syndrome (SARS)-related coronavirus 2) to assess infection dynamics and host response. During the resulting subclinical infection, viral RNA was monitored between 2 and 21 days post-inoculation (dpi), and reached a peak in the upper respiratory cavity between 4 and 6 dpi. Viral genomic sequence analysis in samples from three animals identified the Y453F nucleotide substitution relative to the inoculum. Viral RNA was also detected in environmental samples, specifically in swabs of ferret fur. Microscopy analysis revealed viral protein and RNA in upper respiratory tract tissues, notably in cells of the respiratory and olfactory mucosae of the nasal turbinates, including olfactory neuronal cells. Antibody responses to the spike and nucleoprotein were detected from 21 dpi, but virus-neutralizing activity was low. A second intranasal inoculation (re-exposure) of two ferrets after a 17-day interval did not produce re-initiation of viral RNA shedding, but did amplify the humoral response in one animal. Therefore, ferrets can be experimentally infected with SARS-CoV-2 to model human asymptomatic infection.
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Allan, G. M., F. McNeilly, I. Walker, T. Linne, J. Moreno-Lopez, P. Hernandez, S. Kennedy, et al. "A Sequential Study of Experimental Porcine Paramyxovirus (LPMV) Infection of Pigs: Immunostaining of Cryostat Sections and Virus Isolation." Journal of Veterinary Diagnostic Investigation 8, no. 4 (October 1996): 405–13. http://dx.doi.org/10.1177/104063879600800401.
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La Piedad Michoacan Paramyxovirus (LPMV) is a recently recognized paramyxovirus infecting pigs throughout Mexico. Disease syndromes observed in field cases associated with LPMV infection include neurologic, respiratory, and reproductive disorders. Clinical signs and the distribution of LPMV virus and antigen in tissue samples from pigs experimentally infected with LPMV by natural routes were studied. Severe neurologic disease and death occurred following experimental inoculation of 3- and 17-day-old pigs. All of the pigs inoculated at 3 days of age were either dead or moribund by 8 days after inoculation, whereas 30% of the pigs inoculated at 17 days of age were affected. Virus was consistently recovered from or demonstrated in tissues from the respiratory tract of both groups of pigs. LPMV and antigen were also demonstrated in central nervous system (CNS) tissues from these pigs; however, differences in virus distribution within the CNS were demonstrated in the 2 groups. In the pigs inoculated at 17 days of age, isolation of LPMV was restricted to the olfactory bulb and midbrain. In contrast, in the pigs inoculated at 3 days of age, isolation of LPMV was more widespread throughout the CNS tissue examined. Virus excretion studies indicated that nasal spread of LPMV was more important than fecal spread. Comparatively large quantities of infectious LPMV were consistently recovered from urine samples of experimentally infected pigs.
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Alvites, Rui D., Mariana V. Branquinho, Ana R. Caseiro, Irina Amorim, Sílvia Santos Pedrosa, Alexandra Rêma, Fátima Faria, et al. "Rat Olfactory Mucosa Mesenchymal Stem/Stromal Cells (OM-MSCs): A Characterization Study." International Journal of Cell Biology 2020 (January 29, 2020): 1–21. http://dx.doi.org/10.1155/2020/2938258.
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Stem/stromal cell-based therapies are a branch of regenerative medicine and stand as an attractive option to promote the repair of damaged or dysfunctional tissues and organs. Olfactory mucosa mesenchymal stem/stromal cells have been regarded as a promising tool in regenerative therapies because of their several favorable properties such as multipotency, high proliferation rate, helpful location, and few associated ethical issues. These cells are easily accessible in the nasal cavity of most mammals, including the rat, can be easily applied in autologous treatments, and do not cope with most of the obstacles associated with the use of other stem cells. Despite this, its application in preclinical trials and in both human and animal patients is still limited because of the small number of studies performed so far and to the nonexistence of a standard and unambiguous protocol for collection, isolation, and therapeutic application. In the present work a validation of a protocol for isolation, culture, expansion, freezing, and thawing of olfactory mucosa mesenchymal stem/stromal cells was performed, applied to the rat model, as well as a biological characterization of these cells. To investigate the therapeutic potential of OM-MSCs and their eventual safe application in preclinical trials, the main characteristics of OMSC stemness were addressed.
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Mandal, Surjyanarayan, Snigdha Das Mandal, Krishna Chuttani, and Bharat Bhushan Subudhi. "Mucoadhesive microemulsion of ibuprofen: design and evaluation for brain targeting efficiency through intranasal route." Brazilian Journal of Pharmaceutical Sciences 51, no. 3 (September 2015): 721–31. http://dx.doi.org/10.1590/s1984-82502015000300024.
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This study aimed at designing mucoadhesive microemulsion gel to enhance the brain uptake of Ibuprofen through intranasal route. Ibuprofen loaded mucoadhesive microemulsion (MMEI) was developed by incorporating polycarbophil as mucoadhesive polymer into Capmul MCM based optimal microemulsion (MEI) and was subjected to characterization, stability, mucoadhesion and naso-ciliotoxicity study. Brain uptake of ibuprofen via nasal route was studied by performing biodistribution study in Swiss albino rats. MEI was found to be transparent, stable and non ciliotoxic with 66.29 ± 4.15 nm, -20.9 ± 3.98 mV and 98.66 ± 1.01% as average globule size, zeta potential and drug content respectively. Transmission Electron Microscopy (TEM) study revealed the narrow globule size distribution of MEI. Following single intranasal administration of MMEI and MEI at a dose of 2.86 mg/kg, uptake of ibuprofen in the olfactory bulb was around 3.0 and 1.7 folds compared with intravenous injection of ibuprofen solution (IDS). The ratios of AUC in brain tissues to that in plasma obtained after nasal administration of MMEI were significantly higher than those after intravenous administration of IDS. Findings of the present investigation revealed that the developed mucoadhesive microemulsion gel could be a promising approach for brain targeting of ibuprofen through intranasal route.
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Son, Bomin, Wesuk Kang, Soyoon Park, Dabin Choi, and Taesun Park. "Dermal Olfactory Receptor OR51B5 Is Essential for Survival and Collagen Synthesis in Human Dermal Fibroblast (Hs68 Cells)." International Journal of Molecular Sciences 22, no. 17 (August 27, 2021): 9273. http://dx.doi.org/10.3390/ijms22179273.
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Skin dermis comprises extracellular matrix components, mainly collagen fibers. A decrease in collagen synthesis caused by several factors, including ultraviolet (UV) irradiation and stress, eventually causes extrinsic skin aging. Olfactory receptors (ORs) were initially considered to be specifically expressed in nasal tissue, but several ORs have been reported to be present in other tissues, and their biological roles have recently received increasing attention. In this study, we aimed to characterize the role of ORs in cell survival and collagen synthesis in dermal fibroblasts. We confirmed that UVB irradiation and dexamethasone exposure significantly decreased cell survival and collagen synthesis in Hs68 dermal fibroblasts. Moreover, we demonstrated that the mRNA expression of 10 ORs detectable in Hs68 cells was significantly downregulated in aged conditions compared with that in normal conditions. Thereafter, by individual knockdown of the 10 candidate ORs, we identified that only OR51B5 knockdown leads to a reduction of cell survival and collagen synthesis. OR51B5 knockdown decreased cAMP levels and dampened the downstream protein kinase A/cAMP-response element binding protein pathway, downregulating the survival- and collagen synthesis-related genes in the dermal fibroblasts. Therefore, OR51B5 may be an interesting candidate that plays a role in cell survival and collagen synthesis.
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Stanek, Jerzy, Gabrielle de Courten-Myers, Abbot G. Spaulding, William Strub, and Robert J. Hopkin. "Case of Complex Craniofacial Anomalies, Bilateral Nasal Proboscides, Palatal Pituitary, Upper Limbs Reduction, and Amnion Rupture Sequence: Disorganization Phenotype?" Pediatric and Developmental Pathology 4, no. 2 (March 2001): 192–202. http://dx.doi.org/10.1007/s100240010131.
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We report a case of a dizygotic twin with complex abnormalities of head, body, and limbs. The anomalies include the following: lateral and midline cleft upper lip, ectopic palatal pituitary, natal teeth, bilateral nasal proboscides with an absent nose, left microphthalmia with conjunctival-lined cyst, right ocular dysgenesis, bilateral retinal dysplasia, platybasia with skull asymmetry, hydrocephalus secondary to aqueductal atresia, brain hemispheric asymmetry with a parietal–occipital cortical flap, agenesis of posterior corpus callosum, absence of the olfactory nerves and left anterior cerebral artery, leptomeningeal and intraventricular heterotopias, right radial longitudinal terminal meromelia with constriction rings of fingers, partial syndactyly of the third and fourth left fingers, dorsiflexed great toes and pes equinovarus bilaterally, and multiple skin tags with a sacral appendage. Additionally, this twin's placental disc and extraplacental membranes were devoid of amnion. We regard these anomalies as a possible expression of the human homologue of the disorganization phenotype or another gene mutation. Nevertheless, an abnormality of blastogenesis with early damage to organizing tissues of the frontonasal region and limbs, or a vascular disruption, cannot be excluded. Early amnion rupture sequence (possible extraamniotic pregnancy with amniotic bands, limb reduction defects with Streeter bands, and multiple skin tags tapering into amniotic bands) was also present in this case, and may have acted as a contributing factor.
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Gorka, Marco, Jan Schinköthe, Reiner Ulrich, Kevin Ciminski, Martin Schwemmle, Martin Beer, and Donata Hoffmann. "Characterization of Experimental Oro-Nasal Inoculation of Seba’s Short-Tailed Bats (Carollia perspicillata) with Bat Influenza A Virus H18N11." Viruses 12, no. 2 (February 19, 2020): 232. http://dx.doi.org/10.3390/v12020232.
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In 2012 and 2013, the genomic sequences of two novel influenza A virus (IAV) subtypes, designated H17N10 and H18N11, were identified via next-generation sequencing in the feces of the little yellow-shouldered fruit bat (Sturnira lilium) and the flat-faced fruit-eating bat (Artibeus planirostris), respectively. The pathogenesis caused by these viruses in their respective host species is currently insufficiently understood, which is primarily due to the inability to obtain and keep these bat species under appropriate environmental and biosafety conditions. Seba’s short-tailed bats (Carollia perspicillata), in contrast, are close relatives and a natural H18N11 reservoir species, with the advantage of established animal husbandry conditions in academic research. To study viral pathogenesis in more detail, we here oro-nasally inoculated Seba’s short-tailed bats with the bat IAV H18N11 subtype. Following inoculation, bats appeared clinically healthy, but the histologic examination of tissues revealed a mild necrotizing rhinitis. Consistently, IAV-matrix protein and H18-RNA positive cells were seen in lesioned respiratory and olfactory nasal epithelia, as well as in intestinal tissues. A RT-qPCR analysis confirmed viral replication in the conchae and intestines as well as the presence of viral RNA in the excreted feces, without horizontal transmission to naïve contact animals. Moreover, all inoculated animals seroconverted with low titers of neutralizing antibodies.
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Kondoh, Daisuke, Yusuke Tanaka, Yusuke K. Kawai, Takayuki Mineshige, Kenichi Watanabe, and Yoshiyasu Kobayashi. "Morphological and Histological Features of the Vomeronasal Organ in African Pygmy Hedgehog (Atelerix albiventris)." Animals 11, no. 5 (May 19, 2021): 1462. http://dx.doi.org/10.3390/ani11051462.
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The vomeronasal organ (VNO) detects specific chemicals such as pheromones and kairomones. Hedgehogs (Eulipotyphla: Erinaceidae) have a well-developed accessory olfactory bulb that receives projections from the VNO, but little is known about the hedgehog VNO. Here, we studied the histological features of the VNO in five individual African pygmy hedgehogs by hematoxylin-eosin, periodic acid-Schiff, and Alcian blue stains. The hedgehog VNO comprises a hyaline cartilage capsule, soft tissue and epithelial lumen, and it branches from the site just before the incisive duct opening into the nasal cavity. The soft tissues contain several small mucous (or mucoserous) glands and a large serous gland, and many venous sinuses all around the lumen. The VNO lumen is round to oval throughout the hedgehog VNO, and the sensory epithelium lines almost the entire rostral part and medial wall of the middle part. These findings indicate that the VNO is functional and plays an important role in the hedgehog. Notably, the VNO apparently has a characteristic flushing mechanism with serous secretions like those of gustatory glands, which the hedgehog might frequently use to recognize the external environment.
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Hartmann, Antje, Eberhard Ludewig, Kerstin von Pückler, Martin Kramer, Martin J. Schmidt, and Charlotte Söffler. "Magnetic resonance imaging features of esthesio - neuroblastoma in three dogs and one cat." Tierärztliche Praxis Ausgabe K: Kleintiere / Heimtiere 44, no. 05 (2016): 333–40. http://dx.doi.org/10.15654/tpk-150963.
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SummaryObjective: Esthesioneuroblastoma is a rare malignant intranasal tu - mor that originates from the olfactory neuroepithelium of the upper nasal cavity, and can destroy the cribriform plate and expand into the neurocranium. Descriptions of the magnetic resonance features of esthesioneuroblastomas in animals are scarce. The objectives of this study were to report the magnetic resonance imaging features of esthesioneuroblastomas in order to determine distinct imaging characteristics that may help distinguish it from other intracranial tumor types. Material and methods: Magnetic resonance images of four patients with confirmed esthesioneuroblastomas were reviewed and compared with previously reported cases. Results: The esthesioneu - roblastomas appeared as oval-shaped, solitary lesions in the caudal nasal cavity that caused osteolysis of the cribriform plate and extended into the brain in all cases. Signal intensity was variable. Contrast enhancement was mild and varied from homogeneous to heterogeneous. A peripheral cystic component was found in two patients and was reported in only one previous case. Mass effect and white matter edema were marked to severe. Osteolysis of facial bones and extension into the facial soft tissues or retrobulbar space were not present in any of the cases, although this has been reported in the litera ture. Conclusion: A definitive diagnosis of esthesioneuroblastoma based on signal intensity or contrast behavior was not possible. Nevertheless, the presence of a mass in the caudal nasal cavity with extension into the neurocranium seems to be a feature highly suspicious of esthesioneuroblastoma. In contrast to other extra-cranial le - sions, the extra-cranial mass was relatively small and destruction of facial bones seems to be rare.
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Mariani, Luigi, Benoit Schaller, Joachim Weis, Christoph Ozdoba, and Rolf W. Seiler. "Esthesioneuroblastoma of the pituitary gland: a clinicopathological entity?" Journal of Neurosurgery 101, no. 6 (December 2004): 1049–52. http://dx.doi.org/10.3171/jns.2004.101.6.1049.
Full textAbstract:
✓ Esthesioneuroblastoma (olfactory neuroblastoma) is a rare, malignant neoplasm that typically arises in the nasal vault, invades adjacent tissues, and causes locoregional (cervical lymph nodes) and distant metastases. Only two cases of tumors arising in the sellar region that had the histological characteristics of esthesioneuroblastoma have been reported in the literature to date. The authors present the case of a 35-year-old woman with secondary amenorrhea and a rapidly growing tumor located in the adenohypophysis. After total removal of the lesion through a transseptal—transsphenoidal approach, the histological examination revealed an esthesioneuroblastoma Grade II/III according to Hyams. Considering the particular location of the lesion and the absence of residual tumor on postoperative magnetic resonance imaging, no adjuvant therapy was performed. The patient remained free from tumor recurrence 2 years postoperatively. Because all published cases of this esthestoneuroblastoma have been large neuroblastic tumors of the pituitary gland arising in middle-aged women, pituitary neuroblastoma might represent a rare, specific clinicopathological entity.
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Alexander, Kathleen A., Peter N. Laver, Mark C. Williams, Claire E. Sanderson, Carly Kanipe, and Mitchell V. Palmer. "Pathology of the Emerging Mycobacterium tuberculosis Complex Pathogen, Mycobacterium mungi, in the Banded Mongoose (Mungos mungo)." Veterinary Pathology 55, no. 2 (December 19, 2017): 303–9. http://dx.doi.org/10.1177/0300985817741730.
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Wild banded mongooses ( Mungos mungo) in northeastern Botswana and northwest Zimbabwe are infected with a novel Mycobacterium tuberculosis complex (MTC) pathogen, Mycobacterium mungi. We evaluated gross and histologic lesions in 62 infected mongooses (1999–2017). Many tissues contained multifocal irregular, lymphohistiocytic to granulomatous infiltrates and/or multifocal or coalescing noncaseating to caseating granulomas with variable numbers of intralesional acid-fast bacilli. Over one-third of nasal turbinates examined had submucosal lymphohistiocytic to granulomatous infiltrates, erosion and ulceration of the nasal mucosa, bony remodeling, and nasal distortion. Similar inflammatory cell infiltrates expanded the dermis of the nasal planum with frequent ulceration. However, even in cases with intact epidermis, acid-fast bacilli were present in variable numbers among dermal infiltrates and on the epidermal surface among desquamated cells and debris, most commonly in small crevices or folds. In general, tissue involvement varied among cases but was highest in lymph nodes (50/54, 93%), liver (39/53, 74%), spleen (37/51, 73%), and anal glands/sacs (6/8, 75%). Pulmonary lesions were present in 67% of sampled mongooses (35/52) but only in advanced disseminated disease. The pathological presentation of M. mungi in the banded mongoose is consistent with pathogen shedding occurring through scent-marking behaviors (urine and anal gland secretions) with new infections arising from contact with these contaminated olfactory secretions and percutaneous movement of the pathogen through breaks in the skin, nasal planum, and/or skin of the snout. Given the character and distribution of lesions and the presence of intracellular acid-fast bacilli, we hypothesize that pathogen spread occurs within the body through a hematogenous and/or lymphatic route. Features of prototypical granulomas such as multinucleated giant cells and peripheral fibrosis were rarely present in affected mongooses. Acid-fast bacilli were consistently found intracellularly, even in regions of necrosis. The mongoose genome has a unique deletion (RD1mon) that includes part of the encoding region for PPE68 (Rv3873), a gene co-operonic with PE35. These proteins can influence the host’s cellular immune response to mycobacterial infections, and it remains uncertain how this deletion might contribute to observed patterns of pathology. M. mungi infection in banded mongooses is characterized by both a unique transmission and exposure route, as well as accompanying pathological features, providing an opportunity to increase our understanding of MTC pathogenesis across host-pathogen systems.
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Dye, J. A., K. T. Morgan, D. L. Neldon, J. S. Tepper, G. R. Burleson, and D. L. Costa. "Characterization of Upper Respiratory Disease in Rats Following Neonatal Inoculation with a Rat-adapted Influenza Virus." Veterinary Pathology 33, no. 1 (January 1996): 43–54. http://dx.doi.org/10.1177/030098589603300105.
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Neonatal F344 rats were infected with a rat-adapted influenza virus (RAIV) to use as a potential model to study the combined effects of air pollutant exposure with early life respiratory viral infections. Initially, 6-day-old pups were intranasally inoculated with RAIV or medium alone, and nasal and lower respiratory tract (LRT) tissues were assessed histologically at 1, 3, 6, and 13 days postinoculation (DPI). Immunologic assessments included thymic lymphocyte quantification and anti-RAIV immunoglobulin production. Pups then received two inoculations (at 6 and 30 days of age), with histologic and immunologic assessment 6 and 13 days after the second inoculation and bronchoprovocation testing 5-8 weeks later. Following the single RAIV inoculation, IgM and IgG1 measurements increased at 6, 11, and 15 DPI, with IgG1 being greater at 11 and 15 DPI. Nasal lesions were evident as early as 1 DPI and primarily involved the anterior dorsal medial meatus and adjacent dorsal atrio- and nasoturbinates. Alterations included epithelial cell exfoliation and necrosis, mild erosions, suppurative and nonsuppurative inflammation, intraepithelial neutrophil accumulations, and intraluminal exudate. By 3 DPI, olfactory epithelial damage was multifocal or locally diffuse, with degeneration of sensory cells and variable inflammation. By 13 DPI, lesions were essentially repaired. Minimal changes were apparent in the LRT despite evidence of viral replication in the lungs 24 hours after inoculation (>3 log10 plaque-forming units/lung). Pups reinoculated with RAIV at 30 days of age did not develop significant histologic lesions, nor did they exhibit increased airway responsiveness when assessed as young adults. In spite of their immature immune status at the time of initial infection, 13 days after the second RAIV inoculation, IgG, increased substantially. Thus, neonatal RAIV infection resulted in acute nasal epithelial injury and inflammation, alterations that may allow subsequent evaluation of viral disease-air pollutant interactions.
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Wang, Bo, and Yanli Du. "Cadmium and Its Neurotoxic Effects." Oxidative Medicine and Cellular Longevity 2013 (2013): 1–12. http://dx.doi.org/10.1155/2013/898034.
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Cadmium (Cd) is a heavy metal that has received considerable concern environmentally and occupationally. Cd has a long biological half-life mainly due to its low rate of excretion from the body. Thus, prolonged exposure to Cd will cause toxic effect due to its accumulation over time in a variety of tissues, including kidneys, liver, central nervous system (CNS), and peripheral neuronal systems. Cd can be uptaken from the nasal mucosa or olfactory pathways into the peripheral and central neurons; for the latter, Cd can increase the blood brain barrier (BBB) permeability. However, mechanisms underlying Cd neurotoxicity remain not completely understood. Effect of Cd neurotransmitter, oxidative damage, interaction with other metals such as cobalt and zinc, estrogen-like, effect and epigenetic modification may all be the underlying mechanisms. Here, we review thein vitroandin vivoevidence of neurotoxic effects of Cd. The available finding indicates the neurotoxic effects of Cd that was associated with both biochemical changes of the cell and functional changes of central nervous system, suggesting that neurotoxic effects may play a role in the systemic toxic effects of the exposure to Cd, particularly the long-term exposure.
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Horiuchi, Yasue, Shin-ichi Kano, Koko Ishizuka, Nicola G. Cascella, Seiji Ishii, C. Conover Talbot, Andrew E. Jaffe, et al. "Olfactory cells via nasal biopsy reflect the developing brain in gene expression profiles: Utility and limitation of the surrogate tissues in research for brain disorders." Neuroscience Research 77, no. 4 (December 2013): 247–50. http://dx.doi.org/10.1016/j.neures.2013.09.010.
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Meacci, Elisabetta, Mercedes Garcia-Gil, and Federica Pierucci. "SARS-CoV-2 Infection: A Role for S1P/S1P Receptor Signaling in the Nervous System?" International Journal of Molecular Sciences 21, no. 18 (September 15, 2020): 6773. http://dx.doi.org/10.3390/ijms21186773.
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The recent coronavirus disease (COVID-19) is still spreading worldwide. The severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), the virus responsible for COVID-19, binds to its receptor angiotensin-converting enzyme 2 (ACE2), and replicates within the cells of the nasal cavity, then spreads along the airway tracts, causing mild clinical manifestations, and, in a majority of patients, a persisting loss of smell. In some individuals, SARS-CoV-2 reaches and infects several organs, including the lung, leading to severe pulmonary disease. SARS-CoV-2 induces neurological symptoms, likely contributing to morbidity and mortality through unknown mechanisms. Sphingosine 1-phosphate (S1P) is a bioactive sphingolipid with pleiotropic properties and functions in many tissues, including the nervous system. S1P regulates neurogenesis and inflammation and it is implicated in multiple sclerosis (MS). Notably, Fingolimod (FTY720), a modulator of S1P receptors, has been approved for the treatment of MS and is being tested for COVID-19. Here, we discuss the putative role of S1P on viral infection and in the modulation of inflammation and survival in the stem cell niche of the olfactory epithelium. This could help to design therapeutic strategies based on S1P-mediated signaling to limit or overcome the host–virus interaction, virus propagation and the pathogenesis and complications involving the nervous system.
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Bonferoni, Maria Cristina, Giovanna Rassu, Elisabetta Gavini, Milena Sorrenti, Laura Catenacci, and Paolo Giunchedi. "Nose-to-Brain Delivery of Antioxidants as a Potential Tool for the Therapy of Neurological Diseases." Pharmaceutics 12, no. 12 (December 21, 2020): 1246. http://dx.doi.org/10.3390/pharmaceutics12121246.
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Oxidative stress has a key role in the pathogenesis of neurodegenerative disorders such as Alzheimer’s, Parkinson’s, and Huntington’s diseases and can be an important cause of the damages in cerebral ischemia. Oxidative stress arises from high levels of reactive oxygen species (ROS). Consequently, on this rational base, antioxidants (many of natural origin) are proposed as potential drugs to prevent ROS noxious actions because they can protect the target tissues from the oxidative stress. However, the potential of antioxidants is limited, owing to the presence of the blood–brain barrier (BBB), which is difficult to cross with a consequent low bioavailability of the drug into the brain after systemic (intravenous, intraperitoneal, oral) administrations. One strategy to improve the delivery of antioxidants to the brain involves the use of the so-called nose-to-brain route, with the administration of the antioxidant in specific nasal formulations and its passage to the central nervous system (CNS) mainly through the olfactory nerve way. In the current literature, many examples show encouraging results in studies carried out in cell cultures and in animal models about the potential neuroprotective effects of antioxidants when administered through the nose. This review concerns the nose-to-brain route for the brain targeting of antioxidants as a potential tool for the therapy of neurological diseases.
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HOOPER, John D., Luisa CAMPAGNOLO, Goodarz GOODARZI, Tony N. TRUONG, Heidi STUHLMANN, and James P. QUIGLEY. "Mouse matriptase-2: identification, characterization and comparative mRNA expression analysis with mouse hepsin in adult and embryonic tissues." Biochemical Journal 373, no. 3 (August 1, 2003): 689–702. http://dx.doi.org/10.1042/bj20030390.
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We report the identification and characterization of mouse matriptase-2 (m-matriptase-2), an 811-amino-acid protein composed of an N-terminal cytoplasmic domain, a membrane-spanning domain, two CUB (complement protein subcomponents C1r/C1s, urchin embryonic growth factor and bone morphogenetic protein 1) domains, three LDLR (low-density-lipoprotein receptor class A) domains and a C-terminal serine-protease domain. All m-matriptase-2 protein domain boundaries corresponded with intron/exon junctions of the encoding gene, which spans approx. 29 kb and comprises 18 exons. Matriptase-2 is highly conserved in human, mouse and rat, with the rat matriptase-2 gene (r-maltriptase-2) predicted to encode transmembrane and soluble isoforms. Western-blot analysis indicated that m-matriptase-2 migrates close to its theoretical molecular mass of 91 kDa, and immunofluorescence analysis was consistent with the proposed surface membrane localization of this protein. Reverse-transcription PCR and in-situ-hybridization analysis indicated that m-matriptase-2 expression overlaps with the distribution of mouse hepsin (m-hepsin, a cell-surface serine protease identified in hepatoma cells) in adult tissues and during embryonic development. In adult tissues both are expressed at highest levels in liver, kidney and uterus. During embryogenesis m-matriptase-2 expression peaked between days 12.5 and 15.5. m-hepsin expression was biphasic, with peaks at day 7.5 to 8.5 and again between days 12.5 and 15.5. In situ hybridization of embryonic tissues indicated abundant expression of both m-matriptase-2 and m-hepsin in the developing liver and at lower levels in developing pharyngo–tympanic tubes. While m-hepsin was detected in the residual embryonic yolk sac and with lower intensity in lung, heart, gastrointestinal tract, developing kidney tubules and epithelium of the oral cavity, m-matriptase-2 was absent in these tissues, but strongly expressed within the nasal cavity by olfactory epithelial cells. Mechanistic insight into the potential role of this new transmembrane serine protease is provided by its novel expression profile in embryonic and adult mouse.
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Bhutta, M. F., S. Al-Shaikh, M. Latif, R. Lee, and J. Uraiby. "Nasal polyps do not contain olfactory structures." Rhinology journal 49, no. 2 (June 1, 2011): 185–89. http://dx.doi.org/10.4193/rhino09.171.
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BACKGROUND: Nasal polyposis can lead to olfactory dysfunction, either due to physical obstruction of the olfactory cleft or physiological disruption of the olfactory neuroepithelium. Where medical therapy has failed to relieve symptoms of nasal polyposis, surgical excision can be considered. However, removal of polyps medial to the middle turbinate is controversial: some believe this will relieve physical obstruction to odourants, others state that removal here risks excising olfactory neuroepithelium. METHODS: We stained 25 nasal polypectomy samples from the area medial to the middle turbinate with olfactory marker protein. RESULTS: We confirmed that our staining method worked on normal olfactory tissue. However, no positive staining of nasal polyps was demonstrated. CONCLUSION: We conclude that nasal polyps medial to the middle turbinate do not contain olfactory neurons, and surgical excision is not contraindicated.
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Stefania Erra and Ennio Nano B D. "Olfactory neuroblastoma: case report and focus on cancerogenesis." World Journal of Biology Pharmacy and Health Sciences 6, no. 3 (June 30, 2021): 035–39. http://dx.doi.org/10.30574/wjbphs.2021.6.3.0060.
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Background: Neuroendocrine neoplasms (NENs) of the nasal cavity, paranasal sinuses and nasopharynx account for a wide spectrum of histotypes. They can range from indolent form to highly aggressive tumors. Olfactory neuroblastoma, like most sino-nasal NENs, represents a rare neoplasm that prompts diagnostic pitfalls. From a morphological perspective, olfactory neuroblastoma can mimic many nasal neoplasms but a proper recognition is mandatory for its aggressive behaviour. Case presentation: A case of olfactory neuroblastoma in a 85 years old woman is reported. The neoplasm has been surgical removed from the nasal cavity with a clinical and radiographic diagnosis of nasal polyp. Correct diagnostic definition has needed a complete histological and immunohistochemical characterization of the tumoral tissue in surgical pathology laboratory. Conclusion: The correct diagnosis of olfactory neuroblastoma directs the clinical management that is unique for this neoplasm in comparison to other nasal ones. Bicranial-facial surgery or a trephination procedure represent the most common approach for the treatment of this malignancy. Their success determine disease prognosis.
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Corona, Cristiano, Chiara Porcario, Francesca Martucci, Barbara Iulini, Barbara Manea, Marina Gallo, Claudia Palmitessa, et al. "Olfactory System Involvement in Natural Scrapie Disease." Journal of Virology 83, no. 8 (January 21, 2009): 3657–67. http://dx.doi.org/10.1128/jvi.01966-08.
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ABSTRACT The olfactory system (OS) is involved in many infectious and neurodegenerative diseases, both human and animal, and it has recently been investigated in regard to transmissible spongiform encephalopathies. Previous assessments of nasal mucosa infection by prions following intracerebral challenge suggested a potential centrifugal spread along the olfactory nerve fibers of the pathological prion protein (PrPSc). Whether the nasal cavity may be a route for centripetal prion infection to the brain has also been experimentally studied. With the present study, we wanted to determine whether prion deposition in the OS occurs also under field conditions and what type of anatomical localization PrPSc might display there. We report here on detection by different techniques of PrPSc in the nasal mucosa and in the OS-related brain areas of sheep affected by natural scrapie. PrPSc was detected in the perineurium of the olfactory nerve bundles in the medial nasal concha and in nasal-associated lymphoid tissue. Olfactory receptor neurons did not show PrPSc immunostaining. PrPSc deposition was found in the brain areas of olfactory fiber projection, chiefly in the olfactory bulb and the olfactory cortex. The prevalent PrPSc deposition patterns were subependymal, perivascular, and submeningeal. This finding, together with the discovery of an intense PrPSc immunostaining in the meningeal layer of the olfactory nerve perineurium, at the border with the subdural space extension surrounding the nerve rootlets, strongly suggests a probable role of cerebrospinal fluid in conveying prion infectivity to the nasal submucosa.
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Yu, H., Y. Hu, A. J. Pask, G. Shaw, and M. B. Renfree. "245. Aristaless-related homeobox gene is involved in early development and spermatogenesis in mammals." Reproduction, Fertility and Development 20, no. 9 (2008): 45. http://dx.doi.org/10.1071/srb08abs245.
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The aristaless homeobox gene, ARX, belongs to a large family of homeodomain transcription factors with essential roles in forebrain, pancreas, muscle tissues and testes development in human and mouse. Mutation of ARX in humans results in mental retardation with or without ambiguous genitalia. We used comparative analyses to examine the evolutionary conservation of the mammalian ARX gene. We characterised ARX in a marsupial, the tammar wallaby, to determine if this gene is highly conserved in the homeodomain, aristaless domain, octapeptide motif and polyalanine tracts of all mammals. We further investigated the mRNA distribution in the developing head of tammar with in situ hybridisation, and found that it is expressed in forebrain and olfactory bulb as expected. Besides these regions, very strong expression was detected in the epithelium of the tongue and nasal pits. In the gonads, there is very strong staining in the interstitial cells and some of the germ cells in the developing ovary; strong staining was also seen in the cytoplasm of Sertoli cells and some of the germ cells, weak staining was also detected in the interstitium of the testis, possibly within the vessel endothelial cells and interstitial fibroblast-like cells. In addition, we investigated mRNA distribution in adult testes based on a very strong signal observed with northern blotting. Interestingly, mRNA expression was restricted to the round spermatids, and was not seen before or after this stage. In order to confirm this new role for ARX in the adult testis, we further investigated mRNA distribution of Arx in adult mouse testis, and found the same expression pattern, which implies a conserved function for ARX in spermatogenesis and may explain why humans with ARX mutations are infertile. This is the first report that ARX gene is involved in spermatogenesis in addition to its conserved roles in early mammalian development.
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Turk, M. A. M., W. G. Henk, and W. Flory. "3-Methylindole-Induced Nasal Mucosal Damage in Mice." Veterinary Pathology 24, no. 5 (September 1987): 400–403. http://dx.doi.org/10.1177/030098588702400506.
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3-Methylindole (3MI) damages nasal olfactory epithelium in mice. Lesions were studied histologically from 30 minutes to 28 days after intraperitoneal injection of 400 mg 3MI/kg. Cellular swelling was apparent in olfactory epithelium by 6 hours after injection of 3MI, while respiratory epithelium was normal. Necrosis of olfactory epithelium and subepithelial glands was diffuse by 48 hours. Subsequent ulceration resulted in epithelial hyperplasia, squamous metaplasia, fibroplasia, and ossification. Partially occlusive intranasal fibrous and osseous tissue persisted through 28 days after 3MI injection.
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Getchell, Marilyn L., Ying Chen, Xinxin Ding, D. Larry Sparks, and Thomas V. Getchell. "Immunohistochemical Localization of a Cytochrome P-450 Isozyme in Human Nasal Mucosa: Age-Related Trends." Annals of Otology, Rhinology & Laryngology 102, no. 5 (May 1993): 368–74. http://dx.doi.org/10.1177/000348949310200509.
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Immunoperoxidase staining with an antibody to cytochrome P-450 (NMa) was used to investigate the localization of this isozyme in the human nasal mucosa. Olfactory mucosa was identified by staining of olfactory receptor cells with an antibody to olfactory marker protein. Immunoreactivity to NMa was localized in sustentacular cells in the olfactory epithelium, and in Bowman's gland acinar cells and vascular endothelial cells in the lamina propria. In the respiratory mucosa, ciliated epithelial cells, as well as serous gland acinar cells and vascular endothelial cells in the lamina propria, were immunoreactive for this isozyme. An age-related decrement in the intensity and extent of immunoreactivity within these cells was noted in nasal tissue from patients 60 years of age and over when compared with that of patients under 60 years of age. These results identify sites of xenobiotic metabolism or activation in human nasal mucosa.