Journal articles: 'Olfactory tissue'

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Nishizaki, Kazunori. "Olfactory Tissue and Regeneration Medicine." Practica Oto-Rhino-Laryngologica 104, no. 5 (2011): 309–15. http://dx.doi.org/10.5631/jibirin.104.309.

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Makino, N., S. Ookawara, S. Madoiwa, Y. Ohta, T. Ishikawa, K. Katoh, S. Takigami, et al. "Morphological assessment of the luminal surface of olfactory epithelium in mice deficient in tissue plasminogen activator following bulbectomy." Journal of Laryngology & Otology 126, no. 11 (September 19, 2012): 1114–20. http://dx.doi.org/10.1017/s002221511200206x.

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AbstractObjective:This study aimed to investigate the function of tissue plasminogen activator in the olfactory epithelium of mice following neural injury.Method:Transmission electron microscopy was used to study the changes in the morphology of the olfactory epithelium 1–7 days after surgical ablation of the olfactory bulb (bulbectomy).Results:Prior to bulbectomy, a uniformly fine material was observed within some regions of the olfactory epithelium of mice deficient in tissue plasminogen activator. At 2–3 days after bulbectomy, there were degenerative changes in the olfactory epithelium. At 5–7 days after bulbectomy, we noted drastic differences in olfactory epithelium morphology between mice deficient in tissue plasminogen activator and wild-type mice (comparisons were made using findings from a previous study). The microvilli seemed to be normal and olfactory vesicles and receptor neuron dendrites were largely intact in the olfactory epithelium of mice deficient in tissue plasminogen activator.Conclusion:The tissue plasminogen activator plasmin system may inhibit the regeneration of the olfactory epithelium in the early stages following neural injury.

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Biedlingmaier, John F., and Philip J. Whelan. "Analysis for Olfactory Epithelium using Olfactory Marker Protein on Endoscopically Harvested Middle Turbinates." American Journal of Rhinology 10, no. 4 (July 1996): 221–24. http://dx.doi.org/10.2500/105065896782103144.

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The middle turbinate is thought to play a key role in olfaction, and many surgeons have cautioned against removal of the middle turbinate during endoscopic sinus surgery. We reviewed 110 patients having 198 partial middle turbinate resections and found that only one patient complained of postoperative anosmia (0.9%). To further investigate the presence of olfactory tissue on the middle turbinate, 36 sections from 12 endoscopically resected turbinate specimens were stained for olfactory tissue, using olfactory marker protein (OMP). Cadaveric olfactory cleft specimens served as positive controls. Neither olfactory epithelium nor olfactory receptor cells were identified in the surgical specimens. The clinical rarity of anosmia suggests that partial resections must not adversely affect airflow to the olfactory cleft. The histologic data suggest that conservative partial turbinate resections should not affect olfaction directly, either because olfactory tissue is not removed by this maneuver, or because the amount of olfactory tissue in this segment is minimal.

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Menco, Bert Ph M. "Ultrastructural aspects of olfactory signal transduction and its development." Proceedings, annual meeting, Electron Microscopy Society of America 52 (1994): 142–43. http://dx.doi.org/10.1017/s042482010016844x.

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Vertebrate olfactory receptor cells are specialized neurons that have numerous long tapering cilia. The distal parts of these cilia line the interface between the external odorous environment and the luminal surface of the olfactory epithelium. The length and number of these cilia results in a large surface area that presumably increases the chance that an odor molecule will meet a receptor cell. Advanced methods of cryoprepration and immuno-gold labeling were particularly useful to preserve the delicate ultrastructural and immunocytochemical features of olfactory cilia required for localization of molecules involved in olfactory signal-transduction. We subjected olfactory tissues to freeze-substitution in acetone (unfixed tissues) or methanol (fixed tissues) followed by low temperature embedding in Lowicryl K11M for that purpose. Tissue sections were immunoreacted with several antibodies against proteins that are presumably important in olfactory signal-transduction.

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Sindwani, R. "Immunohistochemical Characterization of Human Olfactory Tissue." Yearbook of Otolaryngology-Head and Neck Surgery 2012 (January 2012): 190–92. http://dx.doi.org/10.1016/j.yoto.2012.03.020.

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Holbrook, Eric H., Enming Wu, William T. Curry, Derrick T. Lin, and James E. Schwob. "Immunohistochemical characterization of human olfactory tissue." Laryngoscope 121, no. 8 (July 25, 2011): 1687–701. http://dx.doi.org/10.1002/lary.21856.

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SCHULZE, D. H., M. PYRSKI, A. RUKNUDIN, J. W. MARGOLIS, S. K. POLUMURI, and F. L. MARGOLIS. "Sodium-Calcium Exchangers in Olfactory Tissue." Annals of the New York Academy of Sciences 976, no. 1 (January 24, 2006): 67–72. http://dx.doi.org/10.1111/j.1749-6632.2002.tb04716.x.

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McClintock, Timothy S., Chad E. Glasser, Soma C. Bose, and Daniel A. Bergman. "Tissue expression patterns identify mouse cilia genes." Physiological Genomics 32, no. 2 (January 2008): 198–206. http://dx.doi.org/10.1152/physiolgenomics.00128.2007.

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In mammals, cilia are critical for development, sensation, cell signaling, sperm motility, and fluid movement. Defects in cilia are causes of several congenital syndromes, providing additional reasons to identify cilia-related genes. We hypothesized that mRNAs selectively abundant in tissues rich in highly ciliated cells encode cilia proteins. Selective abundance in olfactory epithelium, testes, vomeronasal organ, trachea, and lung proved to be an expression pattern uniquely effective in identifying documented cilia-related genes. Known and suspected cilia-related genes were statistically overrepresented among the 99 genes identified, but the majority encoded proteins of unknown function, thereby predicting new cilia-related proteins. Evidence of expression in a highly ciliated cell, the olfactory sensory neuron, exists for 73 of the genes. In situ hybridization for 17 mRNAs confirmed expression of all 17 in olfactory sensory neurons. Most were also detected in vomeronasal sensory neurons and in neighboring tissues rich in ciliated cells such as respiratory epithelium. Immunoreactivity for one of the proteins identified, Spa17, colocalized with acetylated tubulin in the cilia layer of the olfactory epithelium. In contrast, the ciliary rootlet protein, Crocc, was located in discrete structures whose position was consistent with the dendritic knobs of the olfactory sensory neurons. A compilation of >2,000 mouse genes predicted to encode cilia-related proteins revealed a strong correlation ( R = 0.99) between the number of studies predicting a gene's involvement in cilia and documented evidence of such involvement, a fact that simplifies the selection of genes for further study of the physiology of cilia.

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Reed, C. J., E. A. Lock, and F. De Matteis. "NADPH: cytochrome P-450 reductase in olfactory epithelium Relevance to cytochrome P-450-dependent reactions." Biochemical Journal 240, no. 2 (December 1, 1986): 585–92. http://dx.doi.org/10.1042/bj2400585.

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The presence of a very active cytochrome P-450-dependent drug-metabolizing system in the olfactory epithelium has been confirmed by using 7-ethoxycoumarin, 7-ethoxyresorufin, hexobarbitone and aniline as substrates, and the reasons for the marked activity of the cytochrome P-450 in this tissue have been investigated. The spectral interaction of hexobarbitone and aniline with hepatic and olfactory microsomes has been examined. By this criterion there was no evidence for marked differences in the spin state of the cytochromes of the two tissues, or for the olfactory epithelium containing a greater amount of cytochrome capable of binding hexobarbitone, a very actively metabolized substrate. Rates of NADPH and NADH: cytochrome c reductase activity were found to be higher in the olfactory epithelium than in the liver, and direct evidence was obtained for a greater amount of the NADPH-dependent flavoprotein in the olfactory microsomes. Investigation of male rats and male and female mice, as well as male hamsters, demonstrated that, in all cases, the cytochrome P-450 levels of the olfactory epithelium were lower than those of the liver, while the 7-ethoxycoumarin de-ethylase and NADPH:cytochrome c reductase activities were higher. A correlation was found between 7-ethoxycoumarin de-ethylase and NADPH:cytochrome c reductase activities for both tissues in all species examined. The ratio of reductase to cytochrome P-450 was found to be considerably higher in the olfactory epithelium (1:2-1:3) than in the liver (1:11-1:15), regardless of the species examined, suggesting that facilitated electron flow may contribute significantly to the cytochrome P-450 catalytic turnover in the olfactory tissue.

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Harrison, Paul J. H., Holly S. Cate, Pascal Steullet, and Charles D. Derby. "Structural plasticity in the olfactory system of adult spiny lobsters: postembryonic development permits life-long growth, turnover, and regeneration." Marine and Freshwater Research 52, no. 8 (2001): 1357. http://dx.doi.org/10.1071/mf01103.

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Caribbean spiny lobsters (Panulirus argus) rely on their sense of olfaction for many behaviours. Growth of their olfactory systems, and maintenance of olfactory function, is ensured by structural change that occurs continuously throughout life. In this paper, we review recent studies on postembryonic development in the olfactory system of P. argus and several other decapod species. Major structural change occurs in both the peripheral and central olfactory systems; it includes addition and loss of olfactory receptor neurons (ORNs), aesthetasc and other sensilla, and interneurons associated with the olfactory lobes of the brain. From these studies it is clear that continuous growth and turnover of olfactory tissue is a normal process in decapod crustaceans. In addition, we describe for the first time mechanisms that enable the peripheral olfactory system of spiny lobsters to regenerate after injury. We monitored the regeneration of olfactory tissue usingin vivo incorporation of the cell proliferation marker 5- bromo-2′-deoxyuridine (BrdU). Our results show that regeneration after partial antennular amputation, which reduces the length of the antennule and thereby the number of ORNs, occurs as a result of upregulation of the normal mode of ORN addition and down-regulation of loss. In contrast, localized injury to aesthetasc sensilla, which causes the associated ORNs to degenerate but does not reduce antennular length, is followed by local regeneration of olfactory tissue.

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Yagi, Sayaka, and Richard M. Costanzo. "Grafting the Olfactory Epithelium to the Olfactory Bulb." American Journal of Rhinology & Allergy 23, no. 3 (May 2009): 239–43. http://dx.doi.org/10.2500/ajra.2009.23.3307.

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Background Impaired olfactory function leads to a decrease in the quality of life for many patients. Surgical treatment options are limited, especially for those suffering from hyposmia or anosmia after posttraumatic injury to the olfactory nerves. Stem cells located in the olfactory epithelium (OE) have the capacity to grow new neurons, making the OE an ideal candidate for restorative tissue grafting. This study was performed to determine if strips of OE survive transplantation directly to the olfactory bulb (OB). Methods Transgenic mice, expressing a green fluorescent protein (GFP), were used to obtain the donor graft tissue. Strips of OE from GFP donor mice were transplanted directly to sites in the OB and cerebral cortex (CC; control sites) of wild-type mice. Graft survival rates at 30 days were determined for transplant sites in the OB and CC. Results Strips of OE from transgenic mice survived transplantation to the OB and continued to express the GFP marker protein. The 30-day survival rate in the OB (83%, 5 of 6 grafts) was the same as in the CC (10 of 12 grafts). The morphology of the graft revealed characteristics found in normal OE. Conclusion We showed that strips of OE can be successfully grafted to both the OB and CC. Grafts of the OE, if strategically positioned on the ventral surface of the bulb and given access to the nasal cavity, could provide the basis for new surgical treatments to restore olfactory function.

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Ranzani, Marco, Vivek Iyer, Ximena Ibarra-Soria, Martin Del Castillo Velasco-Herrera, Mathew Garnett, Darren Logan, and David J. Adams. "Revisiting olfactory receptors as putative drivers of cancer." Wellcome Open Research 2 (February 10, 2017): 9. http://dx.doi.org/10.12688/wellcomeopenres.10646.1.

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Background: Olfactory receptors (ORs) recognize odorant molecules and activate a signal transduction pathway that ultimately leads to the perception of smell. This process also modulates the apoptotic cycle of olfactory sensory neurons in an olfactory receptor-specific manner. Recent reports indicate that some olfactory receptors are expressed in tissues other than the olfactory epithelium suggesting that they may have pleiotropic roles. Methods: We investigated the expression of 301 olfactory receptor genes in a comprehensive panel of 968 cancer cell lines. Results: Forty-nine per cent of cell lines show expression of at least one olfactory receptor gene. Some receptors display a broad pattern of expression across tumour types, while others were expressed in cell lines from a particular tissue. Additionally, most of the cancer cell lines expressing olfactory receptors express the effectors necessary for OR-mediated signal transduction. Remarkably, among cancer cell lines, OR2C3 is exclusively expressed in melanoma lines. We also confirmed the expression of OR2C3 in human melanomas, but not in normal melanocytes. Conclusions: The pattern of OR2C3 expression is suggestive of a functional role in the development and/or progression of melanoma. Some olfactory receptors may contribute to tumorigenesis.

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Jafek, Bruce W., Pamela M. Eller, Edward W. Johnson, Mary M. Chapman, and Christopher M. Filley. "Ultrastructural Changes of the Olfactory Epithelium in Alzheimer's Disease." American Journal of Rhinology 6, no. 6 (November 1992): 219–25. http://dx.doi.org/10.2500/105065892781976646.

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Recent studies have demonstrated an association between abnormalities in the sense of smell and Alzheimer's disease (AD). In our laboratory we have shown that olfactory dysfunction is accompanied by histopathological changes in the olfactory epithelium. These findings led us to believe that there were changes in the olfactory epithelium in AD that resulted in altered olfactory function. In the present study we have done biopsies of tissue from 12 patients who have been screened thoroughly and diagnosed with probable AD. Olfactory epithelium from 10 of these patients has been examined at the electron microscopic level. The overall appearance of the epithelium is altered from that seen in normosmic, age-matched controls. The ultrastructural appearance of olfactory receptor cells and support cells is disrupted. In addition, a crystallinelike material has been observed over the surface of the olfactory epithelium in six patients. This material was not observed in the respiratory epithelium of the same patients and has not been seen by us in any other pathological or normal tissues we have examined. The overall appearance of the olfactory epithelium in these probable AD patients seems to be unique when compared with other pathological states examined so far. The present study suggests that olfactory epithelium biopsy may be useful in the early detection of AD.

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Wang, M. M., R. Y. Tsai, K. A. Schrader, and R. R. Reed. "Genes encoding components of the olfactory signal transduction cascade contain a DNA binding site that may direct neuronal expression." Molecular and Cellular Biology 13, no. 9 (September 1993): 5805–13. http://dx.doi.org/10.1128/mcb.13.9.5805.

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Genes which mediate odorant signal transduction are expressed at high levels in neurons of the olfactory epithelium. The molecular mechanism governing the restricted expression of these genes likely involves tissue-specific DNA binding proteins which coordinately activate transcription through sequence-specific interactions with olfactory promoter regions. We have identified binding sites for the olfactory neuron-specific transcription factor, Olf-1, in the sequences surrounding the transcriptional initiation site of five olfactory neuron-specific genes. The Olf-1 binding sites described define the consensus sequence YTCCCYRGGGAR. In addition, we have identified a second binding site, the U site, in the olfactory cyclic nucleotide gated channel and type III cyclase promoters, which binds factors present in all tissue examined. These experiments support a model in which expression of Olf-1 in the sensory neurons coordinately activates a set of olfactory neuron-specific genes. Furthermore, expression of a subset of these genes may be modulated by additional binding factors.

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Wang, M. M., R. Y. Tsai, K. A. Schrader, and R. R. Reed. "Genes encoding components of the olfactory signal transduction cascade contain a DNA binding site that may direct neuronal expression." Molecular and Cellular Biology 13, no. 9 (September 1993): 5805–13. http://dx.doi.org/10.1128/mcb.13.9.5805-5813.1993.

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Genes which mediate odorant signal transduction are expressed at high levels in neurons of the olfactory epithelium. The molecular mechanism governing the restricted expression of these genes likely involves tissue-specific DNA binding proteins which coordinately activate transcription through sequence-specific interactions with olfactory promoter regions. We have identified binding sites for the olfactory neuron-specific transcription factor, Olf-1, in the sequences surrounding the transcriptional initiation site of five olfactory neuron-specific genes. The Olf-1 binding sites described define the consensus sequence YTCCCYRGGGAR. In addition, we have identified a second binding site, the U site, in the olfactory cyclic nucleotide gated channel and type III cyclase promoters, which binds factors present in all tissue examined. These experiments support a model in which expression of Olf-1 in the sensory neurons coordinately activates a set of olfactory neuron-specific genes. Furthermore, expression of a subset of these genes may be modulated by additional binding factors.

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Maßberg, Désirée, and Hanns Hatt. "Human Olfactory Receptors: Novel Cellular Functions Outside of the Nose." Physiological Reviews 98, no. 3 (July 1, 2018): 1739–63. http://dx.doi.org/10.1152/physrev.00013.2017.

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Olfactory receptors (ORs) are not exclusively expressed in the olfactory sensory neurons; they are also observed outside of the olfactory system in all other human tissues tested to date, including the testis, lung, intestine, skin, heart, and blood. Within these tissues, certain ORs have been determined to be exclusively expressed in only one tissue, whereas other ORs are more widely distributed in many different tissues throughout the human body. For most of the ectopically expressed ORs, limited data are available for their functional roles. They have been shown to be involved in the modulation of cell-cell recognition, migration, proliferation, the apoptotic cycle, exocytosis, and pathfinding processes. Additionally, there is a growing body of evidence that they have the potential to serve as diagnostic and therapeutic tools, as ORs are highly expressed in different cancer tissues. Interestingly, in addition to the canonical signaling pathways activated by ORs in olfactory sensory neurons, alternative pathways have been demonstrated in nonolfactory tissues. In this review, the existing data concerning the expression, as well as the physiological and pathophysiological functions, of ORs outside of the nose are highlighted to provide insights into future lines of research.

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Le Bon, Anne Marie, Nicolas Deprêtre, Estelle Sibille, Stéphanie Cabaret, Stéphane Grégoire, Vanessa Soubeyre, Elodie Masson, et al. "Comprehensive study of rodent olfactory tissue lipid composition." Prostaglandins, Leukotrienes and Essential Fatty Acids 131 (April 2018): 32–43. http://dx.doi.org/10.1016/j.plefa.2018.03.008.

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Nagra, Gurjit, Lena Koh, Andrei Zakharov, Dianna Armstrong, and Miles Johnston. "Quantification of cerebrospinal fluid transport across the cribriform plate into lymphatics in rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 291, no. 5 (November 2006): R1383—R1389. http://dx.doi.org/10.1152/ajpregu.00235.2006.

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A major pathway by which cerebrospinal fluid (CSF) is removed from the cranium is transport through the cribriform plate in association with the olfactory nerves. CSF is then absorbed into lymphatics located in the submucosa of the olfactory epithelium (olfactory turbinates). In an attempt to provide a quantitative measure of this transport,125I-human serum albumin (HSA) was injected into the lateral ventricles of adult Fisher 344 rats. The animals were killed at 10, 20, 30, 40, and 60 min after injection, and tissue samples, including blood (from heart puncture), skeletal muscle, spleen, liver, kidney, and tail were excised for radioactive assessment. The remains were frozen. To sample the olfactory turbinates, angled coronal tissue sections anterior to the cribriform plate were prepared from the frozen heads. The average concentration of125I-HSA was higher in the middle olfactory turbinates than in any other tissue with peak concentrations achieved 30 min after injection. At this point, the recoveries of injected tracer (percent injected dose/g tissue) were 9.4% middle turbinates, 1.6% blood, 0.04% skeletal muscle, 0.2% spleen, 0.3% liver, 0.3% kidney, and 0.09% tail. The current belief that arachnoid projections are responsible for CSF drainage fails to explain some important issues related to the pathogenesis of CSF disorders. The rapid movement of the CSF tracer into the olfactory turbinates further supports a role for lymphatics in CSF absorption and provides the basis of a method to investigate the novel concept that diseases associated with the CSF system may involve impaired lymphatic CSF transport.

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Ayala-Grosso, Carlos, Rosalinda Pieruzzini, Leslie Vargas-Saturno, and José E. Cardier. "Human olfactory mesenchymal stromal cells co-expressing horizontal basal and ensheathing cell proteins in culture." Biomédica 40, no. 1 (March 1, 2020): 72–88. http://dx.doi.org/10.7705/biomedica.4762.

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Introduction: The olfactory neuro-epithelium has an intrinsic capability of renewal during lifetime provided by the existence of globose and horizontal olfactory precursor cells. Additionally, mesenchymal stromal olfactory cells also support the homeostasis of the olfactory mucosa cell population. Under in vitro culture conditions with Dulbecco modified eagle/F12 medium supplemented with 10% fetal bovine serum, tissue biopsies from upper turbinate have generated an adherent population of cells expressing mainly mesenchymal stromal phenotypic markers. A closer examination of these cells has also found co-expression of olfactory precursors and ensheathing cell phenotypic markers. These results were suggestive of a unique property of olfactory mesenchymal stromal cells as potentially olfactory progenitor cells.Objective: To study whether the expression of these proteins in mesenchymal stromal cells is modulated upon neuronal differentiation.Materials and methods: We observed the phenotype of olfactory stromal cells under DMEM/F12 plus 10% fetal bovine serum in comparison to cells from spheres induced by serum-free medium plus growth factors inducers of neural progenitors.Results: The expression of mesenchymal stromal (CD29+, CD73+, CD90+, CD45-), horizontal basal (ICAM-1/CD54+, p63+, p75NGFr+), and ensheathing progenitor cell (nestin+, GFAP+) proteins was determined in the cultured population by flow cytometry. The determination of Oct 3/4, Sox-2, and Mash-1 transcription factors, as well as the neurotrophins BDNF, NT3, and NT4 by RT-PCR in cells, was indicative of functional heterogeneity of the olfactory mucosa tissue sample. Conclusions: Mesenchymal and olfactory precursor proteins were downregulated by serum-free medium and promoted differentiation of mesenchymal stromal cells into neurons and astroglial cells.

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Frings, S. "Protein kinase C sensitizes olfactory adenylate cyclase." Journal of General Physiology 101, no. 2 (February 1, 1993): 183–205. http://dx.doi.org/10.1085/jgp.101.2.183.

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Effects of neurotransmitters on cAMP-mediated signal transduction in frog olfactory receptor cells (ORCs) were studied using in situ spike recordings and radioimmunoassays. Carbachol, applied to the mucosal side of olfactory epithelium, amplified the electrical response of ORCs to cAMP-generating odorants, but did not affect unstimulated cells. A similar augmentation of odorant response was observed in the presence of phorbol dibutyrate (PDBu), an activator of protein kinase C (PKC). The electrical response to forskolin, an activator of adenylate cyclase (AC), was also enhanced by PDBu, and it was attenuated by the PKC inhibitor Goe 6983. Forskolin-induced accumulation of cAMP in olfactory tissue was potentiated by carbachol, serotonin, and PDBu to a similar extent. Potentiation was completely suppressed by the PKC inhibitors Goe 6983, staurosporine, and polymyxin B, suggesting that the sensitivity of olfactory AC to stimulation by odorants and forskolin was increased by PKC. Experiments with deciliated olfactory tissue indicated that sensitization of AC was restricted to sensory cilia of ORCs. To study the effects of cell Ca2+ on these mechanisms, the intracellular Ca2+ concentration of olfactory tissue was either increased by ionomycin or decreased by BAPTA/AM. Increasing cell Ca2+ had two effects on cAMP production: (a) the basal cAMP production was enhanced by a mechanism sensitive to inhibitors of calmodulin; and (b) similar to phorbol ester, cell Ca2+ caused sensitization of AC to stimulation by forskolin, an effect sensitive to Goe 6983. Decreasing cell Ca2+ below basal levels rendered AC unresponsive to stimulation by forskolin. These data suggest that a crosstalk mechanism is functional in frog ORCs, linking the sensitivity of AC to the activity of PKC. At increased activity of PKC, olfactory AC becomes more responsive to stimulation by odorants, forskolin, and cell Ca2+. Neurotransmitters appear to use this crosstalk mechanism to regulate olfactory sensitivity.

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Agrawal, Smriti M., and Robert J. Omeljaniuk. "Levels of specifically bound [3H]ketanserin compared with levels of serotonin (5HT) in the brain regions of juvenile and sexually recrudescing female rainbow trout, Oncorhynchus mykiss." Canadian Journal of Physiology and Pharmacology 78, no. 3 (March 1, 2000): 228–36. http://dx.doi.org/10.1139/y99-135.

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This study compared the distribution of specifically bound [3H]ketanserin (Bsp) with serotonin (5HT) in brain regions of juvenile and sexually recrudescing female trout. Amounts of Bsp varied widely among brain regions and consistently differed between juvenile and sexually recrudescing females. Levels of Bsp were significantly greater in the hypothalamus than the olfactory lobe, which were at least threefold greater than in all other tissues examined (Kruskal-Wallis test, p < 0.05). Bsp densities in the hypothalamus, preoptic area, and optic lobe were significantly greater in juveniles compared with corresponding tissues from sexually recrudescing females (Mann-Whitney U test, p < 0.05); in contrast, Bsp in olfactory lobe and spinal cord did not differ significantly between the two classes of fish. 5HT concentration was determined by high performance liquid chromatography - electrochemical detection (HPLC-EC) analysis. Biogenic amine standards eluted in a stereotypic pattern, with peaks consistently separable in time. 5HT concentration was significantly greater in hypothalamus than in olfactory lobe and undetectable in the pituitary (Kruskal-Wallis test, p < 0.05). Trends in distribution of Bsp and 5HT were comparable in the hypothalamus and preoptic area in juvenile and sexually recrudescing females. In general, density of specific [3H]ketanserin binding sites was directly related to 5HT content of brain regions in juvenile and sexually recrudescing females. 5HT concentrations (pmol/g tissue) were approximately 900-fold greater than Bsp (fmol/g tissue) in all brain regions, and approximately 300-fold greater than Bsp in the olfactory lobe. These results suggest important regulatory role(s) for 5HT in the trout preoptic-hypothalamo-hypophysial axis, which may differ from 5HT role(s) in trout olfactory lobe.Key words: high performance liquid chromatography - electrochemical detection, [3H]ketanserin, sexually recrudescing female trout.

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Grosu-Bularda, Andreea, Claudiu Manea, and Ioan Lascar. "The role of olfactory ensheating cells in regenerative medicine: review of the literature." Romanian Journal of Rhinology 5, no. 18 (June 1, 2015): 75–80. http://dx.doi.org/10.1515/rjr-2015-0008.

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Abstract Olfactory ensheathing cells (OECs) join olfactory axons in their entrance to the central nervous system, representing a unique population of glial cells with functions in olfactory neurogenesis, axonal growth and olfactory bulb formation. Olfactory ensheathing cells have a great potential to induce repair for neural injuries, in central nervous system and peripheral nervous system, existing numerous experimental and clinical studies lately, reporting beneficial effects in anatomical and functional recovery. Studies are also conducted in order to establish possible pro-regenerative effects of the OECs, their potential in tissue repair and ability to modulate the immune system. The aim of this paper was to review the properties of olfactory ensheathing cells and their potential therapeutic role in regenerative medicine.

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Liu, Qingjun, Weiwei Ye, Hui Yu, Ning Hu, Liping Du, Ping Wang, and Mo Yang. "Olfactory mucosa tissue-based biosensor: A bioelectronic nose with receptor cells in intact olfactory epithelium." Sensors and Actuators B: Chemical 146, no. 2 (April 29, 2010): 527–33. http://dx.doi.org/10.1016/j.snb.2009.12.032.

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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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Smutzer, Gregory, John E. Zimmerman, Chang-Gyu Hahn, Delta D. Ruscheinsky, Amaris Rodrı́guez, Li-Ying Han, and Steven E. Arnold. "Inositol 1,4,5-trisphosphate receptor expression in mammalian olfactory tissue." Molecular Brain Research 44, no. 2 (March 1997): 347–54. http://dx.doi.org/10.1016/s0169-328x(96)00282-3.

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van Ginkel, F. W., J. R. McGhee, J. M. Watt, A. Campos-Torres, L. A. Parish, and D. E. Briles. "Pneumococcal carriage results in ganglioside-mediated olfactory tissue infection." Proceedings of the National Academy of Sciences 100, no. 24 (November 10, 2003): 14363–67. http://dx.doi.org/10.1073/pnas.2235844100.

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Say, Phillip, Donald Leopold, Gregory Cochran, Lynette Smith, and Tim Greiner. "Resection of the Inferior Superior Turbinate: Does it Affect Olfactory Ability or Contain Olfactory Neuronal Tissue?" American Journal of Rhinology 18, no. 3 (May 2004): 157–60. http://dx.doi.org/10.1177/194589240401800305.

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Lacroix, Marie-Christine, Monique Caillol, Didier Durieux, Régine Monnerie, Denise Grebert, Luc Pellerin, Cendrine Repond, Virginie Tolle, Philippe Zizzari, and Christine Baly. "Long-Lasting Metabolic Imbalance Related to Obesity Alters Olfactory Tissue Homeostasis and Impairs Olfactory-Driven Behaviors." Chemical Senses 40, no. 8 (July 23, 2015): 537–56. http://dx.doi.org/10.1093/chemse/bjv039.

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Bickle, Ian C. "Olfactory Neuroblastoma." Philippine Journal of Otolaryngology-Head and Neck Surgery 31, no. 1 (June 24, 2016): 65–66. http://dx.doi.org/10.32412/pjohns.v31i1.327.

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This 57 year-old woman presented with a seizure. She had a history of attending the ENT and neurosurgical departments for more than a decade. At the time of her initial presentation many years prior, her main complaint was of nasal congestion. A nasopharyngeal biopsy confirmed an olfactory neuroblastoma. Olfactory neuroblastoma is an uncommon slow growing tumour of the nasal cavity with no established etiological basis. With a neuroectodermal origin, it arises from the olfactory epithelium of the upper nasal cavity.1 Most cases arise from the cribriform plate, upper third of the nasal septum, superior turbinates or anterior ethmoidal air cells. However, it typically presents late when multiple structures are involved, which may include the orbits and intracranial compartments.2 Accounting for approximately 2% of sinonasal tumors, although often late to present, ironically only a minority of patients experience anosmia.3 The commonest complaint at initial presentation is nasal blockage accounting for nearly a quarter of cases, with headache and epistaxis the next most frequent symptoms.1 Multi-modality imaging is essential in that the most recognized management of this infrequent tumor is a combination of craniofacial surgery and radiotherapy. The imaging pathway in this case was typical, with CT and MRI complementing each other in maximizing tumor delineation. Computed Tomography has superior definition is reviewing bony involvement which is a typical finding, whereas MRI has superiority in evaluating the extent of soft tissue invasion and establishing tumor boundaries against post obstruction fluid in the paranasal sinuses.3 In this case the CT illustrates the gross destruction of the skull base, orbital and sinus margins. (Figure 1-4) The MRI outlines the extension of disease involving the pituitary fossa, brainstem and frontal sinus invasion. (Figures 5 and 6)

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Kim, Boo-Young, Ju Yeon Park, and EuiJin Kim. "Differences in Mechanisms of Steroid Therapy and Olfactory Training for Olfactory Loss in Mice." American Journal of Rhinology & Allergy 34, no. 6 (June 20, 2020): 810–21. http://dx.doi.org/10.1177/1945892420930945.

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Objective Steroid therapy and olfactory training are common treatments for olfactory loss. Systemic steroid treatment is the most effective approach for treating sinonasal olfactory loss. Olfactory training is typically effective for treating sensorineural olfactory loss. However, the differences in mechanisms of steroid therapy and olfactory training for olfactory dysfunction are unclear. The aim of this study was thus to evaluate the differences in mechanisms of olfactory training and steroid therapy. Subjects and Methods Mice in each group were administered 3-methylindole at a dose of 300 mg/kg. Olfactory function was evaluated with a food-finding test once a week. The olfactory neuroepithelium was harvested for histologic examination and protein analysis. Subsequently, data analysis, gene ontology and pathway analysis, quantitative real-time polymerase chain reaction of mRNA, and western blot analysis were conducted. Results Mice were divided into four groups according to treatment. Control, anosmia, training, and steroid groups resumed food-finding. MMP27, CCL22 and IL18rap mRNA expression were significantly increased in the training group compared to that in the steroid group. IL1R2 mRNA expression was significantly higher in the olfactory neuroepithelium of steroid-treated mice than in that of the training group mice. Conclusions Steroid therapy improved olfactory function via anti-inflammatory effects, unlike olfactory training which involved cell regeneration and tissue remodeling. Protein and gene analyses revealed that steroid therapy and olfactory training are underpinned by distinct mechanisms. Selection of the most appropriate treatment will be dependent on the cause of olfactory loss.

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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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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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Warner, M., P. Tollet, M. Strömstedt, K. Carlström, and J. Å. Gustafsson. "Endocrine regulation of cytochrome P-450 in the rat brain and pituitary gland." Journal of Endocrinology 122, no. 1 (July 1989): 341–49. http://dx.doi.org/10.1677/joe.0.1220341.

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ABSTRACT In an effort to understand the physiological functions of cytochrome P-450 in the central nervous system and pituitary gland, we evaluated changes in the level of the enzyme as a function of the endocrine status of rats and the ability of these tissues to synthesize or degrade steroids. The P-450 content of microsomes prepared from the hypothalamic preoptic area (HPOA), the olfactory lobes and the cerebrum was 0·040 ± 0·009 and in the pituitary gland 2·2 ± 0·6 (s.d.) nmol/g tissue. The P-450 content of the HPOA and olfactory lobes, but not of the rest of the cerebrum, was influenced by the endocrine status of rats. In microsomes it increased five- to tenfold over control levels during late pregnancy in the olfactory lobes and during lactation in the HPOA, and in both brain regions treatment of rats with 5α-dihydrotestosterone (DHT) caused an eight- to tenfold increase in the P-450 content. Androstenedione was not a good substrate for brain P-450. The level of androstenedione 19-hydroxylase in the olfactory lobe microsomal fraction was 0·50± 0·06 nmol 19-hydroxyandrostenedione formed/g tissue per h. This activity was tenfold lower in other brain areas and was not detectable in the pituitary gland. The rate of aromatization of androstenedione to oestradiol in the HPOA and olfactory lobe of lactating rats was 0·46 ± 0·14 and 0·38 ± 0·05 pmol/oestradiol formed/g tissue per h respectively. 5α-Androstane-3β,17β-diol (A-5α-3β,17β-diol) was a much better substrate for P-450 throughout the brain and pituitary gland. Catalytic activity was 125 ± 46 and 307 ±108 nmol triols formed/g tissue per h in the brain and pituitary gland respectively. The P-450 responsible for this catalytic activity was isolated and its substrate specificity examined. In addition to A-5α-3β,17β-diol, 5-androstene-3β,17β-diol, dehydroepiandrosterone and DHT were also substrates, with turnover numbers of 27, 8, 12 and 1 mol product/mol P-450 per min respectively. None of these catalytic activities was induced in the rat brain during pregnancy, lactation or DHT treatment. The enzyme was also present in the brains of mice but not guinea-pigs. The yield of P-450 from the mitochondrial fraction of the HPOA and olfactory lobes in control rats was 0·01–0·02 nmol/g tissue. This increased tenfold during pregnancy. Immunological evidence for the presence of the cholesterol side-chain cleavage enzyme P-450 SCC was found in the HPOA and olfactory lobes of pregnant but not of control rats. However, no SCC catalytic activity was detectable in these brain mitochondrial P-450 fractions. From these studies we conclude that there is a major influence of the endocrine system on the content and quality of P-450 in the brain. However, the function and substrate specificities of these P-450s as well as of those in the pituitary gland remain to be characterized. Journal of Endocrinology (1989) 122, 341–349

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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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Smutzer, Gregory, Virginia M. Y. Lee, John Q. Trojanowski, and Steven E. Arnold. "Human Olfactory Mucosa in Schizophrenia." Annals of Otology, Rhinology & Laryngology 107, no. 4 (April 1998): 349–55. http://dx.doi.org/10.1177/000348949810700415.

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Recent evidence indicates that developmental anomalies may underlie some symptoms of schizophrenia, while psychophysical studies have demonstrated olfactory deficits in this disease. The postmortem olfactory mucosa of elderly schizophrenic patients was examined to characterize the molecular phenotype of this tissue. The distribution of developmentally regulated cytoskeletal proteins, a synaptic vesicle protein, a neural marker protein, a receptor for trophic molecules, axonal guidance and cell migration proteins, and neuronal and glial cytoskeletal proteins of various degrees of phosphorylation was examined by immunohistochemistry. Both schizophrenic and control subjects exhibited dystrophic neurites that were immunoreactive for synaptophysin, microtubule-associated proteins (MAP1B), and neurofilament proteins. No major histochemical or morphologic differences in either the expression or distribution of these proteins were observed in the olfactory epithelium of schizophrenic compared to control subjects. These studies indicated that dystrophic neurites frequently occurred in the olfactory mucosa of both schizophrenics and neurologically normal adults. The absence of major immunocytochemical abnormalities suggested that olfactory deficits in schizophrenia may be due to more subtle cellular or molecular differences or to abnormalities in olfactory regions of the central nervous system rather than in the olfactory epithelium.

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Kudrycki, K., C. Stein-Izsak, C. Behn, M. Grillo, R. Akeson, and F. L. Margolis. "Olf-1-binding site: characterization of an olfactory neuron-specific promoter motif." Molecular and Cellular Biology 13, no. 5 (May 1993): 3002–14. http://dx.doi.org/10.1128/mcb.13.5.3002.

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We report characterization of several domains within the 5' flanking region of the olfactory marker protein (OMP) gene that may participate in regulating transcription of this and other olfactory neuron-specific genes. Analysis by electrophoretic mobility shift assay and DNase I footprinting identifies two regions that contain a novel sequence motif. Interactions between this motif and nuclear proteins were detected only with nuclear protein extracts derived from olfactory neuroepithelium, and this activity is more abundant in olfactory epithelium enriched in immature neurons. We have designated a factor(s) involved in this binding as Olf-1. The Olf-1-binding motif consensus sequence was defined as TCCCC(A/T)NGGAG. Studies with transgenic mice indicate that a 0.3-kb fragment of the OMP gene containing one Olf-1 motif is sufficient for olfactory tissue-specific expression of the reporter gene. Some of the other identified sequence motifs also interact specifically with olfactory nuclear protein extracts. We propose that Olf-1 is a novel, olfactory neuron-specific trans-acting factor involved in the cell-specific expression of OMP.

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Kudrycki, K., C. Stein-Izsak, C. Behn, M. Grillo, R. Akeson, and F. L. Margolis. "Olf-1-binding site: characterization of an olfactory neuron-specific promoter motif." Molecular and Cellular Biology 13, no. 5 (May 1993): 3002–14. http://dx.doi.org/10.1128/mcb.13.5.3002-3014.1993.

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We report characterization of several domains within the 5' flanking region of the olfactory marker protein (OMP) gene that may participate in regulating transcription of this and other olfactory neuron-specific genes. Analysis by electrophoretic mobility shift assay and DNase I footprinting identifies two regions that contain a novel sequence motif. Interactions between this motif and nuclear proteins were detected only with nuclear protein extracts derived from olfactory neuroepithelium, and this activity is more abundant in olfactory epithelium enriched in immature neurons. We have designated a factor(s) involved in this binding as Olf-1. The Olf-1-binding motif consensus sequence was defined as TCCCC(A/T)NGGAG. Studies with transgenic mice indicate that a 0.3-kb fragment of the OMP gene containing one Olf-1 motif is sufficient for olfactory tissue-specific expression of the reporter gene. Some of the other identified sequence motifs also interact specifically with olfactory nuclear protein extracts. We propose that Olf-1 is a novel, olfactory neuron-specific trans-acting factor involved in the cell-specific expression of OMP.

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Reed, C. J., E. A. Lock, and F. De Matteis. "Olfactory cytochrome P-450. Studies with suicide substrates of the haemoprotein." Biochemical Journal 253, no. 2 (July 15, 1988): 569–76. http://dx.doi.org/10.1042/bj2530569.

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1. The olfactory epithelium of male hamsters has been found to be extremely active in the cumene hydroperoxide-supported oxidation of tetramethylphenylenediamine, and this peroxidase activity has been shown to be cytochrome P-450-dependent. 2. The interaction of a series of suicide substrates of cytochrome P-450 with the hepatic and olfactory mono-oxygenase systems has been assessed by determination of peroxidase, 7-ethoxycoumarin O-de-ethylase (ECOD) and 7-ethoxyresorufin O-de-ethylase (EROD) activities after treatment in vivo with these compounds. Chloramphenicol, OOS-trimethylphosphorothiolate and two dihydropyridines [DDC (3,5-diethoxycarbonyl-1,4-dihydrocollidine) and 4-ethyl DDC (3,5-diethoxycarbonyl-4-ethyl-1,4-dihydro-2,6-dimethylpyridine)] all caused similar percentage inhibitions of hepatic and olfactory activities, but the absolute amounts of enzymic activity lost were considerably greater in the latter tissue. In contrast, halothane had little effect upon hepatic cytochrome P-450-dependent reactions, whereas it severely inhibited those of the olfactory epithelium. 3. The time course of loss and recovery of hepatic and olfactory peroxidase, ECOD and EROD activities after a single dose of 4-ethyl DDC was studied. The rates of loss of activity observed were very similar, irrespective of tissue or reaction examined. In the olfactory epithelium, all three activities recovered concurrently and at a rate similar to that of the hepatic peroxidase activity. In contrast, the hepatic de-ethylation of 7-ethoxycoumarin and 7-ethoxy-resorufin recovered significantly more rapidly. 4. It is suggested that this behaviour is due to 4-ethyl DDC acting not only as a suicidal inhibitor but also as an inducer of certain forms of cytochrome P-450 in the liver; in the olfactory epithelium, however, inactivation, but not induction, occurs. Classical inducing agents were reported to have no effect upon olfactory cytochrome P-450, and in the present study neither phenobarbitone nor beta-naphthoflavone treatment had any effect upon olfactory cytochrome P-450-dependent reactions, although it induced those of the liver.

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Camargo, Antonio P., Thiago S. Nakahara, Luiz E. R. Firmino, Paulo H. M. Netto, João B. P. do Nascimento, Elisa R. Donnard, Pedro A. F. Galante, Marcelo F. Carazzolle, Bettina Malnic, and Fabio Papes. "Uncovering the mouse olfactory long non-coding transcriptome with a novel machine-learning model." DNA Research 26, no. 4 (July 18, 2019): 365–78. http://dx.doi.org/10.1093/dnares/dsz015.

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Abstract Very little is known about long non-coding RNAs (lncRNAs) in the mammalian olfactory sensory epithelia. Deciphering the non-coding transcriptome in olfaction is relevant because these RNAs have been shown to play a role in chromatin modification and nuclear architecture reorganization, processes that accompany olfactory differentiation and olfactory receptor gene choice, one of the most poorly understood gene regulatory processes in mammals. In this study, we used a combination of in silico and ex vivo approaches to uncover a comprehensive catalogue of olfactory lncRNAs and to investigate their expression in the mouse olfactory organs. Initially, we used a novel machine-learning lncRNA classifier to discover hundreds of annotated and unannotated lncRNAs, some of which were predicted to be preferentially expressed in the main olfactory epithelium and the vomeronasal organ, the most important olfactory structures in the mouse. Moreover, we used whole-tissue and single-cell RNA sequencing data to discover lncRNAs expressed in mature sensory neurons of the main epithelium. Candidate lncRNAs were further validated by in situ hybridization and RT-PCR, leading to the identification of lncRNAs found throughout the olfactory epithelia, as well as others exquisitely expressed in subsets of mature olfactory neurons or progenitor cells.

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Wu, Chunsheng, Peter B. Lillehoj, and Ping Wang. "Bioanalytical and chemical sensors using living taste, olfactory, and neural cells and tissues: a short review." Analyst 140, no. 21 (2015): 7048–61. http://dx.doi.org/10.1039/c5an01288k.

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Hauser, Roman, Marek Wiergowski, Michał Kaliszan, Tomasz Gos, Gerhard Kernbach-Wighton, Michał Studniarek, Zbigniew Jankowski, and Jacek Namieśnik. "Olfactory and tissue markers of fear in mammals including humans." Medical Hypotheses 77, no. 6 (December 2011): 1062–67. http://dx.doi.org/10.1016/j.mehy.2011.09.003.

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BLAND, ROSEMARY, STAN LOVETT, and GEORGE H. DODD. "Studies on the role of ascorbic acid in olfactory tissue." Biochemical Society Transactions 20, no. 2 (May 1, 1992): 199S. http://dx.doi.org/10.1042/bst020199s.

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Qasba, Pankaj, and Randall R. Reed. "Tissue and Zonal-Specific Expression of an Olfactory Receptor Transgene." Journal of Neuroscience 18, no. 1 (January 1, 1998): 227–36. http://dx.doi.org/10.1523/jneurosci.18-01-00227.1998.

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Hauser, Leah J., Rakesh K. Chandra, Ping Li, and Justin H. Turner. "Role of tissue eosinophils in chronic rhinosinusitis-associated olfactory loss." International Forum of Allergy & Rhinology 7, no. 10 (July 25, 2017): 957–62. http://dx.doi.org/10.1002/alr.21994.

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Steele, K. E., K. J. Davis, K. Stephan, W. Kell, P. Vogel, and M. K. Hart. "Comparative Neurovirulence and Tissue Tropism of Wild-type and Attenuated Strains of Venezuelan Equine Encephalitis Virus Administered by Aerosol in C3H/HeN and BALB/c Mice." Veterinary Pathology 35, no. 5 (September 1998): 386–97. http://dx.doi.org/10.1177/030098589803500508.

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To assess the potential for aerosol administration of vaccines for Venezuelan equine encephalitis virus (VEE), we compared the neurovirulence and tissue tropism of the wild-type Trinidad donkey (TrD) strain to those of the attenuated TC83 and V3526 strains of VEE in mice. Six to 8-week-old female C3H/HeN and BALB/c mice were aerosol exposed to one of the three VEE strains. Three mice of each strain were euthanatized at different times and their tissues were processed and stained using hematoxylin and eosin, immunohistochemistry, and in situ hybridization. All three viral strains infected the brains of mice and induced encephalitis. TrD spread caudally from the olfactory bulbs to all regions of the brain, caused widespread necrotizing panencephalitis by day 5, and resulted in 100% mortality (geometric mean = 7 days) in both mouse strains. By comparison, TC83 relatively spared the caudal regions of the brain but still caused 100% mortality in the C3H/HeN mice (geometric mean = 12 days), yet it did not kill any BALB/c mice. V3526 infectivity of the brain was the most limited, mainly affecting the neocortex and diencephalon. This virus was not lethal in either mouse strain. The TrD strain also infected the olfactory neuroepithelium, local lymphoid tissues, teeth, and vomeronasal organs, whereas the affinity of TC83 and V3526 outside the brain was essentially limited to the olfactory neuroepithelium. Attenuated VEE strains administered to mice by aerosol have restricted tissue tropism as compared with wild-type virus; however, even attenuated strains can infect the brain and induce encephalitis.

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Liadi, Modinat, Andrew Collins, Ying Li, and Daqing Li. "The Impact of Tissue Storage Conditions on Rat Olfactory Ensheathing Cell Yield and the Future Clinical Implications." Cell Transplantation 27, no. 9 (August 10, 2018): 1320–27. http://dx.doi.org/10.1177/0963689718787762.

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Trauma causes spinal cord injury, and the devastating consequences of the injury are due to the failure of the damaged central nervous system (CNS) axons to regenerate. Previous studies have shown that olfactory ensheathing cells (OECs) are a unique type of glial cell and they can promote regeneration of CNS axons to aid recovery after spinal cord injury. Transplantation of OECs, in particular from the olfactory bulb (OB), is considered one of the most promising therapeutic strategies for the repair of CNS injuries, including spinal cord injury. Transplantation of OECs can be autologous or allogenic. Here we focused on the less invasive and more error-proof allograft approach which needs a collection of donor OB tissue for OEC production. In this study, we investigated the effects on the yield and proportions of OECs and olfactory nerve fibroblasts (ONFs) from storing OB tissue in various media for periods of 24 and 48 hours. The OEC yield contributes to the viability of a successful cell transplant. We concluded that storing OB tissue for a period longer than 24 hours negatively impacted the total cell number and subsequently the OEC population. This study provides useful information for future clinical applications.

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Ghosh, Saroj Kumar. "The morphohistology and fine anatomy of the olfactory organ in pabda catfish, Ompok bimaculatus (Bloch, 1794)." Our Nature 18, no. 1 (December 30, 2020): 10–15. http://dx.doi.org/10.3126/on.v18i1.34237.

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The organization of the olfactory system in Ompok bimaculatus (Siluriformes: Siluridae) were investigated by histological and ultrastructural analysis. The nasal chamber was totally engrossed by a boat shaped elongated olfactory rosette with numerous lamella. Histomicroscopically, each lamella was comprised of central core bounded on both sides by the cellular elements of olfactory epithelium. The central core was composed of thick connective tissue, nerve fibres and blood capillaries. The cellular components of the olfactory epithelium were identified based on their staining vigour, architecture, structural characteristics and surface features. The sensory epithelium contained morphologically recognizable ciliated, microvillous and rod receptor neurons. Labyrinth cells, scattered lymphatic cells, secretory mucous cells, stratified epithelial cells bearing microfolds and condensed ciliated supporting cells were observed in the indifferent epithelia. The basal cells were submerged in the deeper zone of mucosa above the basal lamina. Different sensory and nonsensory cells of the olfactory lining were associated with chemical stimulation of the fish studied. This species acquires a well developed olfactory sense for exploring the aquatic environment and able to determine the chemical changes in the surroundings.

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Greer, Charles A., Juan C. Bartolomei, and Jeffrey M. Dembner. "Organization of primary afferent and local-circuit synapses in the olfactory glomerulus." Proceedings, annual meeting, Electron Microscopy Society of America 52 (1994): 148–49. http://dx.doi.org/10.1017/s0424820100168475.

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Odorant molecules are transduced by olfactory receptor cells whose axons join to form the olfactory nerve which distributes across the surface of the olfactory bulb (OB). Axons exit the nerve layer to terminate within the glomerular neuropil of the OB. While there appears a gross topography between the epithelium and OB4, it is clear that extensive topographic reorganization of axons occurs within the olfactory nerve. To better understand the mechanisms that may contribute to the establishment of glomerular-specific fascicles and functional domains within the OB, we have investigated axonal organization within the nerve and the intraglomerular distribution of primary afferent synapses using light, confocal and electron microscopy.Sprague-Dawley rats, 30 to 50 days postnatal, were anesthetized, lightly perfused with 0.9% NaCl and the OBs removed. Crystals of the lipophilic dye, Dil, were inserted into the olfactory nerve layer and the tissue placed in 4% paraformaldehyde at room temperature for 10 - 30 days.

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Mezler, M., S. Konzelmann, J. Freitag, P. Rossler, and H. Breer. "Expression of olfactory receptors during development in Xenopus laevis." Journal of Experimental Biology 202, no. 4 (February 15, 1999): 365–76. http://dx.doi.org/10.1242/jeb.202.4.365.

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A coordinated expression of tissue- and cell-specific genes during development is required to establish the complex functional organization of the vertebrate olfactory system. Owing to the unique features of its olfactory system and the well-characterized phases of its development, Xenopus laevis was chosen as a model organism to study the onset and the temporal and spatial patterns of expression of olfactory-specific genes. Using RT-PCR and in situ hybridization, it was found that expression of Xenopus olfactory marker protein and of class I receptors, which are thought to be responsible for the perception of water-soluble odorants, was detectable as early as stage 32, less than 2 days after fertilization. In contrast, expression of class II receptors, which are thought to recognize airborne odours, was not detected before stage 49, approximately 12 days after fertilization. The results indicate that the expression of olfactory receptors and marker protein is governed by temporally regulated cues during development.

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Vogt, R. G., S. M. Lindsay, C. A. Byrd, and M. Sun. "Spatial patterns of olfactory neurons expressing specific odor receptor genes in 48-hour-old embryos of zebrafish Danio rerio." Journal of Experimental Biology 200, no. 3 (February 1, 1997): 433–43. http://dx.doi.org/10.1242/jeb.200.3.433.

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Olfactory neurons have a complex phenotype characterized by their expression of a specific odor receptor (OR) gene and their targeting of an equally specific locus in the olfactory bulb. In the adult fish, olfactory neurons expressing specific ORs are broadly distributed in the epithelium, intermingling with neurons expressing other OR phenotypes. This distributed adult pattern has led to the suggestion that olfactory neuron phenotype is determined by a stochastic process, independent of external positional cues. However, when the fish olfactory system is established during embryogenesis it is simple in its organization, with few olfactory neurons and an olfactory epithelium that has not yet folded into the adult morphology. It is possible that positional cues might act in the embryo to establish an initial population and pattern of olfactory neuron phenotypes and that subsequent morphogenesis and neuronal addition lead to the randomized distribution of neurons. To test this possibility, we examined the spatial patterns of olfactory neurons expressing specific OR genes in 48 h embryos, a time of relative simplicity in the developing olfactory epithelium. Three-dimensional plots of neuron distributions were made, and comparison of OR expression patterns were made between right and left epithelia, between individual animals and between different OR genes. The patterns of OR gene expression were not conserved in these comparison. Mathematical analysis of 21 epithelia for the degree of order in the distribution of olfactory neurons argued strongly that the neurons expressing given ORs are randomly distributed in the 48 h embryos. These results are consistent with those observed from adult tissue and support models suggesting that extrinsic positional cues do not have a major role in specifying olfactory neuron phenotypes.

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Journal articles on the topic 'Olfactory tissue'

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