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The role of inflammatory mediators in the pathogenesis of nasal polyposis: Literature review

cells are at the interface of innate and adaptive immunity. Curr Opin Immunol., 2007;19(6):711-720. 10. Di Lorenzo G., Drago A., Esposito Pellitteri M., Candore G., Colombo A., Gervasi F., Pacor M.L., Purello D’Ambrosio F., Caruso C. - Measurement of inflammatory mediators of mast cells and eosinophils in native nasal lavage fluid in nasal polyposis. Int Arch Allergy Immunol., 2001;125(2):164-175. 11. Erbek S.S., Yurtcu E., Erbek S., Atac F.B., Sahin F.I., Cakmak O. - Proinflammatory cytokine single nucleotide polymorphisms in nasal

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Polcalcins as pollen panallergens in allergic rhinitis

Abstract

Polcalcins are highly cross-reactive calcium-binding allergen components specifically expressed in pollen from trees, grasses and weeds. The grass allergen component rPhl p 7, a recombinant non-glycosylated calcium-binding protein of 2-EF-hand type, is the most cross-reactive polcalcin and may be used as a polcalcin biomarker of IgE-mediated hypersensitivity. Polcalcin sensitization, which appears to be linked to geographical factors, level and time of pollen exposure, has to be assessed in allergic rhinitis patients with multiple pollen sensitizations and may be useful for a better targeted prescription of allergen immunotherapy.

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The cranial nerve zero – mini review

Abstract

The terminal nerve (cranial nerve zero, cranial nerve XIII, the nerve “N”) was discovered in fish in 1894. In the early 90’s, it was found in human embryos and human adults. In the anterior fossa, it courses on the inner side of the olfactory tract and bulb; it then spreads fibers through the cribriform plate to distribute beneath the nasal septum mucosa. Being provided with intrinsic ganglion cells, its functions are weakly suggested by studies in different species. It may be connected with the visual system, it could act upon the intracranial vascular system, or it could ensure the pathway for pheromone-mediated behaviours. The cranial nerve zero deserves a better attention equally from anatomists and ENT specialists.

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Hereditary angioedema - an otolaryngologist’s perspective

Abstract

Hereditary angioedema (HAE) is a rare autosomal dominant disease consisting of recurrent angioedema attacks, varying in severity, possibly life-threatening and with frequent involvement of the head and neck areas. The patophysiology of HAE differs from histamine-mediated allergic angioedema. Three types of reduced quality or quantity in various complement or coagulation factors, leading to massive release of bradykinin, increase vascular permeability and produce capilary leakage. Clinical manifestations of HAE include swelling located predominantly in the head and neck area, hands, feet and urogenital area and abdominal pain caused by edema of the gastrointestinal tract mucosa. Diagnosis requires laboratory tests for complement components and genetic tests. A timely and correct diagnosis in the emergency room is of utmost importance, the medical treatment of HAE being substantially different from that of allergic angioedema. Although new therapies are available and in development, airway intervention and surgery are still life-saving procedures and the ENT surgeon is an important part of the multidisciplinary team managing an HAE attack.

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A paradigm shift: “Defect of the fontanel” instead of “Accessory ostium” and classified nasal septal deformities instead of “septal deviation”

. International Consensus Statement on Allergy and Rhinology: Rhinosinusitis. Int Forum Allergy Rhinol. 2016;6 Suppl 1:S22-209. DOI: 10.1002/alr.21695. 9. Mladina R, Skitarelić N, Carić T, Raguž M. Type 5 and 6 nasal septal deformities: Could we predict and prevent acute coronary syndrome attacks in the future? Med Hypotheses. 2015;85(5):640-4. DOI: 10.1016/j.mehy.2015.08.001. 10. Liang P, Xu Y, Zhang X, Ding C, Huang R, Zhang Z, et al. CRISPR/Cas9-mediated gene editing in human tripronuclear zygotes. Protein Cell. 2015;6(5):363-72. DOI: http://dx.doi.org/10.1007/s

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Endoscopic and histological staging: Deciding factors in the treatment of chronic rhinosinusitis

HMGB1 protein in chronic rhinosinusitis with nazal polyposis - is it a real proinflammatory mediator? Romanian Journal of Rhinology, 2013;3(10):71-80. 12. Fransson M., Benson M., Wennergren G., Cardell L.O. - A role for neutrophils in intermittent allergic rhinitis. Acta Otolaryngol., 2004 Jun;124(5):616-620. 13. Bellussi L.M., Chen L., Chen D., Passali F.M., Passali D. - The role of high mobility group box 1 chromosomal protein in the pathogenesis of chronic sinusitis and nasal polyposis Acta Otorhinolaryngol Ital., 2012

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Oxidative stress-related pathophysiology in chronic rhinosinusitis with nasal polyps: research challenges

. Free radicals in nasal and paranasal diseases. In: Miller J, Le Prell CG, Rybak L, editors. Free radicals in ENT pathology. Humana Press; 2015, p.479–92. 13. Esmatinia F, Bakhshaei M. Recurrent sinonasal polyposis after the endoscopic sinus surgery. Rev Clin Med. 2014;1(2):86-92. DOI: 10.17463/RCM.2014.02.010. 14. Burgess A, Shah K, Hough O, Hynynen K. Focused ultrasound-mediated drug delivery through the blood-brain barrier. Expert Rev Neurother. 2015;15(5):477–91. DOI: 10.1586/14737175.2015.1028369. 15. Cheng YK, Hwang GY, Lin CD, Tsai MH, Tsai SW

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Multicentric study on the efficacy and tolerability of Streptococcus salivarius 24SMB and Streptococcus oralis 89a in respiratory tract infections

-Yochay G, Trzcinski K, Thompson CM, Malley R, Lipsitch M. Interference between Streptococcus pneumoniae and Staphylococcus aureus: in vitro hydrogen peroxide-mediated killing by Streptococcus pneumoniae. J Bacteriol. 2006;188(13):4996–5001. DOI: 10.1128/JB.00317-06. 4. Dobson A, Cotter PD, Ross RP, Hill C. Bacteriocin production: a probiotic trait? Appl Environ Microbiol. 2012;78(1):1–6. DOI: 10.1128/AEM.05576-11. Epub 2011 Oct 28. 5. Dillon RJ, Vennard CT, Buckling A, Charnley AK. Diversity of locust gut bacteria protects against pathogen invasion. Ecol Lett

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Olfaction and traumatic head injury - Is it possible to discriminate between malingering and patients with smell disorders based on nowadays knowledge?

;41(23):7241-7252. doi: 10.1021/bi015916c. 9. Larsson M., Backman L. - Modality memory across the adult life span: evidence for selective age-related olfactory deficits. Exp Aging Res., 1998;24(1):63-82. doi: 10.1080/036107398244364. 10. Hummel T., Futschik T., Frasnelli J., Huttenbrink K.B. - Effects of olfactory function, age, and gender on trigeminally mediated sensations: a study based on the lateralization of chemosensory stimuli. Toxicol Lett., 2003;140-141:273-280. 11. Hummel T. - Assessment of intranasal trigeminal function. Int

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Cystic fibrosis - general review on sinonasal complications and case report

chronic sinus diseases by measurement of inflammatory mediators. Allergy, 2006;61(11):1280–1289. 15. Welsh M.J., Smith A.E. - Molecular mechanisms of CFTR chloride channel dysfunction in cystic fibrosis. Cell, 1993;73(7):1251–1254. 16. Accurso F.J., Rowe S.M., Clancy J.P., et al. - Effect of VX-770 in persons with cystic fibrosis and the G551D-CFTR mutation. N Engl J Med., 2010;363(21):1991–2003. doi: 10.1056/NEJmoa0909825. 17. Gan K.H., Veeze H.J., van den Ouweland A., et al. - A cystic fibrosis mutation associated with mild lung disease. N Engl J Med

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