コーパス検索結果 (1語後でソート)
通し番号をクリックするとPubMedの該当ページを表示します
1 ncluding mechanical stimulation and chemical irritants.
2 iggers such as allergens, microorganisms and irritants.
3 and the presence of inhalable pollutants and irritants.
4 tinel for structurally diverse electrophilic irritants.
5 f environmental exposures like allergens and irritants.
6 ough and a heightened sensitivity to inhaled irritants.
7 ether with neurons to identify itch-inducing irritants.
8 airway defense against inhaled pathogens and irritants.
9 of different weak sensitizers / addition of irritants.
10 econd study focused on EHR use and daily EHR irritants.
11 to a plethora of pathogens and environmental irritants.
12 eference contact allergens and nonallergenic irritants.
13 in increased penetrability to allergens and irritants.
14 xposure to allergens, pathogens, or chemical irritants.
15 rs chronically exposed to moderate levels of irritants.
16 after chronic exposure to moderate levels of irritants.
17 ons or exposure to allergic and non-allergic irritants.
18 hagous fluids, environmental xenobiotics and irritants.
19 ent of TRPA1, a key sensor for environmental irritants.
20 matory responses to cutaneous and peritoneal irritants.
21 y airway exposures to allergens and chemical irritants.
22 ell as environmental and endogenous chemical irritants.
23 pungent natural compounds and environmental irritants.
24 y for behavioral responses to these chemical irritants.
25 nd mediates behavioral responses to chemical irritants.
26 pungent natural compounds, and environmental irritants.
27 ion of nociceptors by endogenous and natural irritants.
28 mach less susceptible to damage from luminal irritants.
29 lvents, welding fumes, and other respiratory irritants.
30 hich respond to numerous odorants as well as irritants.
31 tinocytes treated with certain allergens and irritants.
32 es to protect the host against pathogens and irritants.
33 oxyethylene) ammonium chloride (ITDOP); mild irritants: 5% 3-decyloxypropyl-bis(polyoxyethylene) amin
35 o enhance permeability and susceptibility to irritants; accordingly, increased attention should be gi
36 rritation response in mice elicited by smoke irritants (acrolein, acetic acid, and cyclohexanone).
38 ral, bacterial, and nonmicrobial (toxins and irritants) agents, resulting in production of many diffe
40 rosols with increasing doses of the chemical irritants allyl isothiocyanate (AITC; also known as must
42 s can affect airway inflammatory response to irritants and allergens, but the importance of stress in
44 uction machinery through which environmental irritants and endogenous proalgesic agents depolarize no
46 cautions should be taken against respiratory irritants and molds and to prevent children from becomin
50 tion following long-term exposure to harmful irritants and pollutants, particularly in the airways.
51 el is the molecular target for environmental irritants and pungent chemicals, such as cinnamaldehyde
53 catnip and nepetalactone as insect-selective irritants and suggest that, despite TRPA1's broad conser
57 t recognize pathogens, chemical and physical irritants, and damaged cells subsequently initiating a w
58 associated molecular patterns, environmental irritants, and endogenous stimuli released from dying ce
59 host from toxins, xenobiotics, environmental irritants, and helminthic parasites, and (3) IgE-stimula
60 er that allows the penetration of allergens, irritants, and microbes into a cutaneous milieu that fac
62 of the circadian clock, escape responses to irritants, and multi-parameter day-night locomotor behav
63 PCR analyses of multiple chemical allergens, irritants, and non-sensitizers have identified 10 genes
64 entions to reduce exposures to allergens and irritants, and research on the underlying mechanisms tha
65 unters with allergens, pathogens, wounds and irritants, and to react more quickly to the next experie
66 multiple symptomatic high-level exposures to irritants; and (iii) possible IIA, that is asthma occurr
68 ctivated by noxious heat, acid, and alkaloid irritants as well as several endogenous ligands and is s
69 to a wide spectrum of noxious electrophilic irritants, as well as cold, heat, and mechanosensation.
71 side' world from potentially harmful toxins, irritants, bacteria and other pathogens that also exist
72 gions in the mouth are uniquely sensitive to irritants because they can penetrate through the tissue
73 s sensory detection of pathogens, toxins and irritants; breakdown of the epithelial barrier is associ
74 ubstances, toxins, venoms, and environmental irritants but that also trigger exuberant allergic react
75 diverse array of environmental and microbial irritants by forming the barrier of epithelial cells int
78 rs after treatment, mild and moderate ocular irritants caused a significant increase in corneal thick
79 he epithelium, whereas the mild and moderate irritants caused complete epithelial cell loss with incr
81 nflammation via hapten-specific T cells) and irritants (chemicals that are toxic to epidermal cells).
83 and bulb may provide an avenue whereby nasal irritants could affect processing of coincident olfactor
84 nasal epithelium, requiring that trigeminal irritants diffuse through the junctional barrier at the
85 s are activated by noxious stimuli including irritants (e.g. TRPV1 agonist capsaicin) and inflammator
86 ave been identified, including environmental irritants (e.g., acrolein) and ingredients of pungent na
87 (e.g., allyl isothiocyanate), environmental irritants (e.g., acrolein), and endogenous ligands (4-hy
88 nerve endings can detect certain lipophilic irritants (e.g., mints, ammonia), the epithelium also ho
93 s, microbial products and sterile endogenous irritants governs whether the outcome will be with suppr
97 oreign organisms, damaged cells and physical irritants; however, inappropriately triggered or sustain
98 o screen the existence of gingivitis and its irritants, i.e., dental calculus and soft deposits, from
99 vironmental and occupational sensitizers and irritants in its pathogenesis and the interaction with b
101 exposed to a range of physical and chemical irritants in the environment that are known to trigger a
103 igeminally mediated reflex reactions to some irritants including acyl-homoserine lactone bacterial qu
104 rrier to allergens as well as other external irritants including infectious agents, and atmospheric p
106 where it acts as a sensor for environmental irritants, including acrolein, and some pungent plant in
108 nd to contain significantly more respiratory irritants, including NO(x), CO, and CO(2), and a larger
109 ensor for structurally diverse electrophilic irritants, including small volatile environmental toxica
110 mediators and to a diverse array of volatile irritants, including those found in tear gas and garlic.
114 ature of bronchial asthma, and inhalation of irritants may facilitate development of nonallergic AHR.
116 , but not prevented, by elimination of local irritants, meticulous oral hygiene, and regular periodon
117 ave examined in vivo and in vitro effects of irritants, most focused on events developing hours to da
119 itial management includes avoiding causative irritants or allergens (e.g., by wearing impermeable glo
121 s) may increase the risk of LRI by acting as irritants or through increasing susceptibility to infect
122 and clears the airways and lungs of inhaled irritants, particulates, pathogens, and accumulated secr
125 eated skin contact with contact allergens or irritants, resulting in allergic contact dermatitis (ACD
126 endogenous danger signals and environmental irritants, resulting in the formation and activation of
128 ess C5aRs and that exposure to environmental irritants such as cigarette smoke modulates the expressi
131 de range of allergens, infectious agents and irritants (such as pollutants) occurring indoors and out
132 s and responds to a wide variety of chemical irritants, such as acrolein in smoke or isothiocyanates
134 This contrasts with most other common oral irritants, such as cinnamaldehyde, capsaicin, and alcoho
137 ildren are exposed to multiple environmental irritants, such as viruses and allergens, that are commo
138 emically disparate animal- and plant-derived irritants target the same key allosteric regulatory site
139 cle beginning on page 2574), have identified irritants that activate transient receptor potential cat
143 can be activated by exogenous electrophilic irritants through direct covalent modification, we reaso
144 ized epithelial chemosensors that respond to irritants through the canonical taste transduction casca
145 vivo CM revealed corneal injury with slight irritants to be restricted to the epithelium, whereas th
146 ted by reactive environmental and endogenous irritants to initiate pain perception, local inflammatio
147 Thus, in CF, the reduced ability of mucosal irritants to stimulate airway gland secretion via SubP m
149 , that is activated by a variety of reactive irritants via the covalent modification of cysteine resi
151 hannels are activated by chemically reactive irritants, whereas snake and Drosophila TRPA1 orthologs
152 single or multiple high-level exposure(s) to irritants, whereas this relationship can only be inferre
153 n were induced by both contact allergens and irritants; whereas only contact allergens prompted stron