ライフサイエンスコーパス: inhalant

1 nd nasally administered as Nasacort AQ nasal inhalant.

2 dust mite (10 trials), grass pollen or other inhalants.

3 ding to potential exposure to asthma-causing inhalants.

4 Until recently, inhalant abuse and dependence have been overlooked as se

5 ping prevention and treatment programmes for inhalant abuse and dependence.

6 demonstrated a decrease in the prevalence of inhalant abuse, but overall rates remain high.

7 eviews the most recent epidemiologic data on inhalant abuse, summarizes the types of substances used

8 delivered signal to promote sensitization to inhalant aeroallergen, which may account for one mechani

9 IgE stimulated by a cross-reactive inhalant allergen can result in diverse patterns of alle

10 The prevalence of inhalant allergen sensitization increased during childho

11 Sensitization to at least one food or inhalant allergen was found in 319 of 765 (41.7%), and t

12 (637 vs 177 IU/mL, P = .002), and nonfungal inhalant allergen-specific IgE.

13 e and multiplicity of sensitization (food vs inhalant), allergen combinations, and sIgE levels.

14 rticipants had higher median specific IgE to inhalant allergens (41.4 kUA /L, IQR 10.1-118.4) compare

15 AC of the diet and incident sensitization to inhalant allergens (adjusted odds ratio: 0.73, 95% confi

16 ecific IgE concentrations to selected common inhalant allergens (dust mite (Dematophagoides farinae),

17 assessment of sensitization to 24 foods, 14 inhalant allergens and 55 allergenic molecules; and conf

18 re the relationship between sensitization to inhalant allergens and adult asthma, we performed two ne

19 fic IgE >/=0.35 kUA /l to common food and/or inhalant allergens at any time point.

20 with specific IgE against 13 common food and inhalant allergens at the ages of (1/2), 1(1/2), 4, and

21 ent of asthma, rhinitis and sensitization to inhalant allergens between 8 and 16 years, and to assess

22 ease the risk of developing sensitization to inhalant allergens from childhood to adolescence.

23 er proteins from pollens and fruits, certain inhalant allergens from house dust mites and cockroaches

24 A clear benefit for inhalant allergens has not yet been shown.

25 sign on the IgE sensitization profile toward inhalant allergens in patients with respiratory allergy

26 tic potential of allergen immunotherapy with inhalant allergens in pollen-related food allergy is not

27 rum IgE antibodies toward four food and four inhalant allergens measured at the age of 5 years.

28 ed by AD skin could promote sensitization to inhalant allergens remains elusive.

29 , maternal specific serum IgE against eight inhalant allergens was sampled after the children's birt

30 Specific IgE levels for 6 food and 13 common inhalant allergens were assessed in cord blood and 1-yea

31 25(OH)D and specific IgE against four common inhalant allergens were measured by standard procedures.

32 IgE antibodies to food and inhalant allergens were measured in children with active

33 ng function and serum specific IgE levels to inhalant allergens were measured, and information on ast

34 nsitization was assessed by skin prick test (inhalant allergens) and specific IgE levels (food allerg

35 erotoxin IgE antibodies, but not IgE against inhalant allergens, are risk factors for asthma severity

36 been suggested that sensitization to common inhalant allergens, which is developed in a majority of

37 al IgE and specific IgE to SEs, and food and inhalant allergens.

38 llergens in homes as well as specific IgE to inhalant allergens.

39 assessed by measuring serum IgE specific to inhalant allergens.

40 ed-U shape) associated with sensitization to inhalant allergens.

41 used combining questionnaire data and IgE to inhalant allergens.

42 sociated with poly-sensitization to food and inhalant allergens.

43 ioimmunosorbent test in response to standard inhalant allergens.

44 n of peripheral blood mononuclear cells from inhalant allergic patients was followed by an increased

45 At age 10 years, inhalant allergic sensitization and food-allergic sensit

46 (SIT) represents an effective treatment for inhalant allergies; however, successful birch pollen SIT

47 Inhalant allergy can present as chronically severe asthm

48 nhalant allergy without asthma; furthermore, inhalant allergy in one parent also conferred additional

49 s than in families where only one parent had inhalant allergy without asthma; furthermore, inhalant a

50 ly separated the cases into four groups: (i) inhalant allergy, (ii) fungal sensitization with or with

51 es and specific IgE levels against 12 common inhalant and 10 food allergens were assessed longitudina

52 IgE and IgG responses to 47 inhalant and food allergen components were analyzed in s

53 were linked to levels of IgE against common inhalant and food allergens at 4 and 8 years of age.

54 s were assessed simultaneously for 16 common inhalant and food allergens at age (1/2), 1(1/2), 4, and

55 ssociation of specific IgE levels to several inhalant and food allergens compared with HEU participan

56 the overall risk of sensitization to common inhalant and food allergens up to school age, but sensit

57 Allergic sensitization against 28 inhalant and food allergens was assessed at (1/2), 1(1/2

58 Allergic sensitization against common inhalant and food allergens was determined longitudinall

59 /= 0.35 kU/l to at least one of 15 evaluated inhalant and food allergens), current rhinitis, and curr

60 was assessed by skin prick test (SPT) using inhalant and food allergens.

61 by skin-prick testing with a panel of common inhalant and food allergens.

62 re tested for serum specific IgEs (sIgEs) to inhalant and food allergens; participants 6 years or old

63 ement between the two methods for diagnosing inhalant and food allergic sensitization at the four age

64 by skin prick tests, and physician-diagnosed inhalant and food allergy by a postal questionnaire.

65 ated with allergic sensitization, especially inhalant and seasonal allergens, rather than food allerg

66 Serum immunoglobulin E against eight common inhalant and six food allergens was assessed at ages 4,

67 oss-reacting allergenic structures shared by inhalants and foods.

68 ing for use of non-glucocorticoid-containing inhalants, and confirmed results by addressing confoundi

69 ee of the 10 substances considered (alcohol, inhalants, and heroin).

70 pping molecular sites of action for ethanol, inhalants, and volatile anesthetics on glycine receptors

71 glycemic clamps were performed in dogs under inhalant anesthesia with deep hindlimb lymphatic samplin

72 non-neuronal cell populations involved with inhalant biotransformation, detoxification, and maintena

73 ng effects of ethanol but not anesthetics or inhalants, demonstrated antagonism of anesthetic and inh

74 s, demonstrated antagonism of anesthetic and inhalant effects on this receptor.

75 ring of vaccines of pharmaceutical grade for inhalant, food, and venom allergens.

76 Use of inhalants for obstructive airway diseases (PR = 0.79; 95

77 nt of metabolic syndrome-related conditions, inhalants for obstructive airway diseases and glucocorti

78 Inhalants have the potential to result in serious organ

79 ced by airway sensitization and challenge to inhalant house dust mite (HDM), we demonstrate that the

80 nizes the nasopharynx and is thus exposed to inhalants, including cigarette smoke.

81 Inhalants, including toluene, target the addiction neuro

82 Environmental and occupational inhalants may induce a large number of pulmonary disease

83 individuals may be especially susceptible to inhalant occupational exposures.

84 children concomitantly sensitized to common inhalant or food allergens (-136.9 ml; 95% confidence in

85 licited by the negative control to any of 10 inhalant or food allergens.

86 d particularly in those sensitized to common inhalant or food allergens.

87 eding with childhood allergic sensitization, inhalant or food allergy and eczema, and whether any ass

88 Assays for inhalants provide greater opportunities for accurate dia

89 Inhalants remain one of the most commonly abused substan

90 as the milk and egg dominated and peanut and inhalant(s) groups were not (ORs of 1.6 [95% CI, 0.8-3.0

91 and egg dominated" (15.3%), and "peanut and inhalant(s)" (5.1%).

92 Since toluene and other abused inhalants share many behavioral effects with ethanol, it

93 All three inhalants significantly and reversibly enhanced neurotra

94 scles (OSMs), which control the exhalant and inhalant siphons, respectively, also requires Mrf We cha

95 nsidered these to be avoidance receptors for inhalants that, when activated, lead to ASM contraction

96 In addition to known medical consequences of inhalant use (including death), other risks associated w

97 ncluding death), other risks associated with inhalant use and addiction include addiction to other su

98 d psychological damage that can be caused by inhalant use argues for much greater attention to be pai

99 pioid, sedative/tranquilizer, and/or solvent/inhalant use disorders.

100 dels have cast light on how reinforcement of inhalant use occurs, and on mechanisms of development of

101 consequences, pharmacology, and etiology of inhalant use, and how we might develop preventive and ma