ライフサイエンスコーパス: glucocorticosteroid

1 ably without the systemic adverse effects of glucocorticosteroids.

2 nflammatory mediators, and respond poorly to glucocorticosteroids.

3 All patients had been treated with glucocorticosteroids.

4 d a favourable initial response to high dose glucocorticosteroids.

5 improvement accompanied clinical response to glucocorticosteroids.

6 85% oral antihistamines, and 89% received IV glucocorticosteroids.

7 scientific rationale for the combined use of glucocorticosteroids and beta-2-adrenoreceptor (beta2AR)

8 nd immunosuppressive medications, especially glucocorticosteroids and calcineurin inhibitors.

9 ing the unstratified model, had limitations, glucocorticosteroids and cyclosporine were the most prom

10 controlled by administering a combination of glucocorticosteroids and dapsone.

11 Topical glucocorticosteroids are considered an efficient treatme

12 Current forms of treatment of SLE including glucocorticosteroids are often inadequate and induce sev

13 Calcineurin inhibitors and glucocorticosteroids are the mainstays of most regimens

14 t, intravenous immunoglobulins, and systemic glucocorticosteroids because of limited evidence.

15 inhaled bronchodilator and anti-inflammatory glucocorticosteroid, but those with severe disease often

16 Our study indicates that even low-potency glucocorticosteroids can broadly affect immune and barri

17 n-1beta induced CCL27 production whereas the glucocorticosteroid clobetasol propionate suppressed it.

18 Following the administration of inhaled glucocorticosteroids combined with protease inhibitor-ba

19 Glucocorticosteroids continue to be the mainstay of trea

20 The effect of the glucocorticosteroid, dexamethasone, on arachidonic acid

21 We demonstrate that glucocorticosteroids differentially affect mast cell num

22 patients who remained relapse-free while the glucocorticosteroid dosage was tapered to 10 mg/d.

23 it increase the proportion of patients whose glucocorticosteroid dosages were tapered to 10 mg/d with

24 ime to first relapse, biomarkers, cumulative glucocorticosteroid dose, and the number of patients who

25 tifying the factors responsible for relative glucocorticosteroid (GC) resistance present in patients

26 -cell-associated genes and their response to glucocorticosteroid (GC) treatment in Chinese patients w

27 nd excess inflammation is also refractory to glucocorticosteroids (GC).

28 The mainstay of asthma therapy, glucocorticosteroids (GCs) have among their therapeutic

29 ecretion, survival, and their sensitivity to glucocorticosteroids (GCS), agents that normally induce

30 or not receiving (n = 10) long-term inhaled glucocorticosteroid (GS) therapy.

31 (1) before and after inhaled albuterol in 19 glucocorticosteroid (GS)-naive patients with mild interm

32 Topically applied glucocorticosteroids (GS) have been shown to cause local

33 mmatory response with broadly active, potent glucocorticosteroids has proved useful as an adjunct to

34 High-dose glucocorticosteroid hormones are a mainstay in the treat

35 Glucocorticosteroid hormones, including dexamethasone, h

36 Inhaled glucocorticosteroids (ICS) are commonly prescribed for c

37 Inhaled glucocorticosteroids (ICS) are the mainstay of treatment

38 The effect of inhaled glucocorticosteroids (ICS) on bone metabolism and subseq

39 severity, smoking status, and use of inhaled glucocorticosteroids (ICS).

40 e in the lungs of patients with COPD who are glucocorticosteroid insensitive with a density of 1.036

41 Glucocorticosteroid insensitivity was selective for proi

42 stemic immunomodulating therapies, including glucocorticosteroids, intravenous immunoglobulins, cyclo

43 long-term (16 weeks) application of topical glucocorticosteroids on AD skin and define response biom

44 ys prior to bone marrow transplant (BMT), of glucocorticosteroids on the day of BMT, or a combination

45 We evaluated the effect of inhaled glucocorticosteroids on these phenomena.

46 bronchoprotection can be restored by inhaled glucocorticosteroids only in individuals with mild hyper

47 ucocorticosteroid taper and required chronic glucocorticosteroid or other immunosuppressive therapy.

48 e (epinephrine), H1-antihistamines, systemic glucocorticosteroids or methylxanthines to manage anaphy

49 ticosteroid plus placebo, and 28 patients to glucocorticosteroid plus infliximab.

50 Sixteen patients were assigned to glucocorticosteroid plus placebo, and 28 patients to glu

51 ator, improved asthma control during inhaled glucocorticosteroid reduction in patients with allergic

52 To define the mechanisms by which inhaled glucocorticosteroid regulates allergen-induced airway in

53 ession closely predicted individual clinical glucocorticosteroid responses at 16 weeks of treatment.

54 dermatitis (AD), but a global assessment of glucocorticosteroid responses on key disease circuits up

55 investigating the mechanisms of beta2AR and glucocorticosteroids signaling and their molecular inter

56 Patients routinely worsened following glucocorticosteroid taper and required chronic glucocort

57 Budesonide is a highly potent topical glucocorticosteroid that is characterized by low systemi

58 d moisturizing therapies, local and systemic glucocorticosteroid therapies.

59 e allergic asthma receiving standard inhaled glucocorticosteroid therapy with or without LABAs.

60 sufficiently controlled on standard inhaled glucocorticosteroid therapy with/without long-acting bet

61 least 3 months of conventional therapy with glucocorticosteroids, thiopurines, or methotrexate.

62 hed for a way to deliver ultra high doses of glucocorticosteroids to the CNS of rats with experimenta

63 he rate of exacerbations that were moderate (glucocorticosteroid-treated) or severe.

64 protein levels in HeLa cells independent of glucocorticosteroid treatment could also produce an effe

65 Topical glucocorticosteroid use in patients with AD resulted in

66 Glucocorticosteroids were associated with a survival ben

67 exception is adrenal insufficiency caused by glucocorticosteroids which, although transient, can be l