戻る
「早戻しボタン」を押すと検索画面に戻ります。 [閉じる]

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 85% oral antihistamines, and 89% received IV glucocorticosteroids.
2 ably without the systemic adverse effects of glucocorticosteroids.
3 nflammatory mediators, and respond poorly to glucocorticosteroids.
4           All patients had been treated with glucocorticosteroids.
5 d a favourable initial response to high dose glucocorticosteroids.
6 improvement accompanied clinical response to 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 and influenced by concomitant treatment with glucocorticosteroids, and by the presence of recognized
12                                      Topical glucocorticosteroids are considered an efficient treatme
13  Current forms of treatment of SLE including glucocorticosteroids are often inadequate and induce sev
14                   Calcineurin inhibitors and glucocorticosteroids are the mainstays of most regimens
15 certainty about the effects of using topical glucocorticosteroids as maintenance therapy.
16 t, intravenous immunoglobulins, and systemic glucocorticosteroids because of limited evidence.
17 inhaled bronchodilator and anti-inflammatory glucocorticosteroid, but those with severe disease often
18    Our study indicates that even low-potency glucocorticosteroids can broadly affect immune and barri
19 n-1beta induced CCL27 production whereas the glucocorticosteroid clobetasol propionate suppressed it.
20      Following the administration of inhaled glucocorticosteroids combined with protease inhibitor-ba
21                                              Glucocorticosteroids continue to be the mainstay of trea
22                            The effect of the glucocorticosteroid, dexamethasone, on arachidonic acid
23                          We demonstrate that glucocorticosteroids differentially affect mast cell num
24 patients who remained relapse-free while the glucocorticosteroid dosage was tapered to 10 mg/d.
25                                              Glucocorticosteroid dosages could be reduced for all pat
26 it increase the proportion of patients whose glucocorticosteroid dosages were tapered to 10 mg/d with
27 ime to first relapse, biomarkers, cumulative glucocorticosteroid dose, and the number of patients who
28 erate certainty in the evidence that topical glucocorticosteroids effectively reduce esophageal eosin
29 tifying the factors responsible for relative glucocorticosteroid (GC) resistance present in patients
30 -cell-associated genes and their response to glucocorticosteroid (GC) treatment in Chinese patients w
31                                              Glucocorticosteroids (GC) are standard-of-care treatment
32 nd excess inflammation is also refractory to glucocorticosteroids (GC).
33              The mainstay of asthma therapy, glucocorticosteroids (GCs) have among their therapeutic
34 ecretion, survival, and their sensitivity to glucocorticosteroids (GCS), agents that normally induce
35  or not receiving (n = 10) long-term inhaled glucocorticosteroid (GS) therapy.
36 (1) before and after inhaled albuterol in 19 glucocorticosteroid (GS)-naive patients with mild interm
37                            Topically applied glucocorticosteroids (GS) have been shown to cause local
38 mmatory response with broadly active, potent glucocorticosteroids has proved useful as an adjunct to
39                                    High-dose glucocorticosteroid hormones are a mainstay in the treat
40                                              Glucocorticosteroid hormones, including dexamethasone, h
41                                      Inhaled glucocorticosteroids (ICS) are commonly prescribed for c
42                                      Inhaled glucocorticosteroids (ICS) are the mainstay of treatment
43                        The effect of inhaled glucocorticosteroids (ICS) on bone metabolism and subseq
44 severity, smoking status, and use of inhaled glucocorticosteroids (ICS).
45 istamines, leukotriene receptor antagonists, glucocorticosteroids, immunosuppressive agents, and omal
46                                              Glucocorticosteroids in increasing doses are recommended
47 ating them appropriately, and not increasing glucocorticosteroids in patients who do not have obvious
48 e in the lungs of patients with COPD who are glucocorticosteroid insensitive with a density of 1.036
49                                              Glucocorticosteroid insensitivity was selective for proi
50 stemic immunomodulating therapies, including glucocorticosteroids, intravenous immunoglobulins, cyclo
51            The patient received therapy with glucocorticosteroids intravenously, followed by intramus
52 trategies such as fluid replacement, oxygen, glucocorticosteroids, methylxanthines, bronchodilators,
53  long-term (16 weeks) application of topical glucocorticosteroids on AD skin and define response biom
54 ys prior to bone marrow transplant (BMT), of glucocorticosteroids on the day of BMT, or a combination
55           We evaluated the effect of inhaled glucocorticosteroids on these phenomena.
56 bronchoprotection can be restored by inhaled glucocorticosteroids only in individuals with mild hyper
57 ucocorticosteroid taper and required chronic glucocorticosteroid or other immunosuppressive therapy.
58 e (epinephrine), H1-antihistamines, systemic glucocorticosteroids or methylxanthines to manage anaphy
59 ticosteroid plus placebo, and 28 patients to glucocorticosteroid plus infliximab.
60            Sixteen patients were assigned to glucocorticosteroid plus placebo, and 28 patients to glu
61 common mental disorder at baseline, need for glucocorticosteroid prescription or flare (hazard ratio
62 mptoms of a common mental disorder, rates of glucocorticosteroid prescription or flare (HR, 2.48; 95%
63                                              Glucocorticosteroid prescription or flare, escalation, h
64 , trichostatin A, nuclear factor-kappaB, and glucocorticosteroid receptor were replicated in the sali
65 ostatin A and the nuclear factor-kappaB, the glucocorticosteroid receptor, and CCAAT/enhancer-binding
66 f trichostatin A, nuclear factor-kappaB, the glucocorticosteroid receptor, and CCAAT/enhancer-binding
67 ator, improved asthma control during inhaled glucocorticosteroid reduction in patients with allergic
68    To define the mechanisms by which inhaled glucocorticosteroid regulates allergen-induced airway in
69 ession closely predicted individual clinical glucocorticosteroid responses at 16 weeks of treatment.
70  dermatitis (AD), but a global assessment of glucocorticosteroid responses on key disease circuits up
71  investigating the mechanisms of beta2AR and glucocorticosteroids signaling and their molecular inter
72        Patients routinely worsened following glucocorticosteroid taper and required chronic glucocort
73        Budesonide is a highly potent topical glucocorticosteroid that is characterized by low systemi
74 d moisturizing therapies, local and systemic glucocorticosteroid therapies.
75 e allergic asthma receiving standard inhaled glucocorticosteroid therapy with or without LABAs.
76  sufficiently controlled on standard inhaled glucocorticosteroid therapy with/without long-acting bet
77  least 3 months of conventional therapy with glucocorticosteroids, thiopurines, or methotrexate.
78 rporeal photopheresis (ECP) but reduced with glucocorticosteroids, TNFalpha blockade, and alpha4beta7
79 hed for a way to deliver ultra high doses of glucocorticosteroids to the CNS of rats with experimenta
80 he rate of exacerbations that were moderate (glucocorticosteroid-treated) or severe.
81  protein levels in HeLa cells independent of glucocorticosteroid treatment could also produce an effe
82                                      Topical glucocorticosteroid use in patients with AD resulted in
83                                              Glucocorticosteroids were associated with a survival ben
84 exception is adrenal insufficiency caused by glucocorticosteroids which, although transient, can be l