ライフサイエンスコーパス: steroid-resistant

1 id resistant (SR, abbreviation derived from "steroid resistant").

2 that elastase-induced airway neutrophilia is steroid resistant.

3 pa B) and tyrosine kinase activation and was steroid resistant.

4 d; in contrast, TGF-beta1 mRNA synthesis was steroid resistant.

5 Rejection episodes are most often steroid resistant.

6 TNF-alpha, CXCL1, CXCL2, and CXCL5, and was steroid resistant.

7 ent Group II P=0.002) and significantly less steroid resistant acute rejection episodes (3.1% in Grou

8 Sirolimus should be considered for use in steroid-resistant acute and chronic GVHD.

9 p, four of five recipients developed severe, steroid-resistant acute cellular rejection, whereas FR10

10 igate the clinical outcomes of patients with steroid-resistant acute exacerbation of idiopathic inter

11 n used clinically for two decades to reverse steroid-resistant acute graft rejection.

12 Treatment for steroid-resistant acute graft-versus-host disease (GVHD)

13 Treatment of steroid-resistant acute graft-versus-host disease (GVHD)

14 Survival after steroid-resistant acute GVHD continues to be problematic

15 , multicenter, randomized clinical trial for steroid-resistant acute GVHD serves as a model for futur

16 ntithymocyte globulin (ATG) for treatment of steroid-resistant acute GVHD was conducted in 95 patient

17 ll tolerated and active for the treatment of steroid-resistant acute GVHD, particularly with gastroin

18 vidence for the benefit of MSC treatments in steroid-resistant acute GVHD.

19 eriments, sirolimus provides good control of steroid-resistant acute or chronic GVHD.

20 moglobulin) as induction therapy or to treat steroid-resistant acute or chronic rejection.

21 Steroid-resistant acute rejection is a risk factor for i

22 icial in liver transplantation for reversing steroid-resistant acute rejection, and for controlling t

23 even of 94 patients (50%) were converted for steroid-resistant acute rejection.

24 mediated ILC2 numbers, TH2 cell numbers, and steroid-resistant AHR.

25 s IL-27 production, which has been linked to steroid-resistant airway hyperresponsiveness (AHR).

26 r IL-27 significantly suppressed RSV-induced steroid-resistant airway hyperresponsiveness and airway

27 rophil depletion suppressed IL-1beta-induced steroid-resistant airway hyperresponsiveness.

28 n the search for new therapies to reduce the steroid-resistant airway inflammation evident in COPD.

29 nfection-mediated, ovalbumin-induced severe, steroid-resistant allergic airway disease.

30 trophilic airway phenotype was shown to be a steroid-resistant allergic respiratory variant that was

31 of all rejection episodes in both eras were steroid resistant and required antibody therapy.

32 it is not surprising that well-characterised steroid-resistant and steroid-dependent asthma have mult

33 By this criterion, nephrotic FSGS is usually steroid-resistant and, if not controlled by more aggress

34 he six patients, of which three were severe (steroid-resistant) and five were late (>90 days).

35 reatment for asthma, a subset of patients is steroid resistant, and chronic steroid use causes side e

36 Production of IFN-gamma and IL-27 was steroid-resistant, and neutralization of IFN-gamma or IL

37 mmasome responses drive experimental severe, steroid-resistant asthma and are potential therapeutic t

38 The causes of steroid-resistant asthma are multifactorial and result f

39 Steroid-resistant asthma comprises an important source o

40 ) has suggested that severe asthma, of which steroid-resistant asthma is a component, consists of at

41 RATIONALE: Severe, steroid-resistant asthma is the major unmet need in asth

42 d IL-1beta responses in experimental severe, steroid-resistant asthma were examined using a highly se

43 e NLRP3 inflammasome and IL-1beta in severe, steroid-resistant asthma.

44 ucus metaplasia in a mixed Th2/Th17 model of steroid-resistant asthma.

45 ent asthma phenotypes as virus-associated or steroid-resistant asthma.

46 oorly understood, and are unknown in severe, steroid-resistant asthma.

47 icating a potential role for T(H)17 cells in steroid-resistant asthma.

48 aT-catenin (CTNNA3) that correlate with both steroid-resistant atopic asthma and asthmatic exacerbati

49 We additionally looked for TDF-R in steroid-resistant BT-549 cells and human dermal fibrobla

50 DMP is commonly steroid-resistant but may slowly resolve.

51 ys during airway inflammation and identify a steroid-resistant cascade of Wnt5a, Tgm2, and LTs, which

52 rway disease and identify T2M cells as a new steroid-resistant cell population.

53 The reversible steroid-resistant character of the iPHIL neutrophilic ai

54 to immunosuppressive agents in children with steroid-resistant disease (0% of patients with alteratio

55 genetic cause in 32.3% of the children with steroid-resistant disease but zero of 38 children with s

56 Standard initial treatment for steroid-resistant disease is to add a single immunosuppr

57 vity and has been implicated in a variety of steroid-resistant diseases.

58 ein (cyto mu) was transfected into cyto mu-, steroid-resistant early B cell lines.

59 The underlying mechanisms associated with steroid-resistant exacerbations remain largely unknown.

60 pressed IL-1beta responses and the important steroid-resistant features of disease in mice, whereas I

61 blished causes of both familial and sporadic steroid-resistant focal segmental glomerulosclerosis (FS

62 rotein A9, which significantly discriminated steroid resistant from steroid-responsive rejections (P<

63 Significant control of steroid-resistant FSGS has not been achieved with limite

64 orable toxicity profile and response rate in steroid-resistant GVHD, a multicenter, double-blinded, r

65 provement over ATG in the treatment of acute steroid-resistant GVHD.

66 cal model and could suggest parallels in the steroid-resistant human disease.

67 ell-mediated airway inflammation and AHR are steroid resistant, indicating a potential role for T(H)1

68 s) play essential roles in the generation of steroid-resistant inflammation and AHR secondary to alle

69 mation, particularly in clinical settings of steroid resistant inflammatory disease.

70 hus, LIGHT and LTalphabeta induce a distinct steroid-resistant inflammatory signature in airway epith

71 teroid responsiveness and perhaps converting steroid-resistant leukemia to a hormone-responsive pheno

72 IL-33 is a relatively steroid-resistant mediator that promotes airway remodeli

73 VEGF164 overexpression after birth induces a steroid-resistant minimal change like-disease in mice.

74 y defects of coenzyme Q10 biosynthesis cause steroid-resistant nephrotic syndrome (SRNS) as part of m

75 Steroid-resistant nephrotic syndrome (SRNS) causes 15% o

76 Steroid-resistant nephrotic syndrome (SRNS) causes 15% o

77 splantation appears reduced in patients with steroid-resistant nephrotic syndrome (SRNS) due to monog

78 Identification of single-gene causes of steroid-resistant nephrotic syndrome (SRNS) has furthere

79 Steroid-resistant nephrotic syndrome (SRNS) is a frequen

80 Steroid-resistant nephrotic syndrome (SRNS) is a frequen

81 Steroid-resistant nephrotic syndrome (SRNS) is the secon

82 Steroid-resistant nephrotic syndrome (SRNS) leads to end

83 Steroid-resistant nephrotic syndrome (SRNS), a frequent

84 Steroid-resistant nephrotic syndrome (SRNS), a heterogen

85 ered the understanding of pathomechanisms in steroid-resistant nephrotic syndrome (SRNS), not even a

86 ng podocin (NPHS2) cause autosomal recessive steroid-resistant nephrotic syndrome (SRNS).

87 a cohort of 31 children affected by sporadic steroid-resistant nephrotic syndrome and 38 patients who

88 a primary adrenal insufficiency syndrome and steroid-resistant nephrotic syndrome caused by loss-of-f

89 Steroid-resistant nephrotic syndrome has a poor prognosi

90 Steroid-resistant nephrotic syndrome is characterized by

91 esting a potential therapy for patients with steroid-resistant nephrotic syndrome with ADCK4 mutation

92 tions in the NPHS2 gene are a major cause of steroid-resistant nephrotic syndrome, a severe human kid

93 filter, leads to proteinuria, edema and, in steroid-resistant nephrotic syndrome, end-stage kidney d

94 ave been shown to be single-gene defects-eg, steroid-resistant nephrotic syndrome, which is caused by

95 cin, the gene mutated in autosomal recessive steroid-resistant nephrotic syndrome.

96 ne whose mutations cause autosomal recessive steroid-resistant nephrotic syndrome.

97 -term renal outcome in children with primary steroid-resistant nephrotic syndrome.

98 term outcome, respectively, in children with steroid-resistant nephrotic syndrome.

99 containing kinase 4 (ADCK4) gene that cause steroid-resistant nephrotic syndrome.

100 odoNet, the Europe-based consortium studying steroid-resistant nephrotic syndrome.

101 P3, caspase-1, IL-1beta responses that drive steroid-resistant neutrophilic inflammation and airway h

102 Steroid-resistant NS (SRNS) is defined by primary resist

103 divided into steroid-sensitive NS (SSNS) and steroid-resistant NS (SRNS).

104 This is the first study in children with steroid-resistant NS who underwent kidney transplantatio

105 onclude that vitamin D-resistant and gonadal steroid-resistant NWP cells contain a protein(s) that ma

106 ody treatment was required to reverse either steroid-resistant or Banff grades II or III acute reject

107 histological changes (disease recurrence and steroid-resistant or late rejections) were comparable in

108 ma-treated intestinal epithelial cells via a steroid-resistant pathway involving NF-kappa B and tyros

109 oliferation count in 91% (10/11) of in vitro steroid-resistant patients (P = 0.003).

110 -6 levels elevated to 197 +/- 20 pg/ml among steroid-resistant patients and normalized to 20 +/- 5 pg

111 Similarly, 91% (10/11) of in vitro steroid-resistant patients failed to show a significant

112 In all, 82% (9/11) of in vitro steroid-resistant patients were dead at 6 months as comp

113 set, and pathologic findings were similar in steroid-resistant patients with and without alterations.

114 e-day prednisone, and an alkylating agent in steroid-resistant pediatric FSGS has produced the highes

115 a large minority of patients with CRS have a steroid-resistant phenotype, identification of which wil

116 S1P induces a steroid-resistant, pro-remodelling pathway in ASM cells.

117 ry CsA therapy of which 70 required OKT3 for steroid resistant rejection and 29 required tacrolimus r

118 gimen was associated with the lowest rate of steroid resistant rejection requiring antilymphocyte the

119 The incidence of steroid resistant rejection requiring antilymphocyte the

120 Steroid resistant rejection was similar (BD 19%, ED 17%)

121 The treatment of steroid-resistant rejection (SRR) is associated with sev

122 with decreased rates of acute rejection and steroid-resistant rejection after OLT.

123 Twelve patients who experienced steroid-resistant rejection after primary liver transpla

124 lograft infiltrates has been associated with steroid-resistant rejection and poor graft survival.

125 as the primary therapy for the treatment of steroid-resistant rejection and provides a rapid and sus

126 owel diseases and as rescue therapy in acute steroid-resistant rejection in selected settings in clin

127 omonab-CD3) revolutionized the management of steroid-resistant rejection in transplant patients.

128 e less likely than CLT recipients to develop steroid-resistant rejection or ductopenic rejection.

129 te the recent advances in immunosuppression, steroid-resistant rejection remains a difficult problem

130 The incidence of steroid-resistant rejection was 5%.

131 e of rejection was 49%, and the incidence of steroid-resistant rejection was 6%.

132 isodes were initially treated with steroids; steroid-resistant rejection was managed with an antibody

133 However, steroid-resistant rejection was significantly less frequ

134 Steroid-resistant rejection was treated with OKT3 or FK5

135 graft recipients undergoing OKT3 therapy for steroid-resistant rejection were randomized to receive O

136 severe histologic rejection and were free of steroid-resistant rejection when compared with SIM-treat

137 unologic safety assessed by the incidence of steroid-resistant rejection within the first 30 days aft

138 low incidence of late acute rejection, late steroid-resistant rejection, and death or graft loss rel

139 patients received antilymphocyte therapy for steroid-resistant rejection, five of whom are now off st

140 tacrolimus, when used as rescue therapy for steroid-resistant rejection, were associated with a comp

141 was ineffective and can potentially lead to steroid-resistant rejection.

142 dy was required in eight (13%) patients with steroid-resistant rejection.

143 reduces the frequency of acute cellular and steroid-resistant rejection.

144 eoral group required treatment with OKT3 for steroid-resistant rejection.

145 18/60), with four patients (7%) experiencing steroid-resistant rejection.

146 Steroid-resistant rejections decreased from 48% to 15%.

147 There were more steroid-resistant rejections in antibody-positive than i

148 No steroid-resistant rejections occurred within 30 days.

149 prevent the occurrence of difficult to treat steroid-resistant rejections, thereby leading to improve

150 e particularly effective in neutrophil-rich, steroid-resistant severe asthma.

151 o standard steroid therapy, and this type of steroid-resistant, severe asthma has been linked to the

152 lunts T cell responses to glucocorticoids in steroid resistant (SR) asthma by reducing glucocorticoid

153 Blood tests are needed to identify steroid-resistant (SR) asthmatic patients early so that

154 fferences between steroid-sensitive (SS) and steroid-resistant (SR) asthmatics.

155 a role in the pathology of asthma, including steroid-resistant (SR) disease.

156 association with complete response (CR) and steroid-resistant (SR) GVHD.

157 n D regulation of responses in patients with steroid-resistant (SR) versus steroid-sensitive (SS) ast

158 elapses are common, and some patients become steroid-resistant (SR), steroid-dependent (SD), or frequ

159 asthma does not respond to glucocorticoids (steroid resistant [SR]).

160 ly divided into steroid-sensitive (SSNS) and steroid-resistant (SRNS) forms.

161 ive in treating steroid-dependent (SDNS) and steroid-resistant (SRNS) nephrotic syndrome (NS) in chil

162 RC-1 switches steroid-responsive tumors to a steroid-resistant state in which the SRC-1 target gene A

163 Targeting steroid-resistant Th1 responses will be necessary to res

164 ty is more severe in FSGS than in MCD and in steroid-resistant than in steroid-dependent NS, regardle

165 linded study in active steroid dependent and steroid resistant UC patients on concomitant steroid the

166 we found that the murine cell line (HT-2) is steroid resistant when incubated with IL-2, but steroid

167 tic patients with increased TSLP levels were steroid resistant, which was reversed by clinically avai