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 steroid-dependent/frequently relapsing, 22% steroid-resistant, 85% previously treated with two or mo

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

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

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

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

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

13 vestigated in diverse diseases(1), including steroid-resistant acute graft versus host disease (SR-aG

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

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

16 cells was conducted in 15 participants with steroid-resistant acute graft-versus-host disease.

17 h previously reported outcomes in studies of steroid-resistant acute graft-versus-host disease.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

32 In this study, we used a murine model of steroid-resistant airway inflammation and report that co

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

34 luate the clinical features of patients with steroid-resistant airway type 2 inflammation.

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

36 ired during dexamethasone/IL-27 treatment of steroid-resistant allergic inflammation, and importantly

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

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

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

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

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

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

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

44 lammation and AHR in a mouse model of severe steroid resistant asthma, potentially through the accumu

45 ew treatment options exist for patients with steroid resistant asthma.

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

47 reatments, offering a promising strategy for steroid-resistant asthma and potentially other respirato

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

49 Steroid-resistant asthma comprises an important source o

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

51 Steroid-resistant asthma is often characterized by high

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

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

54 gressively emerged as adjunctive therapy for steroid-resistant asthma, there remains a clinical need

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

56 omising therapeutic approach for people with steroid-resistant asthma.

57 etin nanobody (mnbTSLP) for the treatment of steroid-resistant asthma.

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

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

60 therapeutic agent in allergic and especially steroid-resistant asthma.

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

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

63 ionally, mnbTSLP restores the sensitivity of steroid-resistant asthmatic mice to budesonide by inhibi

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

65 Thus, the treatment of inhaled steroid-resistant bronchial asthma with dupilumab can al

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

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

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

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

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

71 Some patients develop a steroid-resistant condition, yet, the cellular and molec

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

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

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

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

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

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

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

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

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

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

82 y biopsy; FSGS-CT included 132 patients with steroid-resistant FSGS randomized to cyclosporine vs dex

83 odulin plasma concentrations are elevated in steroid-resistant graft-versus-host disease (GVHD), impl

84 Efforts to improve the prognosis of steroid-resistant gut acute graft-versus-host-disease (S

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

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

87 way pathology and lung function in the acute steroid-resistant house dust mite extract model.

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

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

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

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

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

93 le in publicly available datasets, including steroid-resistant interferon pathway expression in the r

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

95 rome [BOS]) and proinflammatory cytokines by steroid-resistant lymphocytes.

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

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

98 betac cytokines drive steroid-resistant mixed myeloid cell airway inflammation

99 iliopathies (seven out of nine individuals), steroid-resistant nephrotic syndrome (nine out of 21 ind

100 ines were also generated from a patient with steroid-resistant nephrotic syndrome (p.R168H homozygote

101 osis (FSGS) is the main pathology underlying steroid-resistant nephrotic syndrome (SRNS) and a leadin

102 studies have identified >55 genes as causing steroid-resistant nephrotic syndrome (SRNS) and localize

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

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

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

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

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

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

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

110 Steroid-resistant nephrotic syndrome (SRNS) is character

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

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

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

114 Exome sequencing was performed on 187 Steroid-Resistant Nephrotic Syndrome (SRNS) paediatric p

115 ch to rescue wild-type podocin expression in steroid-resistant nephrotic syndrome (SRNS) patient deri

116 fficacy and safety of rituximab in childhood steroid-resistant nephrotic syndrome (SRNS) remains uncl

117 While 44-83% of children with steroid-resistant nephrotic syndrome (SRNS) without a pr

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

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

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

121 encing to identify novel monogenic causes of steroid-resistant nephrotic syndrome (SRNS).

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

123 Mutations in MYO1E are associated with steroid-resistant nephrotic syndrome (SRNS).

124 pment of FSGS and other morphologic types of steroid-resistant nephrotic syndrome (SRNS).

125 dentified CRB2 mutations as a novel cause of steroid-resistant nephrotic syndrome (SRNS).

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

127 ty and depletion, and in human biopsies from steroid-resistant nephrotic syndrome and from human auto

128 cessive disease characterized by early-onset steroid-resistant nephrotic syndrome and microcephaly.

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

130 Steroid-resistant nephrotic syndrome has a poor prognosi

131 Conversely, up to a third of cases of steroid-resistant nephrotic syndrome have a monogenic or

132 NPHS2 variants are the most common cause of steroid-resistant nephrotic syndrome in children >1 mont

133 Steroid-resistant nephrotic syndrome is characterized by

134 of albuminuria, glomerular diseases such as steroid-resistant nephrotic syndrome or Alport syndrome

135 lities cause podocytopathies associated with steroid-resistant nephrotic syndrome or severe proteinur

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

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

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

139 ildren who do not respond, defined as having steroid-resistant nephrotic syndrome, most respond to se

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

141 The etiology of steroid-resistant nephrotic syndrome, which manifests as

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

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

144 ve nephropathy, which typically manifests as steroid-resistant nephrotic syndrome.

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

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

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

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

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

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

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

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

153 formin DAAM2 in four unrelated families with steroid-resistant NS.

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

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

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

157 eads to superior vision outcomes in cases of steroid-resistant or recurrent sympathetic ophthalmia.

158 Steroid-resistant or steroid-refractory acute graft-vers

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

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

161 -6 levels elevated to 197 +/- 20 pg/ml among steroid-resistant patients and normalized to 20 +/- 5 pg

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

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

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

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

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

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

168 Treating steroid resistant/refractory cGVHD remains challenging.

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

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

171 The incidence of steroid resistant rejection requiring antilymphocyte the

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

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

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

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

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

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

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

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

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

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

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

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

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

185 However, steroid-resistant rejection was significantly less frequ

186 Steroid-resistant rejection was treated with OKT3 or FK5

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

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

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

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

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

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

193 18/60), with four patients (7%) experiencing steroid-resistant rejection.

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

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

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

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

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

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

200 No steroid-resistant rejections occurred within 30 days.

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

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

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

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

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

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

207 icant mortality and morbidity, especially in steroid-resistant (SR) cases.

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

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

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

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

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

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

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

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

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

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

218 f to classify steroid-treated type 2-low and steroid-resistant type 2-high (srT2-high) subgroups.

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

220 Two hundred seventy patients with steroid-resistant ulcerative colitis were randomised to

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

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