ライフサイエンスコーパス: glucocorticoid

1 ethylprednisolone acetate (MPA), a synthetic glucocorticoid.

2 -kinase in mediating the metabolic action of glucocorticoids.

3 ns, nonsteroidal anti-inflammatory drugs, or glucocorticoids.

4 ade that culminates in systemic secretion of glucocorticoids.

5 ed of tacrolimus, mycophenolate mofetil, and glucocorticoids.

6 -deficient A549 cells that were treated with glucocorticoids.

7 e mainstay of treatment of CRS, specifically glucocorticoids.

8 ontributes to the tissue-specific actions of glucocorticoids.

9 with hearing disorders who are refractory to glucocorticoids.

10 ortisol metabolism, and tissue resistance to glucocorticoids.

11 agonists and medium-to-high doses of inhaled glucocorticoids.

12 s fetal exposure to stress hormones, such as glucocorticoids.

13 we describe a role for CBR1 in metabolism of glucocorticoids.

14 against hip fracture in older patients using glucocorticoids.

15 Collectively, these data show that glucocorticoids act directly on activated glomerular par

16 It is commonly assumed that glucocorticoids act primarily by dampening the immune re

17 Interactions between stress exposure (via glucocorticoid actions) and infection impose resource tr

18 Glucocorticoids activate the glucocorticoid receptor, a

19 this nongenomic signaling pathway, in which glucocorticoids activate Wnt pathway via mbGR, provides

20 were associated with paracrine regulation of glucocorticoid activity because global deletion of 11bet

21 r proliferation and pathways associated with glucocorticoid activity.

22 function was also observed in the setting of glucocorticoid addition, which is a strong atrophy-induc

23 for parental ethnicity and smoking, prenatal glucocorticoid administration, preeclampsia, gestational

24 mg/dL) manifested 6 weeks after the start of glucocorticoid administration, whereas 100% of the mice

25 hat may govern the epigenetics of stress and glucocorticoids along the lifespan: first, the presence

26 ids is believed to occur due to insufficient glucocorticoid alpha-mediated anti-inflammatory activity

27 However, the mechanisms by which glucocorticoids ameliorate proteinuria and glomerular di

28 In this group, expression of glucocorticoid and androgen receptor genes explained the

29 plying that therapeutic normalization of the glucocorticoid and catecholamine imbalance in SCI patien

30 the basis for improved in vivo monitoring of glucocorticoid and insulin action.

31 Our data suggest that concurrent glucocorticoid and noradrenergic activity prompts an ali

32 ndro), respectively, critical for generating glucocorticoids and androgens.

33 The direct modulation of BCAs by glucocorticoids and insulin may provide the basis for im

34 story of rheumatoid arthritis who was taking glucocorticoids and methotrexate presented to the emerge

35 oA/ROCK signaling, which can be activated by glucocorticoids and was found in our previous work to be

36 ic approach in crescentic nephritis, that of glucocorticoid antagonism, which was at least as effecti

37 Because glucocorticoids are administered to ALL patients during

38 c explanation for the empirical finding that glucocorticoids are effective in the treatment of B-lymp

39 We hypothesized that glucocorticoids are lower in maternal and cord blood at

40 Giant-cell arteritis commonly relapses when glucocorticoids are tapered, and the prolonged use of gl

41 Although glucocorticoids are used to manage exacerbations, some p

42 Glucocorticoids are vital for lung maturation.

43 metabolic and immunological consequences of glucocorticoid-associated interventions in a mouse model

44 However, glucocorticoids at physiological levels are essential fo

45 for signaling pathways regulating estrogen, glucocorticoid, B-cell receptor signaling, and ATM signa

46 or severe exacerbations while taking inhaled glucocorticoid-based triple maintenance therapy.

47 lucocorticoids leads to rapid restoration of glucocorticoid biosynthesis gene expression coincident w

48 anscriptomic profiling marked suppression of glucocorticoid biosynthesis in the epidermis of psoriati

49 D human epidermis model, we demonstrate that glucocorticoid biosynthesis is suppressed by proinflamma

50 nzymatically amplified feedback loop whereby glucocorticoids boost cAMP to maintain insulin secretion

51 ydrogenase type 2, the "barrier" to maternal glucocorticoids), by pregnant women was associated with

52 Although glucocorticoids can repress inflammatory gene expression

53 drome, and other human diseases modulated by glucocorticoid control.

54 In glucocorticoid-treated mice, we find that glucocorticoids coordinately suppress expression of seve

55 We first report that exposure to the primary glucocorticoid corticosterone (CORT) in adolescent mice

56 Glucocorticoids (cortisol and corticosterone) and their

57 en together, our data suggest that localized glucocorticoid deficiency in psoriatic skin interferes w

58 ressed by proinflammatory cytokines and that glucocorticoid deficiency promotes inflammatory response

59 ation and systemic neutrophil activity via a glucocorticoid-dependent pathway.

60 time to first relapse and the average daily glucocorticoid dose (during weeks 48 through 52).

61 point was the percentage change in the oral glucocorticoid dose from baseline to week 28.

62 tic with area under the curve for predicting glucocorticoid dose of >0.9 with FDR adjusted P values i

63 The odds of a reduction in the oral glucocorticoid dose were more than 4 times as high with

64 versus placebo on the reduction in the oral glucocorticoid dose while asthma control was maintained

65 significantly reduced the median final oral glucocorticoid doses from baseline by 75%, as compared w

66 compared with a reduction of 25% in the oral glucocorticoid doses in the placebo group (P<0.001 for b

67 tabolites amongst groups receiving different glucocorticoid doses revealed a clear distinction betwee

68 muscle, resulting in hepatic ketogenesis and glucocorticoid-driven muscle catabolism, which are preve

69 Despite ongoing research, high glucocorticoid efficacy and widespread usage in medicine

70 renalectomy completely prevented SCI-induced glucocorticoid excess and lymphocyte depletion but did n

71 nism may contribute to diabetes in states of glucocorticoid excess, such as Cushing syndrome, which a

72 Excessive glucocorticoid exposure has been shown to be deleterious

73 Prenatal glucocorticoid exposure influences the timing of puberty

74 Novel treatments aim to reduce glucocorticoid exposure, improve excess hormone control,

75 deaths occurred in 311 patients treated with glucocorticoids for 1 year or longer compared with 11 (1

76 ignificantly longer in patients treated with glucocorticoids for 1 year or longer than in patients tr

77 he primary outcome was the rate of sustained glucocorticoid-free remission at week 52 in each tociliz

78 pering plus placebo with regard to sustained glucocorticoid-free remission in patients with giant-cel

79 ed expression of FKBP5, implicating aberrant glucocorticoid functioning in PTSD.

80 Glucocorticoid (GC) and hypoxic transcriptional response

81 Jozic et al. describe mechanisms of glucocorticoid (GC) downregulation of wound healing by i

82 n of small-molecule compounds, we identified glucocorticoid (GC) hormone signaling as an activator of

83 We have identified the glucocorticoid (GC) hormones as critical for optimal mob

84 The mechanisms driving glucocorticoid (GC) insensitivity in patients with sever

85 The glucocorticoid (GC) receptor (GR) suppresses inflammatio

86 de-inducible clone 5 (Hic-5) is required for glucocorticoid (GC) regulation of some genes but not oth

87 typically treated with an empiric course of glucocorticoid (Gc) therapy; a class of steroids that ar

88 (T-ALL) patients often display resistance to glucocorticoid (GC) treatment.

89 Using a mouse model of glucocorticoid (GC)-induced glaucoma, primary human TM c

90 Glucocorticoid (GC)-induced ocular hypertension (OHT) is

91 Glucocorticoid (GC)-refractory acute rejection (AR) is a

92 Glucocorticoids (GC) are the primary steroids that regul

93 Although glucocorticoids (GCs) are a mainstay in the clinical man

94 Glucocorticoids (GCs) are important regulators of system

95 The synthetic glucocorticoids (GCs) dexamethasone, mometasone furoate,

96 Glucocorticoids (GCs), including dexamethasone (dex), ar

97 Glucocorticoids (GCs), key mediators of stress signals,

98 Despite the widespread use of glucocorticoids (GCs), their anti-inflammatory effects a

99 Glucocorticoids (GCs)-ligands of the glucocorticoid rece

100 Glucocorticoids (GCs; referred to clinically as corticos

101 For several decades, glucocorticoids have been used empirically to treat rapi

102 Glucocorticoids have been used to treat hearing loss and

103 edical therapies, which primarily consist of glucocorticoids, have limited efficacy and present safet

104 Chronic stress and elevated glucocorticoid hormone are associated with decreases in

105 re to corticosterone, the dominant amphibian glucocorticoid hormone, mediates development and immune

106 Glucocorticoid hormones (GCs) are used to treat a variet

107 Thyroid and glucocorticoid hormones are critical for heart maturatio

108 Both new neurons and glucocorticoid hormones are required for the enhancement

109 st a permissive role of combined thyroid and glucocorticoid hormones during the cardiac differentiati

110 ar factors that govern tissue specificity of glucocorticoids, however, are poorly understood.

111 cule AMPK inhibitor strongly synergized with glucocorticoids, identifying TXNIP, CNR2 and AMPK as pot

112 ot only shed light on the mechanism by which glucocorticoid imparts its beneficial effect on dystroph

113 g all kinds of immunosuppressive treatments, glucocorticoid in combination with bDMARDs and synthetic

114 Glucocorticoids in aquatic systems originating from natu

115 ve a functional relationship with mGluR5 and glucocorticoids in PTSD.

116 f KLF15 in mediating the salutary effects of glucocorticoids in the podocyte.

117 vacopan was effective in replacing high-dose glucocorticoids in treating vasculitis.

118 regulatory subunits of PKA were increased by glucocorticoids in wild-type mice.

119 luding estrogens, androgens, progestins, and glucocorticoids, in hospital wastewaters, river water, a

120 Here, we found that glucocorticoids increased HSL phosphorylation, but not P

121 Glucocorticoid-induced lipolysis requires the phosphoryl

122 ular mechanism, plays a critical role in the glucocorticoid-induced osteonecrosis.

123 is contained in the GRE, which may modulate glucocorticoid-induced sST2 expression.

124 A recent publication has shown that anti-glucocorticoid-induced TNFR family-related protein agoni

125 of DTA-1 did not affect receptor binding and glucocorticoid-induced TNFR family-related protein-induc

126 ssion of the Aldo-induced protein serum- and glucocorticoid-inducible kinase 1 (SGK1), NCC and alphaE

127 hat MTA1 is a novel corepressor of serum and glucocorticoid-inducible kinase 1 (SGK1).

128 rn, leads to increased activity of serum and glucocorticoid-inducible kinase 1 (SGK1).

129 Here, we report that serum- and glucocorticoid-inducible kinase 3 (SGK3), a kinase trans

130 rt that GRIP1 loss in macrophages attenuates glucocorticoid induction of several anti-inflammatory ta

131 In agreement with reduced WAT lipolysis, glucocorticoid- initiated hepatic steatosis and hypertri

132 To assess the efficacy of a single glucocorticoid intradiscal injection (GC IDI) in patient

133 icoids are tapered, and the prolonged use of glucocorticoids is associated with side effects.

134 uring critical illness, tissue resistance to glucocorticoids is believed to occur due to insufficient

135 In utero exposure to glucocorticoids (iuGC) triggers prominent motivation def

136 itro and in vivo that treatment with topical glucocorticoids leads to rapid restoration of glucocorti

137 nger-term effects of fetal exposure to lower glucocorticoid levels during obese pregnancy.

138 sover design to produce low, medium and high glucocorticoid levels.

139 revealing a negative feedback loop by which glucocorticoids limit MDFIC activity.

140 regulation, which indicates that mixtures of glucocorticoids may be of concern for developing fish.

141 istal promoter are involved in UC and affect glucocorticoid-mediated ST2 expression.

142 Glucocorticoid-mediated ST2 production was evaluated in

143 Molecular regulation of glucocorticoid-mediated ST2 was assessed by RT-qPCR, ChI

144 11betaHSD2 is known to regulate glucocorticoid metabolism by converting active cortisol

145 enzymes involved in cholesterol epoxide and glucocorticoid metabolism or GR may be novel strategies

146 ck, patients can have various alterations in glucocorticoid, mineralocorticoid, and sex steroid produ

147 tance to multiple steroid hormones including glucocorticoids observed in a patient with 16p11.2 micro

148 nt feedback of local proopiomelanocortin and glucocorticoids on cutaneous immunity contributes to inf

149 We examined the long-term effects of glucocorticoids on milestone-related disease progression

150 y potential negative effects of low maternal glucocorticoids on the fetus in the short-term.

151 iseases, understanding the direct effects of glucocorticoids on the podocyte, independent of the immu

152 tal adrenal hyperplasia include avoidance of glucocorticoid overtreatment and control of sex hormone

153 ry-adrenal (HPA) axis, triggering endogenous glucocorticoid production.

154 Glucocorticoids promote lipolysis in white adipose tissu

155 Conversely, MAPKs, which are inhibited by glucocorticoids, provide feedforward control to limit ex

156 receptors (activated by epinephrine) and the glucocorticoid receptor (activated by corticosterone).

157 We also showed a loss of glucocorticoid receptor (GCR) in proinflammatory lymphoc

158 rovide insight into the molecular effects of glucocorticoid receptor (GR) activation at a clinically

159 investigations have examined the effects of glucocorticoid receptor (GR) activation prior to inflamm

160 d in vitro estrogen (ER), androgen (AR), and glucocorticoid receptor (GR) activity, along with a broa

161 which activates transcription factors (TFs) glucocorticoid receptor (GR) and CREB within minutes and

162 ls through its molecular targeting of AR and glucocorticoid receptor (GR) and downstream pro-oxidant

163 The nonselective glucocorticoid receptor (GR) antagonist mifepristone has

164 ome-wide regulatory actions of ZNF764 on the glucocorticoid receptor (GR) in HeLa cells as a model sy

165 te corticosteroid efficacy, interacting with glucocorticoid receptor (GR) in patients with chronic rh

166 g frequencies via promiscuous binding to the glucocorticoid receptor (GR) in T cells.

167 antitatively explore the organization of the glucocorticoid receptor (GR) in the interphase nucleus o

168 ytoskeletal organization, interacts with the glucocorticoid receptor (GR) in the nucleus of human pod

169 The glucocorticoid receptor (GR) is a ligand-regulated trans

170 The glucocorticoid receptor (GR) is essential for the stress

171 The glucocorticoid receptor (GR) is the major receptor for t

172 Emerging data suggest that the glucocorticoid receptor (GR) is upregulated in this cont

173 The podocyte-specific glucocorticoid receptor (GR) knockout mice had similar r

174 The steroid hormone-activated glucocorticoid receptor (GR) regulates cellular stress p

175 ted by dexamethasone because it contains two glucocorticoid receptor (GR) response elements (GREs).

176 steroids that are activating ligands for the glucocorticoid receptor (GR) transcription factor.

177 The genomic loci bound by the glucocorticoid receptor (GR), a hormone-activated transc

178 These drugs bind to the glucocorticoid receptor (GR), a ligand-activated transcr

179 our key TFs regulating the fasting response: glucocorticoid receptor (GR), cAMP responsive element bi

180 like transcription factor 15 (KLF15) and the glucocorticoid receptor (GR), cooperate to stimulate pro

181 Dexamethasone (DEX), a synthetic ligand for glucocorticoid receptor (GR), is routinely used to stimu

182 stimulates BC cell growth by binding to the glucocorticoid receptor (GR), the nuclear receptor of en

183 of an alternative nuclear hormone receptor, glucocorticoid receptor (GR), which has similar DNA-bind

184 Glucocorticoids (GCs)-ligands of the glucocorticoid receptor (GR)-are widely used to treat in

185 Finally, we show that glucocorticoid receptor (GR)-regulated genes are signifi

186 HF is a weak endogenous agonist of the human glucocorticoid receptor (GR).

187 hosphate (FPP) and cortisol, ligands for the glucocorticoid receptor (GR).

188 optosis in lymphoid malignancies through the glucocorticoid receptor (GR).

189 ss of androgen receptor (AR) blockade by the glucocorticoid receptor (GR).

190 inter-regional variations relate to those in glucocorticoid receptor (HPA) and androgen receptor (HPG

191 ling, we investigated the role of membranous glucocorticoid receptor (mbGR) by using cell-impermeable

192 of functional variants and haplotypes in the glucocorticoid receptor (NR3C1) and mineralocorticoid re

193 ants in NR3C1 that alter the activity of the glucocorticoid receptor (rs56149945, rs41423247, and rs6

194 t signaling through heterologously expressed glucocorticoid receptor and degradation of a permanently

195 Interestingly, the glucocorticoid receptor and its cofactors affect each ot

196 tectable plasma HIV-1 RNA), co-regulates the glucocorticoid receptor and PPARgamma and transduces hep

197 intron functions as a genomic enhancer where glucocorticoid receptor binding regulates Kappa expressi

198 Mechanistically, activated glucocorticoid receptor binds directly to a glucocortico

199 A disordered region at the N-terminus of the glucocorticoid receptor can fine tune how cells respond

200 and fear-circuit dysfunction, inflammation, glucocorticoid receptor hypersensitivity) in addition to

201 viors, as well as hyperactive fear circuits, glucocorticoid receptor hypersensitivity, and response t

202 ry we present an in silico simulation of the glucocorticoid receptor interaction network, linked to d

203 We conclude that the podocyte glucocorticoid receptor is important for limiting protei

204 and also by compound A, a novel nonsteroidal glucocorticoid receptor ligand.

205 nonsteroidal, selective indazole ether-based glucocorticoid receptor modulators (SGRMs) was developed

206 ds can repress inflammatory gene expression, glucocorticoid receptor recruitment increases expression

207 Induction of glucocorticoid receptor signaling or forkhead box (FOXO)

208 ated cortisol stress, both of which activate glucocorticoid receptor signaling.

209 sulating more interactions/genes involved in glucocorticoid receptor signalling.

210 dentified Pik3r1 (also called p85alpha) as a glucocorticoid receptor target gene.

211 We demonstrate that human glucocorticoid receptor tunes this signaling in vivo by

212 (Ser203, 211, and 226) located in the human glucocorticoid receptor's (GR's) ID AF1 domain.

213 entified the products of NR3C1 (encoding the glucocorticoid receptor), TXNIP (encoding a glucose-feed

214 Glucocorticoids activate the glucocorticoid receptor, a ubiquitous nuclear receptor t

215 (androgen receptor, estrogen receptor alpha, glucocorticoid receptor, mineralocorticoid receptor, and

216 model with podocyte-specific deletion of the glucocorticoid receptor.

217 ical symptoms and variation in genes, NR3C1 (glucocorticoid receptor; GR) and NR3C2 (mineralocorticoi

218 hanisms underlying the opposing functions of glucocorticoid receptors (GRs) and estrogen receptor alp

219 ough interaction with ubiquitously expressed glucocorticoid receptors (GRs), this steroid hormone has

220 ous glucocorticoidogenesis and expression of glucocorticoid receptors are inhibited in psoriatic skin

221 channel NaV1.5 in the heart by the serum and glucocorticoid regulated kinase-1 (SGK1).

222 Glucocorticoid regulation of human ILC2s is largely unkn

223 e strongly associated with inflammation, and glucocorticoid regulation of the inflammatory response w

224 from noradrenergic overactivation and excess glucocorticoid release via hypothalamus-pituitary-adrena

225 balance by rhythmical mineralocorticoid and glucocorticoid release, endogenous accrual of surplus bo

226 bsorption were counterbalanced by rhythmical glucocorticoid release, with excretion of endogenous osm

227 alocorticoid release and elevated rhythmical glucocorticoid release.

228 minimal change disease and primary FSGS, and glucocorticoids remain the initial and often, the primar

229 Glucocorticoids remain the mainstay of therapy in most c

230 ers readily discriminates supraphysiological glucocorticoid replacement doses in patients with CAH.

231 Glucocorticoid replacement therapy is the mainstay of tr

232 hydroxylase deficiency receiving their usual glucocorticoid replacement therapy who were part of the

233 polymyalgia rheumatica that is refractory to glucocorticoids requires further investigation.

234 has been reported to play a critical role in glucocorticoid resistance.

235 easing evidence supports that Th17 cells are glucocorticoid resistant.

236 topoietic stem cells to differentiate into a glucocorticoid-resistant and primed myeloid lineage immu

237 useful for developing approaches to overcome glucocorticoid-resistant immunopathology.

238 nase phosphatase 1 expression, and increased glucocorticoid response element activation.

239 glucocorticoid receptor binds directly to a glucocorticoid response element in the CXCR4 promoter an

240 Human/rat CLDN1 promoters contain glucocorticoid response elements (GREs) and adjacent tra

241 This increased expression was dependent on glucocorticoid response elements upstream of annexins an

242 2 transcription through interaction with the glucocorticoid-response element (GRE) carrying rs6543115

243 binding and transcriptional activity on the glucocorticoid-responsive genes.

244 from human biopsy specimens correlated with glucocorticoid responsiveness in 35 patients with minima

245 Several studies showed that treatment with glucocorticoids restores podocyte differentiation marker

246 n the cytoplasm of cells, and treatment with glucocorticoids resulted in the dissociation of the GR-M

247 We compare glucocorticoid sensitive and resistant immunological dis

248 cells in psoriasis and related diseases are glucocorticoid sensitive.

249 cts of aminophylline on HDAC2 expression and glucocorticoid sensitivity in lipopolysaccharide (LPS)-i

250 fy molecular pathways that are implicated in glucocorticoid sensitivity of Th17 cells in the literatu

251 veral aspects in Th17-related diseases alter glucocorticoid sensitivity of Th17 cells.

252 We hypothesized that the clinical glucocorticoid sensitivity of these asthmatics is reflec

253 udy indicates that aminophylline can restore glucocorticoid sensitivity, which provides a new approac

254 a set of 100 biomarkers primarily related to glucocorticoid signaling and immune function.

255 determined whether disruption of endogenous glucocorticoid signaling in chondrocytes also modulates

256 Endogenous glucocorticoid signaling in chondrocytes attenuates join

257 revious studies demonstrated that endogenous glucocorticoid signaling in osteoblasts promotes inflamm

258 Restoration of efficient endogenous glucocorticoid signaling represents a realistic goal in

259 ortisol concentrations, nor genes regulating glucocorticoid signalling (HSD11B-1, HSD11B-2, NR3C1, NR

260 Understanding the mechanisms of glucocorticoid signalling and how resistance may arise i

261 e Cox proportional hazard models showed that glucocorticoid significantly increased the risk of HBVr.

262 ubjected to treatment with prednisone and/or glucocorticoid-sparing agents.

263 exacerbations, was also effective as an oral glucocorticoid-sparing therapy in patients relying on or

264 uggest that intermittent, rather than daily, glucocorticoid steroid regimen promotes sarcolemmal repa

265 ry at baseline and after 2 weeks of systemic glucocorticoid (steroid) treatment to identify immunolog

266 These data indicate that dosing frequency of glucocorticoid steroids affects muscle remodeling in non

267 ing in mice and found that a single pulse of glucocorticoid steroids improved sarcolemmal repair thro

268 Glucocorticoid steroids such as prednisone are prescribe

269 Glucocorticoid steroids, like prednisone, are known to d

270 ether experimentally elevating levels of the glucocorticoid stress hormone, corticosterone, in broile

271 r tocilizumab on the rates of relapse during glucocorticoid tapering was studied in patients with gia

272 the identification of targets downstream of glucocorticoids that minimize toxicity without compromis

273 ain symptomatic despite prolonged, high-dose glucocorticoid therapy.

274 agonists and medium-to-high doses of inhaled glucocorticoids, those who received tezepelumab had lowe

275 dministrating dexamethasone, a commonly used glucocorticoid to prevent brain edema in GBM patients, s

276 -sparing therapy in patients relying on oral glucocorticoids to manage severe asthma associated with

277 any patients with severe asthma rely on oral glucocorticoids to manage their disease.

278 In glucocorticoid-treated mice, we find that glucocorticoid

279 We then studied whether glucocorticoid treatment can be improved by co-administr

280 Glucocorticoid treatment for 1 year or longer was associ

281 We used Kaplan-Meier analyses to compare glucocorticoid treatment groups for time to stand from s

282 the combination of RhoA/ROCK inhibition and glucocorticoid treatment in dystrophic muscle have a syn

283 Oral glucocorticoid treatment increases fracture risk, and ev

284 Glucocorticoid treatment is recommended as a standard of

285 We compared no glucocorticoid treatment or cumulative treatment duratio

286 Glucocorticoid treatment represents a standard palliativ

287 nergistic effect of RhoA/ROCK inhibition and glucocorticoid treatment, which could lead to the develo

288 s of patients who have severe asthma despite glucocorticoid treatment; these cells are associated wit

289 l structure of GR in complex with the potent glucocorticoid triamcinolone acetonide (TA) and a fragme

290 salt-driven changes in mineralocorticoid and glucocorticoid urinary excretion on day-to-day osmolyte

291 9%) deaths in 58 patients with no history of glucocorticoid use (odds ratio 0.47, 95% CI 0.22-1.00; p

292 than did placebo, thus allowing for reduced glucocorticoid use.

293 nhalants for obstructive airway diseases and glucocorticoid use.

294 However, glucocorticoids used as treatment contribute to the morb

295 ory drug users, 0.97 (95% CI, 0.82-1.14) for glucocorticoid users, and 1.05 (95% CI, 0.90-1.21) for c

296 y drug users, 17.4% (95% CI, 15.4-19.5%) for glucocorticoid users, and 19.0% (95% CI, 16.3-20.2%) for

297 uction of bone formation may be regulated by glucocorticoids via inhibition of TGF-beta gene expressi

298 thyroid AAbs in CSU are linked to the use of glucocorticoids (weak evidence) but not to disease durat

299 as managed conservatively with high doses of glucocorticoids, which resulted in prompt resolution of

300 e C5a receptor inhibitor, could replace oral glucocorticoids without compromising efficacy.