ライフサイエンスコーパス: glucocorticoid

1 r greater than 10 mg/d (all P < 0.001 vs. no glucocorticoids).

2 r greater than 10 mg/d (all P < 0.001 vs. no glucocorticoids).

3 red the sensitivity of gene transcription to glucocorticoids.

4 t were induced by androgens, progestins, and glucocorticoids.

5 s and 39.5% of Optum patients were receiving glucocorticoids.

6 imaging, before and after administration of glucocorticoids.

7 bute to the cell type-specific activities of glucocorticoids.

8 rbated in people receiving LABA or LABA plus glucocorticoids.

9 and, when indicated, supplemental oxygen and glucocorticoids.

10 uppressive properties commonly attributed to glucocorticoids.

11 oup versus 47% in the control group received glucocorticoids 2 years after transplantation (P=0.04).

12 the muscle, and is known to be responsive to glucocorticoid, a class of anti-inflammatory drugs commo

13 One of the main mechanisms by which glucocorticoids achieve such deleterious outcome in bone

14 The connection between adipose glucocorticoid action and whole-body metabolism is incom

15 Thus, LABAs modulate glucocorticoid action, and comparable transcriptome-wide

16 s sensitive to small, physiologic changes in glucocorticoid activity, as evidenced by the lack of cir

17 Associations persisted after oral glucocorticoid adjustment.

18 sponse of circulating eosinophils to in vivo glucocorticoid administration in 3 species and found tha

19 owing for aggressive clinical management and glucocorticoid administration, which have been shown to

20 which we used to test a protective role for glucocorticoids against stress.

21 mptoms, as well as the protective effects of glucocorticoids against their development.

22 cocorticoids, leading us to hypothesize that glucocorticoids alone can swiftly increase the 3',5'-cyc

23 Glucocorticoids also inhibit osteoblastogenesis and prom

24 enolate mofetil or cyclophosphamide and with glucocorticoids, although these treatments are not unifo

25 edge) to systematically investigate specific glucocorticoid and catecholamine actions on the porcine

26 To conclude, this study identified a set of glucocorticoid and immune-related genes in association w

27 gest that transcriptional cross-talk between glucocorticoid and steroid sex hormone signaling represe

28 , monocyte-macrophage lineage cells produced glucocorticoids and genetic ablation of steroidogenesis

29 egmental glomerulosclerosis lesions includes glucocorticoids and other immunosuppressive drugs; indiv

30 val, albeit with considerable morbidity from glucocorticoids and other immunosuppressive medications.

31 angement that is differentially regulated by glucocorticoids and specialized proresolving mediators t

32 Careful use of glucocorticoids and the application of preventive strate

33 ntially confounding medications (fluorinated glucocorticoids and/or intravenous immunoglobulin) after

34 in, norepinephrine, hypocretin, vasopressin, glucocorticoids, and neuroimmune factors) in the extende

35 As glucocorticoids are associated with important adverse ef

36 Glucocorticoids are considered first-line therapy in a v

37 Glucocorticoids are effective, but adverse effects occur

38 Low-dose glucocorticoids are frequently used for the management o

39 Glucocorticoids are indispensable for PD-1 induction on

40 Antihistamines and/or glucocorticoids are not reliable interventions to preven

41 Glucocorticoids are potent endogenous anti-inflammatory

42 Glucocorticoids are powerful, broad-spectrum anti-inflam

43 Glucocorticoids are primary stress hormones that regulat

44 Glucocorticoids are the cornerstone of treatment for GCA

45 Glucocorticoids are the mainstay of treatment; however,

46 Glucocorticoids are widely used for the suppression of i

47 Glucocorticoids are widely used to reduce disease activi

48 Glucocorticoids are widely used to suppress inflammation

49 er, only few pediatric studies have examined glucocorticoid associations with hippocampal subfield vo

50 ace when intestinal epithelia are exposed to glucocorticoids at birth.

51 onary neutrophilia persists without rhythmic glucocorticoid availability.

52 oid progenitor and provide new insights into glucocorticoid-based therapeutic strategies for the trea

53 ell as localized pharmacologic inhibition of glucocorticoid biosynthesis improved tumor growth contro

54 nd many of these changes were reduced by the glucocorticoid budesonide.

55 Persistent disruption of homeostatic glucocorticoid circadian rhythmicity due to chronic stre

56 In response to stress, maternal glucocorticoid circuit activation corresponded with indi

57 human skin transcriptome induced by topical glucocorticoid clobetasol propionate (CBP) in healthy vo

58 rsity led to a 9 to 14% increase in females' glucocorticoid concentrations across adulthood.

59 e direct effects of early adversity on adult glucocorticoid concentrations were 11 times stronger tha

60 Body temperature may affect glucocorticoid concentrations, particularly in ectotherm

61 to explain the effects of early adversity on glucocorticoid concentrations.

62 Altogether, our work reveals that IL7 and glucocorticoids coordinately drive aberrant activation o

63 evelopment and function, we investigated the glucocorticoid/CXCR4 axis in mice.

64 tions of person-years spent at each level of glucocorticoid daily exposure were 80% for non-use, 6.0%

65 inhibition versus stimulation and do so via glucocorticoid-dependent and -independent mechanisms, re

66 potentiate cocaine seeking in male rats via glucocorticoid-dependent cannabinoid type-1 receptor (CB

67 Frontline therapy for HLH consists of the glucocorticoid dexamethasone (DEX) and the chemotherapeu

68 In this study, in human NK cells, the glucocorticoid dexamethasone downregulated LIMK expressi

69 Our results indicate that glucocorticoids directly up-regulate DPP4 expression and

70 Associations between glucocorticoid dose (none, <=5 mg/d, >5 to 10 mg/d, and

71 is uncertain whether or not low to moderate glucocorticoid dose increases cardiovascular risk.

72 ed an increased risk of CVDs associated with glucocorticoid dose intake even at lower doses (<5 mg) i

73 6% versus 11.0% (95% CI, 10.6% to 11.5%) for glucocorticoid dose of 5 mg or less per day, 14.4% (CI,

74 was 4.0% versus 5.2% (CI, 4.7% to 5.8%) for glucocorticoid dose of 5 mg or less per day, 8.1% (CI, 7

75 We aimed to quantify glucocorticoid dose-dependent cardiovascular risk in peo

76 esidual confounding and misclassification of glucocorticoid dose.

77 d use of primary prevention treatment at all glucocorticoid doses.

78 This is important because glucocorticoid-driven maturational changes in fetal card

79 hormones, including estrogens, androgens or glucocorticoids during pregnancy results in chronic cond

80 Glucocorticoids (e.g. prednisolone) remain the only drug

81 ment with dexamethasone, a classic synthetic glucocorticoid, enhanced survival of critically ill pati

82 Thus, glucocorticoids exert bimodal restraints on inflammation

83 Here, we report that perinatal glucocorticoid exposure had long-term consequences and r

84 We found that perinatal glucocorticoid exposure resulted in persistent alteratio

85 Intranasal treatment with the synthetic glucocorticoid fluticasone propionate prevented chitosan

86 e (AD), associated with elevated circulating glucocorticoids (GC) and glucocorticoid receptors (GR) s

87 Glucocorticoids (GC) are a controversial yet commonly us

88 ic health, the impacts of maternal excessive glucocorticoids (GC) on fetal brown adipose tissue (BAT)

89 Despite their notorious adverse effects, glucocorticoids (GC, potent anti-inflammatory drugs) are

90 Glucocorticoids (GCs) are a central component of therapy

91 Glucocorticoids (GCs) are potent anti-inflammatory drugs

92 Glucocorticoids (GCs) are small lipid hormones produced

93 be mediated in part via enhanced exposure to glucocorticoids (GCs), which are known to impact neuroge

94 confers susceptibility to anti-inflammatory glucocorticoids (GCs).

95 Patients in the glucocorticoid group also displayed less frequent organ

96 Although hormones such as glucocorticoids have been broadly accepted in recent dec

97 cal therapy and intraarticular injections of glucocorticoids have been shown to confer clinical benef

98 Therapeutic glucocorticoids have been widely used in rheumatic disea

99 Paradoxically, glucocorticoids have only a limited efficacy in controll

100 elective drugs on the basis of the action of glucocorticoids have proven difficult.

101 The specific cellular mechanisms by which glucocorticoids have their therapeutic action have been

102 Of note, glucocorticoids highly stimulated macrophage mobility; u

103 how that stress promotes VOEs by eliciting a glucocorticoid hormonal response that augments gut perme

104 versity, adult social bonds, and adult fecal glucocorticoid hormone concentrations (a measure of hypo

105 There is extensive evidence that glucocorticoid hormones enhance memory consolidation, he

106 Variation in the regulation of glucocorticoid hormones, which mediate the phenotypic re

107 rature on plasma corticosterone (predominant glucocorticoid in reptiles) in eastern fence lizards (Sc

108 enous immune globulin was used in 144 (77%), glucocorticoids in 91 (49%), and interleukin-6 or 1RA in

109 osinopenia has been the basis for the use of glucocorticoids in eosinophilic disorders, and it has in

110 vide insight into the mechanism of action of glucocorticoids in eosinophilic disorders, with implicat

111 method was successfully applied to determine glucocorticoids in industrial canal water.

112 in the understanding of the central role of glucocorticoids in preparing the fetus for life after bi

113 the cell types and intracellular targets of glucocorticoids in rheumatic diseases have not been full

114 g some signs of decline, the use of systemic glucocorticoids in rheumatology is likely to continue to

115 The safety and efficacy of antenatal glucocorticoids in women in low-resource countries who a

116 Changes in the levels of metabolic hormones (glucocorticoids) in response to variation in food and de

117 Glucocorticoids increased the heart rate and muscle cont

118 We show that glucocorticoids induce KLF9 expression in the human airw

119 A549 and BEAS-2B pulmonary epithelial cells, glucocorticoids induce KLF9 expression with similar kine

120 Glucocorticoids induced rapid bone marrow homing of eosi

121 each GBS into luciferase reporters revealed glucocorticoid-induced activity requiring a glucocortico

122 a2), compared with control matrices (VehMs), glucocorticoid-induced cell-derived matrices (GIMs) trig

123 coid signaling and the mechanisms underlying glucocorticoid-induced developmental programming.

124 Moreover, glucocorticoid-induced DPP4 activation was also observed

125 Additionally, we show that glucocorticoid-induced DPP4 expression is blocked by the

126 The kinetics of glucocorticoid-induced eosinopenia and bone marrow migra

127 The phenomenon of glucocorticoid-induced eosinopenia has been the basis fo

128 Our results indicate that glucocorticoid-induced eosinopenia results from CXCR4-de

129 and BEAS-2B ChIP-seq data reveal four common glucocorticoid-induced GR binding sites (GBSs).

130 report that stress elicits glucocorticoid-induced gut permeability, in turn trigger

131 ed aldosterone-induced gene is the serum and glucocorticoid-induced kinase (SGK1), which acts downstr

132 sitol-3 kinase (PI(3) -Kinase)/AKT/Serum and glucocorticoid-induced kinase-1(SGK-1) pathway resulted

133 ge mobility; unexpectedly, DPP4 mediated the glucocorticoid-induced macrophage migration, and siRNA-m

134 mportant and common iatrogenic complication, glucocorticoid-induced osteoporosis, in a substantial pr

135 hormone, are involved in the pathogenesis of glucocorticoid-induced osteoporosis.

136 ithin the fetal lung, causing a break in the glucocorticoid-induced positive feedforward loop.

137 ade of CXCR4 reduced or eliminated the early glucocorticoid-induced reduction in blood eosinophils.

138 When subjected to either restraint- or glucocorticoid-induced stress paradigms.

139 , and stress responses, including stress and glucocorticoid-induced suppression of pulsatile luteiniz

140 Furthermore inhibition of glucocorticoid-induced TNF-receptor-related and Ebi3 par

141 NF-receptor-superfamily-member 18 (TNFRSF18, glucocorticoid-induced TNF-receptor-related) and EBV-ind

142 Glucocorticoid-induced TNFR family related gene (GITR) i

143 rthermore, we found that BD(L) expression of glucocorticoid-induced tumor necrosis factor ligand (GIT

144 Chorein upregulates the serum and glucocorticoid inducible kinase SGK1.

145 Serum- and glucocorticoid-inducible kinase 1 (SGK1) transcription,

146 PR-4/neuropeptide receptor, SGK-1/serum- and glucocorticoid-inducible kinase, and specific isoforms o

147 nse in dendritic cells-the activation of the glucocorticoid-inducible transcriptional regulator TSC22

148 Moreover, glucocorticoid induction of 11beta-hsd1, C/ebpalpha and

149 Glucocorticoids inhibit adrenal androgen production.

150 Physical therapy versus glucocorticoid injection for osteoarthritis of the knee.

151 seline WOMAC scores were 108.8+/-47.1 in the glucocorticoid injection group and 107.1+/-42.4 in the p

152 mized trial to compare physical therapy with glucocorticoid injection in the primary care setting in

153 andomly assigned in a 1:1 ratio to receive a glucocorticoid injection or to undergo physical therapy.

154 than patients who received an intraarticular glucocorticoid injection.

155 One patient fainted while receiving a glucocorticoid injection.

156 The glucocorticoid-insensitive hyperrresponsiveness in isola

157 e of a novel immune suppressive mechanism of glucocorticoids involving the transcriptional and transl

158 This analysis revealed that the response to glucocorticoids is highly cell type dependent, in terms

159 for all patients with long-term use of oral glucocorticoids is required.

160 e kinase 3 (PI3K/GSK3) signaling, with serum-glucocorticoid kinase 1 (SGK1), an inhibitor of glycogen

161 High doses and long-term use of glucocorticoids lead to an important and common iatrogen

162 ell signaling effects have been reported for glucocorticoids, leading us to hypothesize that glucocor

163 campal subregions were related to cumulative glucocorticoid levels (hair cortisol), parenting stress,

164 o the powerful effects of early adversity on glucocorticoid levels in adulthood.

165 Glucocorticoids mainly increase bone resorption during t

166 Glucocorticoids may modulate inflammation-mediated lung

167 als have proposed that the administration of glucocorticoids may modulate this effect.

168 Overall, a model for glucocorticoid-mediated regulation of KLF9 involving mul

169 ated miRNAs by luciferase reporter assays of glucocorticoid-mediated transrepression and predicted re

170 of stereotypies, as well as on body weight, glucocorticoid metabolite concentrations, and behavior i

171 lucocorticoid receptor (GR) elicits variable glucocorticoid-modulated transcriptomes in different cel

172 lative to other organ systems, maturation by glucocorticoids of the fetal cardiovascular system has b

173 Several indirect effects of glucocorticoids on bone metabolism, such as suppression

174 Here, we review the effects of glucocorticoids on fetal basal cardiovascular function a

175 giotensin-aldosterone system and the adrenal glucocorticoid pathway, with a smaller fraction caused b

176 he drug anakinra, but not treatment with the glucocorticoid prednisolone, prevented these changes.

177 estimated time-variant daily and cumulative glucocorticoid prednisolone-equivalent dose-related risk

178 midine, secondary bile acid, and neuroactive glucocorticoid/pregnanolone-type steroidal metabolites.

179 nce supports a role for antihistamine and/or glucocorticoid premedication in specific chemotherapy pr

180 ional zonation, with induction of Cyp11b2 in glucocorticoid-producing zona fasciculata cells.

181 leads to enhanced sympathetic signaling and glucocorticoid production, which influences neutrophil a

182 vary within and across steroid classes (i.e. glucocorticoids, progestogens, sex steroids), emphasizin

183 Glucocorticoids promote CXCR4 expression by T cells, mon

184 related to stress adaptation, including the glucocorticoid receptor (encoded by NR3C1).

185 The glucocorticoid receptor (GR) and KLF15 form a feed-forwa

186 meostasis through two nuclear receptors, the glucocorticoid receptor (GR) and mineralocorticoid recep

187 al expression of tyrosine hydroxylase (Th)], glucocorticoid receptor (GR) and plasma corticosterone,

188 Glucocorticoid receptor (GR) and STAT3 bind to the same

189 tiinflammatory corticosteroids targeting the glucocorticoid receptor (GR) are the current standard of

190 tures to MIEs for androgen receptor (AR) and glucocorticoid receptor (GR) binding using ToxCast data.

191 Activation of the glucocorticoid receptor (GR) by the synthetic corticoste

192 Ligand-activated glucocorticoid receptor (GR) elicits variable glucocorti

193 haracterized by high levels of expression of glucocorticoid receptor (GR) encoded by NR3C1.

194 Here, we identified a gradient of increasing glucocorticoid receptor (GR) expression and signaling fr

195 ad reduced glucose transporter 1 (GLUT1) and glucocorticoid receptor (GR) expression in response to D

196 To assess the role of the Glucocorticoid Receptor (GR) in such programming, we use

197 ng studies revealed that PI3Ks act to reduce glucocorticoid receptor (GR) levels, which are rescued b

198 of inactive 11-dehydrocorticosterone to the glucocorticoid receptor (GR) ligand, corticosterone.

199 Noninvasive methods to study glucocorticoid receptor (GR) signaling are urgently need

200 m latency, in part because activation of the glucocorticoid receptor (GR) stimulates productive infec

201 etic, and epigenetic research has linked the glucocorticoid receptor (GR) to memory processes, and to

202 steroid levels, leading to activation of the glucocorticoid receptor (GR), a pioneer transcription fa

203 2) Glucocorticoid receptor (GR), an immunity-modulating tra

204 oliferator-activated receptor gamma (PPARG), glucocorticoid receptor (GR), and thyroid hormone recept

205 atory molecules, and their cognate receptor, glucocorticoid receptor (GR), is expressed in nearly all

206 ia corticosteroid-mediated activation of the glucocorticoid receptor (GR), stimulates viral gene expr

207 cals, hormones, and estrogen-receptor (ER)-, glucocorticoid receptor (GR)-, and peroxisome proliferat

208 increased corticosteroid levels activate the glucocorticoid receptor (GR).

209 d direct podocyte protective effects via the glucocorticoid receptor (GR).

210 of the circadian clock and repressors of the glucocorticoid receptor (GR).

211 Phosphorylation of the glucocorticoid receptor (GR:NR3C1) and activation of NR4

212 uantified the dynamics of the cell cycle and glucocorticoid receptor activation, and explored their i

213 n regulating transcriptional activity of the glucocorticoid receptor and has multiple functions relat

214 otropin-releasing factor antagonists and the glucocorticoid receptor antagonist mifepristone, the HPT

215 Treatment of mutant mice with the glucocorticoid receptor antagonist RU486 restored KLF15

216 particular, Fkbp5 mRNA, which codes for the glucocorticoid receptor co-chaperone protein FKBP51, was

217 activity in transgenic plants bearing an ANT-glucocorticoid receptor fusion construct.

218 In mammals, methylation of the glucocorticoid receptor gene Nr3c1 has been implicated a

219 First, S1PR1 regulates NFkappaB and nuclear glucocorticoid receptor pathways to suppress inflammatio

220 There were no effects on sperm count and glucocorticoid receptor protein levels within the epidid

221 ith phosphorylated CREB and ligand-activated glucocorticoid receptor to directly control the inductio

222 Driving minimal promoters with exogenous (glucocorticoid receptor) or synthetic transcription fact

223 and synaptic function, immune signaling, and glucocorticoid receptor/stress response showed enrichmen

224 levated circulating glucocorticoids (GC) and glucocorticoid receptors (GR) signaling impairment.

225 Using a novel strain of mice lacking glucocorticoid receptors (GRs) specifically in B cells,

226 story we present began with the discovery of glucocorticoid receptors in hippocampus and has extended

227 he effect of tissue-specific manipulation of glucocorticoid receptors in mouse models of inflammation

228 spring, including ones in white matter/glia, glucocorticoid receptors, neuroimmune outcomes, cerebrov

229 in patients 12 years of age or older who had glucocorticoid-refractory acute GVHD after allogeneic st

230 , showed potential efficacy in patients with glucocorticoid-refractory acute GVHD.

231 We propose that endogenous glucocorticoids regulate a dynamic mode of B cell migrat

232 ges, and eosinophils, but it is not known if glucocorticoids regulate CXCR4 in B cells.

233 n anemia (DBA), the mechanisms through which glucocorticoids regulate human erythropoiesis remain poo

234 arental Holocaust exposure were enriched for glucocorticoid-regulated genes and immune pathways with

235 Among glucocorticoid-regulated genes, we identified the exopep

236 mTORC1 and mTORC2-specific serum/glucocorticoid-regulated kinase 1 (SGK1) are constitutiv

237 ective pressures in driving the evolution of glucocorticoid regulation.

238 the dependence of the memory enhancement on glucocorticoid release during the immediate posttraining

239 ei of the stria terminalis (avBST) regulates glucocorticoid release, suggesting the potential for avB

240 isorders, with implications for the study of glucocorticoid resistance and the development of more ta

241 glucocorticoid-induced activity requiring a glucocorticoid response element (GRE) within each distal

242 ding increased interferon response genes and glucocorticoid response genes.

243 LP treatment induced the expression of glucocorticoid responsive gene Fkbp5 in the allograft.

244 onsistent with those of the induction of the glucocorticoid-responsive chemokine receptor CXCR4, and

245 duces DPP4 gene expression by binding to two glucocorticoid-responsive elements (GREs) within the DPP

246 dipeptidyl peptidase-4 (DPP4) as a critical glucocorticoid-responsive gene in THP1-MPhi.

247 hy volunteers identified numerous unreported glucocorticoid-responsive genes, including over a thousa

248 Altogether, these data identify a unique glucocorticoid-responsive human erythroid progenitor and

249 aberrant overexpression of Tsc22d3 (GILZ), a glucocorticoid-responsive transcription factor not norma

250 to support the role of antihistamines and/or glucocorticoid routine premedication in patients receivi

251 e differences are in part driven by aberrant glucocorticoid secretion during development, with strong

252 RFRP neuronal activation markedly stimulated glucocorticoid secretion, demonstrating a feedback loop

253 ation, whereas neither manipulation affected glucocorticoid secretion.

254 normally associated with diurnal patterns of glucocorticoid secretion.

255 The actions of glucocorticoids seem to be highly cell-type and context

256 5 methylation was associated with indices of glucocorticoid sensitivity but not with basal FKBP5 gene

257 A membrane- impermeable glucocorticoid showed similarly rapid stimulation of cAM

258 Glucocorticoid signaling also acutely recruits BDNF to e

259 work of differentially methylated regions in glucocorticoid signaling and inflammation-related genes

260 for investigating the developmental roles of glucocorticoid signaling and the mechanisms underlying g

261 Active glucocorticoid signaling associated with failure to resp

262 us showed dysregulation of genes involved in glucocorticoid signaling pathway (HPA axis) in the ventr

263 BAT ALK7 results in excessive activation of glucocorticoid signaling upon fasting.

264 esults in reduced 11beta-HSD1 expression and glucocorticoid signaling within the fetal lung, causing

265 knockdown of G(alphas) virtually eliminated glucocorticoid-stimulated cAMP responses, suggesting tha

266 The glucocorticoid stress response is frequently used to ind

267 Pretreatment with a glucocorticoid synthesis inhibitor blocked the memory en

268 Importantly, the inhibition of glucocorticoids synthesis, blockade of IL-17A, or deplet

269 ociated with differential methylation in the glucocorticoid system that might influence stress and in

270 had little effect on responses to any of the glucocorticoids tested.

271 ular health of the preterm baby of antenatal glucocorticoid therapy administered to pregnant women th

272 ent, we discuss the immunological impacts of glucocorticoid therapy for COVID-19.

273 n in macrophages, potentially explaining why glucocorticoid therapy is less effective in controlling

274 Antenatal glucocorticoid therapy reduces mortality in the preterm

275 imal GBSs drove modest reporter induction by glucocorticoids, this region exhibited basal eRNA produc

276 at least in part, mediated by the ability of glucocorticoids to cause transcriptional upregulation of

277 Mechanistically, glucocorticoids together with IL-12, IL-15, and IL-18 no

278 rd of the gene expression changes induced by glucocorticoid treatment and shifts the view of how this

279 gical pathways associated with low BMD after glucocorticoid treatment in asthmatics using gene expres

280 Asthma resistance to glucocorticoid treatment is a major health problem with

281 ents with (GC) and without (noGC) daily oral glucocorticoid treatment was determined (n = 318).

282 Post glucocorticoid treatment, interactions between distal an

283 tive disease; acute blindness is rare during glucocorticoid treatment.

284 not all patients have a response to standard glucocorticoid treatment.

285 We demonstrate that glucocorticoids upregulate CXCR4 mRNA and protein in mou

286 Compared to periods of non-glucocorticoid use, those with <5.0 mg daily prednisolon

287 ; 95% CI, 3.57 to 6.56), height, weight, and glucocorticoid use.

288 Here, we isolated direct effects of glucocorticoids using the chicken embryo, a model system

289 th Dexamethasone (mAv-Dex), a broad-spectrum glucocorticoid, using a combination of hydrolysable este

290 ed infection in Optum patients not receiving glucocorticoids was 4.0% versus 5.2% (CI, 4.7% to 5.8%)

291 infection in Medicare patients not receiving glucocorticoids was 8.6% versus 11.0% (95% CI, 10.6% to

292 , and analysis for the determination of nine glucocorticoids was developed.

293 part, because the effect of social bonds on glucocorticoids was weak compared to the powerful effect

294 Dasatinib plus glucocorticoids were administered, followed by two cycle

295 ents with RA receiving stable DMARD therapy, glucocorticoids were associated with a dose-dependent in

296 The limits of detection for the glucocorticoids were between 0.03 and 0.17 ng/mL, wherea

297 Glucocorticoids were reported to upregulate 11beta-HSD1

298 y therapies for many glomerular diseases are glucocorticoids, which exert their immunosuppressive and

299 Multiple environmental stressors induce glucocorticoids, which prompted us to investigate their

300 ians should balance the benefits of low-dose glucocorticoids with this potential risk.