ライフサイエンスコーパス: adrenal

1 D3, 1,20,25(OH)3D3 and 1,20,26(OH)3D3 in the adrenals.

2 m 100 pmol/g to 500 pmol/g) independent of adrenals.

3 in complex with progesterone, a substrate in adrenal 21-hydroxylation.

4 the eyes (4.5 %ID/g) or (68)Ga-avebetrin in adrenals (25.9 %ID/g), respectively, were found, which w

5 ction during the RF active phase reflects an adrenal aberrant activation of CREB signaling, which sel

6 the mass was a pheochromocytoma, a cortical adrenal adenoma was histologically proven.

7 The relationship between age and adrenal aldosterone synthase (CYP11B2) expression was ev

8 rst steroid, pregnenolone, is synthesized in adrenal and gonadal tissues to initiate steroid synthesi

9 the activation of the hypothalamic-pituitary-adrenal and hypothalamic-pituitary-thyroid axes, as well

10 In primary adrenal and non-transfected H295R cells, compound 8 decr

11 Two malignant (adrenal and renal carcinoma) lesions and one precancerou

12 Our results show increased adrenal and renal expression of hCYP11B2 in transgenic m

13 teristics of the human disease with abnormal adrenal and renal morphology.

14 rine growth restriction (IUGR) with gonadal, adrenal, and bone marrow failure, predisposition to infe

15 patients (91%) had familial, multiple, extra-adrenal, and/or malignant tumors and/or were younger tha

16 The brain and adrenal are critical control centers that maintain body

17 The adrenals are a major endocrine site of production/secret

18 As expected, Sim1CrhKO mice exhibit adrenal atrophy as well as decreased basal, diurnal and

19 h propranolol and the hypothalamic-pituitary-adrenal axis (HPA) with mifepristone.

20 ons with demonstrable hypothalamic-pituitary-adrenal axis abnormalities.

21 nstead of consecutive hypothalamus-pituitary-adrenal axis activation, we report that acute SCI in mic

22 Increased hypothalamic-pituitary-adrenal axis activity leads to increased levels of gluco

23 anxiety behavior and hypothalamic-pituitary-adrenal axis activity, likely through modulation of hipp

24 ession, and increased hypothalamic-pituitary-adrenal axis activity.

25 diated attenuation of hypothalamic-pituitary-adrenal axis activity.

26 ation, or exacerbated hypothalamic-pituitary-adrenal axis activity.

27 ghrelin regulates the hypothalamic-pituitary-adrenal axis and affects anxiety and mood disorders, suc

28 N Sirt1 activates the hypothalamic-pituitary-adrenal axis and basal GC levels by enhancing the produc

29 ted by inhibiting the hypothalamic-pituitary-adrenal axis and inflammatory responses to stress.

30 al that impairment of hypothalamic-pituitary-adrenal axis during depression can lead to olfactory def

31 oendocrine markers of hypothalamic-pituitary-adrenal axis function were examined in a sample of 122 c

32 s without influencing hypothalamic-pituitary-adrenal axis function.

33 rgic, neurons induced hypothalamic-pituitary-adrenal axis hyperactivity and reduced fear- and anxiety

34 glial activation, and hypothalamic-pituitary-adrenal axis hyperactivity in stress vulnerability.

35 The hypothalamic-pituitary-adrenal axis is a dynamic system regulating glucocortico

36 The hypothalamic-pituitary-adrenal axis is a pivotal component of an organism's res

37 The hypothalamus-pituitary-adrenal axis is sensitive to changes in the early-life e

38 catecholaminergic and hypothalamic-pituitary-adrenal axis leads to splenic atrophy and contraction of

39 sion to study whether hypothalamic-pituitary-adrenal axis perturbation could be sufficient to provoke

40 central component of hypothalamic-pituitary-adrenal axis regulation that prepares the organism for s

41 ein 51 is involved in hypothalamic-pituitary-adrenal axis regulation.

42 with an insufficient hypothalamic-pituitary-adrenal axis response and the optimum treatment for this

43 Evaluation of the hypothalamic-pituitary-adrenal axis response in these animals revealed an incre

44 knockdown had reduced hypothalamic-pituitary-adrenal axis responses to both acute and chronic stress

45 group showed altered hypothalamus-pituitary-adrenal axis responses to stress, evidenced by lower ACT

46 stimuli activate the hypothalamic-pituitary-adrenal axis resulting in increased steroidogenic activi

47 corticoid release via hypothalamus-pituitary-adrenal axis stimulation.

48 gnificantly increased hypothalamic-pituitary-adrenal axis stress response and impaired sensorimotor g

49 ic nervous system and hypothalamic-pituitary-adrenal axis) transcription factor activation.

50 omote arousal via the hypothalamic-pituitary-adrenal axis, but rather probably acts via brainstem crh

51 s hormone system, the hypothalamic-pituitary-adrenal axis, contributes to variability in stress-relat

52 abnormalities in the hypothalamic-pituitary-adrenal axis, including signaling by corticotropin-relea

53 nic stress alters the hypothalamic-pituitary-adrenal axis, increases gut motility, and increases the

54 nsmitter systems, the hypothalamic-pituitary-adrenal axis, metabolic hormonal pathways, inflammatory

55 C), the amygdala, and hypothalamic-pituitary-adrenal axis, the precise genetic and experiential contr

56 the regulation of the hypothalamic-pituitary-adrenal axis, thereby affecting an individual's ability

57 d inactivation of the hypothalamic-pituitary-adrenal axis, without affecting energy expenditure or gl

58 region modulating the hypothalamic-pituitary-adrenal axis-and somatosensory, viscerosensory, and inte

59 the amygdala and the hypothalamic-pituitary-adrenal axis.

60 ons, by affecting the hypothalamic-pituitary-adrenal axis.

61 ajor regulator of the hypothalamic-pituitary-adrenal axis.

62 ng hormone (CRH) and then stimulation of the adrenal by ACTH.

63 Conclusion Adrenal calcifications identified on CT scans are common

64 The prevalence of adrenal calcifications in patients with fCCM was compare

65 Adrenal calcifications in patients with fCCM were more f

66 Purpose To determine if adrenal calcifications seen at computed tomography (CT)

67 Thus, the adrenal capsule acts as a central signaling center that

68 ed in lysosomes of cortical cells, a type of adrenal cell present in the culture.

69 Adrenal cell transplantation and the restoration of HPA

70 improved significantly both the capacity of adrenal cells for stable, long-term basal hormone releas

71 rometry (ToF-SIMS) to image chemically fixed adrenal cells prepared for transmission electron microsc

72 In adrenal cells, MRAP is essential for adrenocorticotropic

73 tical cell line, H295R, and in primary human adrenal cells.

74 We investigated this question in mouse adrenal chromaffin cells and found that SNAP-25 inhibits

75 Using adrenal chromaffin cells and neurons, we now find that b

76 ystem that controls epinephrine release from adrenal chromaffin cells and, consequently, hepatic gluc

77 examined secretion from Munc18-1-null mouse adrenal chromaffin cells expressing Munc18-1 mutants des

78 h electrophysiological measurements in mouse adrenal chromaffin cells, we show that PI(4,5)P2 uncagin

79 les in two sequential priming steps in mouse adrenal chromaffin cells.

80 ephrine uptake at the synaptic terminals and adrenal chromaffin cells.

81 esent the electrochemical response to single adrenal chromaffin vesicles filled with catecholamine ho

82 one tenth of the catecholamine compared with adrenal chromaffin vesicles.

83 and subtype differentiation was performed by adrenal computed tomography scanning and adrenal vein sa

84 In support of the brain-adrenal connection in stress, many (but not all) depress

85 high levels in peripheral tissues, including adrenal cortex (E16-E21) and cochlear ganglia (E19-P3),

86 g in increased steroidogenic activity in the adrenal cortex and an elevation of cortisol levels in th

87 pituitary-adrenal (LHPA) axis, with enlarged adrenal cortex and increased glucocorticoid levels.

88 rect Sf1 expression exclusively in the fetal adrenal cortex and is bound by both Sf1 and Dax1.

89 Aldosterone, synthesized in the adrenal cortex by the enzyme CYP11B2, induces positive s

90 Adrenal Cortex Carcinoma (ACC) is an aggressive tumour w

91 logical control of cortisol synthesis in the adrenal cortex involves stimulation of adrenocorticotrop

92 Glucocorticoid production in the adrenal cortex is activated in response to an increase i

93 nduced and maintained and how renewal of the adrenal cortex is ensured remain a mystery.

94 gh levels of glucocorticoids produced by the adrenal cortex of the stressed subject reduce neurogenes

95 Adrenal cortex physiology relies on functional zonation,

96 that PKA acts as a tumour suppressor in the adrenal cortex, through repression of WNT signalling.

97 5 may have tumor suppressor functions in the adrenal cortex.

98 n or by autonomous cortisol release from the adrenal cortex.

99 During stress, adrenal corticosterone and hippocampal corticotropin-rel

100 ere also able to demonstrate increased intra-adrenal corticosterone levels and an increase in steroid

101 l subjects were given metyrapone (to inhibit adrenal cortisol secretion) + /- hydrocortisone (HC) in

102 this plasticity requires neuropeptide Y, an adrenal cotransmitter and the activation of adrenal Y5 r

103 pin-releasing hormone/hypothalamic-pituitary-adrenal (CRH/HPA) axis and the sympathomedullary system.

104 ther tissues local metabolism of ovarian and adrenal-derived androgens regulate AR-dependent gene exp

105 A fetal adrenal enhancer (FAdE) in the Sf1 gene was previously i

106 and brain lesion count were associated with adrenal findings in patients with fCCM.

107 amples of human serum and epidermis, and pig adrenals for the presence of intermediates and products

108 APCCs were studied in 42 normal adrenals from kidney donors.

109 th, cardiovascular development and pituitary-adrenal function of isolated chronic developmental hypox

110 tion, thereby underscoring the importance of adrenal function on survival.

111 dations include greater vigilance in testing adrenal function than current standard practice.

112 FCs in the left adrenal gland than the right adrenal gland and 50 of the 61 observed SFCs (82%) found

113 essory protein (MRAP) is highly expressed in adrenal gland and adipose tissue.

114 nance imaging excluded common lesions of the adrenal gland and showed lymphadenopathy around the majo

115 Zona glomerulosa cells (ZG) of the adrenal gland constantly integrate fluctuating ionic, ho

116 al in fetal development, T-cell function and adrenal gland growth homeostasis, and that the functions

117 These mice also develop adrenal gland hyperplasia in old age.

118 ssociated with risks of primary macronodular adrenal gland hyperplasia.

119 ed with controls, aged HCM females exhibited adrenal gland hypertrophy, reduced volume in mood-relate

120 high-thoracic level (Th1) SCI disconnecting adrenal gland innervation, compared with low-thoracic le

121 of 19 patients having more SFCs in the left adrenal gland than the right adrenal gland and 50 of the

122 ing adenomas (APAs) are benign tumors of the adrenal gland that constitutively produce the salt-retai

123 ation of fresh frozen mouse liver and rabbit adrenal gland tissue sections with a range of higher spa

124 s and the morphologic characteristics of the adrenal gland were recorded.

125 l motor nerve to the vicinity of the forming adrenal gland, where they detach from the nerve and form

126 pinal mediastinum, retroperitoneum, neck and adrenal gland.

127 tal secretory events from thin slices of the adrenal gland.

128 the 61 observed SFCs (82%) found in the left adrenal gland.

129 n human serum and epidermis, and the porcine adrenal gland.

130 in addition to involvement of kidneys and/or adrenal glands (CNS-IPI).

131 thesized from cholesterol in mitochondria of adrenal glands and gonads/ovaries.

132 Adrenal glands are zonated endocrine organs that are ess

133 11B2) expression was evaluated in 127 normal adrenal glands from deceased kidney donors (age, 9 month

134 ns (SFCs) (</=5 mm) were seen in one or both adrenal glands in 19 of the 38 patients with fCCM (50%),

135 leukocyte infiltration and hemorrhage in the adrenal glands of deceased mice.

136 ed by removal of the catecholamine-producing adrenal glands prior to endotoxic shock.

137 mized mice were transplanted with denervated adrenal glands to restore physiologic glucocorticoid lev

138 X disease occurred almost exclusively in the adrenal glands with frequently bilateral tumors.

139 697 (42.9%) in the liver, 138 (8.5%) in the adrenal glands, 38 (2.3%) in the pancreas, 109 (6.7%) in

140 Spleen, liver, and adrenal glands, common targets for acute infection, appe

141 eting, resulting in effective imaging of the adrenal glands, pituitary gland, lymph nodes, pancreas,

142 nduces a strong inflammatory response in the adrenal glands, which is accompanied by cell death and h

143 ons including the central nervous system and adrenal glands.

144 ting glucocorticoid hormone synthesis in the adrenal glands.

145 aldosterone synthesis that acts directly on adrenal glomerulosa cells to increase CYP11B2 expression

146 ) regulates neuroendocrine functions such as adrenal glucocorticoid release, whereas extra-hypothalam

147 onnection between stress, brain function and adrenal has been further expanded by two recent, indepen

148 Interestingly, the adrenal hormone cortisol was predominantly produced in m

149 ition may involve the hypothalamic-pituitary-adrenal (HPA) and hypothalamic-pituitary-gonadal (HPG) a

150 cular consequences of hypothalamic-pituitary-adrenal (HPA) axis activation by exogenous adrenocortico

151 aining stress-induced hypothalamic-pituitary-adrenal (HPA) axis activation by inhibiting hypophysiotr

152 rfont potently blocks hypothalamic-pituitary adrenal (HPA) axis activation in adrenalectomized rats.

153 hat the potential for hypothalamic-pituitary-adrenal (HPA) axis activation might be mitigated.

154 t of their effects on hypothalamic pituitary-adrenal (HPA) axis activation, aversive conditioning, or

155 measure of long-term hypothalamus-pituitary-adrenal (HPA) axis activity.

156 well as regulation of hypothalamic-pituitary-adrenal (HPA) axis activity.

157 ing activation of the hypothalamic-pituitary-adrenal (HPA) axis and increases in anxiety behavior, wh

158 y between the central hypothalamic-pituitary-adrenal (HPA) axis and the skin HPA axis analog, in the

159 sturbance and promote hypothalamic-pituitary-adrenal (HPA) axis dysregulation, a key feature of affec

160 eestablishment of the hypothalamic-pituitary-adrenal (HPA) axis feedback and corticosterone circadian

161 The hypothalamic-pituitary-adrenal (HPA) axis has been implicated in the pathophysi

162 variation within the hypothalamic-pituitary-adrenal (HPA) axis has been linked to risk for depressio

163 vous system (SNS) and hypothalamic-pituitary-adrenal (HPA) axis in rodents, evidence from human studi

164 e control loop of the hypothalamic-pituitary-adrenal (HPA) axis is closed by negative feedback of cor

165 The stress-responsive hypothalamo-pituitary-adrenal (HPA) axis plays a central role in promoting ada

166 e relationship of the hypothalamic-pituitary-adrenal (HPA) axis to suicidal behavior and its risk fac

167 e on behavior and the hypothalamic-pituitary-adrenal (HPA) axis were abolished.

168 dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis, altered cortisol metabolism, and tis

169 ormal function of the hypothalamic-pituitary-adrenal (HPA) axis, and resultant glucocorticoid (GC) se

170 ough regulation of the hypothalamo-pituitary-adrenal (HPA) axis, the neuroendocrine system that contr

171 to activation of the hypothalamic-pituitary-adrenal (HPA) axis, the sympathetic nervous system throu

172 tokines stimulate the hypothalamic-pituitary-adrenal (HPA) axis, triggering endogenous glucocorticoid

173 energic input and the hypothalamus-pituitary-adrenal (HPA) axis.

174 rmonal priming of the hypothalamic-pituitary-adrenal (HPA) axis.

175 ish equivalent of the hypothalamic-pituitary-adrenal (HPA) axis.

176 ress response via the hypothalamic-pituitary-adrenal (HPA) axis.

177 e limbic forebrain and hypothalamo-pituitary-adrenal (HPA) effector neurons in the paraventricular hy

178 the amygdala and the hypothalamic-pituitary-adrenal (HPA) stress axis, both required for lifelong co

179 nocorticotropic hormone, indicating primary (adrenal) hypercortisolism.

180 terone-producing adenoma (APA) and bilateral adrenal hyperplasia (BAH), remains a matter of debate.

181 is the mainstay of treatment for congenital adrenal hyperplasia (CAH) but has a narrow therapeutic i

182 of female genital virilization is congenital adrenal hyperplasia (CAH), in which excess androgen prod

183 Congenital adrenal hyperplasia (CAH), resulting from mutations in C

184 100 CYP21A2 variants give rise to congenital adrenal hyperplasia (CAH).

185 nadequately treated patients with congenital adrenal hyperplasia (CAH).

186 ntly been discovered in primary macronodular adrenal hyperplasia (PMAH), a cause of Cushing syndrome.

187 Challenges in the treatment of congenital adrenal hyperplasia include avoidance of glucocorticoid

188 Congenital adrenal hyperplasia is a group of autosomal recessive di

189 Material/Forty-one patients with congenital adrenal hyperplasia were evaluated by gray-scale and col

190 l lipodystrophy and non classical congenital adrenal hyperplasia, and an essential splice site mutati

191 ficiency, the most common type of congenital adrenal hyperplasia, is in place in many countries, howe

192 21A2, the disease-causing gene in congenital adrenal hyperplasia, we now provide a full structural ex

193 st tumors (TART) in patients with congenital adrenal hyperplasia.

194 reduction in dosage-sensitive sex reversal, adrenal hypoplasia critical region, on chromosome X, gen

195 Our data suggest that mortality and adrenal incapacitation are associated with the degree of

196 The present study investigates the impact of adrenal inflammation in septic mice challenged with ceca

197 pacitation are associated with the degree of adrenal inflammation, thereby underscoring the importanc

198 neumonitis (two [5%] and one [3%] patients), adrenal insufficiency (one [3%] and two [5%] patients),

199 ufficiency but harms septic patients without adrenal insufficiency and encourage further efforts to t

200 enger receptor BI mice as the first relative adrenal insufficiency animal model, we found that cortic

201 corticosteroid treatment benefits mice with adrenal insufficiency but harms mice without adrenal ins

202 erapy for a subgroup of septic patients with adrenal insufficiency but harms septic patients without

203 The frequency of secondary adrenal insufficiency in sepsis remains open to debate a

204 Primary adrenal insufficiency is life threatening and can presen

205 In such patients, adrenal insufficiency must be treated with hydrocortison

206 Adrenal insufficiency occurs most in patients taking the

207 psis using genetic or surgical initiation of adrenal insufficiency resulted in increased mortality, b

208 Here, we have described a primary adrenal insufficiency syndrome and steroid-resistant nep

209 milies with SRNS and facultative ichthyosis, adrenal insufficiency, immunodeficiency, and neurologica

210 -related serious adverse events (pemphigoid, adrenal insufficiency, liver disorder).

211 had immune-related SAEs, including two with adrenal insufficiency, two with pneumonitis, and one wit

212 The most serious potential adverse effect is adrenal insufficiency, which can be life threatening.

213 on the type of lymphoma and/ or presence of adrenal insufficiency.

214 seful therapeutic strategy for patients with adrenal insufficiency.

215 adrenal insufficiency but harms mice without adrenal insufficiency.

216 HSPC numbers via the hypothalamic-pituitary-adrenal/interrenal (HPA/I) stress response axis.

217 decreases the limbic-hypothalamic-pituitary-adrenal (LHPA) axis activity in the offspring.

218 ponents of the limbic-hypothalamic-pituitary-adrenal (LHPA) axis, with enlarged adrenal cortex and in

219 Case Report: We present a case of unilateral adrenal lymphoma that was initially diagnosed as an infe

220 ow biopsy confirmed the diagnosis of primary adrenal lymphoma without bone marrow metastasis.

221 Primary adrenal lymphomas are a very rare type of extranodal lym

222 ity for differentiating lymphomas from other adrenal malignancies; however, histopathology is conside

223 uation of a patient with melanoma in whom an adrenal mass was detected on CT and MR during follow-up

224 describe a patient with melanoma in whom an adrenal mass was detected on CT and MRI during post-surg

225 Ultrasonography detected an adrenal mass, and magnetic resonance imaging excluded co

226 Chromaffin cells of the adrenal medulla (AM) represent the main neuroendocrine a

227 ve oxygen species (ROS) levels in the CB and adrenal medulla (AM).

228 Sympathetic ganglion and adrenal medulla volume and the expression level of Let-7

229 ce develop carcinoma in the thymus, stomach, adrenal medulla, and mammary gland but not in other orga

230 dial wall cortical regions projecting to the adrenal medulla, positively correlated with increases in

231 ile neuroblastoma is often RD3-positive, the adrenal medulla, where many neuroblastomas originate, is

232 ve oxygen species (ROS) levels in the CB and adrenal medulla, which were a result of DNA methylation-

233 cognition, and affect to the function of the adrenal medulla.

234 ks in the cerebral cortex have access to the adrenal medulla.

235 tions with a major sympathetic effector, the adrenal medulla.

236 a childhood tumor in sympathetic ganglia and adrenal medulla.

237 alignant tumors and/or cysts of the kidneys, adrenal medullae and sympathetic paraganglia, endolympha

238 epinephrine and norepinephrine released from adrenal medullary chromaffin cells and norepinephrine re

239 y axis), heart rate variability (sympathetic adrenal medullary system), EEG event-related potentials

240 h steroidogenic mouse Leydig MA-10 and human adrenal NCI cells.

241 For each adrenal nodule, nonenhanced attenuation values were reco

242 ing expression in central nervous system and adrenal or pancreas tissues are strongly enriched for as

243 we provide new insights into the underlying adrenal pathology.

244 duces the activity of hypothalamic-pituitary-adrenal pathways via actions in specific brain regions,

245 in-1beta, and tumor necrosis factor-alpha in adrenal protein extracts of nonsurvivors compared with s

246 factors, normalizing hypothalamic-pituitary-adrenal reactivity, and the reduction of neuroinflammati

247 ify a maladaptive sympathetic-neuroendocrine adrenal reflex mediating immunosuppression after SCI, im

248 he lactose [(13)C]ureide breath test and the adrenal response to CRF was assessed by serial salivary

249 he dynamics of normal hypothalamic-pituitary-adrenal responses to major surgery will provide us with

250 shed their heightened hypothalamic-pituitary-adrenal responsivity and reduced stress-induced cognitiv

251 y suggestive for the diagnosis of testicular adrenal rest tissues on ultrasonography.

252 esonance (MR) imaging features of testicular adrenal rest tumors (TART) in patients with congenital a

253 Totally eighteen adrenal rest tumors in 9 patients were diagnosed TART on

254 testicular masses, a diagnosis of testicular adrenal rest tumour was made; biopsy was deferred and ho

255 Testicular adrenal rest tumours (TARTs) are benign testicular masse

256 Prompt diagnosis of testicular adrenal rest tumours is essential, as it only indicates

257 el, we were able to show that this increased adrenal sensitivity results from changes in the regulati

258 ion of both stimulatory and inhibitory intra-adrenal signaling pathways.

259 was low (0.12 and 0.3 Hz, respectively, for adrenal slices and cultured cells) and increased up to 0

260 ic events from cultured chromaffin cells and adrenal slices.

261 in lumbar sympathetic nerve activity (SNA), adrenal SNA and ABP than equi-osmotic sorbitol (2.0 osmo

262 1.0 m NaCl significantly raised lumbar SNA, adrenal SNA and ABP.

263 ours post cecal ligation and puncture; using adrenal-specific scavenger receptor BI mice as an induci

264 Scavenger receptor BI null and adrenal-specific scavenger receptor BI null mice.

265 elucidate the effects of stress on brain and adrenal stem cells, showing similarities in the way that

266 Significant suppression of multiple adrenal steroid hormones was also seen in treated childr

267 Starting with the discovery of adrenal steroid, and later, estrogen receptors in the hi

268 ders encompassing enzyme deficiencies in the adrenal steroidogenesis pathway that lead to impaired co

269 Many key factors within the adrenal steroidogenic pathway have been identified and s

270 is, we developed a mathematical model of the adrenal steroidogenic regulatory network that accounts f

271 Subsequent findings that adrenal stress hormones activated by learning experience

272 ssion of genes in the hypothalamic-pituitary-adrenal/stress system (e.g., Crhr1) is one of them.

273 vironment Study, and the Pharmacogenetics of Adrenal Suppression with Inhaled Steroid Study).

274 increases lumbar sympathetic nerve activity, adrenal sympathetic nerve activity and arterial blood pr

275 g steroid hormone in humans, produced by the adrenals, the gonads and the brain.

276 ethylated in CPA than in adjacent unaffected adrenal tissue and white blood cells.

277 ulosa, zona fasciculata, and tumour in human adrenal tissue, and investigated the functional role of

278 In adrenal tissue, the total CYP11B2-expressing area was ne

279 NFATs ("exposed"; n = 166) and those with no adrenal tumor ("unexposed"; n = 740), with at least 3 ye

280 cident composite diabetes than those without adrenal tumors (30 of 110 [27.3%] vs. 72 of 615 [11.7%]

281 o evaluate the hypothesis that nonfunctional adrenal tumors (NFATs) increase risk for cardiometabolic

282 Background: Benign adrenal tumors are commonly discovered on abdominal imag

283 ment of whether the classification of benign adrenal tumors as "nonfunctional" adequately reflects th

284 Extra-adrenal tumors occurred in 28 mutation carriers (48%) an

285 higher risk for diabetes than those without adrenal tumors.

286 ometabolic outcomes compared with absence of adrenal tumors.

287 ional imaging is recommended to characterize adrenal tumors; however, mistakes may occur and therefor

288 ish between pheochromocytoma and physiologic adrenal uptake.

289 t appropriate criteria for interpretation of adrenal vein cannulation and lateralisation, the use of

290 ropriate way to prepare the patient, whether adrenal vein sampling can be avoided for some subgroups

291 , and strategies to improve success rates of adrenal vein sampling in centres with little experience.

292 Adrenal vein sampling is recognised by Endocrine Society

293 PA and conclusive subtype differentiation by adrenal vein sampling was made in 91 patients (27 patien

294 by adrenal computed tomography scanning and adrenal vein sampling, using strict criteria to define s

295 sed with unilateral primary aldosteronism by adrenal venous sampling who had undergone a total adrena

296 hours of exposure, plasma, skin, brain, and adrenals were collected and processed to measure cortico

297 ed blood flow favouring the brain, heart and adrenals, whereas HA fetuses showed a blunted cardiovasc

298 We created a bioartificial adrenal with 3D cell culture conditions by encapsulation

299 nclusion, transplantation of a bioartificial adrenal with xenogeneic cells may be a treatment option

300 adrenal cotransmitter and the activation of adrenal Y5 receptors.