ライフサイエンスコーパス: endocrine

1 ovascular, hematology, pulmonary, renal, and endocrine).

2 5 cardiac (4.3 [3.5-5.4] and 5.6 [4.5-7.1]), endocrine (3.9 [2.9-5.1] and 6.4 [5.1-8.0]), and musculo

3 Furthermore, endocrine activity in vitro assays were performed.

4 d within the lamina terminalis in regulating endocrine and behavioral responses that are involved in

5 -like 1 (DLL1) controls the decision between endocrine and exocrine fates of multipotent progenitors

6 we demonstrate high viability and preserved endocrine and exocrine function in HPS for at least 10 d

7 To date, the endocrine and exocrine pancreas have been studied separa

8 The endocrine and exocrine pancreas have been studied separa

9 as the bidirectional blood flow between the endocrine and exocrine pancreas, not necessarily a unidi

10 gration of the capillary network between the endocrine and exocrine pancreas.

11 CTORIAL enables harmonized assessment of the endocrine and metabolic disrupting activity of chemicals

12 mood, and anxiety disorders and demonstrate endocrine and molecular alterations compared to controls

13 clinical trials using senolytics for several endocrine and non-endocrine diseases.

14 in overlapping and distinct patterns in both endocrine and non-endocrine tissues in late pancreas dev

15 e-releasing hormone antagonist with superior endocrine and tolerability profiles and positive outcome

16 ctroceuticals as the intersection of neural, endocrine, and immune systems.

17 cute exposure to DiNP dysregulates cellular, endocrine, and immunological aspects in the colon of adu

18 gence of acquired drug resistance (chemo and endocrine) as well as radio resistance, it is essential

19 Endocrine assays and chromatin accessibility and conform

20 Blood pressure is controlled by endocrine, autonomic, and behavioral responses that main

21 ion of the thyroid, somatotropic and adrenal endocrine axes, possibly influencing homeostatic and str

22 s of ALDH2, BRAP and CUX2 in the liver-brain endocrine axis connecting metabolic shifts with excessiv

23 s maintaining quiescence of the reproductive endocrine axis during childhood before its reawakening a

24 nges associate with various cardiometabolic, endocrine, bone- and energy-related comorbidities of Rel

25 t also to the CNS effects of hormones on non-endocrine brain circuitry.

26 ous oscillations in neurological, metabolic, endocrine, cardiovascular and immune functions.

27 Whilst all were similarly associated with endocrine causes of infant deaths (NO2, 2.167 [1.539, 3.

28 und that nine are dispensable for pancreatic endocrine cell development.

29 insulin- and glucagon-producing cells during endocrine cell development.

30 1 inhibition, suggesting that LSD1 regulates endocrine cell differentiation by limiting the duration

31 her determine that RA-mediated regulation of endocrine cell differentiation occurs through Wnt pathwa

32 identify a transient requirement for LSD1 in endocrine cell differentiation spanning a short time-win

33 SPR/Cas9-mediated gene editing, coupled with endocrine cell differentiation strategies, we dissect th

34 st time, we address the role of cell size in endocrine cell electrical activity, finding that larger

35 sms by which RA signaling directs pancreatic endocrine cell fate.

36 show how pervasive epigenetic priming steers endocrine cell fates.

37 implying continued essential roles in mature endocrine cell function.

38 local bone environment by functioning as an endocrine cell that controls phosphate reabsorption in t

39 mal and ectodermal epithelia to generate all endocrine cell types.

40 s suggests direct interactions between islet endocrine cells and surrounding cells as well as the bid

41 In contrast, Prox1-positive endocrine cells appear as primary sensors of cholinergic

42 These data suggest that clustering of endocrine cells during islet morphogenesis is guided, at

43 y for monitoring early changes in pancreatic endocrine cells eventually leading to T1D.

44 vel cAMP effector, expressed in neuronal and endocrine cells in adult mammals, that is required for D

45 bryogenesis but become much more enriched in endocrine cells in adults, implying continued essential

46 derived peptides that are released from gut endocrine cells in response to nutrient intake.

47 eostasis is coordinated by hormone-secreting endocrine cells in the pancreas, as well as glucose util

48 Endocrine cells in the pituitary gland typically display

49 etabolism, and diabetes onset, but how islet endocrine cells interact with sensory neurons has not be

50 s with MRS specifically impairs formation of endocrine cells of the pancreas head and tail.

51 Endocrine cells of the pancreatic islet interact with th

52 Since endocrine cells only contain a handful of these channels

53 nabled pseudo-entry virus infects pancreatic endocrine cells, liver organoids, cardiomyocytes, and do

54 iduals with MRS specifically lack pancreatic endocrine cells, we micro-CT imaged a 12-week-old foetus

55 hESC-gut tube intermediates into pancreatic endocrine cells.

56 are secretory vesicles found in neurons and endocrine cells.

57 ies in the exocrine pancreas that may induce endocrine cellular stress as a trigger for autoimmunity.

58 of Australia were investigated for seasonal endocrine changes associated with reproduction.

59 cells that also uniquely harbor neuronal and endocrine characteristics.

60 Thus, the ApoJ-LRP2 axis is a novel endocrine circuit that is central to the maintenance of

61 d type 2 diabetes mellitus, as well as other endocrine conditions.

62 neural substrates and mechanisms behind the endocrine control of metabolism during dietary protein d

63 ntified in patients with neurological but no endocrine defects, we show that the effect on SG formati

64 investigated whether chronic and endogenous endocrine delivery of extracellular miR-210 to pulmonary

65 very and PH, thus demonstrating a pathogenic endocrine delivery of extracellular miR-210.

66 ing that the exocrine glands, similar to the endocrine, develop from the same primordia that give ris

67 nt a powerful tool to model human pancreatic endocrine development and associated disease pathophysio

68 the produced microproteins, is required for endocrine development.

69 ancreas, and loss of Dll1 leads to premature endocrine differentiation.

70 eton strongly inhibited neurogenin 3-induced endocrine differentiation.

71 e role of cellular senescence in a number of endocrine diseases, including osteoporosis, metabolic sy

72 ing senolytics for several endocrine and non-endocrine diseases.

73 Subclinical hypothyroidism (SCH) is a common endocrine disorder affecting women of reproductive age.

74 imary hyperparathyroidism (PHPT) is a common endocrine disorder, definitive treatment usually requiri

75 antly, dysfunctional SBP2 is associated with endocrine disorders in humans.

76 - and hypothyroidism, are the most prevalent endocrine disorders.

77 Using a rat model for exposure to an endocrine disrupting chemical (EDC), we show that early-

78 Early exposure to such endocrine disrupting chemicals (EDC) may affect brain de

79 idence suggests that gestational exposure to endocrine disrupting chemicals (EDCs) may interfere with

80 Of particular concern are endocrine disrupting chemicals (EDCs).

81 Endocrine disrupting chemicals are common in our environ

82 Framework for the Testing and Assessment of Endocrine Disrupting Chemicals as a guide.

83 The ubiquitous presence of endocrine disrupting chemicals, parabens, and their meta

84 Bisphenol-A (BPA), a potent endocrine disrupting compound, is a synthetic ingredient

85 Bisphenol A, an endocrine disrupting compound, is widely used in food an

86 ith a mixture of 12 environmentally relevant endocrine disrupting compounds (EDmix).

87 t some SPAs may cause hepatic toxicity, have endocrine disrupting effects, or even be carcinogenic.

88 sed in polyvinyl chloride products, exhibits endocrine-disrupting capabilities.

89 tal processes to pathologies associated with endocrine-disrupting chemical (EDC) exposure are poorly

90 Endocrine-disrupting chemicals (EDCs) are exogenous chem

91 exposure to environmental pollutants such as endocrine-disrupting chemicals (EDCs) during critical pe

92 The presence and distribution of endocrine-disrupting chemicals (EDCs) in the mariculture

93 s on the endocrine system are referred to as endocrine-disrupting chemicals (EDCs).

94 w studies have investigated the link between endocrine-disrupting chemicals and autistic traits.

95 Many commercial plasticizers are toxic endocrine-disrupting chemicals that are added to plastic

96 resulted from historical contamination with endocrine-disrupting pesticides.

97 d, accurate, and sensitive assessment of the endocrine-disrupting potential of benchmark chemicals ba

98 els, allow for a more holistic assessment of endocrine-disrupting potential of chemicals with limited

99 g many species through, among other effects, endocrine disruption and reproductive impairment.

100 model group selected for further studies of endocrine disruption consisted of continuous AC(50) data

101 Respondents agreed that endocrine disruption is still a significant issue and no

102 e summarize the major literature findings of endocrine disruption of neurodevelopment and concomitant

103 en receptor (AR) is a target of interest for endocrine disruption research, as altered signaling can

104 agonist pathways to prioritize chemicals for endocrine disruption testing.

105 Therefore, predicting potential endocrine disruption via exogenous chemicals requires th

106 veractivation of hPXR is linked to potential endocrine disruption, oxidative stress, hepatic steatosi

107 brain is a critical target for developmental endocrine disruption, resulting in altered neuroendocrin

108 ific selection including at genes related to endocrine disruption, there was no strong evidence that

109 and can also be applied to other targets of endocrine disruption.

110 s or using biomarkers specific to vertebrate endocrine disruption.

111 oncomitant changes in behavior by four major endocrine disruptor classes:bisphenol A, polychlorinated

112 pesticide with antiandrogenic activity as an endocrine disruptor compound.

113 In support of the Endocrine Disruptor Screening Program, the U.S. Environm

114 e that is from a male that was exposed to an endocrine disruptor will display a more severe reproduct

115 (di(2-ethylhexyl)phthalate) (DEHP), a known endocrine disruptor, contributed by approximately half o

116 ration animals were exposed prenatally to an endocrine disruptor, di-2-ethylhexyl phthalate (DEHP), a

117 relations between maternal/fetal exposure to endocrine disruptors and incidence of neurodevelopmental

118 Net demographic effects of exposure to endocrine disruptors may often be strongly underestimate

119 The incidence of endocrine disruptors, both possible (glyphosate and gluf

120 widespread persistent organic pollutants and endocrine disruptors.

121 romic repeats (CRISPR) screens to understand endocrine drug resistance, we discovered ARID1A and othe

122 storm represents a rare but life-threatening endocrine emergency.

123 d plasma insulin and altered glucoregulatory endocrines, exaggerated sympathoadrenal activity and red

124 with a unique constellation of neurological, endocrine, exocrine, and haematological findings that is

125 in the tumor microenvironment and implicate endocrine-exocrine signaling beyond insulin in PDAC deve

126 ct with adjacent cells and via paracrine and endocrine factors that affect cells in the bone marrow m

127 increased delivery of oxygen, nutrients, and endocrine factors to organs during the active period and

128 DAC inhibitor valproic acid and a variety of endocrine factors, xenobiotic chemicals, or metabolites

129 okines") have emerged as a distinct class of endocrine factors.

130 GF21 expressed by adipocytes and upstream of endocrine FGF21 expressed by hepatocytes.

131 The three members of the endocrine-fibroblast growth factor (FGF) family, FGF19,

132 1 diabetes research efforts have focused on endocrine function and autoimmunity, recent studies iden

133 sulin delivery systems that mimic pancreatic endocrine function could enhance health and improve qual

134 etic peptide (BNP), thereby demonstrating an endocrine function for the heart.

135 y and may orchestrate the sex differences in endocrine function observed during pubertal transition.

136 henozoospermic men aged 20-45 y, with normal endocrine function.

137 bsorption preferences, microbe defenses, and endocrine function.

138 effect of prenatal hormonal milieu on adult endocrine functioning.

139 GI microbiome activities are known to affect endocrine functions(6,7), the intestinal microbiome of i

140 ort, protein transport, metabolic functions, endocrine functions) showed that different lines may be

141 pressed by signaling from gastrin-expressing endocrine (G) cells.

142 The corpus luteum is an endocrine gland that synthesizes and secretes progestero

143 The corpus luteum is a transient endocrine gland that synthesizes and secretes the steroi

144 EN1 cohort of the Groupe d'etude des Tumeurs Endocrines (GTE).

145 hat has a key role in maintaining immune and endocrine homeostasis.

146 les resembling those of exocrine zymogen and endocrine hormone secreting cells; and (ii) elevated pre

147 ne colocalization of dopamine receptors with endocrine hormones in HC and T1DM pancreatic tissue.

148 ated peptides urocortins 1-3 (UCN1-UCN3) are endocrine hormones that control the stress responses by

149 During stress, endocrine IL-6 is the required instructive signal for me

150 Tumor-induced perturbations in the endocrine, immune and nervous systems drive anorexia and

151 in A to depolymerize the cytoskeleton during endocrine induction, we developed a two-dimensional diff

152 Sex is a proxy for multiple genetic and endocrine influences on behavior, including how environm

153 ampullary tumor and can lead to exocrine and endocrine insufficiency such as malnutrition and diabete

154 retofore unknown role of Ogt in exocrine and endocrine islet development.

155 The anterior-most placode generates the endocrine lobe [adenohypophysis (ADH)] of the pituitary,

156 roid cancer (PTC) is the most common type of endocrine malignancy.

157 ular organisms via autocrine, paracrine, and endocrine mechanisms.

158 monstrates an important direct metabolic and endocrine mechanistic link to the viral disease process.

159 ample, microorganisms can serve as microbial endocrine mediators and can respond to stimuli and produ

160 isrupted in psychiatric disorders, including endocrine, metabolic, and hormonal systems.

161 ompared the relationships between peripheral endocrine, metabolic, and immune signaling and brain act

162 rgan systems, including the central nervous, endocrine, metabolic, hematopoietic, immune and, finally

163 ess that controls the function of the heart, endocrine, muscles, and neuronal tissues.

164 8%), genitourinary (8.7%), digestive (8.3%), endocrine, nutritional or metabolic (8.3%), and respirat

165 missions for 7 major disease categories: (1) endocrine, nutritional, and metabolic diseases; (2) nerv

166 particularly, genitourinary, digestive, and endocrine, nutritional, and metabolic illnesses.

167 l necessary to perhaps manipulate the female endocrine of the black tiger shrimp.

168 brown adipose tissue as a stress-responsive endocrine organ and mechanistic insight into targeting t

169 abolic homeostasis and its prominent role as endocrine organ is now well recognized.

170 strointestinal tract is known as the largest endocrine organ that encounters and integrates various i

171 xpenditure, adipose tissue is also a dynamic endocrine organ that secretes bioactive factors into blo

172 s stored in them identified the atrium as an endocrine organ.

173 ecent studies have also identified BAT as an endocrine organ.

174 s (e.g., gastrointestinal mucosa or skin) or endocrine organs, although any organ system can be affec

175 ulin metabolism and cell cycle regulation in endocrine pancreas (miR-15a and miR-17).

176 Early pro-inflammatory signaling in the endocrine pancreas involves activation of NF-kappaB, whi

177 that both GLP-1 and CCK are produced in the endocrine pancreas of obese mice.

178 ystematic assessment of the pathology of the endocrine pancreas of patients with LADA and for compari

179 ne pancreas to a pathological process in the endocrine pancreas, suggesting pancreatitis might be a p

180 etic regulation and tumor suppression in the endocrine pancreas; however, intriguing recent data sugg

181 f disease-associated SNPs in the activity of endocrine pancreatic enhancers, including a poorly explo

182 d with type 2 diabetes overlap with putative endocrine pancreatic enhancers, suggesting that these SN

183 Six out of 10 tested sequences are endocrine pancreatic enhancers.

184 imal studies have identified both neural and endocrine pathways, by which the central nervous system

185 bryo function, and to display characteristic endocrine phenotypic patterns, such as the 28-day human

186 Systemic signalling from the endocrine placenta targets the maternal endothelium and

187 Manmade chemicals can interfere with endocrine processes and have permeated many ecosystems.

188 analyzing how the initial physiological and endocrine processes triggered by traumatic stress eventu

189 We also identified an endocrine profile of heightened GLP-1 and PP but lower g

190 Here endocrine profiling, longitudinal observations of known

191 f RA signaling within the NEUROG3-expressing endocrine progenitor population impairs mouse beta cell

192 slet cell mass at birth, caused by decreased endocrine progenitor production and increased beta-cell

193 Pbx directs differentiation of endocrine progenitors into insulin- and glucagon-positiv

194 olves the aggregation of multiple equipotent endocrine progenitors that transition from a phase of st

195 Mice with loss of Sin3a in endocrine progenitors were normal during early postnatal

196 gnificant extracellular matrix and important endocrine properties mediated by adipokines.

197 did not contain more beta cells but a higher endocrine purity (49% versus 36%; P = 0.03).

198 long-term, longitudinal study of pancreatic endocrine regeneration.

199 ) but also with a higher number of total and endocrine-related AEs.

200 An increasing number of mechanisms of endocrine resistance have been reported, including somat

201 trogen-independent proliferation and confers endocrine resistance in ER(+) breast cancers.

202 me remodelling is a key mechanism underlying endocrine resistance in ER+ breast cancer.

203 deacetylase inhibitors (HDACIs) may overcome endocrine resistance in estrogen receptor-positive (ER+)

204 absence of estrogen and are associated with endocrine resistance in metastatic ER-positive (+) breas

205 R(+) breast cancers, but the causal genes to endocrine resistance in this amplicon are unclear.

206 h tamoxifen may experience recurrence due to endocrine resistance, which highlights the need for addi

207 ER pathways accompanying the development of endocrine resistance.

208 xifen (TAM) or aromatase inhibitors leads to endocrine-resistance, whereby physiologic levels of estr

209 Mechanistic studies in endocrine resistant cell lines, suggest an ER-independen

210 ptor Partial Agonists are being evaluated in endocrine-resistant BC clinical trials.

211 evaluation of their pharmacology in numerous endocrine-resistant BC models and an endometrial cancer

212 17beta-estradiol (E(2)) for the treatment of endocrine-resistant BC.

213 nistration of 27 in orthotopic xenografts of endocrine-resistant breast cancer in monotherapy and in

214 are present at a high frequency in advanced endocrine-resistant ER(+) breast cancer.

215 resistant (MCF-7:CFR) cells was confirmed in endocrine-resistant, palbociclib-resistant, and ESR1 mut

216 n governing luminal cell differentiation and endocrine response that underlies breast cancer resistan

217 the modularity and interconnectedness of the endocrine response.

218 In study 2, endocrine responses were measured during the meal.

219 ts of OSE and ER on satiation and associated endocrine responses.

220 Our results identify an endocrine role for BAT to enhance cardiac function that

221 The marrow adipocyte also has an endocrine role in whole body homeostasis through its var

222 DP-NETs, with their numerous lesions and endocrine secretion-related symptoms, continue to be a m

223 hose tumours might have differing degrees of endocrine sensitivity.

224 These findings indicate that muscle-to-brain endocrine signaling mediated by the myokine Dpp regulate

225 gnaling paradigm that connects autocrine and endocrine signaling modes of the same hormone in differe

226 the involvement of evolutionarily conserved endocrine signaling pathways, including the DAF-2/insuli

227 es systemic metabolism through paracrine and endocrine signals(4).

228 In 2017, the Endocrine Society updated its clinical practice guidelin

229 mouse pancreatic mesenchyme to define a pro-endocrine specialized niche.

230 The proportion of endocrine-specific operations increases over time.

231 endocrine surgeons perform a high-volume of endocrine-specific operations, practice patterns are het

232 ice, but also decreases as the proportion of endocrine-specific practice increases.

233 uggest that most surgeons have to grow their endocrine-specific practice over time.

234 emonstrate the importance of RA signaling in endocrine specification and identify conserved mechanism

235 However, the role of RA signaling during endocrine specification has not been fully explored.

236 Age, pre- and post-operative endocrine status, surgical approach, length of surgery,

237 A typical academic endocrine surgeon meets the high-volume threshold for th

238 public still have a limited understanding of endocrine surgeons and what they do.

239 We performed a cross-sectional analysis of endocrine surgeons identified in the Faculty Practice So

240 Although endocrine surgeons perform a high-volume of endocrine-sp

241 One hundred thirty-nine endocrine surgeons practicing in 103 institutions over 4

242 Members of the American Association of Endocrine Surgeons reviewed and commented on preliminary

243 The greatest proportion of endocrine surgeons' patients are insured by commercial p

244 Trends in annual number of endocrine surgeries performed, number of all surgeries p

245 However, 3 decades after the emergence of endocrine surgery as a distinct specialty, the medical c

246 The rate of new, persistent opioid use after endocrine surgery operations is substantial but may be m

247 al data exists regarding opioid misuse after endocrine surgical operations.

248 eripheral immune system, with a focus on the endocrine, sympathetic, parasympathetic, sensory and men

249 vironment, those with adverse effects on the endocrine system are referred to as endocrine-disrupting

250 ine whether differences in the vitamin D-PTH endocrine system contribute to racial disparities in car

251 The endocrine system controls cell growth and metabolism by

252 tabolism, lipid metabolism and digestive and endocrine system pathways in the domesticated fish relat

253 the most frequently occurring cancer of the endocrine system, accounting for 70% of deaths due to en

254 addition to an involvement of the immune and endocrine systems and/or heightened tumour predispositio

255 s attributable not only to the modulation of endocrine systems in the periphery but also to the CNS e

256 D1A in maintaining luminal cell identity and endocrine therapeutic response in ER(+) breast cancer.

257 s in delineating mechanisms of resistance to endocrine therapies and potential strategies to overcome

258 ecommended to determine potential benefit of endocrine therapies to reduce risk of future breast canc

259 ived xenograft samples that are resistant to endocrine therapies.

260 ed at least one dose of CDKI or placebo with endocrine therapy (an aromatase inhibitor [letrozole or

261 gned to chemoendocrine therapy (CT+E) versus endocrine therapy alone (E), allowing us to quantify the

262 eeded to identify patient subgroups for whom endocrine therapy alone might be appropriate for first-l

263 e associated with irreversible-resistance to endocrine therapy and subsequent secondary resistance to

264 as bone marrow that remain quiescent during endocrine therapy and subsequently proliferate to produc

265 nced or metastatic disease should be offered endocrine therapy as first-line therapy, except in cases

266 e findings support future trials of extended endocrine therapy as primary nonoperative treatment of s

267 acknowledges that there are limited data on endocrine therapy benefit for cancers with 1% to 10% of

268 zing ER-targeted drug dosage, and predicting endocrine therapy benefit.

269 east cancer with prior clinical benefit from endocrine therapy but later progression on aromatase inh

270 Primary endocrine therapy for ductal carcinoma in situ (DCIS) as

271 Combination of CDK4/6 inhibitors and endocrine therapy improves clinical outcome in advanced

272 o investigate the benefit of adding CDKIs to endocrine therapy in patients whose tumours might have d

273 Endocrine therapy is usually effective in these hormone-

274 Endocrine therapy resistance frequently develops in estr

275 Multiple mechanisms of endocrine therapy resistance have been identified, inclu

276 l ((18)F-FES) uptake and early assessment of endocrine therapy response using (18)F-FDG and (18)F-flu

277 ctive values of molecular imaging agents for endocrine therapy response.

278 y identification of reduced effectiveness of endocrine therapy resulting from activating ESR1 mutatio

279 Since the addition of CDKI to endocrine therapy seemed to benefit all clinicopathologi

280 reast cancer who are candidates for adjuvant endocrine therapy should be offered tamoxifen for an ini

281 The potential benefit of escalating endocrine therapy versus tamoxifen alone is minimal for

282 erformed before and 7-9 d after the start of endocrine therapy with fulvestrant.

283 r target the ER directly (overall labeled as endocrine therapy).

284 r predicting which patients may benefit from endocrine therapy, and no other assays are recommended f

285 ation factors were age at diagnosis, planned endocrine therapy, and treating centre.

286 binations, especially with immunotherapy and endocrine therapy, seem most promising in the clinical e

287 gnosis associated with neurofibromin loss in endocrine therapy-treated ER(+) breast cancer.

288 e pharmacodynamics of combination HDACIs and endocrine therapy.

289 cer or in patients with tumors refractory to endocrine therapy.

290 ive breast cancer is frequently sensitive to endocrine therapy.

291 val by a number of months when combined with endocrine therapy.

292 t ER(+) breast cancers develop resistance to endocrine therapy; thus, novel targets are needed to tre

293 However, the cell biology of endocrine tissue ageing remains poorly understood.

294 targeting of blood vessels may restore aged endocrine tissue function.

295 owed a different cellular composition of the endocrine tissue, highlighting the tissue dynamics occur

296 distinct patterns in both endocrine and non-endocrine tissues in late pancreas development.

297 ed expression of these genes after 3 months' endocrine treatment of ER+ patients (n = 68) predicted p

298 ve breast cancers (BC) develop resistance to endocrine treatments (ET) and relapse with metastatic di

299 system, accounting for 70% of deaths due to endocrine tumors.

300 of islets by pancreatic ganglia resets these endocrine units, producing synchronization.