ライフサイエンスコーパス: CRF

1 CRF did not differ between the MCD (8.34 +/- 2.12 mm Hg)

2 CRF is an important marker of physical and mental health

3 CRF was significantly reduced in MCD and did not return

4 CRF's fast and potent activation of cholinergic interneu

5 CRF-releasing PVN neurons receive inputs from multiple b

6 otropin-releasing factor receptor subtype 1 (CRF(1)) expressed on MCs.

7 otropin-releasing factor receptor subtype 2 (CRF(2)) as a modulator of stress-induced MC degranulatio

8 ed nucleus vs central nucleus divisions; (2) CRF content of the CEA-DA path; and (3) striatal subregi

9 kg, IP) administration reduced TRAF6 (~20%), CRF (~30%), and MCP-1 (~20%) levels, as well as TLR4 bin

10 arge regional variation in the numbers (0-44 CRFs), types (58 distinct CRFs), and proportions (0-80.5

11 ate groups of rats received intra-NAc AAV2/5-CRF and saline IVSA.

12 ciated vector that overexpressed CRF (AAV2/5-CRF) or green fluorescent protein (AAV2/5-GFP).

13 detected increased over time to 16.7% and 57 CRFs in 2010-15.

14 nd test genetic scores for the response of 6 CRFs (BMI, systolic blood pressure, LDL cholesterol, HDL

15 Our findings identify a CRF(CeA)->CRF(dlBST) circuit for generating anxiety-like

16 we provide evidence suggesting that aberrant CRF expression and function may underlie augmented conne

17 Currently, there remains much unknown about CRF-dependent regulation of cognition, including the sou

18 Adding CRF to standard risk factors resulted in a net reclassif

19 In addition, CRF(2)(-/-) mice exhibited increased serum histamine lev

20 otective effects of ovarian hormones against CRF-induced deficits in sustained attention are also det

21 /34 921 639), bringing the proportion of all CRFs to 16.7% (5 844 113/34 921 639).

22 ons for understanding how discrete amygdalar CRF pathways modulate longer-lasting fear in anxiety- an

23 Mean CH and CRF were 8.52 +/- 1.81 mmHg, and 8.56 +/- 1.59 mmHg, res

24 The CH and CRF were measured with the Ocular Response Analyzer (Rei

25 learning algorithm to train both the DNN and CRF together.

26 antly lower values of corneal hysteresis and CRF than fellow eyes (9.0 +/- 1.8 vs 10.1 +/- 1.8 mm Hg,

27 ed on RNN, convolutional neural networks and CRF alone had lower performance, with a non-timeline bas

28 ific interactions between norepinephrine and CRF, and point to an action by which guanfacine may redu

29 rized persistent effects of repeated NPY and CRF treatment on the structure and function of BLA princ

30 depended on activation of CRF1 receptors and CRF neurons within the dlBST.

31 otropin releasing factor (CRF) signaling and CRF neurons in the bed nucleus of the stria terminalis (

32 -sh) mice systemically engrafted with WT and CRF(2)(-/-) BMMCs demonstrated the functional importance

33 ells (BMMCs) derived from wild-type (WT) and CRF(2)-deficient (CRF(2)(-/-)) mice and RBL-2H3 MCs tran

34 As SSTR2 activation antagonizes CRF-mediated hormone release, this storage/resurfacing m

35 CRF, the tools that are available to assess CRF, the modifiable and nonmodifiable factors influencin

36 THODS AND Between 1987 and 2014, we assessed CRF in 21 080 HF-free subjects (58.3+/-11 years) at the

37 esterol, predicted changes in the associated CRF.

38 Higher baseline CRF and sustained improvements in CRF and weight loss we

39 incidence of myocardial infarction, baseline CRF was not significantly associated with risk of incide

40 tif conservation are seen within and between CRF clades suggesting cis-regulatory regions have been c

41 e is known regarding the association between CRF and incidence of heart failure (HF).

42 dies should examine the interactions between CRF and NOP to elucidate their role in negative reinforc

43 ese findings show that stress activates BNST CRF neurons, and that alpha(2A)-AR activation suppresses

44 The effects of intra-BNST CRF administration were compared with those induced by t

45 that maternal care is impaired by intra-BNST CRF administrations, and these maladaptations are simila

46 Both intra-BNST CRF and LB exposure produced altered maternal care, repr

47 how that stress increases activation of BNST CRF neurons that drive negative affective behavior.

48 e PBN on restraint stress regulation of BNST CRF neurons.

49 duced inhibitory drive onto GluN2D(-/-) BNST-CRF cells ex vivo and increased activity in vivo Using a

50 potentiation, and increased activity in BNST-CRF neurons known to drive negative emotional behavior.

51 ors and increased excitatory drive onto BNST-CRF cells.

52 ion and increased excitatory drive onto BNST-CRF neurons.

53 el with CRFs and that of the model with both CRFs and GRF for BMD prediction.

54 Thus, our findings identify a CeA->BST CRF neuropeptide circuit that generates anxiety-like beh

55 thway to dorsal BST that activates local BST CRF neurons.

56 ) neurons in the CeA is potently enhanced by CRF and that CRFR1 signaling in the CeA is critical for

57 The increase of CIN firing by CRF results in the activation muscarinic acetylcholine r

58 Anxiety-like behavior was mediated by CRF projections from the CeA to the dlBST and depended o

59 Females raised by CRF-infused dams exhibited increased anxiety-like behavi

60 orrelations between corneal properties (CCT, CRF, and CH) and POAG were low (r(g) range -0.18 to 0.11

61 The CCT, CRF, CH, and IOP were compared among the study group.

62 iors is observed after the inhibition of CeA CRF projections to the bed nucleus of the stria terminal

63 at the optogenetic inactivation of these CeA CRF+ neurons prevents recruitment of the neuronal ensemb

64 CeA-CRF neurons transition from responding to the unconditio

65 These results demonstrate CeA-CRF neurons are an important substrate for the persisten

66 Inhibition of CeA-CRF neurons during immediate extinction training is suff

67 Optogenetic silencing of CeAL CRF neurons during contextual fear acquisition disrupted

68 Silencing CeAL CRF projections in the BNSTDL during contextual fear acq

69 (i) first-order to higher-order linear-chain CRFs, and from (ii) first-order to higher-order semi-Mar

70 By contrast, CRF neuronal activity starts to drop within a second of

71 hy via Y(5) receptor activation; conversely, CRF increased excitatory input and induced hypertrophy o

72 g memory via activation of local PKA-coupled CRF receptors, an action associated with robust degradat

73 ral amygdala neurons, and toward non-CRF(+) (CRF(-)) and somatostatin-expressing (SOM(+)) neurons, wh

74 ed from wild-type (WT) and CRF(2)-deficient (CRF(2)(-/-)) mice and RBL-2H3 MCs transfected with CRF(2

75 the physiological principles that determine CRF, the tools that are available to assess CRF, the mod

76 an endurance run test was used to determine CRF.

77 n which the twins in each pair had different CRF (>=1 watt).

78 rised 90,331 nonsibling pairs with different CRF and matched on birth year and year of conscription.

79 vels of conservation exist between different CRFs across land plants, likely occurring through proces

80 the numbers (0-44 CRFs), types (58 distinct CRFs), and proportions (0-80.5%) of HIV-1 recombinants.

81 th the proportion and the number of distinct CRFs detected increased over time to 16.7% and 57 CRFs i

82 that chemogenetic activation of caudal dmPFC CRF neurons elicits a robust degradation of task-related

83 activation of caudal, but not rostral, dmPFC CRF neurons potently impaired working memory, whereas in

84 n, and alpha-tocopherol) in the freeze-dried CRF material was measured over 84 days; the impact of te

85 de interaction study was undertaken for each CRF in women (n ~ 9000) not participating in the dietary

86 Development of a cost-effective CRF measurement process that could readily be incorporat

87 ed and rt-qPCR methods were used to estimate CRF overexpression and changes in CRF receptors (CRFr1,

88 nsistent with a mechanism whereby the excess CRF that characterizes stress-related diseases initiates

89 hestrates the stress response, and excessive CRF is thought to contribute to the pathophysiology of t

90 at striatal cholinergic interneurons express CRF-R1 receptors and are acutely activated by the neurop

91 m corticotropin releasing factor-expressing (CRF(+)) centrolateral amygdala neurons, and toward non-C

92 Corticotropin-releasing factor (CRF) and the three related peptides urocortins 1-3 (UCN1

93 neuropeptide corticotropin-releasing factor (CRF) drive anxiety-like behaviors in rats via a pathway

94 xpression of corticotropin-releasing factor (CRF) in the NAc of female and male rats.

95 neuropeptide corticotropin releasing factor (CRF) is anxiogenic and is produced by subpopulations of

96 Y (NPY) and corticotrophin-releasing factor (CRF) modulate the responses of the basolateral amygdala

97 ontains ~80% corticotropin-releasing factor (CRF) neurons and that the optogenetic inactivation of th

98 n known that corticotropin-releasing factor (CRF) neurons are prominent within the PFC, their role in

99 neuropeptide corticotropin-releasing factor (CRF) on these responses.

100 Corticotropin-releasing factor (CRF) orchestrates the stress response, and excessive CRF

101 The corticotropin-releasing factor (CRF) plays a key role in a variety of behaviours accompa

102 neuropeptide corticotropin releasing factor (CRF) produces a profound and reliable increase in the sp

103 ctivation of corticotropin-releasing factor (CRF) receptors in the caudal dorsomedial PFC (dmPFC) imp

104 Corticotropin releasing factor (CRF) signaling and CRF neurons in the bed nucleus of the

105 ation of the corticotropin-releasing factor (CRF) system potentiates MC degranulation responses durin

106 Corticotropin-releasing factor (CRF) that is released from the paraventricular nucleus (

107 eceptor, and corticotropin-releasing factor (CRF), (CRF1) receptor.

108 europeptide, corticotropin-releasing factor (CRF), that render the locus coeruleus arousal system of

109 mulated with corticotropin releasing factor (CRF), whereupon SSTR2 exits the compartment on syntaxin-

110 tive peptide corticotropin-releasing factor (CRF), which has been identified in critical components o

111 strate that corticotrophin-releasing factor (CRF)-expressing neurons in the central amygdala (CeA) an

112 counteracts corticotropin-releasing factor (CRF)-mediated stress and anxiety symptoms during drug an

113 expressed on corticotropin-releasing factor (CRF)-positive BNST cells implicated in driving negative

114 5, targeting corticotropin-releasing factor (CRF).

115 neuropeptide corticotropin-releasing factor (CRF).

116 erties, including corneal resistance factor (CRF) and corneal hysteresis (CH).

117 steresis (CH) and corneal resistance factor (CRF) between Indian and Chinese populations.

118 hysteresis (CH), corneal resistance factor (CRF), Goldmann- correlated intraocular pressure (IOPg),

119 steresis (CH) and corneal resistance factor (CRF), which were obtained from ocular response analyzer

120 the calculation of corneal resistant factor (CRF), corneal hysteresis, Goldmann-correlated IOP, and c

121 hysteresis [CH], corneal resistance factor [CRF], cup-to-disc ratio [CDR], and primary open-angle gl

122 factors known as Cytokinin Response Factors (CRFs) were examined for conserved motifs across several

123 regression model with clinical risk factors (CRFs) for FN-fracture prediction in Chinese.

124 prediction for cardiometabolic risk factors (CRFs) has been demonstrated using single genetic variant

125 es can improve cardiometabolic risk factors (CRFs), but it is unclear whether the benefits on CRFs ar

126 Cancer-related fatigue (CRF) remains one of the most prevalent and troublesome a

127 g remodels this circuit back toward favoring CRF(+) neurons.

128 hopeptides that were more abundant in female CRF-OE mice were overrepresented in an Alzheimer's disea

129 Controlled-release fertilizers (CRFs) can change the release kinetics of the fertilizer

130 ation based on the conditional random field (CRF) algorithm.

131 prediction using a conditional random field (CRF) based on co-expression relationship.

132 signals from the classical receptive field (CRF) and the extra-classical receptive field (eCRF) in p

133 etwork (CNN), and Conditional Random Fields (CRF) for entity recognition.

134 NN) combined with conditional random fields (CRF) model (RNNCRF) achieved the best performance in rea

135 on and changes in cardiorespiratory fitness (CRF) and body mass index on risk for HF is not well esta

136 sociation between cardiorespiratory fitness (CRF) and cardiovascular disease (CVD) is unknown.

137 Cardiorespiratory fitness (CRF) and endurance performance are characterized by a co

138 Cardiorespiratory fitness (CRF) refers to the capacity of the circulatory and respi

139 flexibility, and cardiorespiratory fitness (CRF) were performed in 22 international space station (I

140 ransmission in the NAc to likely account for CRF facilitation of appetitive behaviors.SIGNIFICANCE ST

141 duced ejection fraction after adjustment for CRF and traditional cardiovascular risk factors.

142 f genome-wide association studies (GWAS) for CRF.

143 forms were the circulating recombinant form (CRF) 02_AG (44% of the analysed sequences), CRF43_02G (1

144 subtypes were circulating recombinant form (CRF) 07_BC (34.6%) and CRF01_AE (32.4%); many unique rec

145 stribution of circulating recombinant forms (CRFs) and unique recombinant forms (URFs) in individual

146 V-1 subtypes, circulating recombinant forms (CRFs), and unique recombinant forms (URFs) in each time

147 V-1 subtypes, circulating recombinant forms (CRFs), and unique recombinant forms (URFs) in individual

148 (33.14%), 20 circulating recombinant forms (CRFs; 11.63%), and 20 unclassified (11.63%) sequences we

149 types (B and circulating recombinant forms [CRFs] CRF01_AE, CRF07_BC, CRF08_BC, and CRF55_01B) in Ch

150 d recovery of its chloroplast-rich fraction (CRF) by centrifugation.

151 nd then juiced; a chloroplast-rich fraction (CRF) was recovered from the juice by centrifugation.

152 n requiring clinical-risk-factor-based FRAX (CRF-FRAX) screening and BMD-based FRAX (BMD-FRAX) screen

153 tics and mechanisms of nutrient release from CRFs.

154 ried to measure contrast response functions (CRF) for all combinations of attention and TMS condition

155 on of several stress-responsive genes (e.g., CRF, POMC, and FKBP5) is altered in the PFC of AUD subje

156 General CRF and lineage specific motifs were identified.

157 se in Arrb2 than females, suggesting greater CRF receptor internalization.

158 Our findings identify a CRF(CeA)->CRF(dlBST) circuit for generating anxiety-like behavior

159 youth are currently believed to have healthy CRF.

160 Crewmembers with higher CRF before spaceflight had a 29% reduced risk of latent

161 ovides critical mechanistic insight into how CRF modulates striatal activity and dopamine transmissio

162 It implements CRFs models, that is discriminative models from (i) firs

163 at diabetes preventive interventions improve CRFs regardless of CAD genetic risk and delivers hypothe

164 0.26; 95% CI, 0.13-0.38; P < .001) improved CRF during and after primary treatment, whereas pharmace

165 is study used a phosphoproteomic approach in CRF-overexpressing (CRF-OE) mice to test the proof of pr

166 o estimate CRF overexpression and changes in CRF receptors (CRFr1, CRFr2) and the CRF receptor intern

167 ronger in pairs with >=60-watt difference in CRF (HR = 0.65, 95% CI: 0.59, 0.71).

168 r in twin pairs with >=60-watt difference in CRF (HR = 0.96, 95% CI: 0.57, 1.64).

169 Elevations in CRF-CRF1 signaling dysregulate FAAH activity, and this g

170 estraint stress increases cFos expression in CRF neurons in the mouse dorsal BNST, consistent with a

171 at CRF assessments (n=3902), improvements in CRF and weight loss over a 4-year follow-up were signifi

172 r baseline CRF and sustained improvements in CRF and weight loss were associated with lower risk of H

173 The increase in CRF gene expression was similar across all groups; howev

174 risk of HF (hazard ratio per 10% increase in CRF, 0.90 [95% CI, 0.82-0.99]; per 10% decrease in body

175 se healthy youth, and the temporal trends in CRF both in the United States and internationally.

176 s prevention strategies on 1-year changes in CRFs in 2,658 Diabetes Prevention Program (DPP) particip

177 iors interact with PRS and affect changes in CRFs in each intervention group.

178 ve response to decreased N/OFQ, or increased CRF transmission, or both.

179 fiable and nonmodifiable factors influencing CRF, the association of CRF with markers of health in ot

180 ow that excitability of genetically isolated CRF-receptive (CRFR1) neurons in the CeA is potently enh

181 as HIV-1 subtypes A, B, C, D, F, G, H, J, K, CRFs, and URFs.

182 s of PFC CRF neurons were dependent on local CRF receptors coupled to protein kinase A.

183 tively, these results demonstrate that local CRF release within the caudal dmPFC impairs frontostriat

184 89); however, both of these groups had lower CRF values than the control (9.76 +/- 1.83 mm Hg, P = .0

185 ral reactivation compared to crew with lower CRF.

186 First, attention lowered CRFs, whereas consciousness raised them.

187 m by pretraining a deep neural network (LSTM-CRF), followed by a rather short fine-tuning phase focus

188 (ii) first-order to higher-order semi-Markov CRFs (semi-CRFs).

189 MC CRF(2) is a negative global modulator of stimuli-induced

190 demonstrated the functional importance of MC CRF(2) in modulating stress-induced pathophysiology.

191 Compared with WT mice, CRF(2)(-/-) mice exhibited greater serum histamine level

192 nd are acutely activated by the neuropeptide CRF that is released in response to salient environmenta

193 s of the release processes and to design new CRFs in a shorter time and with relatively lower cost.

194 rtance for the design and development of new CRFs.

195 ce increased excitatory currents with 100 nM CRF, suggesting dose-effect curve shifts in TMT mice.

196 )O mice following bath application of 300 nM CRF, but only H(2)O mice increased excitatory currents w

197 ntrolateral amygdala neurons, and toward non-CRF(+) (CRF(-)) and somatostatin-expressing (SOM(+)) neu

198 Notably, CRF is strongly modulated by early-life adversity in sev

199 These findings demonstrate a novel CRF gain-control circuit and show separable pathways for

200 ould be grouped into seven potentially novel CRFs.

201 ucleus accumbens (NAc) through activation of CRF type 1 receptors, production of cAMP and reduction i

202 Antagonism of CRF-R1 with CP-154526 caused an accumulation of intracel

203 amilial factors influence the association of CRF with CVD and mortality.

204 factors influencing CRF, the association of CRF with markers of health in otherwise healthy youth, a

205 alamus to DRN-driven serotonergic control of CRF levels in the amygdala may contribute to the transit

206 hift from MRN-driven serotonergic control of CRF levels in the hypothalamus to DRN-driven serotonergi

207 iographic studies to map the distribution of CRF receptor binding sites in the mouse brain.

208 Although the cellular distribution of CRF receptor expression has been well characterized at t

209 We investigated the effects of CRF in the bed nucleus of the stria terminalis (BNST) of

210 Additionally, ectopic excitation of CRF(+) neurons impairs fear memory acquisition and facil

211 LB/cJ dams were exposed to five infusions of CRF or saline into the BNST in the first weeks after bir

212 ith lower preflight CRF and higher levels of CRF deconditioning on return to Earth.

213 The associations of baseline measures of CRF estimated from a maximal treadmill test, body mass i

214 Overexpression of CRF in the NAc increased nicotine IVSA to a larger exten

215 In males, overexpression of CRF produced a larger increase in Arrb2 than females, su

216 oups; however, in females, overexpression of CRF resulted in a larger increase in CRFr1 and CRFr2 rel

217 NIFICANCE STATEMENT Although the presence of CRF receptors in the dorsal and ventral striatum has bee

218 n and the electrophysiological properties of CRF neurons in the paraventricular nucleus of the hypoth

219 The proportion of CRF+ outputs is >50%, and mainly targets the A10 parabra

220 lation of cognition, including the source of CRF for cognition-modulating receptors and the output pa

221 etric analysis of release characteristics of CRFs is of paramount importance for the design and devel

222 f distinct HIV-1 variants and proportions of CRFs and URFs, leading to increases in country level HIV

223 Continued research on CRF mutations will be critical for our future understand

224 ), but it is unclear whether the benefits on CRFs are similar for individuals at different genetic ri

225 om parabrachial nucleus (PBN) afferents onto CRF neurons.

226 essing excitatory drive from PBN inputs onto CRF neurons.SIGNIFICANCE STATEMENT Stress is a major var

227 These structural responses to NPY or CRF required calcineurin or CaMKII, respectively.

228 fected with CRF(2)-overexpressing plasmid or CRF(2) small interfering RNA.

229 Other CRFs accounted for 3.7% (1 309 082/34 921 639), bringing

230 Other CRFs played major roles (>75% of HIV-1 infections) in Es

231 Although other CRFs accounted for small proportions of infections globa

232 ), CRF01_AE for 23.0% (1 838 433), and other CRFs for 16.4% (1 307 270) of all recombinant infections

233 CRF01_AE, other CRFs, and URFs increased, leading to a consistent increa

234 n adeno-associated vector that overexpressed CRF (AAV2/5-CRF) or green fluorescent protein (AAV2/5-GF

235 phoproteomic approach in CRF-overexpressing (CRF-OE) mice to test the proof of principle that when CR

236 Conversely, suppression of constitutive PFC CRF activity improved working memory.

237 to chemogenetically activate or inhibit PFC CRF neurons in working memory-tested male rats.

238 ntly, the cognition-impairing actions of PFC CRF neurons were dependent on local CRF receptors couple

239 em, the present studies demonstrate that PFC CRF neurons impair working memory via activation of loca

240 es were highest in crew with lower preflight CRF and higher levels of CRF deconditioning on return to

241 significantly decreased by manipulating PVN CRF neuronal activity.

242 Here, our recordings of PVN CRF neuronal activity in freely behaving mice revealed t

243 st that the rapid, biphasic responses of PVN CRF neurons encode the positive and negative valences of

244 Optogenetic activation or inhibition of PVN CRF neurons was sufficient to induce a conditioned place

245 nant forms (URFs) (39, 21.8%) and other rare CRFs were observed in the study.

246 er improvement in the majority of recognized CRFs compared with placebo (P < 0.001) irrespective of C

247 ons of infections due to HIV-1 recombinants, CRFs, and URFs and calculated the Shannon diversity inde

248 ike LgA cocaine self-administration, reduced CRF immunodensity in the central nucleus of the amygdala

249 ubtypes A and G, as well as in their related CRFs.

250 Among participants with repeat CRF assessments (n=3902), improvements in CRF and weight

251 However, 81% of the population required CRF-FRAX tests, and 37% required BMD-FRAX tests to achie

252 but the proportions of individuals requiring CRF-FRAX tests and BMD-FRAX tests were reduced by 37% an

253 order to higher-order semi-Markov CRFs (semi-CRFs).

254 Deviations relative to the standard CRF, i.e., gain functions, describe the strength of sign

255 with BMMCs and RBL-2H3 MCs demonstrated that CRF(2) expressed on MCs suppresses store-operated Ca(2+)

256 results were validated by demonstrating that CRF overexpression in females was associated with increa

257 There is also evidence that CRF contributes to maladaptations during the peripartum

258 h are consistent with previous findings that CRF-R1 in the mPFC plays an important role in predator o

259 memory retrieval, supporting the notion that CRF(+) neurons serve to inhibit learned freezing behavio

260 tivity in freely behaving mice revealed that CRF neurons are activated immediately by a range of aver

261 e neurobiology of cognition and suggest that CRF may represent a novel target for the treatment of co

262 nitive and circuit function and suggest that CRF may represent a potential target for treating fronto

263 The CRF isolated from fresh pea vine haulm is a potential so

264 nges in CRF receptors (CRFr1, CRFr2) and the CRF receptor internalizing protein, beta-arrestin2 (Arrb

265 e basis of ligand-binding specificity in the CRF receptor-hormone system, establish a common mechanis

266 scorbic acid) content and composition of the CRF have been determined.

267 terminalis (BNST) and that inhibition of the CRF(CeA-BNST) pathway is mediated by inhibition of the C

268 ST) pathway is mediated by inhibition of the CRF-CRF(1) system and inhibition of BNST cell firing.

269 These results suggest that the CRF(CeA-BNST) pathway could be targeted for the treatmen

270 This effect could only be removed using the CRF-R1 selective antagonist CP-154526, suggesting Ucn1 a

271 t breakdown significantly increased when the CRF samples were exposed to light.

272 Further, systemic pretreatment with the CRF-R1 antagonist CP154526 and bath application with the

273 onist CP154526 and bath application with the CRF-R1 antagonist NBI27914 reduced excitatory transmissi

274 to predict the release of nutrients from the CRFs to elucidate fundamental understanding of the dynam

275 Here we investigated the function of these CRF neurons in stress-induced anxiety using chemogenetic

276 nist CP-154526, suggesting Ucn1 acts through CRF-R1 when promoting chondrocyte survival.

277 atory regions have been conserved throughout CRF evolution.

278 e vulnerable to stress and less adaptable to CRF hypersecretion, a condition found in patients with P

279 releasing factor binds with high affinity to CRF receptor 1 (CRFR1) and is implicated in stress-relat

280 RF, the genetic architecture contributing to CRF remains unclear, especially in non-athlete populatio

281 ndings suggest that exposure to TMT leads to CRF-R1 driven changes in behavior and changes in synapti

282 Binge-induced changes in VTA CRF system protein and messenger RNA were also assessed

283 of binge-like ethanol consumption on the VTA CRF system were assessed following drinking-in-the-dark

284 at ethanol-induced activation of BNST-to-VTA CRF projections is critical in driving binge-like ethano

285 0 degrees C in the presence of air, but when CRF was exposed to light all three nutrients measured we

286 ice to test the proof of principle that when CRF is in excess, sex-biased CRF1 coupling translates in

287 quisition and facilities extinction, whereas CRF(+) neuron inhibition impairs extinction memory retri

288 etween CH with both IOP GAT and IOPcc, while CRF had significant positive association with IOPg.

289 Four loci associated with CRF were identified to reach genome-wide significance (P

290 siological and environmental correlates with CRF, the genetic architecture contributing to CRF remain

291 (-/-)) mice and RBL-2H3 MCs transfected with CRF(2)-overexpressing plasmid or CRF(2) small interferin

292 NPY followed by an identical treatment with CRF, or vice versa, inhibited or reversed all structural

293 CRFs and fracture GRF and by the Model with CRFs and FN-BMD GRF, respectively, as compared to 65.5%

294 k variation were explained by the Model with CRFs and fracture GRF and by the Model with CRFs and FN-

295 er between the performance of the model with CRFs and that of the model with both CRFs and GRF for BM

296 uild a multiple linear regression model with CRFs for BMD prediction in Chinese.

297 vely, as compared to 65.5% in the Model with CRFs only.

298 racture GRF and FN-BMD GRF to the model with CRFs, the area under the receiver operating characterist

299 ogical restraint stress were measured in WT, CRF(2)(-/-), and MC-deficient Kit(W-sh/W-sh) knock-in mi

300 pproach and tested for the prediction of 1-y CRF changes as well as long-term chronic disease develop