ライフサイエンスコーパス: AER

1 AER activity persists longer than normal and is maintain

2 AER among patients with baseline blood eosinophil counts

3 AER correlated positively with mesangial cell number in

4 AER deficits are tied behaviorally to impaired ability t

5 AER expression of reporter constructs in transgenic mice

6 AER formation in Raldh2(-/-) forelimbs is rescued by con

7 AER was marginally lower in green buildings (p=0.109).

8 justed HR, 0.56; 95% CI, 0.33-0.95; P = .03; AER, 6.48/100 person-years; censoring rate, 0.90; 23 eve

9 the inhibitory contribution of the domain 2 AER cluster.

10 3.9; 95% confidence interval [CI], 3.6-4.2; AER, 16.8 per 10,000 person-years).

11 he first year after TC diagnosis (SMR, 5.31; AER, 13.90; n=11) and included cerebrovascular disease (

12 ER, 7.43; n=5) and heart disease (SMR, 3.45; AER, 6.64; n=6).

13 ncluded cerebrovascular disease (SMR, 21.72; AER, 7.43; n=5) and heart disease (SMR, 3.45; AER, 6.64;

14 tudies have compared the effects of aerobic (AER) or resistance (RES) training on hepatic fat content

15 2 (Fgfr2) in the mouse AER to terminate all AER functions; for comparison, we inactivated both Fgfr1

16 rn, indicating that Fgf8 is sufficient among AER-FGFs to sustain normal limb formation.

17 An AER cluster of 13 polymorphisms, located within domain 1

18 the functions of apical ectodermal BMPs, an AER-specific promoter element from the Msx2 gene was use

19 tic module in the anterior region creates an AER-like structure that drives anterior fin expansion.

20 ate that the cetacean hind-limb bud forms an AER and that this structure expresses Fgf8 initially, bu

21 es provided greater GFR (92%; P < 0.005) and AER (95%; P < 0.01) prediction than multiple regression

22 Age, diabetes duration, HbA(1c), and AER were similar among the three centers, but systolic B

23 reprocess to gastroscopes (2.0%, 6/300) and AER reprocess to colonoscopes (0.8%, 1/120).

24 y neoplasms (AER, 5.9 [95% CI, 2.5-9.3]; and AER, 6.0 [95%CI, 2.3-9.6] per 10,000 person-years, respe

25 ing, and greater glycosylated hemoglobin and AER at DCCT closeout but not with waist circumference.

26 smoking status, glycosylated hemoglobin, and AER.

27 the feedback loop between the mesenchyme and AER, and reduces and shifts anteriorly Shh expression in

28 ible for Fgf4 expression in the myotomes and AER, and showed that a conserved E-box is a target for t

29 expression of Fgf4 mRNA in the myotomes and AER.

30 e and independent correlation between PK and AER in univariate and multivariate regression analysis (

31 ough the positive correlation between PK and AER within the subgroups of patients with microalbuminur

32 rin overlap in the hair follicle placode and AER, we postulated that CDH3 could be a direct transcrip

33 fter a progressive rise in relative risk and AER of all solid tumors over time, there was an apparent

34 s, an apparent decrease in relative risk and AER of solid tumors at other sites is suggested.

35 previously characterized functional ZPA and AER enhancers and enrichment for relevant biological ter

36 Our results identify novel ZPA and AER enhancers that could be important regulators of gene

37 veral of these sequences function as ZPA and AER enhancers.

38 tasets show strong correlation with ZPA- and AER-expressed genes, previously characterized functional

39 and early kidney dysfunction was defined as AER >/=7.5 mug/min.

40 distal subectodermal mesoderm that occurs as AER activity attenuates, an event that is essential for

41 Rates of rosuvastatin-associated AERs over its first year of marketing were compared with

42 he increased rate of rosuvastatin-associated AERs relative to other widely used statins was also obse

43 nt limb phenotypes consistent with augmented AER extent and function.

44 cent nonridge ectodermal cells from becoming AER cells; negatively modulate AER activity and thus fin

45 The relationship between AER, MMN to FM tones, and rsfMRI was assessed in the sub

46 ing Fgf4 expression in myotomes and limb bud AER, and that its activity in the myotomes results at le

47 e blastocyst, the myotomes, and the limb bud AER, is regulated by distinct enhancer elements (Hom) in

48 patterning along the PD axis is regulated by AER-FGF signals remains controversial.

49 We substituted seven C1 AER of the FVO strain Plasmodium falciparum AMA1 with al

50 Alanine mutations at the C1 AER had shifted the immune response toward cross-strain-

51 t the hypothesis that immunodampening the C1 AER will divert the immune system toward more conserved

52 consideration of absolute versus categorical AER values, more frequent AER measures, ambulatory BP mo

53 (AER) were determined with average (95% CI) AER of 12 (10-14) per hour, consistent with previous stu

54 egulating morphogenesis of a mature, compact AER along the distal limb apex, from a broad ventral ect

55 structure is indeed a distinct compartment, AER-derived cells are gradually lost after E12.5 and no

56 reacted; AMFs also increased with decreasing AERs and increasing initial ozone-limonene ratios, which

57 ulatory sequences specific to the developing AER, and demonstrate by marking preAER cells that, at st

58 identified a 55-bp enhancer that can direct AER-specific reporter gene expression.

59 -/-) null mutant limb buds reveals disrupted AER morphogenesis.

60 The doubleridge AER is morphologically similar to that of En1 null mice,

61 racts with Wnt/beta-catenin signaling during AER maintenance.

62 l, we compared the 4-month effects of either AER or RES training on insulin sensitivity (by hyperinsu

63 late phase of RA signaling needed to expand AER structure fully along the distal ectoderm.

64 etic protein; FGF, fibroblast growth factor; AER, apical ectodermal ridge; ZPA, zone of polarizing ac

65 , proteinuria, nephropathy, or renal failure AERs.

66 e regression models (81% for GFR and 72% for AER).

67 ion-restricted regulatory loop essential for AER stratification, hence for normal patterning and skel

68 In the mouse, whereas a role for Fgfs for AER establishment and function has been clearly demonstr

69 Rspo2 expression in the AER is required for AER maintenance likely by regulating Wnt/beta-catenin si

70 D patterning process and that a key role for AER-FGF signaling is to facilitate SOX9 function and to

71 both Fgf4 and Fgf8 function in the forelimb AER, we show that limb bud mesenchyme fails to survive i

72 versus categorical AER values, more frequent AER measures, ambulatory BP monitoring, precise GFR meas

73 significantly higher than that obtained from AER reprocess to gastroscopes (2.0%, 6/300) and AER repr

74 significantly higher than that obtained from AERs (1.7%, 7/420).

75 Analysis of markers for functional AER in mouse T(-/-) null mutant limb buds reveals disrup

76 olved in maintenance of a mature functioning AER.

77 Greater AER in African Caribbeans and the absence of association

78 ate was associated with significantly higher AER (1.5% vs. 3.4%, respectively, p = 0.021).

79 -2893) per 100,000 person-years; the highest AERs were found for malignant neoplasms, diseases of dig

80 Genotyping high-impact AER may be useful for classifying AMA-1 strains into inh

81 tudy evaluated neural substrates of impaired AER in schizophrenia using a combined event-related pote

82 deficits contributed in parallel to impaired AER and accounted for approximately 50% of variance in A

83 igates neural mechanisms underlying impaired AER using a combined event-related potential/resting-sta

84 A second important AER cluster was localized to domain 2.

85 ridge (AER), we inactivated Fgf4 and Fgf8 in AER cells or their precursors at different stages of mou

86 odulations in F0M, along with impairments in AER and FM tone discrimination.

87 Greater improvements in AER were seen with benralizumab compared with placebo fo

88 pects of the cellular mechanisms involved in AER formation and in partitioning the ventral ectoderm i

89 Webbing persists in AER-specific inactivations of Bmpr1a and Fgf8 owing to e

90 lative incidence of a sustained reduction in AER to <300 mg/d was 52%, mostly but not entirely under

91 ted for approximately 50% of the variance in AER performance across individuals.

92 counted for approximately 50% of variance in AER performance.

93 In hemoglobin SS disease, increased AER (micro- and macroalbuminuria) occurred in 68% of adu

94 In other sickling disorders, increased AER occurs in 32% of adults, and macroalbuminuria occurs

95 Interstrain AER chimeras can be a way to incorporate inhibitory epit

96 wth factor (FGF) gene family members are key AER-derived signals, with Fgf4, Fgf8, Fgf9 and Fgf17 exp

97 present and required in the developing limb AER for normal autopod development.

98 of association with CHD contrast with lower AER in South Asian men and European women, both strongly

99 [AER] 20-200 microg/min), macroalbuminuria (AER >200 microg/min), ESRD (renal dialysis or transplant

100 s not maintained and progression to a mature AER is blocked.

101 mal factors to the morphogenesis of a mature AER is less clear.

102 , as well as the ultimate fate of the mature AER cells.

103 long-term fate of cells that form the mature AER showed that, although this structure is indeed a dis

104 uration of diabetes was 17 (5) years, median AER was 524 mg/d, and mean (SD) eGFR was 108 (20) ml/min

105 mpr1a in the signaling cascade that mediates AER formation.

106 gfr2 in limb mesenchyme to block mesenchymal AER-FGF signaling.

107 from becoming AER cells; negatively modulate AER activity and thus fine-tune the strength of AER sign

108 ctivated fgf receptor 2 (Fgfr2) in the mouse AER to terminate all AER functions; for comparison, we i

109 GF genes specifically expressed in the mouse AER, Fgf8 is unique not only in its expression pattern,

110 nd Fgf17 expressed specifically in the mouse AER.

111 osinophil counts of 0 or more cells per muL, AER was 0.73 (0.65-0.82); rate ratio versus placebo was

112 genitourinary subsequent primary neoplasms (AER, 5.9 [95% CI, 2.5-9.3]; and AER, 6.0 [95%CI, 2.3-9.6

113 The data presented here identify the non-AER border of dorsal-ventral ectoderm as a new signaling

114 Similarly, we find that a graft of the non-AER D-V border can expand the domain of Shh anteriorly w

115 These data demonstrate that the non-AER D-V border ectoderm is necessary and sufficient for

116 ft chimeras, we find that a graft of the non-AER D-V border ectoderm to a location on the surface of

117 limb mesoderm requires proximity to the non-AER D-V border.

118 ting signal opposing the activity of the non-AER DV border ectoderm.

119 On the basis of AER values, the risk of fine PM exposure was relatively

120 b skeletal phenotypes resulting from loss of AER-FGF signals cannot simply be a consequence of excess

121 However, the mechanism of AER function in limb skeletal patterning has remained un

122 how that T plays a role in the regulation of AER formation, particularly maturation, and suggest that

123 of the AER involves a gradual restriction of AER gene expression from a broad ventral preAER domain t

124 uding WNTs and FGFs, regulate early steps of AER induction.

125 activity and thus fine-tune the strength of AER signaling; and regulate the apoptosis of the distal

126 We showed that FGFR2 promotes survival of AER cells and interacts with Wnt/beta-catenin signaling

127 secondary analyses when other categories of AERs were examined, including adverse events with seriou

128 analysis examined the composite end point of AERs of rhabdomyolysis, proteinuria, nephropathy, or ren

129 e collected from BCs and internal surface of AERs, respectively.

130 samples obtained from the inner surfaces of AERs as the swab samples only indicate whether the AERs

131 f GI endoscopes and the internal surfaces of AERs.

132 wever, expression of Fgf4 in the myotomes or AER of murine embryos does not appear to be essential fo

133 1.5 limbs that fluorescently mark the ZPA or AER, followed by fluorescence-activated cell sorting and

134 removed different combinations of the other AER-FGF genes, we obtained unexpected skeletal phenotype

135 The overall AER was 2803 (95% CI, 2712-2893) per 100,000 person-year

136 rs; censoring rate, 0.92; 17 events; placebo AER, 9.22/100 person-years; censoring rate, 0.85; 32 eve

137 normal intensity, and loss of the posterior AER.

138 We found that premature AER loss in mutant limb buds delayed generation of autop

139 Early inactivation completely prevents AER formation.

140 mber in type 1 diabetic patients with raised AER but normal blood pressure shows no significant reduc

141 The antisaccadic error rate (AER) is increased in Parkinson's disease (PD).

142 imary endpoint was annual exacerbation rate (AER) ratio versus placebo, analysed by baseline eosinoph

143 We linked a mechanistic air exchange rate (AER) model to a mass-balance PM2.5 infiltration model to

144 carbon dioxide (CO2), and air exchange rate (AER) over a seven-day sampling period coincident with su

145 ily determined by vehicle air exchange rate (AER), with AER being mostly a function of ventilation se

146 patients with raised albumin excretion rate (AER) and investigated any change after 3 years in a subg

147 icipants with normal albumin excretion rate (AER) at DCCT closeout developed incident microalbuminuri

148 vels and the urinary albumin excretion rate (AER) was also observed (r = 0.16, P < 0.0001).

149 ia, defined as urine albumin excretion rate (AER)>/=300 mg/d, has long been considered a stage of irr

150 f diabetes, HbA(1c), albumin excretion rate (AER), creatinine clearance, hypertension, body mass inde

151 BP), renal function, albumin excretion rate (AER), glycemia, and other variables, with repeat renal b

152 Albumin excretion rate (AER), the mainstay of early detection of DN, is not a su

153 001) correlated with albumin excretion rate (AER), whereas surface density of peripheral GBM per glom

154 etic retinopathy and albumin excretion rate (AER).

155 CI, 0.25-0.85; P = .01; absolute event rate [AER], 4.79/100 person-years; censoring rate, 0.92; 17 ev

156 of microalbuminuria (albumin excretion rate [AER] 20-200 microg/min), macroalbuminuria (AER >200 micr

157 Air-exchange rates (AER) were determined with average (95% CI) AER of 12 (10

158 ), and high (0.96 h(-1)) air exchange rates (AER) with varying initial ozone-limonene ratios.

159 -beta thalassemia); albumin excretion rates (AER) and renal function (Cockroft-Gault formula) were de

160 ith a wide range of albumin excretion rates (AER).

161 Age-adjusted albumin excretion rates (AER; geometric means, mug/min) were significantly higher

162 Annualized event rates (AERs) were related to the extent/severity of perfusion d

163 Activity-to-exposure ratio (AER) values were calculated to compare relative risks of

164 Deficits in auditory emotion recognition (AER) are a core feature of schizophrenia and a key compo

165 tone of voice [auditory emotion recognition (AER)] that drive impairments in social cognition and glo

166 The reduced AER with GPi DBS could be explained by retrograde stimul

167 ta show that Bmp4 in limb mesoderm regulates AER induction and maturation and implicate signaling fro

168 ectly regulates interdigit PCD by regulating AER-FGFs, which act as survival factors for the interdig

169 IMS Health, rates of adverse event reports (AERs) per million prescriptions were calculated.

170 and using automated endoscope reprocessors (AERs) for disinfecting endoscopes.

171 .5 infiltration model to predict residential AER (Tier 1), infiltration factors (Tier 2), indoor conc

172 these were termed antigenic escape residues (AER).

173 topes function as antigenic escape residues (AER).

174 re expressed in the apical ectodermal ridge (AER) and in various regions of the limb mesenchyme.

175 naling centers, the apical ectodermal ridge (AER) and the zone of polarizing activity (ZPA).

176 is expressed in the apical ectodermal ridge (AER) and underlying mesoderm.

177 rm exclusive of the apical ectodermal ridge (AER) as a new signaling center in the limb bud.

178 is produced by the apical ectodermal ridge (AER) at the distal tip of the limb bud to direct outgrow

179 a century ago, the apical ectodermal ridge (AER) at the distal tip of the tetrapod limb bud was show

180 The apical ectodermal ridge (AER) in the vertebrate limb is required for limb outgrow

181 The apical ectodermal ridge (AER) is a critical signaling center at the tip of the li

182 The apical ectodermal ridge (AER) is a transient embryonic structure essential for th

183 he formation of the apical ectodermal ridge (AER) is critical for the distal outgrowth and patterning

184 ion of the limb bud apical ectodermal ridge (AER) is to produce fibroblast growth factors (FGFs) that

185 digits and expanded apical ectodermal ridge (AER) of Dkk1-deficient mice closely resemble En1 null mi

186 d to defects of the apical ectodermal ridge (AER) of the developing limb buds.

187 ed in the posterior apical ectodermal ridge (AER) of the limb bud in a pattern similar to Fgf4 and th

188 de, but also at the apical ectodermal ridge (AER) of the limb bud.

189 he situation in the apical ectodermal ridge (AER) of the limb.

190 was observed in the apical ectodermal ridge (AER) of the newly forming forelimb buds.

191 d compaction of the apical ectodermal ridge (AER) produces a ridge that is abnormally broad and flat.

192 re signals from the apical ectodermal ridge (AER) that are essential for limb pattern formation along

193 n of Jagged2 in the apical ectodermal ridge (AER) whether the ectodermal or mesenchymal compartment o

194 re expressed in the apical ectodermal ridge (AER), a critical signaling center that directs the outgr

195 lly in the limb bud apical ectodermal ridge (AER), a source of FGF activity.

196 in response to the apical ectodermal ridge (AER), and has the functional potential to be involved in

197 ivity (ZPA) and the apical ectodermal ridge (AER), are known to cause limb malformations and evolutio

198 d epithelium of the apical ectodermal ridge (AER), including three members of the bone morphogenetic

199 One of these, the apical ectodermal ridge (AER), is critical for proximodistal limb outgrowth media

200 ated with a smaller apical ectodermal ridge (AER), referred to here as an apical ectodermal mound (AE

201 esis in the forming apical ectodermal ridge (AER), restricted regions of the central nervous system,

202 ic day 9.5 when the apical ectodermal ridge (AER), the principal site of Megf7 expression at the dist

203 signalling from the apical ectodermal ridge (AER), we inactivated Fgf4 and Fgf8 in AER cells or their

204 development via an apical ectodermal ridge (AER), whereas an alternative Homeobox (Hox)-Fibroblast g

205 al functions of the apical ectodermal ridge (AER), which is required for proper limb bud outgrowth.

206 f the expression of apical ectodermal ridge (AER)-specific genes, including fibroblast growth factor

207 by the newly formed apical ectodermal ridge (AER).

208 ivity (ZPA) and the apical ectodermal ridge (AER).

209 g pathway, from the apical ectodermal ridge (AER).

210 rate ratios (RRs) and absolute excess risks (AERs) were calculated.

211 idence ratios (SIRs), absolute excess risks (AERs), and cumulative incidence of subsequent primary ne

212 os (SMRs) for CVD and absolute excess risks (AERs; number of excess deaths per 10,000 person-years) w

213 at, in addition to sustaining cell survival, AER-FGFs regulate P-D-patterning gene expression during

214 development, providing genetic evidence that AER-FGFs function to specify a distal domain and challen

215 hallenging the long-standing hypothesis that AER-FGF signalling is permissive rather than instructive

216 Our data suggests that AER expression of Bmp2 and Bmp4 is required for digit an

217 The AER at older than 40 years was highest for digestive and

218 The AER clusters map in close proximity to conserved structu

219 The AER for deaths from recurrence declined from 97 extra de

220 The AER is visible from embryonic day 10.5 to 13.5 (E10.5-E1

221 In this study, we genetically ablated the AER by conditionally removing FGFR2 function and found t

222 b, the feedback loop between the ZPA and the AER is interrupted, resulting in abnormal skeletal patte

223 n hair follicle morphogenesis as well as the AER during limb bud outgrowth in humans, whereas it is n

224 es RA to distal ectoderm fated to become the AER.

225 quently in the subridge mesoderm beneath the AER.

226 P < 0.001), to a similar extent, in both the AER and the RES training groups (mean relative reduction

227 cells of the chick limb bud and also by the AER itself.

228 e an ectopic anterior Shh domain expands the AER, promoting additional growth and repatterning.

229 maturation and implicate signaling from the AER in regulation of digit number and identity.

230 Abnormal signaling from the AER precedes ectopic chondrocyte condensation and subseq

231 Importantly, the AER clusters could be split, such that chimeras containi

232 cular level, removal of Bmp2 and Bmp4 in the AER caused an increase in Fgf expression, which correlat

233 nts in each intervention group (23.1% in the AER group and 23.5% in the RES group).

234 Although mice lacking Fgf4 in the AER have normal limbs, limb development is severely affe

235 trongly suggest that Rspo2 expression in the AER is required for AER maintenance likely by regulating

236 Rspo2 is expressed in the AER of all limb buds, however the stunted phenotype is s

237 Cell death in the AER of embryos concurrently exposed to ethanol and EUK-1

238 ation of Engrailed-1 (En1) expression in the AER of limb buds in which Bmp2 and Bmp4 had been removed

239 tigate the role BMP ligands expressed in the AER play in limb development we selectively inactivated

240 Loss of functional Hh signaling in the AER resulted in disruption of the normal digit pattern a

241 nd is driven by misregulation of Fgf8 in the AER, a region lacking Sost and Sostdc1 expression.

242 n factors, Sp8 and Sp9, are expressed in the AER, and regulate Fgf8 expression and limb outgrowth.

243 Both Dlx5 and Sox11 are expressed in the AER, and the proteins encoded by these genes bind to sep

244 ast growth factor 8 (Fgf8), expressed in the AER, downregulates Tbx2 expression.

245 d report that, although it is present in the AER, Fgf8 is undetectable in the genital tubercle.

246 Upon removal of Bmp2 and Bmp4 in the AER, no defects in proximal-distal patterning were obser

247 d Fgf4 are simultaneously inactivated in the AER, the limb does not develop.

248 ences responsible for Msx2 expression in the AER, we characterized the expression of LacZ reporter co

249 which Fgf4 and Fgf8 were inactivated in the AER.

250 ding with the loss of Fgf8 expression in the AER.

251 ucial for maintaining Fgf8 expression in the AER.

252 d that, once a cell is incorporated into the AER, its descendents remain within the AER.

253 Knowing the AER and initial ozone-limonene ratio is crucial to predi

254 Moreover, the AER persisted longer in the Bmp4 mutant limb buds exposi

255 In Sp8 mutants, the AER precursor cells are induced and initially express mu

256 presses Fgf8 initially, but that neither the AER nor Fgf8 expression is maintained.

257 mp signaling pathway in establishment of the AER and regulation of the dorsoventral polarity of the l

258 n chick results in anterior extension of the AER and subsequent limb phenotypes consistent with augme

259 Fgf8 and other markers at the borders of the AER at E11.5 gives the appearance of a double ridge.

260 ermal BMPs may delimit the boundaries of the AER by preventing adjacent nonridge ectodermal cells fro

261 In mouse, formation of the AER involves a gradual restriction of AER gene expressio

262 had delayed induction and maturation of the AER that resulted in expanded Shh signaling.

263 Moreover, we find that grafts of the AER to more proximal locations result in downregulation

264 enotype combining abnormal compaction of the AER with normal dorsal/ventral patterning.

265 owth of the limb depends on formation of the AER, a signaling center that forms at the limb bud apex.

266 he ridge results in the disappearance of the AER, demonstrating the requirement for continued beta-ca

267 efects, characterized by malformation of the AER, diminished Shh expression and the absence of the ma

268 etrical dorsal and ventral expansions of the AER.

269 osterior (AP) expansion in the extent of the AER.

270 a critical role in the establishment of the AER.

271 blishment and perhaps the maintenance of the AER.

272 widely spaced at the posterior margin of the AER.

273 increase in both the width and length of the AER.

274 bthalamic nucleus (STN) has no effect on the AER, but a previous case suggested that DBS of the globu

275 re the effects of STN DBS and GPi DBS on the AER.

276 GPi DBS substantially reduced the AER, restoring lost higher control over oculomotor funct

277 p63 and Dlx5;Dlx6 murine models of SHFM, the AER is poorly stratified and FGF8 expression is severely

278 tion of Tbx2 expression, suggesting that the AER produces a negatively-acting signal opposing the act

279 g normal embryogenesis, BMP signaling to the AER indirectly regulates interdigit PCD by regulating AE

280 oderm is marked at E16.5, in addition to the AER.

281 tend distally to the mesoderm underlying the AER.

282 al tip mesenchyme immediately underneath the AER is preferentially affected in the mutant limb, coinc

283 t, during the same periods of follow-up, the AER for deaths from second primary cancers and circulato

284 ave uncovered a novel mechanism, whereby the AER regulates the number of autopod progenitors by deter

285 f4 and that the induction of Ptc2 within the AER, like that of Fgf4, is mediated via antagonism of BM

286 o the AER, its descendents remain within the AER.

287 er, and swabbing the residual water from the AERs after reprocessing.

288 s the swab samples only indicate whether the AERs are free from microbial contamination or not.

289 Within this AER cluster, antibodies primarily targeted five polymorp

290 ower hemoglobin A1c and BP and regression to AER<300 mg/d were associated with reduced risk of develo

291 rculatory system (18%, 15%, and 14% of total AER, respectively).

292 erson-years, respectively); 36% of the total AER was attributable to these 2 subsequent primary neopl

293 ribution that each FGF can make to the total AER-FGF signal.

294 mutant limbs, we performed double and triple AER-specific inactivations of Bmpr1a, Fgf4 and Fgf8.

295 bud initiation causes an upregulation of two AER-FGFs, Fgf4 and Fgf8, and a loss of interdigital PCD

296 ver, through at least 10 years of follow-up, AER could often be controlled, and GFR frequently remain

297 ned by vehicle air exchange rate (AER), with AER being mostly a function of ventilation setting (reci

298 PK levels are independently correlated with AER and are categorically elevated in patients with macr

299 d assessment of perfusion and function, with AERs of 2.4% (both normal), 5.8% (discordant), and 11.3%

300 , targets for beta-catenin signaling, within AER was greatly reduced in Rspo2(-/-) embryos.