ライフサイエンスコーパス: hypoxia

1 cs that simultaneously target TAMs and tumor hypoxia.

2 in humans at high altitude and in mice under hypoxia.

3 body organs, the brain is most sensitive to hypoxia.

4 ey transcriptional factor in the response to hypoxia.

5 e of muscle homeostasis during adaptation to hypoxia.

6 ckout mouse model characterized by placental hypoxia.

7 utophagy involved in resistance to CTL under hypoxia.

8 al understanding of cellular behavior during hypoxia.

9 decrease, rather than an increase, in tumor hypoxia.

10 xygenated to study the effects of myocardial hypoxia.

11 , and this activity was further augmented by hypoxia.

12 beta-adrenergic receptor function in chronic hypoxia.

13 th decreased NO consumption in physiological hypoxia.

14 simultaneously subjected to hypoglycemia and hypoxia.

15 ciated with reduced polycythemic response to hypoxia.

16 iogenic factors whose synthesis is driven by hypoxia.

17 diffuse white matter injury (DWMI) caused by hypoxia.

18 eading us to question the source of dNTPs in hypoxia.

19 magnitude and spatial distribution of tumor hypoxia.

20 ) is critical for mediating GSC signaling in hypoxia.

21 critical role in arousal to elevated CO2 or hypoxia.

22 n vascular integrity in the face of alveolar hypoxia.

23 ned signaling cascades that are initiated by hypoxia.

24 ervical interneurons (C-INs) also respond to hypoxia.

25 eby preventing vascular leak during alveolar hypoxia.

26 the Drosophila cardiac response to long-term hypoxia.

27 omplexity and tumour heterogeneity caused by hypoxia.

28 umption and inappropriate cell growth during hypoxia.

29 of osteoclastogenesis that is suppressed by hypoxia.

30 duced in p53-proficient CRC cells exposed to hypoxia.

31 ry for efficient metabolic adaptation during hypoxia.

32 noninvasive identification of regional tumor hypoxia.

33 the lifespan of Drosophila during long-term hypoxia.

34 nd prolonged (10 h) poikilocapnic normobaric hypoxia.

35 strengthening adaptive response of cells to hypoxia.

36 , thereby sustaining cancer cell survival in hypoxia.

37 II specifically at the intron retained under hypoxia.

38 ted by aberrant proliferation, necrosis, and hypoxia.

39 se in pregnancy complicated by chronic fetal hypoxia.

40 nt imaging demonstrated increased fractional hypoxia 24 hours after angiography and stenting in place

41 Intermittent hypoxia, a hallmark of OSA, could impose significant lon

42 electrographic seizures, cause brain tissue hypoxia, a measure of ongoing brain injury.

43 Insects can experience functional hypoxia, a situation in which O2 supply is inadequate to

44 A three-week hypoxia acclimation (48 mmHg) resulted in significant up

45 Similarly, hypoxia acclimation resulted in a 20% reduction in whole

46 Evofosfamide is a hypoxia-activated prodrug of bromo-isophosphoramide must

47 rdingly, we hypothesized that during chronic hypoxia, activation of HIF-2alpha may overcome the bone

48 ittent oxygen reductions [acute intermittent hypoxia (AIH)] evokes spinal plasticity.

49 ce (46 +/- 13/h) as well as CBC responses to hypoxia (all P < 0.05 vs. CHF empty virus).

50 These microenvironmental cues, which include hypoxia, also regulate the angiogenic processes within a

51 Interestingly, only the combination of hypoxia and a simulated loss of contractility (2% strain

52 ars caused by respiratory depression-induced hypoxia and a subsequent rise in CO2 that drives fentany

53 persistence under stressful conditions like hypoxia and abets drug tolerance.

54 abrogated the G1 cell cycle checkpoint under hypoxia and analyzed key cell cycle related proteins for

55 The spatial relationship between tumor hypoxia and angiogenesis was assessed by an overlap anal

56 nutrient inputs have led to eutrophication, hypoxia and anoxia, and low pH.

57 ucible method to generate mMSCs by utilizing hypoxia and basic fibroblast growth factor supplementati

58 Hypoxia and chemical repellents impair diving.

59 Hypoxia and dysregulated metabolism are defining feature

60 Q1 could impair the TNBC response induced by hypoxia and exert anti-tumour effects.

61 tified a subgroup of tumours associated with hypoxia and HIF signalling.

62 nce of an air pocket, but limited in time as hypoxia and hypercapnia rapidly develop.

63 Snow properties influence levels of hypoxia and hypercapnia, but their effects on ventilatio

64 led oxygen, produces substantial relief from hypoxia and improves motoneuron and locomotor function a

65 ld incorporate the growing threat of coastal hypoxia and include support for increased detection and

66 e first TCA rewiring occurs in mice in 2-day hypoxia and is mediated by cytosolic malate whereas in 1

67 -grade tumors that associated with increased hypoxia and mRNA expression of Hif1alpha and Vegf and in

68 s work we show that chondrocytes cultured in hypoxia and normoxia can be differentiated by their lipi

69 show that Vasorin is a critical link between hypoxia and Notch signaling in GSCs.

70 ertebrate taxa and may protect cells against hypoxia and oxidative stress.

71 Both positive and negative trends between hypoxia and perfusion were observed in individual lesion

72 utility of multiparametric imaging of tumor hypoxia and perfusion with (18)F-fluoromisonidazole ((18

73 To unravel the respective role of chronic hypoxia and pulmonary inflammation on soleus muscle hype

74 nitoring-mass spectrometry demonstrated that hypoxia and rapamycin treatment increased IGFBP-1 phosph

75 findings are relevant to conditions in which hypoxia and respiratory depression are implicated, inclu

76 Oxygen supplementation could prevent hypoxia and secondary neurological deterioration and thu

77 DII-VENUS and is synergistically enhanced by hypoxia and the auxin transport inhibitor naphthylphthal

78 These findings suggest that hypoxia and, to a far greater extent, exercise independe

79 emely vulnerable to injury during periods of hypoxia and/or ischemia.

80 vated protein kinase (AMPK) is stimulated by hypoxia, and although the AMPKalpha1 catalytic subunit h

81 hey are activated by hypercapnia, but not by hypoxia, and express proton sensors, TASK-2 and Gpr4.

82 ossibly related to adipose cell hypertrophy, hypoxia, and/or intestinal leakage of bacteria and their

83 omal cell-derived factor-1alpha, and reduced hypoxia- and stromal cell-derived factor-1alpha-mediated

84 f antitumor immune response, protection from hypoxia, angiogenesis, DNA repair, cell migration and in

85 IF5A hypusination and cellular resistance to hypoxia/anoxia.

86 (prepubertal children), and the presence of hypoxia are the three main clinical risk factors and are

87 The nanobubbles can also reprogram several hypoxia associated and tumor suppressor genes such as MA

88 different mechanisms, among which the tumor hypoxia-associated radiation resistance is a well-known

89 n the ventrolateral medulla oblongata during hypoxia attenuates the secondary depression.

90 >10% of all coral reefs at elevated risk for hypoxia based on local and global risk factors.

91 th a selective advantage under conditions of hypoxia, but little is known about the mediators of this

92 Responses to hypoxia can be mediated epigenetically, thus we investig

93 Future work is required to determine if hypoxia can be used to prevent and reverse neurodegenera

94 We found that 2 h of hypoxia caused an expected increase in frontal cortical

95 or long-term hypoxia exposure, we found that hypoxia caused heart dysfunction.

96 Gestational hypoxia caused low birth-weight and changes in young adu

97 Here, we provide evidence that hypoxia causes economic impacts on a major fishery.

98 iated following effective signals, including hypoxia, cold shock, heat shock, oxidative stress, exerc

99 g in immunodeficient mice exhibited enhanced hypoxia compared to the original tumours in immunocompet

100 of immunoreactive LEP following exposure to hypoxia, continuing upon return to normoxia.

101 In particular, tissue hypoxia contributes to therapeutic resistance, heterogen

102 We propose that physiological hypoxia coordinates homeostasis of CPCs, providing mecha

103 However, in hypoxia, cytoplasmic accumulation of Tyr359-phosphorylat

104 After 10 h in hypoxia, decreased blood flow to the major nodes of the

105 e report MTA1 regulation of SGK1 expression, hypoxia-dependent MTA1 translocation to the cytoplasm an

106 tive stress, and its dysfunction can lead to hypoxia-dependent pathologies such as ischemia and cance

107 by sugar starvation occurs downstream of the hypoxia-dependent stabilization of ERF-VII proteins and

108 Taken together, our results demonstrate that hypoxia-dependent upregulation of BMX contributes to the

109 Hypoxia did not inhibit BK in inside-out patches.

110 al colonization leads to complex contact and hypoxia driven responses resulting in increased antimicr

111 the hypoxic regions of tumors to weaken the hypoxia-driven pathways and inhibit tumor growth.

112 Nonphysiological hypoxia during early pregnancy induces CHD, but the unde

113 cellular and molecular pathways along which hypoxia exerts effects on nephrogenesis are not well und

114 lmonary granulomas with central necrosis and hypoxia exists.

115 blished Drosophila heart model for long-term hypoxia exposure, we found that hypoxia caused heart dys

116 tillations, associated or not with a chronic hypoxia exposure.

117 We show that the response of the skin to hypoxia feeds back on a wide range of cardiovascular par

118 25%]), fever and infection (four [25%]), and hypoxia (four [25%]); one patient had grade 4 hypoxia re

119 role of G9a in regulating gene expression in hypoxia has not been described extensively.

120 annot distinguish between excitotoxicity and hypoxia, however, because they share common molecular me

121 In animals, intermittent hypoxia (IH) mimicking OSA promotes tumor malignancy bot

122 rom adaptation to repeated episodes of acute hypoxia in a premalignant progression model.

123 re increased in response to inflammation and hypoxia in Caco-2 cells.

124 ssion that occur within hours of exposure to hypoxia in in vivo skeletal muscles remain unexplored.

125 nstrated that the noninvasive measurement of hypoxia in inflammation using (18)F-FAZA and (18)F-FMISO

126 n experiment but were unaffected by chemical hypoxia in Neuro2a cells and in experimental stroke mode

127 urons undergoing ischemic stress mediated by hypoxia in vitro and global cerebral ischemia in rats in

128 uggest that while the ISR protects OPCs from hypoxia in vitro, it does not appear to play a major rol

129 uperoxide release, was detected during acute hypoxia in wild-type but not Cox4i2(-/-) PASMCs.

130 he noticed stimulation of SGK1 expression by hypoxia includes de-repression of SGK1 transcription bec

131 hypothesized effects in the relative prices: Hypoxia increases the relative price of large shrimp com

132 vented excess placental lipid deposition and hypoxia (independent of sex) and insulin resistance in m

133 al analyzer for the measurement of NO2(-) in hypoxia induced H9c2 cardiac cells using ARM microcontro

134 RC cell line and human CRC tissue exposed to hypoxia, induced heat-shock 70-kDa protein-1-like (HSPA1

135 on of BK/Kv strongly limits the magnitude of hypoxia-induced [Ca(2+) ]i rise, with Kv having a much g

136 Hypoxia-induced amoeboid detachment was driven by hypoxi

137 by patch-clamp measurements showed decreased hypoxia-induced cellular membrane depolarization in Cox4

138 will summarize our current understanding of hypoxia-induced changes in cancer cell metabolism, with

139 essors including hypoxia, may play a role in hypoxia-induced DWMI and may represent a novel target fo

140 eurological outcome in preterm neonates with hypoxia-induced DWMI.SIGNIFICANCE STATEMENTDiffuse white

141 EIF2B5: a weak splicing potential at the RI, hypoxia-induced expression and binding of the splicing f

142 y in glioblastoma (GBM) patients may involve hypoxia-induced expression of C-X-C motif chemokine rece

143 PCR demonstrated that 10 microM YC-1 reduced hypoxia-induced expression of HIF-1alpha targets involve

144 Suppression of autophagy via hypoxia-induced expression of the kinase-dead unc-51-lik

145 t, atpenin A5 or myxothiazol does not reduce hypoxia-induced gene expression or RNA editing in monocy

146 JQ1 significantly modulated 44% of hypoxia-induced genes, of which two-thirds were downregu

147 ADORA2A knockdown decreases hypoxia-induced glycolytic enzyme expression, glycolytic

148 , whereas knockdown of LncHIFCAR impairs the hypoxia-induced HIF-1alpha transactivation, sphere-formi

149 lls (PASMCs) from Cox4i2(-/-) mice showed no hypoxia-induced increase of intracellular calcium.

150 mitter within the preBotC contributes to the hypoxia-induced increases in ventilation.

151 th a significant reduction in both tonic and hypoxia-induced lactate release in the cerebral cortex,

152 endently (0.5-50 mg/kg, per os) prevented DM/hypoxia-induced lesions.

153 Nitrite (NO2(-)) supplementation limits hypoxia-induced oxidative stress and activates the alter

154 fic and sustained vasodilation in SUGEN-5416/hypoxia-induced PAH rats than oral, intravenous, or intr

155 In contrast, chronic hypoxia-induced pulmonary hypertension and pulmonary vas

156 adaptation that is triggered upon entry into hypoxia-induced quiescence but facilitates subsequent ce

157 Hypoxia-induced superoxide release which was detected by

158 NCE STATEMENT Exposure to acute intermittent hypoxia induces phrenic long-term facilitation (pLTF), a

159 The role of prolyl hydroxylase (PHD)-3 as a hypoxia inducible factor (HIF)-1alpha cofactor is contro

160 Over-activation of hypoxia inducible factor (HIF)-1alpha has been implicate

161 The hypoxia inducible factor 1 alpha subunit (HIF1A) directl

162 ariant mapped to the EPAS1 gene encoding the hypoxia inducible factor 2alpha.

163 with a focus on its relations with VEGF and hypoxia inducible factor related angiogenesis pathways,

164 (PAECs), expression of transcription factor hypoxia inducible factor-1alpha (HIF-1alpha) is increase

165 nstrate that MUC1-regulated stabilization of hypoxia inducible factor-1alpha (HIF-1alpha) mediates su

166 DF-induced metabolic reprogramming required hypoxia inducible factor-1alpha (HIF-1alpha), downstream

167 Loss of smooth muscle cell hypoxia inducible factor-1alpha underlies increased vasc

168 Hypoxia inducible factors (HIFs) are centrally involved

169 tress management is under the control of the Hypoxia Inducible Factors, whose activity depends on the

170 Hypoxia-inducible factor (HIF) is a key transcriptional

171 demethylating RACK1 protein, a component of hypoxia-inducible factor (HIF) ubiquitination machinery,

172 n regulates cellular function is through the hypoxia-inducible factor (HIF), a transcription factor c

173 factors GATA-binding protein 4 (GATA-4) and hypoxia-inducible factor (HIF)-1alpha and -2alpha in res

174 r atpenin A5 in normoxia robustly stabilizes hypoxia-inducible factor (HIF)-1alpha in primary monocyt

175 Hilpda proved to be a target of hypoxia-inducible factor 1 (Hif-1) and peroxisome prolif

176 ia-induced amoeboid detachment was driven by hypoxia-inducible factor 1 (HIF-1), followed the downreg

177 utyrate (SB) may indirectly (through reduced hypoxia-inducible factor 1 alpha stabilization) decrease

178 , vascular endothelial growth factor (VEGF), hypoxia-inducible factor 1-alpha (HIF-1alpha) and erythr

179 We show that endothelial hypoxia-inducible factor 1alpha (HIF-1alpha) controls gl

180 d growth, blood vessel density, and VEGF and hypoxia-inducible factor 1alpha (HIF-1alpha) expression

181 by the oxygen-sensitive transcription factor hypoxia-inducible factor 1alpha (HIF-1alpha).

182 ow that Parkin is an E3 ubiquitin ligase for hypoxia-inducible factor 1alpha (HIF-1alpha).

183 yl hydroxylase gene (PHD) 1 and 2 and in the hypoxia-inducible factor 2 alpha (HIF2A) were also found

184 in-5-yl}benzonitrile-based inhibitors of the hypoxia-inducible factor prolylhydroxylase domain-1 (PHD

185 HIF (hypoxia-inducible factor)-1alpha is a major determinant

186 y angiogenic growth factors are regulated by hypoxia-inducible factor, and hypoxia-inducible factor-1

187 rotein-1-like (HSPA1L) expression stabilized hypoxia-inducible factor-1alpha (HIF-1alpha) protein and

188 n of the profibrotic markers fibronectin and hypoxia-inducible factor-1alpha and reversed TGF-beta1-i

189 e regulated by hypoxia-inducible factor, and hypoxia-inducible factor-1alpha induction was attenuated

190 s accompanied by nonheme iron deposition and hypoxia-inducible factor-1alpha upregulation in the rena

191 : IL-1R-associated kinase-M, NFkB2/p100, and hypoxia-inducible factor-1alpha.

192 tion in response to oxygen fluctuations, and hypoxia-inducible factors (HIFs) are central mediators o

193 in the VHL tumor suppressor stabilizing the hypoxia-inducible factors (HIFs) are the most prevalent

194 brafish that identifies GCs as activators of hypoxia-inducible factors (HIFs) in the liver.

195 oiesis and leukemogenesis are dependent upon hypoxia-inducible factors (HIFs), a family of essential

196 roteomics and functional analyses identified hypoxia-inducible gene 2 (HIG2), a HIF-1 target, as a ne

197 Here we identify MIR31HG as a hypoxia-inducible lncRNA and therefore we name it LncHIF

198 he adenosine A2a receptor (ADORA2A) promotes hypoxia-inducible transcription factor-1 (HIF-1)-depende

199 They are likely triggered by hypoxia-inducible transcription factors (HIFs), and thei

200 Our findings do not support the view that hypoxia inhibits BK/Kv to initiate or maintain the hypox

201 istance is a well-known one, as there exists hypoxia inside most solid tumors while oxygen is essenti

202 Hypoxia is a commonly found pathologic feature of HGGs.

203 our understanding of human diseases in which hypoxia is a feature.

204 Diffuse white matter injury (DWMI) caused by hypoxia is a leading cause of neurological deficits foll

205 omplication of abdominal surgery, and tissue hypoxia is a main determinant in adhesion formation.

206 Tumor hypoxia is a therapeutic concern since it can reduce the

207 Tumor hypoxia is an established facilitator of survival adapta

208 Increased bone marrow hypoxia is associated with increased recirculation of mu

209 Hypoxia is common in the first few days after acute stro

210 The cellular response to hypoxia is critical for cell survival and is fine-tuned

211 or plasticity elicited by acute intermittent hypoxia is enhanced at disease end-stage, suggesting gre

212 so, whether oxygen given at night only, when hypoxia is most frequent, and oxygen administration is l

213 Hypoxia is often associated with cardiopulmonary disease

214 Although hypoxia is recognized to be an adverse factor in tumor g

215 The ventilatory response to reduced oxygen (hypoxia) is biphasic, comprising an initial increase in

216 vironmental stresses such as those caused by hypoxia, ischemia, and diabetes.

217 We have previously shown that cerebral Hypoxia-ischemia (HI) results in activation of Src kinas

218 rstanding of events associated with cerebral hypoxia-ischemia during cardiopulmonary bypass (CPB) rem

219 early or delayed cell death from hypoxia or hypoxia-ischemia.

220 Reduced oxygen availability (hypoxia) leads to increased production of reactive oxyge

221 gradient from membrane damage, coupled with hypoxia, leads to reduced ATP production by aerobic resp

222 tment rapidly induces a HIF2alpha-associated hypoxia-like transcriptional response followed by an inc

223 As such, oxygen deprivation (hypoxia) limits cholesterol synthesis through incomplete

224 Hypoxia (low O2) is a fundamental microenvironmental det

225 Regions of hypoxia (low oxygen) occur in most solid tumours and cel

226 The response is not mediated by hypoxia, matrix stiffness, or bulk matrix density, but r

227 ovides an anatomical mechanism through which hypoxia may cause deficits in working memory.

228 yotic response to myriad stressors including hypoxia, may play a role in hypoxia-induced DWMI and may

229 that a well-established in vivo mild chronic hypoxia (MCH) mouse model and a new severe acute hypoxia

230 rs, resulting in upregulation of a number of hypoxia mediated signaling pathways including cell proli

231 ken together, our results suggest a role for hypoxia-mediated CCR1 upregulation in driving the egress

232 Here, we report that hypoxia-mediated downregulation of the dual specificity

233 fusion, (18)F-FMISO distribution volume, and hypoxia-mediated entrapment, respectively.

234 It is well suited for understanding hypoxia-mediated mechanisms in cancer disease and other

235 Factor (VEGF) secretion for this pathway of hypoxia-mediated self-renewal.

236 The underlying mechanisms that direct hypoxia-mediated survival in GBM habitats are unclear.

237 TA1 is a stress-responsive gene, but whether hypoxia modulates its function and its role in engaging

238 lly inhibits oxygen consumption, and neither hypoxia nor atpenin A5 in normoxia robustly stabilizes h

239 Stresses such as hypoxia, nutrient deprivation and acidification disturb

240 are highly adapted to life in the hypobaric hypoxia of high altitude.

241 mia) due to the reduced oxygen availability (hypoxia) of residence at high altitude or other conditio

242 Plants respond to hypoxia, often caused by submergence, by expressing a sp

243 tion of c-Myc mimicked the effects of severe hypoxia on CPC proliferation, also triggering quiescence

244 teractions of macrophage differentiation and hypoxia on fibrosis.

245 We investigated the effects of hypoxia on secondary metabolite production and observed

246 tivation is important to BP stability during hypoxia or anesthesia and contributes greatly to the hyp

247 echanisms mediating cell proliferation after hypoxia or HIF-2alpha activation in CRC are unclear.

248 organ pathology in Ndufs4 KO mice exposed to hypoxia or hyperoxia.

249 sistance to early or delayed cell death from hypoxia or hypoxia-ischemia.

250 rise in CBF and associated with brain tissue hypoxia, or higher-frequency PDs may reflect inadequacie

251 e of perturbations that include intermittent hypoxia, oxidative stress, sympathetic activation, and e

252 ned) permeability caused by inflammation and hypoxia (P < 0.0001 and P < 0.05).

253 and function but are not in the response-to-hypoxia pathway.

254 lar for immune responses, IL production, and hypoxia pathways.

255 g traumatic brain injury (TBI), ischemia and hypoxia play a major role in further worsening of the da

256 ation of lung macrophages toward a conserved hypoxia program, with the development of compartment-spe

257 two-hit pathophysiological mechanism without hypoxia provides novel druggable targets to ameliorate a

258 Hypoxia reduces sensitivity to 5-fluorouracil (5-FU)-che

259 Here, we show that NiCl2 (Ni(II)) or hypoxia reduces the protein level and shortens the half-

260 val fraction is calculated to be 80% and the hypoxia reduction factor reaches a maximum value of 2.24

261 Together, our results indicated that hypoxia-regulated autophagy suppresses metastasis in bre

262 ypoxia (four [25%]); one patient had grade 4 hypoxia related to therapy that met protocol-defined cri

263 by subjecting stem villus artery explants to hypoxia-reoxygenation, or inhibiting CSE.

264 an aortic endothelial cells (HAEC) from cold hypoxia/reoxygenation injury more effectively than necro

265 Induction of gene expression under hypoxia requires transcription factors belonging to grou

266 nd -2alpha in response to angiotensin II and hypoxia, respectively, which drive VEGF expression.

267 nes related to ear and tooth development and hypoxia, respectively.

268 s, there was no decrease in HIF-1 binding to hypoxia response elements.

269 ings provide a new insight into HIF-mediated hypoxia response regulation by coupling the FAD dependen

270 e associated with increased inflammatory and hypoxia-response signaling and decreased nutrient transp

271 ne-specific demethylase 1 (LSD1) upregulates hypoxia responses by demethylating RACK1 protein, a comp

272 tumors that show constitutive activation of hypoxia responses.

273 ncreased in hypoxic areas of CRC tissues and hypoxia-responsive miR-21 and miR-30d, but not miR-210,

274 xia (MCH) mouse model and a new severe acute hypoxia (SAH) mouse model of DWMI activates the initial

275 lls, which are neural crest-derived, and the hypoxia-sensitive 'neuroepithelial cells' (NECs) of fish

276 The evolutionary origins of the hypoxia-sensitive cells that trigger amniote respiratory

277 ells, skeletal muscle cells under normal and hypoxia serum starvation conditions) and in vivo experim

278 This hypoxia-specific apoptosis induction by YC-1 involved ex

279 diated by cytosolic malate whereas in 10-day hypoxia the rewiring is mediated by Idh1 and Fasn, suppo

280 These findings suggest that hypoxia, through HIF1A, contributes to the development a

281 lection for genes involved in peroxidase and hypoxia to enable its highland adaptation.

282 head (ONFH) primarily results from ischemia/hypoxia to the femoral head, and one of the cellular man

283 imental RA exhibited a 3-fold enhancement in hypoxia tracer uptake, even in the early disease stages,

284 ications of pregnancy, such as chronic fetal hypoxia, trigger a fetal origin of cardiovascular dysfun

285 expansion, which is conceptually similar to hypoxia-triggered angiogenesis.

286 -repression of SGK1 transcription because of hypoxia-triggered nucleus-to-cytoplasmic translocation o

287 Hypoxia-triggered redistribution of MTA1, SGK1 upregulat

288 P secretion from cancer cells was induced by hypoxia, triggering MAPK signaling in endothelial cells

289 Hypoxia upregulates the core pluripotency factors NANOG,

290 bolism in vitro Correction of stroke-induced hypoxia using supplemental oxygen in vivo lowered Glu le

291 w that G9a protein stability is increased in hypoxia via reduced proline hydroxylation and, hence, in

292 ginal tumours in immunocompetent humans, and hypoxia was reduced by adoptive TH1 transfer.

293 In response to hypoxia, we found an early increase in macrophage number

294 lineate mechanisms of cellular adaptation to hypoxia, we performed RNA-Seq of normoxic and hypoxic he

295 ts of sorafenib led to increased bone marrow hypoxia, which contributed to HIF-dependent BMX upregula

296 Improved perfusion alleviates hypoxia, which reprograms the immunosuppressive tumor mi

297 mpaired arousal responses to hypercarbia and hypoxia, which ultimately leads to asphyxia.

298 nding how tumor and stromal cells respond to hypoxia will allow for the design of innovative cancer t

299 e molecular mechanisms induced by tumor cell hypoxia with a special emphasis on therapeutic resistanc

300 ltiparametric imaging of tumor perfusion and hypoxia with dynamic (18)F-fluoromisonidazole ((18)F-FMI