ライフサイエンスコーパス: hypoxia

1 se be lost as ethanol, for example following hypoxia.

2 he Ly6C(lo) monocyte lineage were exposed to hypoxia.

3 evolved mechanisms to enable survival during hypoxia.

4 e excision repair protein, is upregulated by hypoxia.

5 link acute and chronic adaptive responses to hypoxia.

6 elated negatively with continuous time under hypoxia.

7 coordinate diverse biological outputs during hypoxia.

8 cental insufficiency, which results in fetal hypoxia.

9 ro-environments characterized by acidity and hypoxia.

10 's disease (AD), a condition involving brain hypoxia.

11 of stress-responsive gene transcripts during hypoxia.

12 pability to prevent the progression of tumor hypoxia.

13 in response to energy stress from transient hypoxia.

14 central autonomic respiratory output during hypoxia.

15 erio-occlusive PH in rats exposed to chronic hypoxia.

16 MTA target and help reduce its central basin hypoxia.

17 age and genotype on brain responses to acute hypoxia.

18 essively increasing severity and duration of hypoxia.

19 MPOS (highly metastatic), under normoxia and hypoxia.

20 labeling correlated with MCT1 expression and hypoxia.

21 well at low oxygen and thus are buffered by hypoxia.

22 arget for IUGR in pregnancies complicated by hypoxia.

23 f oxygen sensing and cellular adaptations to hypoxia.

24 ssure (p = 0.004) when comparing normoxia to hypoxia.

25 enocopied in bacteria exposed to atmospheric hypoxia.

26 come, but better yet, exploit intra-tumoural hypoxia.

27 O(2) ), cold (5 degrees C) normoxia, or cold hypoxia.

28 ment characterized by increasing acidity and hypoxia.

29 r after the exposure to short-term sustained hypoxia.

30 shifts exhibited by OS cells in response to hypoxia.

31 2 infected patients, even in the absence of hypoxia.

32 al dominant negative p53 protein and chronic hypoxia.

33 zed by uteroplacental ischaemia and/or fetal hypoxia.

34 s for controlling expiratory activity during hypoxia.

35 We show that hypoxia (1% O(2)) specifically increases matrix disassem

36 fetuses were exposed to normoxia (n = 6) or hypoxia (10% inspired O(2) , n = 9) for the last third o

37 adults to warm (25 degrees C) normoxia, warm hypoxia (12 kPa O(2) ), cold (5 degrees C) normoxia, or

38 ses of stillbirth were perinatal asphyxia or hypoxia (130 [72%] of 180 stillbirths) and congenital in

39 ong selection for the tolerance of low O(2) (hypoxia)(5).

40 e in end-exercise arterial oxygen tension in hypoxia (59 +/- 6 vs. 59 +/- 9 mmHg for controls and HAH

41 sure (P(di) ) of 92 cmH(2) O in normoxia and hypoxia (8% O(2) ) were performed on separate days (>=48

42 Hypoxia-activated prodrugs (HAPs) present a conceptually

43 Hypoxia activates hypoxia-inducible factor-dependent sig

44 Ss) that are microenvironment responsive and hypoxia active are scarcely available and urgently desir

45 asticity during chronic exposure to cold and hypoxia, alone and in combination.

46 could reduce both the occurrence of alveolar hypoxia and absorption atelectasis, thus optimizing the

47 Radial profiling revealed severe hypoxia and c. 0.8 kPa CO(2) within the root vascular cy

48 ent organoid methods are limited by interior hypoxia and cell death due to insufficient surface diffu

49 A stability of a number of mRNAs involved in hypoxia and cell-cycle signaling.

50 mpathetic nerve activity (MSNA) responses to hypoxia and contributes to tonic sympathetic and respira

51 f the blood vasculature, causing cancer cell hypoxia and death in distant avascular regions.

52 companied by ever-present risks of hypobaric hypoxia and decompression sickness.

53 ule-forming cells aimed at alleviating renal hypoxia and enhancing tubulogenesis holds promise as the

54 A lack of PDGFB in platelets led to enhanced hypoxia and epithelial-to-mesenchymal transition in the

55 arction, because of respiratory failure with hypoxia and hemodynamic instability in critically ill pa

56 pathways, and determined sO(2) responses to hypoxia and hyperoxia in the different retinal capillary

57 ce the tumor microenvironment by alleviating hypoxia and improving the antitumor immune response.

58 found in bone marrow niches with the deepest hypoxia and instead are found in hypoxic environments si

59 te PolyhHb is more likely to decrease tissue hypoxia and modulate the metabolic rate of O2 consumptio

60 The Mfsd7c-KO brain exhibited hypoxia and neuronal cell death.

61 of mcp-1 in neurons enhances survival under hypoxia and protects against neurodegeneration in a tauo

62 Exposure of cultured NPCs to hypoxia and sovateltide also showed higher NPC different

63 sleep fragmentation, leading to intermittent hypoxia and subsequent diseases such as cardiovascular,

64 pnoea (OSA) is characterised by intermittent hypoxia and systemic inflammation.

65 ttle is known about the relationship between hypoxia and the type I IFN pathway, which comprises the

66 This study examined effects of hypoxia and tributyltin (TBT) on adult Eastern oysters (

67 types of recurrent episodes of intermittent hypoxia and/or bradycardia, also defined as cardio-respi

68 microenvironment is hypoxic, we assessed if hypoxia and/or interactions with MM cells increases pro-

69 sensitive ecosystems (e.g., coral bleaching, hypoxia) and is expected to have expanding impacts under

70 , and 6-hour variable exposures to sublethal hypoxia, and compared responses for each hypoxia regime

71 e intermediate between normoxia and constant hypoxia, and gonad production correlated negatively with

72 ures of radiosensitivity, HPV status, tumour hypoxia, and microsatellite instability.

73 (SCr), systolic blood pressure (SBP), renal hypoxia, and renal vein levels of pro-inflammatory marke

74 hibition of hyaluronidase activity prevented hypoxia- and oxidant-induced proliferation.

75 Hypoxia appears to be a key factor in adipose tissue dys

76 her plants, molecular responses to exogenous hypoxia are driven by group VII ethylene response factor

77 ent, namely, acidic pH, redox reactants, and hypoxia, are exploited.

78 s relatively common in SCD populations, with hypoxia as a key manifestation, and sequelae including i

79 ontributor to HI effects in the treatment of hypoxia-associated diseases.

80 on of the PPARgamma pathway protects against hypoxia-associated IUGR, we used an experimental murine

81 Elevated hypoxia associates with increased mutational load across

82 fever in the first 24 hours, whereas 41% had hypoxia at admission.

83 s responsible for respiratory control during hypoxia at altitude, by linking genetic factors with car

84 layer revealed hyperoxia during daytime and hypoxia at nighttime resulting from net photosynthesis a

85 The pairing-dubbed happy hypoxia but more precisely termed silent hypoxemia-is es

86 common strategies to cope with high-altitude hypoxia, but some changes require longer evolutionary ti

87 To determine if the sensing of hypoxia by nonclassical monocytes contributes to the dev

88 In plants, hypoxia can be induced by submergence, and the lack of o

89 ion on how extracellular matrix proteins and hypoxia can be utilized to improve MSC retention and the

90 Exposure to hypoxia can decrease individual physiological fitness th

91 tumour cell proliferation or sensitivity to hypoxia, can produce spheroids with similar bulk growth

92 Chronic hypoxia (CH) produces a time-dependent increase of resti

93 Hypoxia was induced in a normobaric hypoxia chamber by decreasing the partial pressure of ox

94 C) of rats treated with chronic intermittent hypoxia (CIH) simulating a severe condition of obstructi

95 tumor initiation and growth, including tumor hypoxia, clonal stem cell selection, and immune cell res

96 When cultured in hypoxia condition, GSCs rapidly exported muscleblind-lik

97 images from the SCD patients in normoxia and hypoxia conditions.

98 at exposure to environmental insults such as hypoxia could explain variable expressivity and penetran

99 nge and cancer cell metabolism that leads to hypoxia, depletion of nutrients, and accumulation of was

100 We also provide evidence that prolonged hypoxia down-regulates kindlin-2 expression, leading to

101 ibitor studies provided further support that hypoxia-driven adaption of pathways associated with glyc

102 ularly roots, can be subjected to periods of hypoxia due to environmental circumstances.

103 The increases in CBF with acute hypoxia during thermal stress were appropriate to mainta

104 n (Pa(CO(2))) blunts the brain's response to hypoxia, effects of disease and age on control of breath

105 tion, its functional and historical roots in hypoxia emphasize a broader evolutionary role.

106 P levels independently of AMPK, and point to hypoxia/energy depletion as potential modifiers of CA4P

107 )-M checkpoint were associated with moderate hypoxia, epithelial-to-mesenchymal transition, and infla

108 research has targeted the effect of oil and hypoxia exposure on developing immune systems.

109 oxia-inducible factor-mediated adaptation to hypoxia, extracellular matrix formation, epigenetic regu

110 Experiments were carried out in hypoxia ( FIO2 = 0.12), whereas convective O(2) delivery

111 It is driven by retinal hypoxia frequently caused by capillary nonperfusion and

112 sion signatures in distinct pathways such as hypoxia, glycolysis, cell metabolism, translation initia

113 sium and copper, further differentiating the hypoxia gradient and validating the protein expression.

114 Both the normoxia and hypoxia groups consisted of seven patients.

115 refore, key adaptive mechanisms to cope with hypoxia have evolved in mammals.

116 These localized shifts toward hypoxia have identified a prominent role for the transcr

117 Hypoxia/HIF-1alpha- and extracellular adenosine/A2 adeno

118 Under inflammation or hypoxia, HMW-HA is degraded by hyaluronidases, such as H

119 In hypoxia, however, glycolysis becomes critical for cytoki

120 ), which release transmitters in response to hypoxia, hypercapnia, and acidemia to activate afferent

121 Acute intermittent hypercapnic hypoxia (IH) induces long-lasting elevations in sympathe

122 ed potential interactions between functional hypoxia imaging and infiltrating lymphocyte levels as a

123 a processes in these models (e.g., placental hypoxia, immune dysfunction, angiogenesis, oxidative str

124 confirmatory experiments, we concluded that hypoxia in IHs is regulated by EPAS1 (HIF-2alpha) instea

125 ure following acute intermittent hypercapnic hypoxia in men.

126 cornerstone of understanding the effects of hypoxia in normal tissues and malignant tumors.

127 a potential strategy to relieve solid tumor hypoxia in order to increase the effectiveness of chemot

128 Imaging of hypoxia in vivo helps with accurate cancer diagnosis and

129 tion rate (GFR), a measure of relative renal hypoxia, in adolescents with and without type 1 diabetes

130 In SOD3-deficient mice, hypoxia increased lung hyaluronidase expression and acti

131 Cold exposure in normoxia or hypoxia increased mitochondrial leak respiration and dec

132 Hypoxia induced increased fibroblast growth factor recep

133 silencing complex) as a crucial regulator in hypoxia-induced angiogenesis.

134 nd YLR086, and knockdown of FGFR1 attenuated hypoxia-induced EGFR TKI resistance in each line.

135 Hypoxia-induced extracellular matrix (ECM) deposition is

136 AMPK activation by AICAR partially prevented hypoxia-induced fetal growth restriction (P < 0.01), due

137 Thus, hypoxia-induced ISL2 regulated ANGPT2, which subsequentl

138 In hypoxia-induced PB the dynamics and coherence between he

139 H-PAAF, IPAH-PASMC) and in vivo (rat chronic hypoxia-induced PH and zebrafish angiogenesis).

140 superoxide dismutase (SOD3) protects against hypoxia-induced PH.

141 To link metastatic propensity to a hypoxia-induced proteotype, we compared the protein prof

142 anisms and function of HE4 overexpression in hypoxia-induced renal fibrosis will provide important in

143 th neuronal activities, which are altered by hypoxia-induced respiratory neuroplasticity.

144 These findings suggest that hypoxia-induced respiratory plasticity was characterized

145 ike features (glioma stem cell, GSC) through hypoxia-induced responses.

146 ly elevated sympathetic nervous activity and hypoxia-induced vascular dysfunction has not been determ

147 Hypoxia induces a vast array of long noncoding RNAs (lnc

148 Our results suggest that hypoxia induces renal fibrosis by upregulating HE4 and a

149 atically alters mitochondrial metabolism and hypoxia inducible factor (HIF) signaling due to iron dep

150 Hypoxia inducible factor (HIFs) signaling contributes to

151 poxia-inducible angiogenic pathway involving hypoxia inducible factor-1 alpha (HIF-1alpha), vascular

152 ter information about the prognostic role of hypoxia-inducible angiogenic pathway in G-AgP.

153 Hypoxia-inducible angiogenic pathway involving hypoxia i

154 d the kidneys have reduced expression of the hypoxia-inducible erythropoietin mRNA.

155 We also observed that depletion of the hypoxia-inducible factor (HIF) genes, HIF1A (encoding HI

156 prominent role for the transcription factor hypoxia-inducible factor (HIF) in the regulation of inna

157 This study compared effects of five hypoxia-inducible factor (HIF) prolyl hydroxylases (PHD)

158 Emerging evidence suggests that hypoxia-inducible factor (HIF) signaling plays a fundame

159 system include the transcriptional regulator hypoxia-inducible factor (HIF), which controls a wide ra

160 dies with the hydroxylase, factor inhibiting hypoxia-inducible factor 1 (FIH-1), we observed increase

161 ugh activation of transcription factors like hypoxia-inducible factor 1 (HIF-1) and c-Myc, yet the im

162 Here, we delineate a pathway controlled by hypoxia-inducible factor 1 (HIF-1) that epigenetically a

163 adhesion molecule 1, IL-10, heme oxygenase 1 hypoxia-inducible factor 1 (HIF-1), monocyte chemotactic

164 nts by activating the transcription factors, hypoxia-inducible factor 1 (HIF1) and HIF2.

165 Increased hypoxia-inducible factor 1-alpha expression in the MP gr

166 Expression of hypoxia-inducible factor 1-alpha peaked in the SCS-group

167 oC activation modulated the stabilization of hypoxia-inducible factor 1alpha (HIF1alpha) to upregulat

168 oxia-inducible factor 2alpha (HIF2alpha) and hypoxia-inducible factor 1alpha (HIF1alpha), were enrich

169 vacuoles within knockout cardiomyocytes; (3) Hypoxia-inducible factor 1alpha protein instability was

170 model, we show that the transcription factor hypoxia-inducible factor 2 alpha (Hif2alpha), which is i

171 portant transcription factor-binding motifs, hypoxia-inducible factor 2alpha (HIF2alpha) and hypoxia-

172 expression changes that suggested increased hypoxia-inducible factor 2alpha signaling.

173 en homeostasis maintaining pathway involving Hypoxia-inducible factor 2alpha.

174 ssion of parenchymal injury transcripts (eg, hypoxia-inducible factor EGLN1).

175 In addition to collagen P4Hs and hypoxia-inducible factor P4Hs, a third P4H-the poorly ch

176 or other 2OG oxygenases, e.g. screens of the hypoxia-inducible factor prolyl-hydroxylase inhibitors r

177 Whether antenatal or postnatal HIF (hypoxia-inducible factor) augmentation can preserve lung

178 A (protein phosphatase 2) regulates the HIF (hypoxia-inducible factor)/PHD-2 (prolyl hydroxylase 2)-c

179 allogeneic recipients resulted in increased hypoxia-inducible factor-1 alpha expression and reduced

180 Here, we report that hypoxia-inducible factor-1alpha (HIF-1alpha) is crucial

181 evelopment of PH, mice lacking expression of hypoxia-inducible factor-1alpha in the Ly6C(lo) monocyte

182 Hypoxia activates hypoxia-inducible factor-dependent signaling, which in t

183 iological processes, including regulation of hypoxia-inducible factor-mediated adaptation to hypoxia,

184 1), AMP-activated protein kinase (AMPK), and hypoxia-inducible factors (HIF-1alpha and HIF-2alpha)-ca

185 esults in the constitutive activation of the hypoxia-inducible factors (HIFs) HIF-1 and HIF-2 and the

186 (PHD1 to PHD3) regulate the activity of the hypoxia-inducible factors (HIFs) HIF-1 and HIF-2, transc

187 This Review focuses on the role of hypoxia-inducible factors (HIFs) in hypertension, type 2

188 l fatty acid (FA) transport, is repressed by hypoxia-inducible factors (HIFs), reducing FA oxidation

189 The response to hypoxia is mediated by hypoxia-inducible factors (HIFs).

190 en through transcriptional regulators called hypoxia-inducible factors (HIFs).

191 Hypoxia-inducible transcription factors (HIFs) directly

192 ibute to the development of therapeutics for hypoxia/inflammatory-related diseases.

193 Malignancy was accompanied by worsened hypoxia inside the tumor mass, creating a positive feedb

194 Hypoxia is a common feature of the tumor microenvironmen

195 Hypoxia is a condition that together with low pH, high a

196 Hypoxia is a key microenvironmental stress in solid tumo

197 Chronic exposure to hypoxia is associated with elevated sympathetic nervous

198 Uteroplacental hypoxia is associated with pregnancy disorders such as i

199 The response to hypoxia is mediated by hypoxia-inducible factors (HIFs).

200 Accordingly, decreased oxygen concentration (hypoxia) is a major stressor that generally subverts lif

201 evant to the natural ecology of NTM, such as hypoxia, is lacking.

202 Chronic hypoxia leads to pathologic remodeling of the pulmonary

203 Induction of EGFR under hypoxia led to an increase in AKT, ERK, and Rb phosphory

204 algorithm to retrieve surrogate measures of hypoxia levels from the images was developed and validat

205 tween these indicator values and MRI-defined hypoxia levels in 63 patients.

206 ing gene expression profiles and MRI-defined hypoxia levels in cancer hallmark analysis, we identifie

207 An additional indicator of hypoxia levels in patient tumors was established on the

208 ted by comparing the MRI-defined levels with hypoxia levels reflected in pimonidazole-stained histolo

209 cs, resulting from the EPR:CR interaction in hypoxia, likely having the most crucial impact on the fu

210 uggest that timing of exposure to oil and/or hypoxia matters, and underscores the need to further inv

211 Hypoxia-mediated induction of ATG9A was lost in cells la

212 ivo optical imaging techniques for assessing hypoxia, microvasculature, and tumor growth.

213 However, HIFalpha stabilization using hypoxia mimetics, does not recapitulate the effect of hy

214 ISTRAV) and/or MItochondrial STress Response Hypoxia (MISTRH).

215 Here, we reveal hypoxia-monitoring function exerted by astrocytes throug

216 cially when considering associations between hypoxia, neoangiogenesis and antitumor activity.

217 ng periods of severe postictal hypoperfusion/hypoxia, not seizures per se, are associated with memory

218 and adapt to many types of stress including hypoxia, nutrient deprivation, metabolic, and oxidative

219 settings may in part reflect the effects of hypoxia on direct PMN-tumor cell interactions.

220 imetics, does not recapitulate the effect of hypoxia on FN matrix reorganization or cell migration.

221 Here we show the detrimental effect of hypoxia on mitochondrial-biogenesis in activated mouse C

222 actor 1 (HIF-1) and c-Myc, yet the impact of hypoxia on negative regulators of angiogenesis is unknow

223 ble resource when assessing the influence of hypoxia on the coastal ecosystem.

224 estic pigs (pASCs) and examine the effect of hypoxia on their proteome and functional characteristics

225 mour cell lines such as their sensitivity to hypoxia or average rate of proliferation, and note that

226 if their cell respiration was obstructed by hypoxia or by chemical inhibition of the electron transp

227 seeds germinating in flooded soils encounter hypoxia or even anoxia leading to poor seed germination

228 fering when the CR activation is achieved by hypoxia or hypercapnia.

229 y, we show that changes in blood flow during hypoxia or hyperoxia could be explained by altered NO de

230 (UtA) isolated from pregnant mice exposed to hypoxia or normoxia from gestational day 14.5 to 18.5.

231 During hypoxia, PB resulted in increased cardiorespiratory cohe

232 Importantly, exposure to hypoxia phase-shifted clocks in a tissue-dependent manne

233 Since the EPR:CR co-activation with hypoxia potentiates the pressor response and restricts b

234 tion using extracellular matrix proteins and hypoxia preconditioning.

235 sion significantly increased CSC survival in hypoxia, proangiogenic factors production and endothelia

236 These data demonstrate that mild hypoxia promotes recovery from preexisting inflammatory

237 udies, we show here that long-term, moderate hypoxia promotes resistance to the EGFR TKI osimertinib

238 ive oxygen species (ROS) accumulation during hypoxia provides the signal that regulates ion channels.

239 ADC and renal hypoxia (R2*) by blood-oxygen-level-dependent MRI were s

240 Two-way ANOVA analyses indicated that hypoxia reduced AMPK activation in the uterine artery an

241 The main findings were (1) chronic hypoxia reduced EDD in lowlanders (changes in forearm va

242 hal hypoxia, and compared responses for each hypoxia regime to normoxic conditions.

243 Together, these findings identify key hypoxia-regulated molecular mechanisms through which PMN

244 size show significantly higher expression of hypoxia-related markers and enhanced chondrogenic differ

245 show that breast cancer cells maintained in hypoxia release small extracellular vesicles (sEVs) that

246 s despite large reductions in CDO(2) Chronic hypoxia renders the brain susceptible to large reduction

247 While hypoxia renders tumours resistant to many conventional t

248 mary cultures of isolated tubular cells in a hypoxia-reoxygenation model.

249 Re-expressing the hypoxia-repressed miR-142-3p, which targets HIF1A, LOX a

250 )-to understand how metabolic status impacts hypoxia resistance, a response that relies on mitochondr

251 Outcomes in the favorable early hypoxia resolution subgroup significantly depended on in

252 unts, with patients who showed both an early hypoxia response and high lymphocyte infiltration levels

253 0.017) compared with patients with an early hypoxia response but low lymphocyte counts.

254 ults comparable to those of patients with no hypoxia response within the first 2 wk of chemoradiation

255 h a regulatory link among circadian rhythms, hypoxia response, fatty acid uptake, and NAFLD.

256 helial growth factor-A165 under control of a hypoxia-response element markedly promotes vascular volu

257 CRISPR/Cas9-mediated deletion of the hypoxia-response element revealed co-regulation of NICI

258 tablished on the basis of expression of nine hypoxia-responsive genes; a strong correlation was found

259 rved and principal component analysis of the hypoxia-responsive proteins indicated that both cell typ

260 applied to comprehensively characterize the hypoxia-responsive proteome profiles in the OS cell phen

261 Exposure to acute hypoxia results in vasodilatation of resistance arteries

262 of endogenous EPO under conditions mimicking hypoxia, ruling out an artifact of heterologous overexpr

263 y act to protect against prolonged placental hypoxia seen in preeclampsia.

264 tility of redox-activated metal complexes as hypoxia-selective H(2) S-releasing agents for use as too

265 xoglutarate-dependent oxygenases that act as hypoxia-sensing components of the HIF system: prolyl-hyd

266 utations accelerate age-dependent changes in hypoxia-sensitive gene expression supporting that ageing

267 dels, LV unloading reduced the expression of hypoxia-sensitive proteins and myocardial damage due to

268 yogenic potential in aging and activation of hypoxia signaling holds promise for rescuing regenerativ

269 y genetic mutations in factors governing the hypoxia signaling pathway, resulting in metabolic dysreg

270 ding of the mechanisms of oxygen sensing and hypoxia signaling that resulted in the development of HI

271 ginates in fetal life and that chronic fetal hypoxia significantly alters it.

272 ersistent fever, and progressive dyspnea and hypoxia, sometimes accompanied by diarrhea and often fol

273 ls residing in low-oxygen microenvironments (hypoxia) such as in the liver, spleen, and lymph nodes.

274 stern and midline shift >=5 mm), presence of hypoxia, systemic hypotension, altitude higher than >500

275 After 8 days of exposure to hypoxia + TBT, oysters substantially up-regulated HIF1-a

276 ndent upon metabolic changes associated with hypoxia that drive the tumor's characteristic epigenetic

277 rcome the effects of both systemic and local hypoxia that occurs as a result of traumatic injury, cel

278 repressor role of SerRS is inactivated under hypoxia through phosphorylation by ataxia telangiectasia

279 Active temperature-dependent hypoxia thus links the biogeography of diverse marine sp

280 ormed maximal exercise tests in normoxia and hypoxia to determine how their altered haemoglobin affin

281 ven pathway that cooperates with laminin and hypoxia to drive resistance to PI3K inhibitors.

282 ical tests focused on determining changes in hypoxia tolerance (pCrit), ventilation rates, and metabo

283 Coculturing a macrophage cell line with hypoxia-treated primary tubules overexpressing periostin

284 Spine regrowth was reduced under all hypoxia treatments, calcification rates under variable h

285 hat is called ventilatory acclimatization to hypoxia (VAH).

286 bited decreased vessel density and increased hypoxia versus pre-resistance, suggesting that resistanc

287 on chromosome 12p13.31 which is regulated by hypoxia via HIF-1 promoter-binding in multiple cell type

288 re capable of rapidly responding to moderate hypoxia via the sensor cation channel transient receptor

289 Hypoxia was induced in a normobaric hypoxia chamber by d

290 reted factors most strongly upregulated upon hypoxia was PCSK6 (proprotein convertase subtilisin/kexi

291 e role of peripheral ORs in triggering brain hypoxia, we used oxygen sensors in freely moving rats to

292 eatments, calcification rates under variable hypoxia were intermediate between normoxia and constant

293 n translocates to the nucleus in response to hypoxia which correlates with increased ubiquitination o

294 Hypoxia, which was exacerbated by EndMT, resulted in inc

295 This study aims to identify thresholds to hypoxia while testing behavioral and physiological respo

296 und the topic of innate immunity and mucosal hypoxia with a focus on transcriptional responses mediat

297 orcine IVD cells under prolonged exposure to hypoxia with physiological glucose concentrations.

298 ing significant, dynamic modulation of tumor hypoxia with the heme-targeting drug treatments create i

299 Roots in flooded soils experience hypoxia, with the least O(2) in the vascular cylinder.

300 POS) - z(POS)|), and "sensitivity" score (|z(Hypoxia) - z(Normoxia)) to quantitatively evaluate the p