ライフサイエンスコーパス: cellular hypoxia

1 creased levels of oxygen under conditions of cellular hypoxia.

2 onmental oxygen levels leading to a state of cellular hypoxia.

3 e response to proinflammatory stimuli during cellular hypoxia.

4 e as (19)F MRI contrast agents for detecting cellular hypoxia.

5 in response to combinations of IFN-gamma and cellular hypoxia.

6 ement, drove transcription, and responded to cellular hypoxia.

7 eduction in pH associated with conditions of cellular hypoxia.

8 nt that there is a multitude of responses to cellular hypoxia.

9 ion of major differentiation markers and the cellular hypoxia adaptive response by contrast with undi

10 ollowing trauma-hemorrhage is independent of cellular hypoxia and activation of HIF-1alpha, but it is

11 t a mechanistic link exists between vascular cellular hypoxia and mediators of inflammation associate

12 cs identical to endogenous HIF-1alpha during cellular hypoxia and reoxygenation.

13 Physiological effects of cellular hypoxia are sensed by prolyl hydroxylase (PHD)

14 unique pattern of development and decline of cellular hypoxia as wound cellularity and proliferation

15 nd microglia phenotype, oxidative stress and cellular hypoxia, autophagy and ubiquitin-proteasome sys

16 ls must resist oxidation damage and adapt to cellular hypoxia, but the mechanisms involved in this pr

17 3) are thought to act as proximal sensors of cellular hypoxia by virtue of their mechanism-based depe

18 mitation, alternative carbon metabolism, and cellular hypoxia, conditions that are thought to exist w

19 Fluorescent probes for the direct imaging of cellular hypoxia could be useful tools that complement r

20 the relative contributions of blood flow and cellular hypoxia (dysoxia) to increases in tissue and ve

21 reproducible model for the study of cerebral cellular hypoxia in healthy individuals.

22 complete Hif1alpha null, results in elevated cellular hypoxia in mouse embryos.

23 Cellular hypoxia induced a time-dependent increase in nu

24 Cellular hypoxia is also found in these conditions.

25 Cellular hypoxia is the common final pathway of brain in

26 Here, we have reprogrammed cellular hypoxia (low O(2)) signaling via gas tunnel eng

27 Cellular hypoxia may be a useful indication of tissue di

28 e tissues such as skeletal muscle, resultant cellular hypoxia necessitates acclimatization to optimiz

29 ulation of macrophage phagocytosis following cellular hypoxia or trauma-hemorrhage.

30 -1alpha) is the central master regulators of cellular hypoxia response and associated with HCM.

31 Cellular hypoxia response is regulated at the level of h

32 eudohypoxic drive-the aberrant activation of cellular hypoxia response pathways despite normal oxygen

33 tion of neural tube formation, regulation of cellular hypoxia response, but also Hepatitis C virus re

34 a and p53 proteins is not coupled during the cellular hypoxia response.

35 Prolonged cellular hypoxia results in energy failure and ultimatel

36 been identified as a factor that influences cellular hypoxia sensing, putatively via an action on th

37 oxamine (DFx) and cobalt chloride, mimics of cellular hypoxia, similarly stimulated VEGF mRNA express

38 le to peripheral tissue hypoperfusion and/or cellular hypoxia, simultaneous measurements of tissue pe

39 tumors and is considered to be a marker for cellular hypoxia that it is not produced in most normal

40 ACE1 blocks the accumulation of HIF1a during cellular hypoxia through decreased protein stability.

41 a message is maintained during conditions of cellular hypoxia through inhibition of IRP-1-dependent r

42 We set out to determine whether cellular hypoxia, via mitochondrial reactive oxygen spec

43 blot analysis and pimonidazole staining for cellular hypoxia, we demonstrate that hypoxia stabilizes