ライフサイエンスコーパス: mechanism is

1 maintenance and suggest that release from this suppressive mechanism is a fundamental requirement for subsequent initiat

2 ions a Low Density Collisionless Shock Acceleration (LDCSA) mechanism is at play, which combines an initial Collisionless

3 Our mechanism is based on the electrically controlled modulation

4 The sensing mechanism is based upon ROS-induced oxidation of the ascorbic

5 s are capable of detecting cisplatin, the signal-on sensing mechanism is better suited for real time analysis of cisplati

6 The feasibility of this reaction mechanism is confirmed from DFT calculations, and the simulat

7 Reverse mutations in Kir1.1 suggest that this mechanism is conserved in other Kir channels.

8 This mechanism is consistent with observations of hybrid earthquak

9 Each mechanism is deemed inadequate to explain the observations of

10 g dominates is thus clearly observed, and the rectification mechanism is discussed in terms of Fermi level pinning and el

11 Furthermore, we demonstrate that this mechanism is disrupted in congenital muscular dystrophy patie

12 The Efr3-dependent CR-anchoring mechanism is distinct from previously reported pathways depen

13 This mechanism is distinct from the BRCA2-dependent fork protectio

14 ctional theory calculations reveal that a stepwise transfer mechanism is dominant in the tautomerization.

15 DHHC7 represents the principal PAT for Glut4 and that this mechanism is essential for insulin-regulated glucose homeosta

16 ies widely among CRISPR-Cas systems, the spacer integration mechanism is essentially identical.

17 While this mechanism is homeostatic we show that it does not achieve glo

18 Remarkably, this mechanism is homoplastic with the evolution of the C4-associa

19 riation in arterial CO2 changes CBF by 3%-4%), the coupling mechanism is incompletely understood.

20 The translocation mechanism is likely conserved for other AAA+ ATPases.

21 We show here that this mechanism is mediated not via cell-autonomous clock propertie

22 We conclude that the inflammatory response mechanism is not active in mouse embryonic stem cells, and in

23 This mechanism is not based on an ordered sarcomeric organization.

24 The exact pathophysiological mechanism is not completely understood and remains controvers

25 memory, autism, and sensitization to cocaine; however, the mechanism is not known.

26 This mechanism is not restricted to the eye, as similar results we

27 Sirt1 can be activated by energy deprivation, but the mechanism is poorly understood.

28 A plausible mechanism is proposed for this cyclization based on the resul

29 A mechanism is proposed in which propionate 2 relays an oxidizi

30 The Rh-PPO mechanism is reminiscent of DNA repair enzymes that displace

31 One such mechanism is senescence.

32 at treatment, is known to cause disastrous failure, but its mechanism is still not completely clear.

33 untington's disease (HD); however, the underlying molecular mechanism is still poorly understood.

34 ly blocks HIV-1 replication in DCs, although the underlying mechanism is still unclear.

35 This demonstrates a central integration mechanism is sufficient to evoke painful thermal TCE, an esse

36 ndant ytterbium(III) cations, a Dexter-type energy transfer mechanism is suggested, which is an important consideration f

37 The proposed mechanism is supported by both experimental and theoretical s

38 es to alternatively transport Na(+) and K(+) This ping-pong mechanism is supported by transient-state studies but contrad

39 Our approach isolates exactly what mechanism is telling us over and above the state variables al

40 sed for the fact that a good fit to data does not imply the mechanism is true: pattern does not equal process.

41 However, the therapeutic mechanism is unclear, with minimal research supporting its us

42 nction prior to Tau aggregate formation, but the underlying mechanism is unclear.

43 amycin complex 1 (mTORC1) activity, although the underlying mechanism is unclear.

44 A itself can modulate AD pathology, although the underlying mechanism is unclear.

45 tions or pathological hypokalaemia, however, the underlying mechanism is unclear.

46 uggests that LBH could modulate the cell cycle, the precise mechanism is unknown and its impact on inflammation in vivo h

47 iferation through inappropriate activation of Cdks, yet the mechanism is unknown.

48 xpression and activity in nonrenal cell types, although the mechanism is unknown.

49 activity in B cell differentiation, although the underlying mechanism is unknown.

50 r toxicity by the anti-leukemic agent asparaginase, but the mechanism is unknown.