ライフサイエンスコーパス: maladaptation

1 sarean section but a higher risk of neonatal maladaptation.

2 he ultimate outcome was either adaptation or maladaptation.

3 s Thbs4(-/-) mice were sensitized to cardiac maladaptation.

4 may be impaired at the high altitude, i.e. a maladaptation.

5 osine response to counteract hypoxia-induced maladaptation.

6 motes stress-induced cellular and behavioral maladaptations.

7 ascular reserve and evaluates the peripheral maladaptations; accordingly, exercise testing has become

8 In diseased cells, maladaptation alters protein structure-function relation

9 provide key information on assessing risk of maladaptation and developing strategies to mitigate clim

10 As (miRNAs) in the regulation of endothelial maladaptation and macrophage failure during atherosclero

11 function, and ultimately behavior, and these maladaptations appear distinct between developmental and

12 Available methods to assess maladaptation are reviewed.

13 typical Afl, action potential duration rate maladaptation at the isthmus may lead to action potentia

14 Greenland has been seen as a classic case of maladaptation by an inflexible temperate zone society ex

15 volutionary time to eliminate the inevitable maladaptations consequent to the profound transformation

16 resynaptic plasticity may represent a neural maladaptation contributing to network instability and ab

17 ta demonstrates that the demographic cost of maladaptation decreases habitat patch occupancy by T. cr

18 Evaluating the expected degree of genetic maladaptation due to climate change will allow forest ma

19 ts a role for PDE V as contributing to renal maladaptation in a model of experimental overt CHF and t

20 to which they were raised, possibly due to a maladaptation in digestion of alternative prey items.

21 This global maladaptation in gene expression at the time of increase

22 H(VTA)) neurons, as well as from more global maladaptation in neurocircuit function.

23 ion suggests a joint role for adaptation and maladaptation in shaping species interactions across nat

24 rthermore, these field experiments show that maladaptation in T. cristinae and consequent increase in

25 eurodevelopmental disorders, perhaps through maladaptations in glutamate signaling and neuroplasticit

26 Whereas cocaine-induced maladaptations in reward circuitry have been extensively

27 ne excitability, may counteract drug-induced maladaptations in the NAc and thus ameliorate the addict

28 ction of the DG is accompanied by structural maladaptations, including dysregulation of adult-generat

29 This maladaptation is also characterized by cell behaviors th

30 population size and that the effect of such maladaptation is comparable to the effects of more tradi

31 a new genetic program has been activated and maladaptation is occurring in the atria, ventricles, or

32 ive feedback between low population size and maladaptation, leading to a sharp range margin.

33 These maladaptations may contribute to the transformation of s

34 eart failure, central cardiac and peripheral maladaptations occur.

35 The maladaptation of endothelial cells to disturbed flow at

36 ns (compared with WKY rats), which indicates maladaptation of energy substrates in the failing heart.

37 s years after an initial insult during which maladaptation of hippocampal circuitries takes place.

38 Treatments to counter maladaptation of p11 levels may provide novel therapeuti

39 lead to metabolic, functional and structural maladaptation of the heart.

40 These findings demonstrate a potential maladaptation of the primary innate response.

41 omes, but it is now clear that mutations and maladaptations of the epigenetic machinery cover a much

42 demonstrated in animal models that metabolic maladaptation plays a pivotal role in contractile dysfun

43 Metabolic maladaptation precedes the onset of severe contractile d

44 ical disease involving lasting, multifaceted maladaptations ranging from gene modulation to synaptic

45 d bird predation support the hypothesis that maladaptation reduces population size through an increas

46 underlying the transition from adaptation to maladaptation remains obscure, however.

47 rmation of reactive interstitial fibrosis, a maladaptation that contributes to left ventricular (LV)

48 ion syndrome as a complex set of hemodynamic maladaptations that include stiff central arteries, norm

49 r disease, perhaps the result of physiologic maladaptation to chronically sleeping and eating at abno

50 e climates, and to estimate relative risk of maladaptation to current and future climates based on ke

51 c glutamatergic transmission may be a common maladaptation to ELS, leading to enhanced excitation of

52 We studied potential genetic maladaptation to future climates in three major European

53 Genetic maladaptation to future climates is likely to become a p

54 ogical basis for a greater susceptibility to maladaptation to night shift work in women.

55 cause murine heart failure, and accelerates maladaptation to pressure overloading.

56 ion and metabolic distress, which potentiate maladaptation to stress and susceptibility to age-relate

57 The aging brain thus displays maladaptation to the loss of monoaminergic input, effect

58 These data suggest that sex-specific maladaptations to hypertensive aging in women may underl

59 od bladder management at the outset, whereas maladaptation was a result of avoidance and denial.

60 of superficial placentation driven by immune maladaptation, with subsequently reduced concentrations