ライフサイエンスコーパス: maladaptation

1 lume endurance training, including potential maladaptation.

2 (measured by telomere length) as a result of maladaptation.

3 es associated with stress-induced behavioral maladaptation.

4 nction (FEV1), and mechanistic correlates of maladaptation.

5 and explored a potential marker of placental maladaptation.

6 stress (i.e., shorter telomeres) because of maladaptation.

7 in breast cancer affected by immune-steroid maladaptation.

8 ipitation extremes return periods leading to maladaptation.

9 usceptibility to vascular maldevelopment and maladaptation.

10 osine response to counteract hypoxia-induced maladaptation.

11 sarean section but a higher risk of neonatal maladaptation.

12 he ultimate outcome was either adaptation or maladaptation.

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

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

15 healthy humans, except in very rare cases of maladaptation.

16 y in terms of lasting cognitive and synaptic maladaptations.

17 motes stress-induced cellular and behavioral maladaptations.

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

19 ertension results from chronic physiological maladaptation against various stressors represented by a

20 Local maladaptation also emerged in control treatments, but it

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

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

23 Mitochondrial maladaptation and dysfunction contribute to the progress

24 To avoid climate-induced maladaptation and extinction, many animal populations wi

25 Right ventricular (RV) maladaptation and failure determine outcome in pulmonary

26 GRK5-mediated pathology in pressure-overload maladaptation and heart failure by expressing in cardiom

27 ignaling through the G protein G(q) triggers maladaptation and heart failure, in part through the act

28 However, evidence for PT maladaptation and its etiological relationship with comp

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

30 estigate the role of inflammation, metabolic maladaptation and mechanical stress.

31 reduced local adaptation, potentially due to maladaptation and relaxed selection, respectively.

32 components can shift long-term adaptation to maladaptation and the development of pathologies.

33 the role of gene loss and pseudogenization, maladaptation and trait loss, and physiological aspects

34 with partial correction of the broad immune maladaptations and protection against severe pneumonia.

35 The inherent association between these 'maladaptations' and sudden cardiac death in the general

36 ction, increased migration distance, climate maladaptation, and consequently greater extinction risk

37 Climate change has reduced fitness, caused maladaptation, and/or led to population declines in at l

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

39 late into tissue maintenance, adaptation, or maladaptation are far from understood.

40 Interspecific conflict and partner-maladaptation are frameworks to explain this variation,

41 Available methods to assess maladaptation are reviewed.

42 ological and behavioural responses and brain maladaptation are the most likely predictors of PPPD, ra

43 by intra-BNST CRF administrations, and these maladaptations are similar to exposure to adverse early

44 nt adaptation to famine and modern metabolic maladaptation associated with nutritional overabundance.

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

46 This maladaptation becomes increasingly evident as subjects f

47 arming households; not only protects against maladaptation but also improves local-level resilience a

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

49 stems, consistent with the idea that climate maladaptation can be an important driver of disease outb

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

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

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

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

54 ere is also evidence that CRF contributes to maladaptations during the peripartum period.

55 ed with the expression of various behavioral maladaptations during withdrawal from binge drinking.

56 that epigenetics-dependent hepatic vascular maladaptation enriches fibrogenic T(H)17 cells to promot

57 Apparent maladaptation in a component of plasticity may be an int

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

59 Maladaptation in balancing internal energy needs and ext

60 Opioids initiate dynamic maladaptation in brain reward and affect circuits that o

61 offer a therapeutic window to leverage redox maladaptation in cancer remains unclear.

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

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

64 iated, at least in part, through a metabolic maladaptation in glutamine metabolism and how the inhibi

65 bution and storage may promote adaptation or maladaptation in homeostatic, maintenance and disease se

66 oot-producing catastrophe would drive global maladaptation in landraces and suggest current adaptive

67 offset methods to predict post-catastrophic maladaptation in landraces over time.

68 irway epithelial injury/repair processes and maladaptation in mediating AA disease severity needs mor

69 mimic clinical observations, and behavioral maladaptation in mice following tolerance to THC.

70 Over time, this may induce several states of maladaptation in myeloid cells.

71 ext century is predicted to cause widespread maladaptation in natural systems.

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

73 s into the understanding of uterine vascular maladaptation in pregnancy complications associated with

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

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

76 chronic, relapsing disorder characterized by maladaptation in the brain mesolimbic and nigrostriatal

77 Chronic stress promotes robust maladaptation in the brain, but the exact intracellular

78 ibiting HIF-1a (HIF1AN) in HA adaptation and maladaptation in three well-characterized groups: highla

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

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

81 mediate striatum-dependent behaviors, while maladaptations in striatal circuitry contribute to menta

82 e current literature on alcohol-mediated SKM maladaptations in the context of comorbidities such as a

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

84 s are both associated with potential cardiac maladaptations, including accelerated coronary artery ca

85 is characterized by myriad cardiac metabolic maladaptations, including altered mitochondrial function

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

87 species mediates bird predation, with local maladaptation increasing predation.

88 s increasingly debated, due to concerns over maladaptation, inter-individual variability, cost and en

89 This maladaptation is also characterized by cell behaviors th

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

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

92 athic pain induced structural and functional maladaptation is therefore critical to understanding its

93 responses in early life, likely due to TRIM maladaptations, lead to aberrant type 2 inflammation-enh

94 rations in cellular processes and associated maladaptation leading to deleterious gastric pathophysio

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

96 ent to which sleep disruption and behavioral maladaptation manifest during abstinence in a mouse mode

97 l regulators) associated with disuse-induced maladaptation, many themselves potently tied to disuse-i

98 These maladaptations may contribute to the transformation of s

99 stimates of climate change vulnerability, or maladaptation, may not only improve prediction power but

100 d molecular network underlying this fibrotic maladaptation might aid in combatting NASH, a growing he

101 ng the gut-brain axis and discuss functional maladaptations observed during metabolic insults, as obs

102 eart failure, central cardiac and peripheral maladaptations occur.

103 e most susceptible to future warming because maladaptation occurs when beetles try to breed at warmer

104 tion, dysregulation of immune responses, and maladaptation of ACE2-related pathways might all contrib

105 d that repeated seizures cause an allostatic maladaptation of AEA signaling in the amygdala that driv

106 Repeated seizures result in a persistent maladaptation of endocannabinoid (eCB) signaling, mediat

107 The maladaptation of endothelial cells to disturbed flow at

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

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

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

111 ntly of epithelial cell lineages, results in maladaptation of resident tissue macrophage differentiat

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

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

114 systemic inflammation and oxidative stress, maladaptation of the renin-angiotensin-aldosterone syste

115 ziness that can lead to chronic symptoms and maladaptation of the vestibular system, but there is no

116 However, maladaptation of this response through microbial dysbios

117 ing 'lipid sensing' mechanisms might lead to maladaptations of the DA system.

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

119 re both peripheral and brain region-specific maladaptations of the immune response to chronic stress

120 r leaflets of those animals, we investigated maladaptation on multiple scales.

121 stinctively different patterns of adaptation/maladaptation or types according to neurobiological pred

122 anxiogenic environments (PD46), and sensory maladaptation (PD47), sustained behavioral effects that

123 In contrast to the PH rats with severe RV maladaptation, PH rats with mild RV maladaptation showed

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

125 Metabolic maladaptation precedes the onset of severe contractile d

126 detect asymptomatic individuals with cardiac maladaptation preceding HF symptoms for it to be a usefu

127 servation actions, including genetic rescue, maladaptation prediction, and assisted gene flow.

128 al target for the amelioration of behavioral maladaptations present in AN patients.

129 adult beta-cell GRK2 delays metabolic islet maladaptation, protecting the heart against obesity-indu

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

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

132 However, brain mechanisms underlying such maladaptations remain elusive.

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

134 fitness trade-offs that turn adaptation into maladaptation, resulting in evolutionary traps.

135 dscape considerably, with various degrees of maladaptation risk.

136 evere RV maladaptation, PH rats with mild RV maladaptation showed a decrease in helical range of fibe

137 'Local maladaptation' suggests that species evolved increased c

138 Chronic mountain sickness (CMS) is a maladaptation syndrome encountered at high altitude (HA)

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

140 detected individuals with subclinical heart maladaptation that precedes HF symptoms by years.

141 increased megamitochondria and mitochondrial maladaptation that promotes AH by mitochondria-mediated

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

143 uggesting that loss of hepatic DRP1 leads to maladaptation to alcohol-induced metabolic stress.

144 in costly fitness trade-offs that result in maladaptation to alternative environments.

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

146 d to measure local adaptation, infer genetic maladaptation to climate, and guide assisted migration.

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

148 epetitive challenges with HDMs revealed that maladaptation to disease triggers may underpin ARC/AA di

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

150 the concept that resilience, adaptation, and maladaptation to environmental disease triggers calibrat

151 wever, LA Ca(2+) signalling is more prone to maladaptation to frequency increases due to less effecti

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

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

154 proving crop yields to predicting population maladaptation to future conditions.

155 a ice habitat to polar bears, we expect that maladaptation to future warming is already widespread ac

156 e pathways responsible for vascular adaption/maladaptation to hypoxia has potential clinical implicat

157 Maladaptation to metabolic stress in HFpEF hearts impair

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

159 n and soybean yields by 33% and 20%, whereas maladaptation to normal conditions reduced yields by 41%

160 NRF2 overactivation causes hepatic metabolic maladaptation to obesity and insulin resistance.

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

162 ethyltransferase 1 (DNMT1) promoted liver EC maladaptation to promote production of angiocrine IGFBP7

163 ate life should first consider psychological maladaptation to situational threats and challenges.

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

165 s scenarios was predicted to lead to further maladaptation to temperature and reduction in growth rat

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

167 d genetic forecasting to measure the risk of maladaptation to warming temperatures and sea ice loss i

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

169 and mutations that underlie adaptation (and maladaptation) to agricultural environments, mitigate ev

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

171 A dominant component of maladaptation was the extracellular matrix increase at R

172 To develop plasma markers of PT maladaptation, we analyzed the plasma proteome in two in

173 Models exploring RV maladaptation were further adjusted for pulmonary vascul

174 der the experimental conditions, they caused maladaptation when light or CO(2) levels were altered, r

175 Finally, we discuss maladaptation which could occur as a result of disaster

176 ering noninvasive markers and associating PT maladaptation with adverse clinical outcomes.

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

178 at-risk alcohol use exhibit skeletal muscle maladaptations, yet data on associated healthcare or pro