ライフサイエンスコーパス: brain dysfunction

1 ma-free days (i.e., fewer days without acute brain dysfunction).

2 he degenerative diseases of aging, including brain dysfunction.

3 rocytic consequences of cirrhosis-associated brain dysfunction.

4 lying synaptic and nonsynaptic mechanisms of brain dysfunction.

5 d reverses neurofibrillary tangle-associated brain dysfunction.

6 ay help prevent and modulate the severity of brain dysfunction.

7 urbs inhibitory synapse formation and causes brain dysfunction.

8 acement, debility, neurologic disorders, and brain dysfunction.

9 ed by H2O2, might contribute to H2O2-induced brain dysfunction.

10 l neurodegenerative diseases and age-related brain dysfunction.

11 whereas recessive mutations lead to skin and brain dysfunction.

12 n and cell death do not play a major role in brain dysfunction.

13 treatment are recommended to prevent ongoing brain dysfunction.

14 care unit survivors at high risk of ongoing brain dysfunction.

15 lth problem in the form of acute and chronic brain dysfunction.

16 arly iron treatment in preventing ID-induced brain dysfunction.

17 tient is not necessarily free of significant brain dysfunction.

18 zepine drugs and may lower the risk of acute brain dysfunction.

19 on of pain in migraine is due to lateralized brain dysfunction.

20 d of mechanisms by which infection can cause brain dysfunction.

21 lular and molecular mechanisms that underlie brain dysfunction.

22 s well as processes that lead to age-related brain dysfunction.

23 sses the blood-brain barrier (BBB) to induce brain dysfunction.

24 vels may contribute to neurodegeneration and brain dysfunction.

25 y present a sensitive measure of HIV-related brain dysfunction.

26 ily a neurological disorder with progressive brain dysfunction.

27 her factors in shaping the risk of postnatal brain dysfunctions.

28 consistent with the concept of developmental brain dysfunction, a term we use to describe the abnorma

29 rium is a highly prevalent syndrome of acute brain dysfunction among critically ill patients that has

30 dosage imbalance for Synj1 may contribute to brain dysfunction and cognitive disabilities in DS.

31 asoprotective role of PGRN may contribute to brain dysfunction and damage in conditions associated wi

32 diovascular disease, which converge to cause brain dysfunction and neurodegeneration.

33 Stroke causes brain dysfunction and neuron death, and the lack of effe

34 crete population of neurons can cause global brain dysfunction and that phenotype severity depends on

35 sorders was to establish the most consistent brain dysfunctions and to address task- and subtype-rela

36 tandard iron indicators to detect ID-induced brain dysfunction, and evaluate the efficacy of early ir

37 e disease with clear pathological hallmarks, brain dysfunction, and unknown etiology.

38 when disorders encompassed by developmental brain dysfunction are considered as a group, the penetra

39 is on micronutrient deficiency, and explores brain dysfunction as a possible mechanism.

40 zheimer transgenic mouse studies demonstrate brain dysfunction, as beta-amyloid levels rise, months b

41 ewborns have a prominently increased risk of brain dysfunctions attributed to white-matter damage, wh

42 vascular reactivity predicts prolonged acute brain dysfunction, but relationships between endothelial

43 e findings imply that regional variations in brain dysfunction can occur in Alzheimer's disease, with

44 information is useful for understanding how brain dysfunctions contribute to movement disorders such

45 phan ratios and presence or absence of acute brain dysfunction (defined as delirium/coma-free days) i

46 nine pathway activity in intensive care unit brain dysfunction (delirium and coma) remains unknown.

47 We assessed patients daily for brain dysfunction (delirium, using Confusion Assessment

48 nuates the development of neuropathology and brain dysfunction during acute and chronic phases includ

49 ry to understand the mechanisms that lead to brain dysfunction during seizures.

50 lay an important role in the pathogenesis of brain dysfunction during sepsis.

51 Delirium is a condition of acute brain dysfunction for which a pre-existing diagnosis of

52 ye movement disorders in patients with focal brain dysfunction have added to our understanding of hum

53 Additionally, possible mechanisms for gut-brain dysfunction have been identified, suggesting prima

54 benzodiazepine drugs may contribute to acute brain dysfunction, ie, delirium and coma, associated wit

55 heral inflammation as potential mediators of brain dysfunction in AD may lead to the development of e

56 yloid plaques and neurofibrillary tangles to brain dysfunction in Alzheimer disease is critical for t

57 ts in synaptic homeostasis may contribute to brain dysfunction in Alzheimer's disease.

58 us but are not bioindicators of brain ID and brain dysfunction in children.

59 bryonic brain development are a component of brain dysfunction in DS.

60 To determine the metabolic substrates of brain dysfunction in DYT1 dystonia, we scanned 7 nonmani

61 stence of different mechanisms of underlying brain dysfunction in familial and sporadic schizophrenia

62 Tat may thus be an important participant in brain dysfunction in HIV dementia.

63 ated with fewer days alive and without acute brain dysfunction in intensive care unit patients.

64 al oscillations, is critical for elucidating brain dysfunction in neuropsychiatric disorders.

65 at all 3 biochemical disturbances underlying brain dysfunction in phenylketonuria can be targeted by

66 to all 3 biochemical disturbances underlying brain dysfunction in phenylketonuria.

67 abuse and abstinence may underlie persistent brain dysfunction in primates and be a target for therap

68 form of plasticity that could contribute to brain dysfunction in psychiatric disease.

69 increasingly popular technique for studying brain dysfunction in psychiatric patients, and is widely

70 data are compatible with the hypothesis that brain dysfunction in RTT is caused by a loss of the MeCP

71 e measures, supporting distributed models of brain dysfunction in schizophrenia.

72 a need to generate serum measures that index brain dysfunction in the preanemic stage of ID, assess t

73 erstanding of the impact of hyperglycemia on brain dysfunction in the zebrafish model.

74 complex but more realistic representation of brain dysfunction in this illness.

75 brain barrier/neurological injury, and acute brain dysfunction, including delirium, remain unexamined

76 cortical pyramidal cells, which perpetuates brain dysfunction into adulthood.

77 cal entity, the pathophysiology resulting in brain dysfunction is not fully understood, although it i

78 Cirrhosis is associated with brain dysfunction known as hepatic encephalopathy (HE).

79 Stroke was defined as focal brain dysfunction lasting >/=24 hours from a vascular ca

80 Brain dysfunction may be the most important and least st

81 Frontal brain dysfunction may underlie depression both in cerebr

82 prenatally and is Altman's model of "minimal brain dysfunction", may be a factor in at least some for

83 lycemia as a putative contributor to several brain dysfunctions observed in diabetes patients, such a

84 rst-episode schizophrenia indicates that the brain dysfunction occurred before clinical presentation.

85 ficantly more neuropsychological evidence of brain dysfunction on the Halstead Impairment Index (P=.0

86 ociation between lowest daily hemoglobin and brain dysfunction (p = 0.69 for delirium), renal dysfunc

87 understanding these disorders indicate that brain dysfunction precedes neurodegeneration, but the ro

88 Diaschisis denotes brain dysfunction remote from a focal brain lesion.

89 Prevention of acute and chronic brain dysfunction requires implementation of a core mode

90 movement disorders, the mechanisms by which brain dysfunction results in dystonia are not understood

91 on, it is argued that evidence of underlying brain dysfunction revealed by these pictures often rests

92 nt records from 5 impairment groups (stroke, brain dysfunction, spinal cord dysfunction, other neurol

93 development and infancy could contribute to brain dysfunction such as that seen in ASD and other dev

94 s, including learning and memory, as well as brain dysfunctions such as drug addiction and psychologi

95 mprinting in a number of syndromes involving brain dysfunction, such as Prader-Willi syndrome, Angelm

96 ing on the site of the lesion, the resultant brain dysfunction, the presentation of depression and ti

97 ese results underline the potential of focal brain dysfunction to produce behavioral improvement and

98 t cerebrovascular effects that contribute to brain dysfunction underlying dementia by limiting the de

99 A few studies tried to identify the brain dysfunction underlying developmental dyscalculia b

100 europathology, and character and severity of brain dysfunction varied substantially among cases.

101 In 10 of these 47 the primary site of brain dysfunction was anterior temporal and orbital-fron

102 ase classification system and the underlying brain dysfunctions, we applied a fully data-driven appro