ライフサイエンスコーパス: abnormal movement

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1 ks relating separately to gene status and to abnormal movement.

2 e orchestration of the modules, resulting in abnormal movements.

3 of the vehicle-treated animals displayed any abnormal movements.

4 he C. elegans unc-33 gene lead to worms with abnormal movements.

5 are characterized by paroxysmal onset of the abnormal movements.

6 , suggesting that both receptors mediate the abnormal movements.

7 y be difficult to differentiate from organic abnormal movements.

8 ionally, the fasting glucose level predicted abnormal movements after the authors controlled for age.

9 e magnitude of the fasting insulin level and abnormal movements after the authors controlled for fast

10 nded survival, reduced associated tremor and abnormal movements and ameliorated weight loss.

11 lity, and simultaneous occurrence of various abnormal movements and dysfunctions.

12 The authors examined the association between abnormal movements and impaired glucose metabolism, whic

13 g how dysfunction in the CNS causes specific abnormal movements and postures.

14 came completely unresponsive with no further abnormal movements and ultimately died.

15 ith catatonic features often associated with abnormal movements, and autonomic and breathing instabil

16 ehavioral and speech problems, seizures, and abnormal movements are common early symptoms.

17 t the striatal cell types that contribute to abnormal movements are poorly defined.

18 ld caution clinicians to not assume that all abnormal movements are seizures.

19 ients report that they do not experience the abnormal movement as voluntary.

20 When treatment began after the appearance of abnormal movements, cystamine extended survival, reduced

21 tients may have cardiovascular syncope, with abnormal movements due to cerebral hypoxia, which may be

22 long-term levodopa therapy, patients develop abnormal movements, dyskinesias, the pathophysiological

23 Mutant mice, which do not display abnormal movements, exhibited significant CbTC tract cha

24 re intimately related to normal movement and abnormal movement in Parkinson's disease (PD), are sculp

25 bserved during normal voluntary movement and abnormal movement in Parkinson's disease (PD).

26 ngitudinal stability of lack of awareness of abnormal movements in schizophrenia.

27 n ability to follow simple commands only and abnormal movements, including myoclonus, tongue and orof

28 ysregulated in proportion to the severity of abnormal movements induced by l-DOPA in a rat model of p

29 delayed epibolic movement of the deep cells, abnormal movement of dorsal forerunner cells, and dissoc

30 nce and extension phenotype, demonstrated by abnormal movement of dorsolateral cells during gastrulat

31 movement notation, we present evidence that abnormal movement patterns can be detected in AS in infa

32 These abnormal movements resemble drug-induced dyskinesia more

33 h impaired glucose tolerance had higher mean abnormal movement scores than those without glucose into

34 secutive glutamines exhibit ataxia, tremors, abnormal movements, seizures, and premature death.

35 ng-term L-DOPA treatment induces involuntary abnormal movements such as dyskinesias.

36 overall locomotor activity and did not cause abnormal movement, such as stereotypy.

37 zebrafish decreased motility while inducing abnormal movements suggestive of seizures.

38 e seen in psychogenic movement disorder, and abnormal movements that would not normally be considered

39 ttention to manifest yet patients report the abnormal movement to be out of their control.

40 The abnormal movements were not associated with kainate-indu

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