ライフサイエンスコーパス: abnormal behavior

1 hippocampus subfields in vivo that underlie abnormal behavior.

2 f these circuits may contribute to normal or abnormal behavior.

3 de developers in recognizing and reacting to abnormal behavior.

4 dostatin, to determine if HemEPCs share this abnormal behavior.

5 n of neural activation may in itself lead to abnormal behavior.

6 yndrome of borderline mental retardation and abnormal behavior.

7 cluding impaired neurocognitive function and abnormal behavior.

8 ouped into three types: normal, delayed, and abnormal behaviors.

9 tissues in the BTBR mice may underlie their abnormal behaviors.

10 but did not alter seizure activity or other abnormal behaviors.

11 uals with autism and may contribute to their abnormal behaviors.

12 through which brain 5-HT deficiency induces abnormal behaviors.

13 ial to screen new transgenic mouse lines for abnormal behavior and physiology, these BAC transgenic m

14 s (GFAP reactivity) was correlated with both abnormal behavior and spontaneous seizures.

15 itor (fluoxetine at 20 mg/kg) attenuates the abnormal behaviors and selectively reverses the circuit

16 They also presented an array of abnormal behaviors and significant weight loss.

17 phane had improvement in social interaction, abnormal behavior, and verbal communication (P = 0.015-0

18 re malformation of the cerebellum as well as abnormal behavior (ataxia).

19 al ventral hippocampal lesion (NVHL) develop abnormal behaviors during or after adolescence, suggesti

20 hanges in cell fate may underlie many of the abnormal behaviors exhibited by cells after loss of PAR-

21 ur previous studies revealed that mucus with abnormal behavior impaired mucociliary transport in newb

22 e neural mechanism for stressed-reared pups' abnormal behavior in a more controlled environment by in

23 s impairment of glycinergic transmission and abnormal behavior in beo mutants.

24 ructure and function of this channel and its abnormal behavior in disease requires knowledge of the n

25 ent of the PFC, which may be associated with abnormal behavior in offsprings.

26 ilization; including perinatal lethality and abnormal behavior in surviving adults.

27 erebroventricular administration ameliorates abnormal behaviors in adult mutant mice.

28 delay during the postnatal period as well as abnormal behaviors in both young and adult animals that

29 hanges in these circuits might contribute to abnormal behaviors in the context of neuropsychiatric di

30 several insights on the etiological basis of abnormal behaviors in these mice, including abnormal cor

31 an FMR1 gene have corrected or overcorrected abnormal behaviors including hyperactivity and altered s

32 that probiotics, when eaten, can improve the abnormal behaviors (including social withdrawal and immo

33 mice showed reduced prepulse inhibition and abnormal behavior, including excessive anxiety, antisoci

34 Beta power is predictive of healthy and abnormal behaviors, including perception, attention and

35 th altered intrahippocampal connectivity and abnormal behavior; including hyperactivity, some defects

36 patterns are observed in PrEE newborns, and abnormal behavior is present in 20-d-old PrEE mice.

37 Group TE now showed only few if any of the abnormal behaviors observed in infancy.

38 The normal and abnormal behavior of a living cell is governed by comple

39 re we investigate the molecular basis of the abnormal behavior of Hectd1 mutant cranial mesenchyme.

40 s therefore provide initial evidence linking abnormal behavior of STAT pathways for cytokine signalin

41 The mechanisms that account for the abnormal behavior of these cells in IDDM are not fully u

42 The abnormal behavior of unc-17(e245) mutants, which have a

43 not induce any overt clinic symptom, such as abnormal behavior, or any neurological signs.

44 ndary passage-inoculated cats have developed abnormal behavior patterns consistent with the early sta

45 amelioration of a subset of PTEN-associated abnormal behaviors, providing evidence that the mTORC1 p

46 investigate whether En2(-/-) mice displayed abnormal behavior relevant to ASD, they were monitored i

47 emonstrate that NRG1-IV/NSE-tTA mice exhibit abnormal behaviors relevant to schizophrenia, including

48 ate output, aggravated a transgene-dependent abnormal behavior (repetitive climbing and leaping) in t

49 In support of this idea, we found that abnormal behaviors resulting from postnatal fluoxetine e

50 free, extra-long interphase MTs that exhibit abnormal behaviors such as cycles of growth and breakage

51 ous knock-out mice display a wide variety of abnormal behaviors that are often considered endophenoty

52 ivity of GABAergic interneurons and produces abnormal behaviors that may be relevant to schizophrenia

53 Several factors may contribute to this abnormal behavior: transcription of LEE genes and type I

54 treated with fluoxetine continued to exhibit abnormal behavior upto 12 days post fertilization due to

55 with protease inhibitors revealed that this abnormal behavior was due to proteolysis.

56 The deafness and abnormal behavior were shown to be inherited as an autos

57 opposing behavioral responses and additional abnormal behaviors were also observed.

58 These abnormal behaviors were consistent with abnormal gamma-a

59 like behaviors in transgenic mice, and these abnormal behaviors were reversible if the expression of

60 s with executive function deficits and other abnormal behaviors, which progress to dementia.

61 d visual imagery abilities and no history of abnormal behavior while they imagined the same scenario