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1  hippocampus subfields in vivo that underlie abnormal behavior.
2 cluding impaired neurocognitive function and abnormal behavior.
3 f these circuits may contribute to normal or abnormal behavior.
4 de developers in recognizing and reacting to abnormal behavior.
5 dostatin, to determine if HemEPCs share this abnormal behavior.
6 n of neural activation may in itself lead to abnormal behavior.
7 yndrome of borderline mental retardation and abnormal behavior.
8  Bengal kitten with intractable seizures and abnormal behavior.
9 ow these circuit changes might contribute to abnormal behaviors.
10 ouped into three types: normal, delayed, and abnormal behaviors.
11 xpressing mice showing schizophrenia-related abnormal behaviors.
12  tissues in the BTBR mice may underlie their abnormal behaviors.
13  but did not alter seizure activity or other abnormal behaviors.
14 uals with autism and may contribute to their abnormal behaviors.
15  through which brain 5-HT deficiency induces abnormal behaviors.
16 nxious psyche and contribute to long-lasting abnormal behaviors.
17          The most common adverse events were abnormal behavior (22 [34%] in the daily prednisone grou
18  microglial numbers has been associated with abnormal behaviors akin to those observed in neurodevelo
19 ial to screen new transgenic mouse lines for abnormal behavior and physiology, these BAC transgenic m
20 s (GFAP reactivity) was correlated with both abnormal behavior and spontaneous seizures.
21                           Importantly, these abnormal behaviors and brain activities were alleviated
22 5 or PKC-gamma inhibitor Go-6983 reduced the abnormal behaviors and elevated relapse-like ethanol dri
23 itor (fluoxetine at 20 mg/kg) attenuates the abnormal behaviors and selectively reverses the circuit
24              They also presented an array of abnormal behaviors and significant weight loss.
25 phane had improvement in social interaction, abnormal behavior, and verbal communication (P = 0.015-0
26 onafluoropentanamide) as capable of inducing abnormal behavior at multiple chemical-concentrations pa
27 re malformation of the cerebellum as well as abnormal behavior (ataxia).
28  genetic variation causes DA dysfunction and abnormal behaviors by stabilizing a HOIF state of the tr
29 al ventral hippocampal lesion (NVHL) develop abnormal behaviors during or after adolescence, suggesti
30 hanges in cell fate may underlie many of the abnormal behaviors exhibited by cells after loss of PAR-
31 ur previous studies revealed that mucus with abnormal behavior impaired mucociliary transport in newb
32 e neural mechanism for stressed-reared pups' abnormal behavior in a more controlled environment by in
33 s impairment of glycinergic transmission and abnormal behavior in beo mutants.
34 ructure and function of this channel and its abnormal behavior in disease requires knowledge of the n
35                        Barbering is a common abnormal behavior in laboratory mice, where mice pluck t
36 rmalize cerebellar myelin content and rescue abnormal behavior in male plKO mice.
37 ent of the PFC, which may be associated with abnormal behavior in offsprings.
38 ilization; including perinatal lethality and abnormal behavior in surviving adults.
39 e off-target edits exhibited no expansion or abnormal behavior in vivo in animals followed for up to
40  mTORC1, ameliorates survival, seizures, and abnormal behaviors in a Pten mutant model, highlighting
41 erebroventricular administration ameliorates abnormal behaviors in adult mutant mice.
42  (EA) therapeutically manage the ACE-induced abnormal behaviors in adulthood.
43 delay during the postnatal period as well as abnormal behaviors in both young and adult animals that
44 eural circuits and ameliorating symptoms and abnormal behaviors in individuals with psychiatric disor
45 sting pathological effect by MIA, leading to abnormal behaviors in offspring mice in a sex-specific m
46  of the link between perinatal cytokines and abnormal behaviors in offspring, human epidemiological s
47 ed as a metric to quantify the occurrence of abnormal behaviors in the arterial oxygen saturation tim
48 hanges in these circuits might contribute to abnormal behaviors in the context of neuropsychiatric di
49 several insights on the etiological basis of abnormal behaviors in these mice, including abnormal cor
50 an FMR1 gene have corrected or overcorrected abnormal behaviors including hyperactivity and altered s
51 that probiotics, when eaten, can improve the abnormal behaviors (including social withdrawal and immo
52  mice showed reduced prepulse inhibition and abnormal behavior, including excessive anxiety, antisoci
53      Beta power is predictive of healthy and abnormal behaviors, including perception, attention and
54 th altered intrahippocampal connectivity and abnormal behavior; including hyperactivity, some defects
55  patterns are observed in PrEE newborns, and abnormal behavior is present in 20-d-old PrEE mice.
56 h DA dysfunction in isolated brains and with abnormal behaviors monitored at high-speed time resoluti
57 anogaster expressing hDAT DeltaN336 and with abnormal behaviors observed at high-time resolution.
58   Group TE now showed only few if any of the abnormal behaviors observed in infancy.
59                               The normal and abnormal behavior of a living cell is governed by comple
60 re we investigate the molecular basis of the abnormal behavior of Hectd1 mutant cranial mesenchyme.
61 s therefore provide initial evidence linking abnormal behavior of STAT pathways for cytokine signalin
62          The mechanisms that account for the abnormal behavior of these cells in IDDM are not fully u
63                                          The abnormal behavior of unc-17(e245) mutants, which have a
64 not induce any overt clinic symptom, such as abnormal behavior, or any neurological signs.
65 ndary passage-inoculated cats have developed abnormal behavior patterns consistent with the early sta
66  amelioration of a subset of PTEN-associated abnormal behaviors, providing evidence that the mTORC1 p
67  investigate whether En2(-/-) mice displayed abnormal behavior relevant to ASD, they were monitored i
68 emonstrate that NRG1-IV/NSE-tTA mice exhibit abnormal behaviors relevant to schizophrenia, including
69 ate output, aggravated a transgene-dependent abnormal behavior (repetitive climbing and leaping) in t
70       In support of this idea, we found that abnormal behaviors resulting from postnatal fluoxetine e
71 lity factors that lead to the development of abnormal behaviors secondary to ZIKV infection early in
72 free, extra-long interphase MTs that exhibit abnormal behaviors such as cycles of growth and breakage
73 sures capture the waves' characteristics and abnormal behaviors, such as atypical periodicity or exce
74 ous knock-out mice display a wide variety of abnormal behaviors that are often considered endophenoty
75 ivity of GABAergic interneurons and produces abnormal behaviors that may be relevant to schizophrenia
76       Several factors may contribute to this abnormal behavior: transcription of LEE genes and type I
77 treated with fluoxetine continued to exhibit abnormal behavior upto 12 days post fertilization due to
78 featuring cognitive impairment, dysmorphism, abnormal behavior, variable epilepsy, white matter abnor
79  with protease inhibitors revealed that this abnormal behavior was due to proteolysis.
80                             The deafness and abnormal behavior were shown to be inherited as an autos
81 opposing behavioral responses and additional abnormal behaviors were also observed.
82                                        These abnormal behaviors were consistent with abnormal gamma-a
83 like behaviors in transgenic mice, and these abnormal behaviors were reversible if the expression of
84 ptic dysfunction and altered plasticity with abnormal behavior, whether similar or other mechanisms c
85 s with executive function deficits and other abnormal behaviors, which progress to dementia.
86 d visual imagery abilities and no history of abnormal behavior while they imagined the same scenario