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1  levels are elevated in postmortem brains of schizophrenics.
2 groups; CA1 only showed changes in the SO of schizophrenics.
3  on 1 meta-analysis and 2 studies of chronic schizophrenics.
4 gh-frequency synchronization in the brain of schizophrenics.
5 iction and the high prevalence of smoking in schizophrenics.
6 eceptor subunits in the prefrontal cortex of schizophrenics.
7 echanisms producing olfactory dysfunction in schizophrenics.
8 receptor complex, may also be upregulated in schizophrenics.
9 n relation to those reported for later-onset schizophrenics.
10    Some unaffected first-degree relatives of schizophrenics also manifest cortical gray-matter defici
11 in the left and right hippocampus between 11 schizophrenics and 13 controls.
12 ause current therapy is ineffective for many schizophrenics and because treatment is often accompanie
13   By contrast, the cerebellar cortex of both schizophrenics and controls contained very high levels o
14 ignificantly different between first-episode schizophrenics and controls over the posterior sagittal
15 loci in a large sample of unrelated Scottish schizophrenics and controls, but failed to replicate the
16               In the cerebral cortex of both schizophrenics and controls, mRNAs for NR1, NR2A, NR2B,
17 ix pairs of individually matched brains from schizophrenics and controls, we measured the volumes and
18 rtex of AT-schizophrenics, as compared to AF-schizophrenics and controls.
19 mporal, and cerebellar cortex of brains from schizophrenics and from neuroleptic-treated and nonmedic
20 xamined in dorsolateral prefrontal cortex of schizophrenics and matched controls by using in situ hyb
21                            Both the familial schizophrenics and their first-degree relatives (but not
22  caused by retinoid dysfunction are found in schizophrenics and their relatives; (ii) those loci that
23 se found in the cerebrospinal fluid (CSF) of schizophrenics, antipsychotic drugs augment NMDA activit
24  was more pronounced in frontal cortex of AT-schizophrenics, as compared to AF-schizophrenics and con
25 al deficits were present in the offspring of schizophrenics at adolescence, to examine their stabilit
26 eased P50 inhibition occurs not only in most schizophrenics, but also in many of their nonschizophren
27 ic mutations in mGlu1 have been described in schizophrenics creating interest in this receptor as a t
28                                First-episode schizophrenics displayed smaller amplitudes over the lef
29 es were divided into 2 groups: 32 studies of schizophrenics enrolled at various illness points (25 57
30                                 Despite many schizophrenics' extremely heavy nicotine use, nicotinic
31                                           In schizophrenics, gamma2S transcripts had fallen to 51.7%
32             Previous studies have shown that schizophrenics have decreased expression of alpha7-nicot
33 both mRNAs were significantly reduced in the schizophrenics, having controlled for the effects of bra
34 s points (25 578 subjects) and 29 studies of schizophrenics identified at either illness onset or fir
35 ctivity of dorsolateral prefrontal cortex in schizophrenics is well known.
36                                     In human schizophrenics, NR2A is selectively reduced in fast-firi
37  (BG) were well visualized in normals and in schizophrenics off medication.
38 sagittal thalamic area was also seen for the schizophrenics (P = .03), which was unchanged at rescan
39 vuII) were more frequent in African American schizophrenics (P = 0.01-0.001).
40                           All 4 offspring of schizophrenics receiving schizophrenia spectrum diagnose
41 ermined to have altered expression levels in schizophrenics relative to controls are involved in a nu
42                                    Childhood schizophrenics showed a significantly greater increase i
43                                        While schizophrenics showed poorer performance than HC in the
44 verlapped with the subregions and laminae in schizophrenics showing the most marked increases of GABA
45 re broadly consistent with the proposal that schizophrenics suffer from enhanced signaling of salienc
46 ted allele had a somewhat lower frequency in schizophrenics than in controls.
47 gnificantly lower relative metabolic rate in schizophrenics than in controls.
48 he frequency of this oscillation is lower in schizophrenics than in healthy individuals.
49                                           In schizophrenics, the alterations in expression of NR2 sub
50                                           In schizophrenics, the BG/CE ratio off medication was 1.54
51                                          For schizophrenics, the distribution differed significantly
52 tributes to clozapine's clinical activity in schizophrenics through modulation of both muscarinic and
53 en-activated protein (MAP) kinase pathway in schizophrenics using postmortem brain samples.
54 nscripts in prefrontal cortex of brains from schizophrenics were reduced by 28.0%, although this redu
55            This study estimates that 4.9% of schizophrenics will commit suicide during their lifetime
56                      Adolescent offspring of schizophrenics with poor neurobehavioral functioning had
57                                 Treatment of schizophrenics with some antipsychotic drugs has been as
58                                              Schizophrenics with the 'at risk' PvuII genotype had low
59 eversible hyperactivity was not a feature of schizophrenics without passivity.