ライフサイエンスコーパス: schizophrenic

1 on 1 meta-analysis and 2 studies of chronic schizophrenics.

2 gh-frequency synchronization in the brain of schizophrenics.

3 levels are elevated in postmortem brains of schizophrenics.

4 iction and the high prevalence of smoking in schizophrenics.

5 echanisms producing olfactory dysfunction in schizophrenics.

6 groups; CA1 only showed changes in the SO of schizophrenics.

7 MDN together were reduced in SPD (0.14%) and schizophrenic (0.15%) patients vs controls (0.16%).

8 needed to attain smoking abstinence among 26 schizophrenic, 26 depressed, and 26 nonpsychiatric heavy

9 Some unaffected first-degree relatives of schizophrenics also manifest cortical gray-matter defici

10 al lobe only in tissue from an additional 10 schizophrenic and 10 matched comparison subjects.

11 ole, formalin-fixed left hemispheres from 14 schizophrenic and 19 normal comparison subjects were ana

12 ity of a categorical distinction between the schizophrenic and affective illnesses.

13 stellate neurons from postmortem samples of schizophrenic and age-matched control brains.

14 (NPC) development in vitro and is altered in schizophrenic and autistic individuals.

15 ns as possible novel sites of dysfunction in schizophrenic and bipolar patients.

16 ression were also observed in the caudate of schizophrenic and bipolar subjects (68--89%).

17 ral prefrontal cortex (Brodmann's area 9) of schizophrenic and bipolar subjects.

18 reactive varicosities did not differ between schizophrenic and comparison subjects in the superficial

19 ontal cortex area 9 from 10 matched pairs of schizophrenic and comparison subjects were processed for

20 in gray matter volume were seen between the schizophrenic and comparison subjects, with selective re

21 sessed and neuropathologically characterized schizophrenic and comparison subjects.

22 nt protein kinase II, did not differ between schizophrenic and control subjects, nor between subjects

23 entified in the CHRNA7 core promoter in both schizophrenic and control subjects.

24 is of the core promoter region for CHRNA7 in schizophrenic and control subjects.

25 Both schizophrenic and depressed participants chose smoking a

26 The study goal was to determine whether schizophrenic and depressed smokers perceive the reinfor

27 Schizophrenic and depressed smokers recognize many drawb

28 tailoring tobacco control interventions for schizophrenic and depressed smokers.

29 misphere thalami obtained at autopsy from 14 schizophrenic and eight comparison subjects were examine

30 s had Alzheimer's type pathology, leaving 10 schizophrenic and five comparison subjects without other

31 Comparison of schizophrenic and healthy control participants revealed

32 ibutions to the variance in liability to the schizophrenic and manic syndromes, but the genetic liabi

33 The authors mapped differences between schizophrenic and normal subjects in gyral asymmetries,

34 Schizophrenic and SPD patients have volume reduction in

35 Four schizophrenic and three comparison subjects had Alzheime

36 al cortex in tissue from an additional three schizophrenic and three matched comparison subjects and

37 loci in a large sample of unrelated Scottish schizophrenics and controls, but failed to replicate the

38 prefrontal cortical tissue from 100 control, schizophrenic, and bipolar subjects.

39 een recorded in language-impaired, autistic, schizophrenic, and other disabled human populations.

40 an epigenetic mechanism that underlies this schizophrenic behavior in malignant glioma.

41 To index schizophrenic behavior, we use the specific inability of

42 n blocking MK-801- and PCP-induced models of schizophrenic behaviors in mice.

43 ls of the 3 proteins of interest in control, schizophrenic, bipolar, and major depression groups (n =

44 smission, the dysfunctional circuitry of the schizophrenic brain (both local circuits and long-loop p

45 nobutyric acid circuits are hallmarks of the schizophrenic brain and its animal models.

46 picture of functional specialization in the schizophrenic brain and its connectional substrates is y

47 Dysbindin expression is reduced in schizophrenic brain tissue, but the molecular mechanisms

48 a soluble fragment at elevated levels in the schizophrenic brain.

49 nown about dysbindin expression in normal or schizophrenic brain.

50 ve been hypothesized to be pathogenic in the schizophrenic brain.

51 ities in the oligodendroglia demonstrated in schizophrenic brains are all examined in light of the hy

52 Numerous recent studies of postmortem schizophrenic brains have reported the presence of struc

53 aller frontal gray matter volume observed in schizophrenic brains suggests that pathology of the fron

54 (71%) in Klenow-positive nuclei was found in schizophrenic but not in bipolar cortexes.

55 in and latency but did not differ from their schizophrenic co-twins on these variables.

56 ty in area 9 exhibited a 12% increase in the schizophrenic cohort, replicating previous findings.

57 hippocampus in the control (unaffected) and schizophrenic conditions, implemented on a 72-processor

58 Capturing different schizophrenic core dysfunctions, functional magnetic res

59 Major theories on the neural basis of schizophrenic core symptoms highlight aberrant salience

60 ic mutations in mGlu1 have been described in schizophrenics creating interest in this receptor as a t

61 chizophrenia and are sensitive predictors of schizophrenic decompensation in healthy adults.

62 two, four, and six, and stratified for sex, schizophrenic diagnosis, and duration of illness.

63 was significantly down-regulated in both the schizophrenic discovery cohort and a second, independent

64 an entorhinal cortex volume of patients with schizophrenic disorders did not differ from that of pati

65 s were diagnosed as having a disorder in the schizophrenic disorders spectrum more frequently than di

66 In patients with schizophrenic disorders, the entorhinal cortex volume po

67 Snap)-25 exocytotic disruption that displays schizophrenic endophenotypes modulated by prenatal facto

68 es were divided into 2 groups: 32 studies of schizophrenics enrolled at various illness points (25 57

69 The sample included subjects from 166 schizophrenic families and 165 controls.

70 Eighteen first episode schizophrenic (FES) patients with AVHs, 18 FES patients

71 ant nonschizophrenic greater than discordant schizophrenic greater than concordant).

72 The schizophrenic group demonstrated significant randomizati

73 nase activities were fourfold greater in the schizophrenic group than in the comparison group.

74 rior vermis was significantly smaller in the schizophrenic group than in the comparison group.

75 The schizophrenic group was neuropsychologically more impair

76 eft hemisphere, with MDN reduced only in the schizophrenic group, and pulvinar in both patient groups

77 ed with localized reduced grey matter in the schizophrenic group.

78 Previous studies have shown that schizophrenics have decreased expression of alpha7-nicot

79 DNF Val(66)Met SNP interface with aspects of schizophrenic hippocampal and frontotemporal dysfunction

80 oral phenotype, which resembles catatonia in schizophrenic humans and tonic immobility in other mamma

81 s points (25 578 subjects) and 29 studies of schizophrenics identified at either illness onset or fir

82 n the prefrontal dysfunction associated with schizophrenic illness.

83 vidence indicates that patients with typical schizophrenic illnesses perform poorly on tests of these

84 responses and functional connectivity to the schizophrenic impairments.

85 sib-pairs (pairs of unaffected siblings and schizophrenic index patients) and the relative risk rati

86 n the offspring similar to those observed in schizophrenic individuals.

87 al dopamine activity in rodents, and induces schizophrenic-like behavior and cognitive deficits in hu

88 s a wide spectrum of antipsychotic-sensitive schizophrenic-like behavioral and psychopharmacological

89 Importantly, selected schizophrenic-like phenotypes and endophenotypes were re

90 ive series of behavioral test screenings for schizophrenic-like symptoms and investigated relevant do

91 gotic pairs and across the three pairings of schizophrenic-manic, schizophrenic-schizoaffective, and

92 However, in the schizophrenic model, increasing DA induces a decrement i

93 In human schizophrenics, NR2A is selectively reduced in fast-firi

94 ase in transmission of the Val allele to the schizophrenic offspring.

95 ging scans of the brain were obtained for 64 schizophrenic or schizoaffective patients (representativ

96 listic to expect the development of, say, a 'schizophrenic' or 'autistic' mouse, mice are unlikely to

97 vuII) were more frequent in African American schizophrenics (P = 0.01-0.001).

98 affected individual or the offspring of two schizophrenic parents.

99 otype effect were more pronounced within the schizophrenic patient group.

100 ssion of miR-19 in human NPCs generated from schizophrenic patient-derived induced pluripotent stem c

101 Asymmetry and shape profiles for 25 schizophrenic patients (15 men) and 28 demographically s

102 When subsamples of schizophrenic patients (n = 10) and patients with SPD (n

103 the patients with SPD and subsamples of the schizophrenic patients (n = 27) and control subjects (n

104 Patients with SPD (n = 16), schizophrenic patients (n = 42), and age- and sex-matche

105 al glucose tolerance tests were performed in schizophrenic patients (n = 48) receiving clozapine, ola

106 Geriatric institutionalized schizophrenic patients (N=124) were assessed three times

107 difference in RGS4 expression levels between schizophrenic patients (or bipolar disorder patients in

108 Healthy adults and schizophrenic patients activate a qualitatively similar

109 onal images of the brain were acquired in 11 schizophrenic patients and 12 healthy control subjects (

110 64-channel event-related potentials from 14 schizophrenic patients and 14 control subjects in a visu

111 n postmortem samples of Broca's area 44 in 9 schizophrenic patients and 14 normal controls.

112 PARTICIPANTS Twenty schizophrenic patients and 17 healthy control participan

113 sorimotor control task in 22 medication-free schizophrenic patients and 22 performance-, age-, and se

114 resonance images obtained on 73 recent-onset schizophrenic patients and 23 controls were analyzed usi

115 opy) were carried out on 25 adolescent-onset schizophrenic patients and 25 healthy adolescents.

116 otal of 54 healthy first-degree relatives of schizophrenic patients and 80 controls matched for demog

117 delineated nuclei) was not different between schizophrenic patients and controls, indicating that the

118 the significance of the differences between schizophrenic patients and healthy comparison subjects a

119 T(1)-weighted images from 20 schizophrenic patients and matched comparison subjects w

120 ting alterations of cortical interneurons in schizophrenic patients and the current notion of schizop

121 , hippocampal volumes did not differ between schizophrenic patients and their nonpsychotic relatives.

122 greater structural brain abnormalities among schizophrenic patients and their nonschizophrenic siblin

123 eater modulation by environmental factors in schizophrenic patients and their relatives.

124 Compared with controls, schizophrenic patients and their unaffected siblings sho

125 nterpretation of the high smoking rate among schizophrenic patients as self-medication has been chall

126 nals) may be particularly affected; although schizophrenic patients can extinguish conditioned fear,

127 t the SNAP25b/SNAP25a ratio was increased in schizophrenic patients carrying the rs6039769 at-risk al

128 Institutionalized schizophrenic patients demonstrated an age-related patte

129 The dorsolateral prefrontal cortex in schizophrenic patients displayed nearly twice the normal

130 frequency range (30-80 Hz) are disturbed in schizophrenic patients during cognitive processes and ma

131 nt of the increased gamma power described in schizophrenic patients during sleep and events of psycho

132 There are ongoing changes in the brains of schizophrenic patients during the initial years after di

133 We now show that schizophrenic patients exhibit abnormally weak center-su

134 nal and structural alterations differentiate schizophrenic patients from healthy controls with 80% se

135 Schizophrenic patients had significantly higher risk for

136 -analysis confirmed that treatment-resistant schizophrenic patients have more favorable outcomes when

137 Because thought disturbances in schizophrenic patients involve language processing, we h

138 The prominence of nicotine addiction in schizophrenic patients is reflected in the normalization

139 ect of alcohol dependence on the thalamus in schizophrenic patients may be mitigated by the type of n

140 evation of kynurenic acid (KYNA) observed in schizophrenic patients may contribute to core symptoms a

141 otion that P300 abnormalities in siblings of schizophrenic patients may involve a widespread network

142 ous expression of claudin-5 in the brains of schizophrenic patients post mortem was observed compared

143 We present a population-based study of 8967 schizophrenic patients receiving major surgery from the

144 Healthy first-degree relatives of schizophrenic patients show altered striatal activation

145 e volume reduction in the pulvinar, but only schizophrenic patients show reduction relative to brain

146 RESULTS During fear conditioning, schizophrenic patients showed blunted autonomic response

147 Schizophrenic patients showed greater overall false reco

148 they had impairments in perceptual closure, schizophrenic patients showed improvement in performance

149 In contrast, the schizophrenic patients showed inappropriately elevated f

150 st detection thresholds, and the unmedicated schizophrenic patients showed visual contrast detection

151 ct, and is contrary to the data from chronic schizophrenic patients suggesting that ketamine effect d

152 eterogeneity of pharmacological responses in schizophrenic patients suggests that additional drug tar

153 tivity disorder and has been associated with schizophrenic patients that do not respond to treatment

154 ltered neurodevelopmental time course in the schizophrenic patients that is particularly salient in a

155 They compared 23 unaffected siblings of schizophrenic patients to 18 matched comparison subjects

156 logy of schizophrenia and the sensitivity of schizophrenic patients to glutamate and glutamatergic dr

157 malities in BP) with our previous studies in schizophrenic patients using the same methodology.

158 e matter tracts in the prefrontal area of 10 schizophrenic patients was determined by diffusion tenso

159 The cognitive and functional status of these schizophrenic patients was fairly stable until late life

160 , but those of non-ill MZ and DZ co-twins of schizophrenic patients were similar.

161 l66Met polymorphism were assessed in Chinese schizophrenic patients with (n = 368) and without (n = 5

162 xamined whether cognitive changes in elderly schizophrenic patients with a history of long-term insti

163 estigate changes of GM volumes of drug-naive schizophrenic patients with and without AVHs.

164 ity after complications were evaluated among schizophrenic patients with different severity.

165 that mirror those observed in the brains of schizophrenic patients with impressive precision.

166 ments in the functional impairments of older schizophrenic patients with increased medical burden.

167 rug of LY404039 (LY2140023) was evaluated in schizophrenic patients with olanzapine as an active cont

168 Studies comparing gray matter (GM) volume of schizophrenic patients with or without auditory verbal h

169 le frontal and inferior parietal cortices of schizophrenic patients with primary negative symptoms.

170 d duration strategies to target subgroups of schizophrenic patients with specific biological deficits

171 task, in ultra-high-risk, early, and chronic schizophrenic patients with the use of functional magnet

172 P300 changes in 66 schizophrenic patients, 115 healthy siblings of schizoph

173 eased expression of CPLXII is seen in HD and schizophrenic patients, a role for CPLXII depletion shou

174 izophrenic patients, 115 healthy siblings of schizophrenic patients, and 89 unrelated controls were s

175 executive functioning in healthy adults and schizophrenic patients, and associates with EEG differen

176 els of NRG1 observed in forebrain regions of schizophrenic patients, exhibit behavioral deficits and

177 icture strongly resembles the one present in schizophrenic patients, highlighting the translational v

178 nsitization support neuroimaging findings in schizophrenic patients, implying that amphetamine sensit

179 Comparison subjects, but not schizophrenic patients, showed error-related activity in

180 n shown to occur in the prefrontal cortex of schizophrenic patients, suggesting that NRG1-erbB signal

181 nd gamma rhythm abnormalities are evident in schizophrenic patients, the approach followed here may f

182 assessed in a large and unselected sample of schizophrenic patients, their healthy siblings, and cont

183 s with SPD and significantly smaller than in schizophrenic patients, while the relative size of the c

184 -surround mechanisms in motion perception of schizophrenic patients.

185 ved from deleterious GRM1 mutations found in schizophrenic patients.

186 but men had larger volumes than women among schizophrenic patients.

187 tical thickness, or somal size in area 44 of schizophrenic patients.

188 , biochemical, and anatomic abnormalities in schizophrenic patients.

189 entials 23 and 25 in the stellate neurons of schizophrenic patients.

190 en olanzapine exposure and hyperlipidemia in schizophrenic patients.

191 glutamate metabolism in brain specimens from schizophrenic patients.

192 ith the severity of negative symptoms in the schizophrenic patients.

193 benefits on the sickest treatment-resistant schizophrenic patients.

194 ve been reported for younger, better-outcome schizophrenic patients.

195 concentration of apoD in serum samples from schizophrenic patients.

196 elevated in patients with SPD and reduced in schizophrenic patients.

197 d with stronger backward masking deficits in schizophrenic patients.

198 startle response similar to that observed in schizophrenic patients.

199 s seen in prodromal, drug-naive, and chronic schizophrenic patients.

200 improves cognition in healthy volunteers and schizophrenic patients.

201 uctural and functional abnormalities in many schizophrenic patients.

202 hosis in humans, and exacerbates symptoms in schizophrenic patients.

203 II) is reduced in selective brain regions in schizophrenic patients.

204 ceptual closure is significantly impaired in schizophrenic patients; however, this deficit in sensory

205 sorder and 17.7% higher than predicted among schizophrenic patients; overall use in no-cap states was

206 w can we hope to explain mechanistically the schizophrenic phenotype?

207 homozygosis and behavioral and morphological schizophrenic phenotypes associated with forebrain defec

208 basis of epidemiological data in normal and schizophrenic populations.

209 ip between positive and negative symptoms of schizophrenic probands and dimensions of schizotypy in t

210 n does not arise from smoking onset during a schizophrenic prodrome and demonstrates a clear dose-res

211 subjects, these diagnostic criteria for the schizophrenic prodrome and the Structured Interview for

212 ially the Iowa Gambling Task (IGT), and with schizophrenic psychopathology including thought disorder

213 ine transmission is thought to contribute to schizophrenic psychosis and drug dependence.

214 The prodromal features had converted to schizophrenic psychosis for 46% of the prodromal patient

215 ria for the prodrome of the first episode of schizophrenic psychosis when based on the Structured Int

216 a priori model of hippocampal dysfunction in schizophrenic psychosis, the authors postulated molecula

217 upporting perception and cognition underlies schizophrenic psychosis.

218 ermined to have altered expression levels in schizophrenics relative to controls are involved in a nu

219 x," n = 28) diagnosed with schizophrenia, 18 schizophrenic relatives, and 48 normal controls.

220 to investigate whether operationally defined schizophrenic, schizoaffective, and manic syndromes shar

221 of overlap in the genes contributing to RDC schizophrenic, schizoaffective, and manic syndromes.

222 Diagnostic Criteria (RDC) for lifetime-ever schizophrenic, schizoaffective, or manic syndrome were a

223 s the three pairings of schizophrenic-manic, schizophrenic-schizoaffective, and schizoaffective-manic

224 Finally, within the schizophrenic/schizoaffective disorder patients, smaller

225 While schizophrenics showed poorer performance than HC in the

226 appropriate animal model for some aspects of schizophrenic social withdrawal.

227 Schizophrenic speech disorder is heterogeneous in form a

228 tained attention and sequencing abilities to schizophrenic speech disorder, measured in terms of comm

229 The schizophrenic subjects age 50 and older were compared to

230 ortex expression of PSD-95 was higher in the schizophrenic subjects and correlated strongly with the

231 est (WCST) and a control task in unmedicated schizophrenic subjects and matched controls.

232 we identified six 3q29 deletions among 7545 schizophrenic subjects and one among 39,748 controls, re

233 immunoblotting in postmortem samples from 14 schizophrenic subjects and their age-, gender-, and auto

234 lex is up-regulated in the frontal cortex of schizophrenic subjects as compared with controls.

235 expression patterns in prefrontal cortex of schizophrenic subjects at different stages of illness, a

236 Oct-6 in the frontal and temporal cortex in schizophrenic subjects but not in comparison subjects.

237 The presence of Oct-6 expression in the schizophrenic subjects but not in the comparison subject

238 basis for increased plasma proline levels in schizophrenic subjects carrying the missense mutation L4

239 HRNA7 is reduced in several brain regions in schizophrenic subjects compared with control subjects.

240 In comparison to the normal adolescents, the schizophrenic subjects demonstrated low prefrontal corte

241 Schizophrenic subjects displayed normal activation of th

242 nd magnetic resonance imaging (MRI) scans of schizophrenic subjects have not consistently revealed fr

243 magnetic resonance imaging (fMRI) studies of schizophrenic subjects may identify brain activity chang

244 hors scanned seven normal subjects and seven schizophrenic subjects on two occasions during performan

245 nd variably improve cognitive functioning in schizophrenic subjects receiving typical antipsychotics.

246 n the dorsolateral prefrontal cortex in more schizophrenic subjects relative to matched controls.

247 tter volume was significantly smaller in the schizophrenic subjects than in the comparison subjects (

248 temporal gyrus showed less activation in the schizophrenic subjects than in the comparison subjects o

249 al white matter volume (6%-8% smaller in the schizophrenic subjects than in the comparison subjects)

250 omoter variants was statistically greater in schizophrenic subjects than in the controls.

251 ng pictorial information at encoding allowed schizophrenic subjects to suppress false recognition to

252 nt study, the differential expression in the schizophrenic subjects was confirmed by quantitative RT-

253 Schizophrenic subjects with predominantly negative sympt

254 ed to compare cerebral metabolic patterns in schizophrenic subjects with predominantly negative sympt

255 Within the schizophrenic subjects, a relationship was observed betw

256 with NMDA-mediated hypofunction observed in schizophrenic subjects, administration of an NMDA antago

257 Within the prefrontal cortex of schizophrenic subjects, alterations in markers of gamma-

258 ingulate cortex from 18 healthy controls, 18 schizophrenic subjects, and 10 bipolar subjects.

259 been found in previous postmortem studies of schizophrenic subjects, and magnetic resonance imaging (

260 For normal, bipolar, depressed, and schizophrenic subjects, COX-1 and COX-2 protein levels d

261 In individual schizophrenic subjects, however, indices of cognitive ac

262 For the schizophrenic subjects, neuronal number in the mediodors

263 In schizophrenic subjects, Oct-6 immunoreactivity was found

264 In post-mortem human brain from untreated schizophrenic subjects, the 2AR is upregulated and the m

265 In the schizophrenic subjects, the relative density of labeled

266 y was present in the temporal lobe in all 10 schizophrenic subjects, while very little or no expressi

267 n the magnitude of cognitive decline for the schizophrenic subjects, with older subjects experiencing

268 cross the medial hemispheric surfaces in the schizophrenic subjects.

269 ns, such as that observed in brain tissue of schizophrenic subjects.

270 ntal cortex of bipolar, but not depressed or schizophrenic subjects.

271 ar disorder, particularly in CA4, but not in schizophrenic subjects.

272 glutamate and GABA metabolism is altered in schizophrenic subjects.

273 a selective reduction in DARPP-32 levels in schizophrenic subjects.

274 an nuclei, were significantly smaller in the schizophrenic subjects.

275 mal neurodevelopment or in tissue from adult schizophrenic subjects.

276 very cohort and a second, independent set of schizophrenic subjects.

277 re broadly consistent with the proposal that schizophrenics suffer from enhanced signaling of salienc

278 sphodiesterase (CNP) are associated with the schizophrenic symptom catatonia in both humans and mouse

279 This provides evidence that these schizophrenic symptom factors (1) are etiologically dist

280 not been established that the dimensions of schizophrenic symptomatology and personality traits in n

281 y interact with hyperdopaminergia to lead to schizophrenic symptomatology remains uncertain.

282 r psychiatric illness with a predominance of schizophrenic symptomatology.

283 renia because of the similarity between some schizophrenic symptoms and symptoms caused by NMDA antag

284 Various schizophrenic symptoms are suggested to be linked to a d

285 ognitive demands may confer vulnerability to schizophrenic symptoms when adult neuroplastic demands a

286 improved efficacy against the full range of schizophrenic symptoms.

287 ion and the pathogenesis of language-related schizophrenic symptoms.

288 in maintenance and repair, contribute to the schizophrenic syndrome.

289 more common in 512 controls compared to 506 schizophrenic (SZ) cases (10.6% vs 7.2%, p=0.007) but th

290 ted allele had a somewhat lower frequency in schizophrenics than in controls.

291 he frequency of this oscillation is lower in schizophrenics than in healthy individuals.

292 For schizophrenics, the distribution differed significantly

293 thus provides novel insights into potential schizophrenic therapeutics that target the endocannabino

294 tributes to clozapine's clinical activity in schizophrenics through modulation of both muscarinic and

295 United Kingdom and Scotland, and a sample of schizophrenic trios from the United States containing pa

296 The schizophrenic twins made more antisaccade reflexive erro

297 Twelve normal volunteers and 18 drug-free schizophrenic volunteers (deficit, N=8; nondeficit, N=10

298 This study estimates that 4.9% of schizophrenics will commit suicide during their lifetime

299 Treatment of schizophrenics with some antipsychotic drugs has been as

300 Schizophrenics with the 'at risk' PvuII genotype had low