ライフサイエンスコーパス: manic

1 an did those whose intake episode was purely manic.

2 ound that 5-nitro-6-methylamino-isocytosine (MANIC; 3), which inhibits another B. anthracis folate sy

3 iatric disorder characterized by episodes of manic and depressed mood states and associated with cort

4 pecificity of the prospective association of manic and depression episodes that is a hallmark of bipo

5 Risks of new manic and depressive episodes were similar but were pred

6 c, predominantly depressive, and across both manic and depressive episodes, showing essentially paral

7 lex and nuanced than simply one of recurring manic and depressive episodes.

8 r placebo were seen in time to recurrence of manic and depressive episodes.

9 a key theory of the pathophysiology of both manic and depressive phases of the illness for over four

10 (BD) is characterized by mood swings between manic and depressive states.

11 bilizer if it has efficacy in treating acute manic and depressive symptoms and in prophylaxis of mani

12 Severity of both manic and depressive symptoms as well as suicidal behavi

13 Manic and depressive symptoms improved equally in both g

14 nd depressive symptoms and in prophylaxis of manic and depressive symptoms in bipolar disorder.

15 ADHD and have greater levels of subthreshold manic and depressive symptoms than children of compariso

16 order, had significantly more severe current manic and depressive symptoms than comparison offspring.

17 d the outcomes of patients with co-occurring manic and depressive symptoms who are treated with antid

18 ionate these into components associated with manic and depressive symptoms, and characterize the impa

19 cts showed greater fear recognition than the manic and euthymic bipolar I disorder subjects.

20 SM-5 criterion A decreases the prevalence of manic and hypomanic episodes but does not affect longitu

21 activity is now considered a core symptom of manic and hypomanic episodes.

22 le modifications at EGF6 and EGF36 (added by Manic and Lunatic but not Radical) inhibited Notch1 acti

23 t time we have demonstrated that, similar to Manic and Lunatic, Radical fringe is also a fucose-speci

24 isorder type I for respondents in which both manic and major depression symptoms were reported (n = 4

25 oups of mood disorders, including psychotic, manic and major depressive episodes (MDEs).

26 suggesting that the familial transmission of manic and major depressive episodes is independent despi

27 pisodes; addition of severity dimensions for manic and major depressive episodes; and removal of the

28 he strong familial specificity of psychotic, manic and MDEs in this largest controlled contemporary f

29 er are more common in bipolar I disorder and manic and psychotic presentations occur earlier in the p

30 ium was associated with both benefit in time manic and worse tolerability compared with placebo.

31 th first-episode affective psychosis (mainly manic), and 14 healthy comparison subjects.

32 inking (74%), mood disturbances (70%,usually manic), and aggression (57%).

33 n/disinhibition, externalizing, subsyndromal manic, and affective lability symptoms.

34 nterviewers for diagnosing major depressive, manic, and hypomanic episodes.

35 Lunatic, Manic, and Radical Fringe (LFNG, MFNG, and RFNG) are N-a

36 Mammals have three Fringes: Lunatic, Manic, and Radical.

37 ion was defined as the absence of psychotic, manic, and severe depressive symptoms for at least 1 wee

38 and neural genetic alterations analogous to manic aspects of bipolar disorders.

39 mechanisms by which neuroinflammation drives manic behavior are not well understood.

40 that the link between neuroinflammation and manic behavior may be mediated by actions on serotonergi

41 together with near-scan PGBI-10M, a score of manic behaviors, depressive behaviors and sex, explained

42 aytime increases in VTA dopamine activity to manic behaviors, we developed a novel optogenetic stimul

43 ipolar disorder are defined as depressive or manic, but depressive and manic symptoms can combine in

44 dability, a number of authors suggested that manic delusions could arise directly from a euphoric moo

45 The most common is related to manic depression, in which neuroleptic drugs should be u

46 e "insanity" similar to dementia praecox and manic depressive illness.

47 Times to symptomatic relapse into manic, depressive, and mixed episodes were all significa

48 comes investigated included risk of relapse (manic, depressive, and total) as well as risk of specifi

49 Nevertheless, true to its manic-depressive behavior, new evidence links TGF-beta w

50 1.05-3.64; P = .03; AR, 6.9/10,000 persons), manic-depressive disorder (HR, 4.35; 95% CI, 1.56-12.09;

51 sk of suicide included male sex, depression, manic-depressive disorder, heavy or binge drinking, and

52 ing which our major diagnostic categories of manic-depressive illness (MDI) and dementia praecox were

53 athophysiology and therapeutic mechanisms of manic-depressive illness are unknown.

54 Manic-depressive illness has been conceptualized as a ne

55 ood modulation, molecular pathophysiology of manic-depressive illness, and therapeutic mechanism of m

56 y used mood stabilizers for the treatment of manic-depressive illness, stimulated the ERK pathway in

57 rebral morphometric deficits associated with manic-depressive illness.

58 n psychiatric nosology that contained DP and manic-depressive insanity (MDI)--Kraepelin's key categor

59 lin's new categories of dementia praecox and manic-depressive insanity were too broad and too heterog

60 trophy and loss in discrete brain regions of manic-depressive patients.

61 Prospective episode duration of manic diagnoses, using onset of mania as baseline date,

62 -IV bipolar I disorder experiencing an acute manic episode (baseline Young Mania Rating Scale score >

63 n view of the efficacy in prevention of both manic episode and depressive episode relapse or recurren

64 5, all patients with a diagnosis of a single manic episode or bipolar disorder between January 1, 199

65 nce of treating bipolar patients, for rating manic episode severity).

66 Individuals with a manic episode showed the greatest reductions in tryptoph

67 tance of long-term prophylaxis after a first manic episode to lessen episode recurrence, allow cognit

68 Immediately following remission of a manic episode treated with the combination of a typical

69 isorder can be diagnosed on the basis of one manic episode); bipolar disorder type II (depressive and

70 After a first manic episode, 1 year of randomized treatment with lithi

71 der, defined by the presence of a syndromal, manic episode, and bipolar II disorder, defined by the p

72 had both a major mental disorder (psychosis, manic episode, or major depressive episode) and a substa

73 was clustered in later adult age groups for manic episode, phobias, alcohol use disorders, and gener

74 otic agent following remission from an acute manic episode.

75 sodes significantly increased risk of Wave 2 manic episodes (AOR: 2.2; 1.7-2.9) and anxiety disorders

76 as associated with psychotic features during manic episodes (P=0.003).

77 .89, 1.45-2.48, p<0.0001), greater number of manic episodes (seven studies, 3909 participants; 1.26,

78 attributable to the familial specificity of manic episodes after adjusting for both proband and rela

79 mong subjects 18.0 years or older, 44.4% had manic episodes and 35.2% had substance use disorders.

80 al focus is warranted on connections between manic episodes and anxiety disorders.

81 between Wave 1 major depressive episode with manic episodes and other psychiatric disorders.

82 the strength of associations between Wave 1 manic episodes and Wave 2 depression, anxiety and substa

83 Manic episodes are one of the major diagnostic symptoms

84 Patients who experienced hypomanic or manic episodes between time points showed abnormal thinn

85 Manual of Mental Disorders, Fourth Edition) manic episodes during the study's 3-year follow-up perio

86 ted in BD-I compared with BD-II and MDD, and manic episodes had focused progressive effect on the CA2

87 Adults with manic episodes have an approximately equivalent relative

88 ian gene disruption and the precipitation of manic episodes in bipolar disorder.

89 recently been approved for stabilization of manic episodes in patients with bipolar disorder.

90 ts capable of triggering both depressive and manic episodes in patients with BPD.

91 y greater number of depressive and hypomanic/manic episodes in the prior year.

92 In multivariable models, Wave 1 manic episodes significantly increased the odds of Wave

93 ects with child BP-I, the 44.4% frequency of manic episodes was 13 to 44 times higher than population

94 ed relapse to mania, and more weeks ill with manic episodes was predicted by low maternal warmth and

95 xed anxiety depression; replacement of mixed manic episodes with a 'mixed features' specifier applica

96 e monotherapy displayed an increased rate of manic episodes within 3 months of medication initiation

97 The preventive effect is clear for manic episodes, although it is equivocal for depressive

98 ducation, numbers of previous depressive and manic episodes, baseline scores on the Hamilton Rating S

99 ipramine, an antidepressant that can trigger manic episodes, increased synaptic expression of GluR1 i

100 d unequivocal evidence for efficacy in acute manic episodes, lithium in acute depressive episodes and

101 ity was greater for depressive episodes than manic episodes, with approximately 74.0% of respondents

102 ssociation between KYNA levels and number of manic episodes.

103 ite polarity symptom levels in depressive or manic episodes.

104 t that impaired sleep can induce and predict manic episodes.

105 had negative correlations with the number of manic episodes.

106 ude: bipolar disorder type I (depressive and manic episodes: this disorder can be diagnosed on the ba

107 19-year-old woman presenting initially with manic excitement followed by a lengthy period of mutism,

108 hanced NOTCH2 activation by DLL1 and -4, and Manic fringe (MFNG) inhibited NOTCH2 activation by JAG1

109 e report that an established Notch modifier, Manic Fringe (Mfng), is expressed in the putative endocr

110 pathways, including Notch (Notch homolog 2, manic fringe homolog), growth factor (FGF intracellular-

111 While Lunatic and Manic Fringe inhibit Notch1 activation from Jagged1 and

112 We found that Lunatic and Manic Fringe modified similar sites on Notch1, while Rad

113 LFNG (Lunatic Fringe) and MFNG (Manic Fringe) transfer N-acetylglucosamine (GlcNAc) to O

114 1, Gbx2), IGF (IGFBP3, IGFBP6, CTGF), Notch (manic fringe, ADAM11), Hedgehog (patched) and Wnt (Frat2

115 s not observed in the published structure of Manic Fringe, and residues predicted to be involved in U

116 e mammalian homologues have been identified, Manic fringe, Lunatic fringe, and Radical fringe.

117 1-Dll4-Notch1 signaling, possibly favored by Manic-Fringe, is specifically required for cardiac epith

118 The manic group also had higher activity in insula and putam

119 GluR1/2 was essential for the development of manic/hedonic-like behaviors such as amphetamine-induced

120 h a 'mixed features' specifier applicable to manic, hypomanic, and major depressive episodes; additio

121 ith bipolar I or II disorder and a DSM-IV-TR manic, hypomanic, depressive, or mixed episode in the pr

122 erior to placebo at prolonging the time to a manic, hypomanic, or mixed episode (P =.006).

123 pisode; of these, 457 subjects switched to a manic, hypomanic, or mixed episode prior to recovery.

124 ignificantly associated with shorter time to manic, hypomanic, or mixed episode recurrence.

125 y from depression and time until switch to a manic, hypomanic, or mixed episode.

126 with bipolar I disorder who presented with a manic, hypomanic, or mixed episode.

127 episodes (298, 34.7%) as those who developed manic, hypomanic, or mixed episodes (118, 13.8%).

128 erience switch from depression directly to a manic, hypomanic, or mixed state.

129 a absent, episodic mania, and chronic mania (manic/hypomanic >1 year).

130 ally identified significant associations for manic/hypomanic states during antidepressant therapy, cu

131 of total follow-up weeks) predominated over manic/hypomanic symptoms (8.9% of weeks) or cycling/mixe

132 ve disorder and correlation between lifetime manic/hypomanic symptoms and depressive symptoms in majo

133 er shifting to bipolar disorders; history of manic/hypomanic symptoms in major depressive disorder an

134 y, primary), depressive episode (RR-dep) and manic/hypomanic/mixed episode (RR-mania), discontinuatio

135 e was 21.4 weeks and until 25% experienced a manic/hypomanic/mixed episode was 85.0 weeks.

136 ilience and in regulating recovery from both manic-like and depression-like behavioral impairments.

137 scribing a patient's experience of cycles of manic-like behavior and depression while on high-dosage

138 roteins (HDACs) are effective in normalizing manic-like behavior, and that class I HDACs (e.g., HDAC1

139 t the PFC, resulted in a profound display of manic-like behavior, characterized by increased stress-i

140 traperitoneally in a system that phenocopies manic-like behavior.

141 s of PLCgamma1 from the forebrain results in manic-like behavior.

142 uronal activity and find that this induces a manic-like behavioral state.

143 8 weeks, and no increased propensity toward manic-like behaviors were reported.

144 g from neuroinflammation in the DR underlies manic-like behaviors.

145 modelling a human SHANK3 duplication exhibit manic-like behaviour and seizures consistent with synapt

146 drug valproate, but not lithium, rescues the manic-like behaviour of Shank3 transgenic mice raising t

147 Delta19 mouse exhibits rapid mood cycling (a manic-like phenotype during the day followed by euthymia

148 exhibit rapid mood-cycling, with a profound manic-like phenotype emerging during the day following a

149 ence in the VTA of wild-type mice produces a manic-like phenotype.

150 report that the compound is able to reverse 'manic-like' behavior in two mouse models: amphetamine-in

151 ssion were used to code polarity at onset as manic, major depressive, or both (mania and major depres

152 e genes: Lunatic (Lfng), Radical (Rfng), and Manic (Mfng).

153 f mammalian fringe proteins (Lunatic [LFng], Manic [MFng], or Radical [RFng] Fringe) increased Delta1

154 tient or outpatient clinics after onset of a manic, mixed, or depressed episode.

155 nia or hypomania (13.3% compared with 1.2%), manic, mixed, or hypomanic episodes (9.2% compared with

156 iagnostic risk factor for the development of manic, mixed, or hypomanic episodes in the offspring of

157 ought to identify diagnostic risk factors of manic, mixed, or hypomanic episodes in the offspring of

158 ratio=2.12) were associated with subsequent manic, mixed, or hypomanic episodes.

159 ay contribute to greater risk of switch into manic, mixed, or hypomanic states.

160 Fifty participants with manic/mixed bipolar disorder (BP group) and 34 healthy c

161 fic treatments may aid in both depressed and manic mood states.

162 disorder (N=227), schizoaffective disorder (manic, N=110; depressed, N=55), their first-degree relat

163 parallel structures of mixed states based on manic or depressive episodes.

164 r severity, improve response to treatment of manic or depressive symptoms, or reduce suicidality.

165 ar disorder (i.e., a history of at least one manic or hypomanic episode with euphoric mood) as well a

166 ntecedents to adolescent depression to index manic or hypomanic episode.

167 disorder, and 310 met DSM-IV criteria for a manic or hypomanic episode.

168 ar I disorder who had recently experienced a manic or hypomanic episode.

169 hat in the high-risk offspring, subthreshold manic or hypomanic episodes (hazard ratio=2.29), major d

170 Only subthreshold manic or hypomanic episodes (hazard ratio=7.57) were ass

171 Subthreshold manic or hypomanic episodes were a diagnostic risk facto

172 ated according to the characteristics of the manic or hypomanic episodes, and present methods for val

173 together are characterised by depressive and manic or hypomanic episodes.

174 e or recurrence of mood episodes in recently manic or hypomanic patients with bipolar I disorder.

175 with tendencies to switch from depressive to manic or hypomanic phases.

176 essive symptoms are at least as disabling as manic or hypomanic symptoms at corresponding severity le

177 The potential for manic or hypomanic symptoms to emerge after sleep depriv

178 al depressive symptoms, but not subsyndromal manic or hypomanic symptoms, are associated with signifi

179 more disabling than corresponding levels of manic or hypomanic symptoms; (2) subsyndromal depressive

180 iagnosis of bipolar I disorder and a current manic or mixed episode (confirmed by the Structured Clin

181 ted during their first hospitalization for a manic or mixed episode and were evaluated using diagnost

182 lacebo for treatment of patients in an acute manic or mixed episode of bipolar disorder.

183 ients achieving symptomatic remission from a manic or mixed episode of bipolar I disorder (Young Mani

184 METHOD: Adults with an acute manic or mixed episode per DSM-IV-TR criteria were enrol

185 ed 262 bipolar disorder patients in an acute manic or mixed episode to aripiprazole, 30 mg/day (reduc

186 ears after their first hospitalization for a manic or mixed episode to assess timing and predictors o

187 s following an initial hospitalization for a manic or mixed episode.

188 adolescents 13-17 years of age with an acute manic or mixed episode.

189 not meet the DSM-IV duration criteria for a manic or mixed episode.

190 -label acute treatment with olanzapine for a manic or mixed episode.

191 atment of bipolar disorder patients in acute manic or mixed episodes and was safe and well tolerated

192 ety of olanzapine for the treatment of acute manic or mixed episodes associated with bipolar disorder

193 mg/day) to divalproex (500-2500 mg/day) for manic or mixed episodes of bipolar disorder (N=251).

194 t of patients hospitalized for acute bipolar manic or mixed episodes.

195 efined as current DSM-IV bipolar I disorder (manic or mixed phase) with at least one cardinal mania c

196 pe was defined as DSM-IV bipolar I disorder (manic or mixed) with at least 1 cardinal symptom (elatio

197 to 18 years of age with bipolar I disorder, manic or mixed, were recruited at 20 centers in the Unit

198 there was at least one family member with a manic or psychotic episode with an onset within 6 weeks

199 time of assessment, bipolar subtype (mixed, manic, or depressed), and treatment group (placebo or va

200 oportion of clinical visits spent depressed, manic, or euthymic in patients with bipolar disorder.

201 robability that an individual was depressed, manic, or euthymic.

202 ely half of visits, patients had depressive, manic, or hypomanic symptoms.

203 tions with attention deficits or depressive, manic, or obsessive-compulsive symptoms.

204 a compound that induces relapse in remitted manic patients and mood elevation in normal subjects.

205 the depressed sample had lower activity than manic patients.

206 nsonism and cognitive decline (P/CD) in some manic patients.

207 nd poor impulse control are hallmarks of the manic phase of bipolar disorder but are also present dur

208 ars with first episode DSM-IV BP-I, mixed or manic phase, with 1 or both cardinal symptoms (elation o

209 ejected the link to prodromal depressive and manic phases, and reduced the emphasis on thought disord

210 ay, and amphetamine hyperlocomotion, an anti-manic predictive assay.

211 ure of mixed states studied as predominantly manic, predominantly depressive, and across both manic a

212 r premorbid occupational status, and initial manic presentation.

213 The CT group also coped better with manic prodromes at 12 months.

214 5 with affective psychosis, 13 of whom had a manic psychosis) and 22 healthy control subjects.

215 wing disorders: major depressive, dysthymic, manic, psychotic, panic, separation anxiety, overanxious

216 The risk of manic relapse was not significantly associated with cont

217 were taking an antidepressant at the time of manic relapse.

218 5 (18%) of the 84 subjects had experienced a manic relapse; only six of these subjects were taking an

219 relative risk=0.65, 95% CI=0.50 to 0.84) and manic relapses (relative risk=0.62, 95% CI=0.40 to 0.95)

220 ening of TH activity during the day reverses manic-related behaviors in ClockDelta19 mice.

221 s were not explained by comorbidity or other manic spectrum symptoms.

222 with stressors or recover from depressive or manic states.

223 The manic subjects showed worse overall recognition of facia

224 examined the risk of antidepressant-induced manic switch in patients with bipolar disorder treated e

225 No patient had a manic switch or was hospitalized for a switch.

226 bitors and bupropion may have lower rates of manic switch than tricyclic and tetracyclic antidepressa

227 Manic switching occurred only in bipolar depression but

228 r BP-I and BP-II and with most increments in manic symptom severity for BP-I.

229 ent with antidepressants may lead to greater manic symptom severity.

230 ich remained significant after adjusting for manic symptom severity.

231 Manic symptomatology, especially syndromal, was less fre

232 red sample of the Longitudinal Assessment of Manic Symptoms (LAM) study.

233 ed youth from the Longitudinal Assessment of Manic Symptoms (LAMS) study (n = 85) and healthy youth (

234 regulation in the Longitudinal Assessment of Manic Symptoms (LAMS) study.

235 ffective lability, and proximal subsyndromal manic symptoms (p<0.05).

236 Forty-two adolescents with three core manic symptoms and no psychiatric diagnosis, and 126 ado

237 -label trial of divalproex sodium to control manic symptoms and to discern the effect of divalproex s

238 ted with mixed amphetamine salts after their manic symptoms are stabilized with divalproex sodium.

239 These data suggest that minimal manic symptoms at baseline coexisting with otherwise ful

240 ric disorders and severity of depressive and manic symptoms at intake in preschool offspring of paren

241 Residual depressive or manic symptoms at recovery and proportion of days depres

242 Residual manic symptoms at recovery and proportion of days of ele

243 spectrum disorder in part through increased manic symptoms at the visit prior to conversion; earlier

244 Accumulating evidence indicates that manic symptoms below the threshold for hypomania (mixed

245 d as depressive or manic, but depressive and manic symptoms can combine in the same episode.

246 Subsyndromal manic symptoms during bipolar I or II depression demarca

247 ine the frequency and clinical correlates of manic symptoms during episodes of bipolar depression.

248 er prevalence of depressive relative to hypo/manic symptoms during the course of BD illness and the h

249 in family-focused treatment had less severe manic symptoms during year 2 than did those in enhanced

250 Children and adolescents who present with manic symptoms frequently do not meet the full DSM-IV cr

251 ipolar II disorder and concurrent ADHD whose manic symptoms had been stabilized through treatment wit

252 ive episodes are accompanied by subsyndromal manic symptoms in bipolar I and II disorders.

253 ness and the high prevalence of subthreshold manic symptoms in both BD and UD depression.

254 there was significantly less fluctuation in manic symptoms in the CT group.

255 tence or rapid alternation of depressive and manic symptoms in the same episode may indicate a more s

256 ention might reduce the risk of hypomanic or manic symptoms in women at risk of developing bipolar di

257 later developed a bipolar spectrum disorder, manic symptoms increased up to the point of conversion.

258 Manic symptoms often accompany bipolar depressive episod

259 d disorder, respectively, and depressive and manic symptoms predicted 2.7-fold and 2.3-fold increases

260 In all disorders, depression improved and manic symptoms remained low across the 20 years.

261 t sample from the Longitudinal Assessment of Manic Symptoms study (LAMS) (n = 55, age = 13.7, SD = 1.

262 ere able to estimate positive, negative, and manic symptoms that showed correlations ranging from r =

263 There was less specificity of manic symptoms that tended to predict all levels of the

264 depression, family history, and the types of manic symptoms that were present during the most serious

265 No significant side effects or worsening of manic symptoms was observed.

266 In the same model, greater severity of manic symptoms was positively associated with higher fra

267 Time with manic symptoms was reduced with lithium, but not lamotri

268 Fractionation revealed that (hypo)manic symptoms were associated with hyperconnectivity in

269 Individuals having manic symptoms were at significantly greater risk for th

270 Participants who had more severe manic symptoms were more likely to receive antiepileptic

271 presented with two or three protocol-defined manic symptoms were randomly assigned to 6 weeks of doub

272 ease in number of visits with depressive and manic symptoms with increased time in study.

273 The Young Mania Rating Scale (for manic symptoms) and the Clinical Global Impression of im

274 res included time to relapse, depressive and manic symptoms, and medication adherence.

275 In bipolar depression accompanied by manic symptoms, antidepressants do not hasten time to re

276 Significant improvement in manic symptoms, assessed by the Young Mania Rating Scale

277 h BP-NOS, subjects with BP-I had more severe manic symptoms, greater overall functional impairment, a

278 h bipolar depressed episodes had concomitant manic symptoms, most often distractibility, flight of id

279 dependence, with no concurrent psychotic or manic symptoms, no use of concurrent psychotropic medica

280 of the most potent and specific triggers of manic symptoms, studies are not available on the effecti

281 ss history at baseline of severe depression, manic symptoms, suicidality, subsyndromal mood episodes,

282 g ketamine and 1 receiving placebo developed manic symptoms.

283 enrollment and were assessed for concomitant manic symptoms.

284 rapy were more effective for depressive than manic symptoms.

285 oup therapy patients had more depressive and manic symptoms.

286 e episode accompanied by > or = 2 concurrent manic symptoms.

287 outcomes included changes in depressive and manic symptoms.

288 had moderate depression and no hypomanic or manic symptoms.

289 ression without increased risk of developing manic symptoms.

290 ticipants were screened at baseline for five manic symptoms: elevated mood, decreased need for sleep,

291 animal behavioral alterations reminiscent of manic symptoms; these complex behaviors probably depend

292 GluR1/2 receptors in mediating facets of the manic syndrome and offer avenues for the development of

293 l disturbance considered foundational to the manic syndrome.

294 nce in liability to mania is specific to the manic syndrome.

295 ng speed, rather than strictly depressive or manic syndromes can provide more homogeneous samples for

296 defined schizophrenic, schizoaffective, and manic syndromes share genetic risk factors.

297 g to RDC schizophrenic, schizoaffective, and manic syndromes.

298 ematic care programs were more effective for manic than depressive symptoms, whereas family therapy a

299 ates of violent crime by clinical subgroups (manic vs depressive or psychotic vs nonpsychotic).

300 order (z=-0.77) to schizoaffective disorder (manic z=-1.08; depressed z=-1.25) to schizophrenia (z=-1