ライフサイエンスコーパス: depressed patient

1 epression (recurrent depressive episodes) in depressed patients.

2 versive sight and taste stimuli in recovered depressed patients.

3 subunit-containing nAChRs (beta2*-nAChRs) in depressed patients.

4 te measures of recurrence risk in previously depressed patients.

5 m structural abnormalities commonly found in depressed patients.

6 Orexins are altered in anxious and depressed patients.

7 nd functional changes in the brains of older depressed patients.

8 not recruit representative treatment-seeking depressed patients.

9 ities in 5-HTT might be present in recovered depressed patients.

10 effects of psilocybin, and are the first in depressed patients.

11 vitamins in the clinical evaluation of older depressed patients.

12 model of depression and in brain tissue from depressed patients.

13 LDN5 expression was also decreased in NAc of depressed patients.

14 pitalization and emergency room visits among depressed patients.

15 sociated with the expression of psychosis in depressed patients.

16 ction as well as to monitor the treatment of depressed patients.

17 may be related to affective dysregulation in depressed patients.

18 ese structures during waking to REM sleep in depressed patients.

19 essed patients tended to be younger than non-depressed patients.

20 se of treatment and determining remission in depressed patients.

21 es and complaints of nonrestorative sleep in depressed patients.

22 extent of this activation was greater in the depressed patients.

23 non-REM sleep differ in healthy subjects and depressed patients.

24 Actors can effectively portray depressed patients.

25 e higher than normal in the basal ganglia of depressed patients.

26 tive protein (CRP)) are reliably elevated in depressed patients.

27 aversive stimuli, which are all abnormal in depressed patients.

28 nitive measures over 8 weeks of treatment in depressed patients.

29 ve episode and the pattern of change seen in depressed patients.

30 y defined medial area of the frontal pole in depressed patients.

31 clinical and cognitive outcomes, in elderly depressed patients.

32 that occurs between healthy participants and depressed patients.

33 ntidepressant actions in treatment-resistant depressed patients.

34 in rodent models and in treatment-refractory depressed patients.

35 frontal cortex, is dramatically increased in depressed patients.

36 raised about the use of rapamycin in immuno-depressed patients.

37 owing treatment with citalopram in currently depressed patients.

38 of SSRI treatment on 5-HT1A autoreceptors in depressed patients.

39 In 65 unmedicated depressed patients 15-min resting-state EEGs were record

40 Twelve late-onset acutely depressed patients, 15 patients fully remitted from majo

41 Of the 18 depressed patients, 16 were considered responders 4-6 mo

42 Ninety-two individuals (68 depressed patients, 24 never-depressed control subjects)

43 Sixty-two medication-free unipolar depressed patients (38 were currently depressed, and 24

44 Sixty-four medication-free unipolar depressed patients: 39 currently depressed and 25 in rem

45 Nineteen treatment-resistant depressed patients, 53% of whom were classified as havin

46 yze magnetic resonance imaging scans from 30 depressed patients 59 to 78 years old and 47 nondepresse

47 e of hippocampal structural abnormalities in depressed patients, abnormal hippocampal functioning has

48 ponse in clinical practice, and talking with depressed patients about the risks and benefits of antid

49 While both healthy and depressed patients activated anterior paralimbic structu

50 art rate variability recovery is impaired in depressed patients after ACS.

51 ine whether symptoms experienced by formerly depressed patients after at least 8 weeks of remission c

52 Depressed patients also exhibited significant bilateral

53 itively correlated with loss aversion in the depressed patients, also implicating impairment in regul

54 sed pharmacotherapy guidelines for suicidal, depressed patients-an important public health population

55 Ten depressed patients and 11 healthy control subjects under

56 utral words were presented to 10 unmedicated depressed patients and 12 healthy comparison subjects in

57 Twelve medication-free depressed patients and 13 healthy subjects underwent pol

58 in 20 unmedicated, fully recovered unipolar depressed patients and 20 age- and gender-matched compar

59 participated: 20 medication-naive currently depressed patients and 20 medication-free recovered pati

60 out the 24H, we studied 26 healthy drug-free depressed patients and 26 healthy age- and sex-matched c

61 Thirty-three elderly depressed patients and 27 nondepressed comparison subjec

62 The study group comprised 45 depressed patients and 45 age- and gender-matched contro

63 ) brain scans were acquired for 15 drug-free depressed patients and 46 age- and gender-matched health

64 orphometric MRI analysis was conducted in 73 depressed patients and 73 matched comparison subjects wi

65 d the ratio of cortisol to DHEA in drug-free depressed patients and a matched comparison group.

66 ontal pole volume was first compared between depressed patients and comparison subjects by subdivisio

67 Depressed patients and comparison subjects did not diffe

68 While the depressed patients and comparison subjects did not diffe

69 of variance techniques were used to compare depressed patients and comparison subjects on hippocampa

70 d subdivisions of human frontal pole between depressed patients and comparison subjects using both un

71 l white matter hyperintensity burden between depressed patients and comparison subjects.

72 We compared reward responsiveness between depressed patients and control subjects, as well as high

73 everal studies reporting differences between depressed patients and controls.

74 The authors investigated whether depressed patients and healthy comparison subjects have

75 potential of [11C]DASB between the recovered depressed patients and healthy comparison subjects in an

76 There were no differences between depressed patients and healthy comparison subjects in hi

77 epressive disorder in a sample consisting of depressed patients and healthy controls.

78 s in parietal cortex compared to nonsuicidal depressed patients and healthy controls.

79 EM sleep relative to presleep wakefulness in depressed patients and healthy subjects.

80 e next hour in 31 medication-free, recovered depressed patients and in 31 matched healthy comparison

81 authors measured this increase in recovered depressed patients and in a healthy comparison group.

82 aternal depression is similar to patterns in depressed patients and in individuals with risk for depr

83 -13 produces rapid antidepressant actions in depressed patients and in preclinical rodent models.

84 at SSRI treatment increases cortical GABA in depressed patients and suggest that this results from an

85 I disorder, 58 age- and sex-matched unipolar depressed patients, and 58 matched healthy controls.

86 th a suicide attempt history, 47 nonsuicidal depressed patients, and 75 healthy controls participated

87 and acute-phase proteins, have been found in depressed patients, and administration of inflammatory s

88 his model: briefly with respect to currently depressed patients, and in more detail with respect to i

89 ymic unipolar patients in remission, acutely depressed patients, and never-depressed volunteers were

90 ive deficits in patients with schizophrenia, depressed patients, and nonpatient comparison subjects.

91 primary care have known that only 10-50% of depressed patients are adequately treated, primarily bec

92 ants offer therapeutic benefit, about 35% of depressed patients are not adequately treated, creating

93 Remission in depressed patients, as defined by a reduction in symptom

94 f SGK1 mRNA in peripheral blood of drug-free depressed patients, as well as in the hippocampus of rat

95 rolled trials to compare suicide rates among depressed patients assigned to an SSRI, other antidepres

96 nadherence in a gradient fashion: 15% of non-depressed patients (BDI score 0 to 4), 29% of mildly dep

97 d patients (BDI score 0 to 4), 29% of mildly depressed patients (BDI score 10 to 16), and 37% of pati

98 ance of an emotion regulation paradigm in 21 depressed patients before and after 2 months of antidepr

99 ance of an emotion regulation paradigm in 21 depressed patients before and after 2 months of antidepr

100 In severely depressed patients before and after electroconvulsive th

101 trations were measured in 11 medication-free depressed patients before initiation of treatment with S

102 ity within and between the DMN and CEN in 17 depressed patients, before and after a 5-week course of

103 ver, whether the same early effect occurs in depressed patients, before changes in mood.

104 Although the average depressed patient benefits moderately from cognitive-beh

105 In the depressed patients, beta2*-nAChR availability was signif

106 amygdala responses to sad faces in currently depressed patients but did not alter responses to fearfu

107 ugs, a mental health referral, or both among depressed patients but had no effect on mental health at

108 In depressed patients but not comparison subjects, volumes

109 st, produces rapid antidepressant effects in depressed patients, but the mechanisms underlying the th

110 apid and sustained antidepressant actions in depressed patients, but the precise cellular mechanisms

111 ct to normalize abnormal neural responses in depressed patients by increasing brain activity to posit

112 t cognitive improvement lasts and to compare depressed patients' cognitive status with that of nondep

113 ty in frontoparietal regions and thalamus in depressed patients compared with healthy subjects.

114 al connectivity to reveal subgroups among 80 depressed patients completing resting state fMRI.

115 The authors' goal was to determine what depressed patients consider important in defining remiss

116 Use of antidepressants by depressed patients declined by 8%; use of antihypertensi

117 flammatory cytokine shown to be increased in depressed patients, decreases neurogenesis in human hipp

118 mbic and anterior paralimbic cortex and that depressed patients demonstrate increases in electroencep

119 In addition, depressed patients demonstrated a different pattern of i

120 Depressed patients demonstrated higher cortisol secretio

121 ve to the comparison subjects, the recovered depressed patients demonstrated significantly higher 5-H

122 Relative to comparison subjects, depressed patients demonstrated significantly less bilat

123 model that white matter ischemia in elderly depressed patients disrupts brain mechanisms of affectiv

124 Most depressed patients don't respond to their first drug tre

125 estigated whether this effect is apparent in depressed patients early in treatment, prior to changes

126 Our findings indicate that depressed patients, especially those with anhedonic feat

127 During the study year, 36% of the depressed patients filled a benzodiazepine prescription

128 The sparse comorbidity map confirmed that depressed patients frequently suffer from both psychiatr

129 Relative to healthy comparison subjects, the depressed patients had attenuated activation in the regi

130 Depressed patients had markedly lower baseline KCCQ summ

131 Severely depressed patients had significant increases in mean aro

132 Compared with healthy controls, depressed patients had significantly increased intracort

133 Depressed patients had smaller right hippocampal volume

134 Severely depressed patients (HAM-D score >24) also received antid

135 of the glucocorticoid receptor (GR) found in depressed patients has been causally implicated in depre

136 pothesized that since psychomotor slowing in depressed patients has been linked to reduced dopaminerg

137 In multivariable modeling, depressed patients have a three-fold greater risk of dyi

138 nal connection in stress, many (but not all) depressed patients have alterations in the components of

139 Depressed patients have been found to have higher levels

140 n brain, but results from studies of acutely depressed patients have been inconsistent.

141 Depressed patients have diminished VZV-CMI responses to

142 Depressed patients have lower beta2*-nAChR availability

143 r, prior hippocampal morphometric studies in depressed patients have neither reported nor controlled

144 al abnormality in this brain structure among depressed patients have produced mixed results.

145 Among currently depressed patients, higher leptin was associated with ke

146 Depressed patients homozygous for the A allele of NTRK2

147 on represents the placebo effect, since many depressed patients improve when treated with either medi

148 EI VFQ-25 scores were significantly lower in depressed patients in all subscales except driving and c

149 tions to better meet the healthcare needs of depressed patients in primary care by improving the reco

150 ive function including executive function in depressed patients in randomised placebo-controlled clin

151 ression subgroup that is distinct from other depressed patients in terms of demographics, psychiatric

152 ological processes that are dysfunctional in depressed patients include alterations in self-referenti

153 natomical and behavioral features similar to depressed patients, including dysregulation of circadian

154 , one of the most efficacious treatments for depressed patients, increases the levels of transcriptio

155 primary care with a heterogeneous sample of depressed patients introduces new challenges related to

156 ntal metabolism from waking to NREM sleep in depressed patients is further evidence for a dynamic sle

157 Antidepressant treatment of depressed patients is strikingly inadequate, even in sui

158 in six regions of postmortem brain tissue of depressed patients matched with controls for time-of-dea

159 Baseline metabolism in successfully treated depressed patients may predict vulnerability to future e

160 tamen, pallidum, and nucleus accumbens in 53 depressed patients (mean age: 44.1 years, 13.8 SD; 52% f

161 functioning, and quality of life (QOL) from depressed patients (N = 2280) at entry and exit of level

162 Depressed patients (n=415) were assessed prospectively f

163 arison of the functional connectivity in 185 depressed patients not receiving medication and 182 pati

164 patients scored significantly worse than non-depressed patients on all components of both the questio

165 across DMN nodes, as previously reported in depressed patients on average.

166 le predicted risk of suicidal behavior among depressed patients over the 2-year period.

167 Of 48,277 depressed patients participating in the trials, 77 commi

168 irments in Theory of Mind (ToM) abilities in depressed patients, particularly in relation to tasks in

169 Depressed patients performed significantly worse than co

170 Depressed patients performed worse than healthy subjects

171 Depressed patients performed worse than healthy subjects

172 ral emotional neural system during waking in depressed patients persists into NREM sleep.

173 Most depressed patients prefer psychotherapy over antidepress

174 ng, long-lasting antidepressant responses in depressed patients provides a unique opportunity to inve

175 Among depressed patients, rates of achieving the primary outco

176 In phase 1, depressed patients received high-dose ECT (at six times

177 ngs support the hypothesis that anhedonia in depressed patients reflects the inability to sustain eng

178 enual cingulate activity was observed in the depressed patients relative to the nondepressed comparis

179 trastriate visual regions was evident in the depressed patients, relative to the comparison subjects.

180 al magnetic stimulation (rTMS) in bipolar II depressed patients remain unclear.

181 of even the "clinically improved" subset of depressed patients remained consistently worse than the

182 ious studies have found that few chronically depressed patients remit with antidepressant medications

183 Depressed patients report alleviation of core symptoms w

184 Depressed patients report the alleviation of major depre

185 tions have been developed, and two-thirds of depressed patients respond to single-modality treatment;

186 Depressed patients scored significantly worse than non-d

187 atients may not be representative of typical depressed patients seeking treatment.

188 Randomized controlled trials in depressed patients selected for elevated suicidal risk a

189 Depressed patients show abnormalities in brain connectiv

190 Our results demonstrate that depressed patients show accelerated cellular aging accor

191 However, depressed patients show impairments in this system.

192 Depressed patients show preferential processing of negat

193 Depressed patients showed attenuated neural responses to

194 For P3b, depressed patients showed decreased right-lateralized ac

195 Additionally, depressed patients showed greater activation in bilatera

196 Depressed patients showed greater REM sleep percentages.

197 However, in post hoc analyses, depressed patients showed hypermetabolism in these areas

198 Consistent with previous findings, depressed patients showed impaired spatial navigation.

199 Depressed patients showed larger decreases than healthy

200 Relative to healthy subjects, depressed patients showed less of a decrease in relative

201 Depressed patients showed smaller decreases than healthy

202 hip in the diagnosis of anxiety disorders in depressed patients, stipulating that anxiety disorders c

203 led an atypical pattern of connectivity in a depressed patient subset that would be overlooked in gro

204 rn of hippocampal surface deformation in the depressed patients suggested specific involvement of the

205 d TPI identified an increased BTP in midlife depressed patients, suggesting early and subtle vascular

206 s aversion correlated with each other in the depressed patients, suggesting that a common pathophysio

207 tamine administration in treatment-resistant depressed patients suggests a possible new approach for

208 Among depressed patients, superiority assessment of the compos

209 died serotonergic response in ventral PFC in depressed patients surviving a high-lethality suicide at

210 Depressed patients tended to be younger than non-depress

211 right superior frontal gyrus white matter of depressed patients than comparison subjects.

212 dial orbitofrontal cortex was thinner in the depressed patients than in the comparison subjects.

213 l-DHEA ratio was significantly higher in the depressed patients than in the healthy comparison subjec

214 navigation deficits previously documented in depressed patients to abnormal hippocampal functioning u

215 portant that we stratify clinical studies of depressed patients to compare melancholic and atypical s

216 udies of antidepressants were applied to the depressed patients to determine how many would have qual

217 his study determined if actors could portray depressed patients to establish the interrater reliabili

218 t that biases in information processing lead depressed patients to make unrealistically negative judg

219 Depressed patients treated in mental health settings com

220 ly by means of telepsychiatry to outcomes of depressed patients treated in person.

221 This study estimated the proportion of depressed patients treated in routine clinical practice

222 d benzodiazepine use among a large sample of depressed patients treated in U.S.

223 measure of spatial memory was assessed in 30 depressed patients (unipolar and bipolar) and 19 normal

224 elevant in antidepressant treatment of adult depressed patients up to 65 years of age.

225 Actors portrayed depressed patients using scripts derived from HDRS asses

226 nistration modulates emotional processing in depressed patients very early in treatment, before chang

227 the pathogenesis of depression and underlies depressed patients' vulnerability to comorbid medical co

228 otential benefits of zinc supplementation in depressed patients, warrant further investigation.

229 Before treatment, functional connectivity in depressed patients was abnormally elevated within the DM

230 ty in the left medial frontal pole volume in depressed patients was demonstrated.

231 After adjustment for potential confounders, depressed patients were at risk for significant worsenin

232 ccipital cortex GABA concentrations in eight depressed patients were measured by using proton magneti

233 Depressed patients were more likely to have sex for mone

234 In this study, thirty-eight bipolar II depressed patients were randomly assigned into three gro

235 Thirty-six depressed patients were randomly assigned to receive DHA

236 Only 16 (22%) of the depressed patients were receiving antidepressant treatme

237 Thirty-three depressed patients were recruited through primary care c

238 ejection fraction or treatment, except that depressed patients were significantly less likely to be

239 Thirty-two currently depressed patients were treated with the antidepressant

240 cotropin secretion levels can be observed in depressed patients, whereas controls show no such effect

241 this drug might be attenuated or blocked in depressed patients who carry the loss of function Met al

242 nts with comorbid medical disorders than for depressed patients who did not have comorbid medical dis

243 Depressed patients who did not improve clinically showed

244 Pupil dilation data suggest that those depressed patients who expend more effort to reappraise

245 f selective serotonin reuptake inhibitors in depressed patients who experience an acute MI might redu

246 participants 60 years or older, including 15 depressed patients who had attempted suicide, 18 depress

247 essed patients who had attempted suicide, 18 depressed patients who had never attempted suicide (depr

248 ychomotor slowing may identify a subgroup of depressed patients who have a dopaminergic deficit that

249 ght advantages over lithium augmentation for depressed patients who have experienced several failed m

250 c and clinical features of a large cohort of depressed patients who met DSM-IV criteria for atypical

251 muscarinic scopolamine occurred in currently depressed patients who predominantly had poor prognoses.

252 For 1,137 depressed patients who received a new antidepressant pre

253 ministration data between 2004 and 2009 from depressed patients who received a prescription for cital

254 Depressed patients who received placebo showed reduced r

255 reporting increased activation in the ACC of depressed patients who respond to a wide range of therap

256 Brain purine levels are low in female depressed patients who respond to treatment with fluoxet

257 acy and were conducted in carefully selected depressed patients who were antidepressant medication fr

258 the North of England, we recruited severely depressed patients, who were diagnosed as having unipola

259 r important clinical questions such as which depressed patients will respond to treatment, which abst

260 Depressed patients with a history of a high-lethality su

261 Depressed patients with a history of suicide attempt sho

262 der risk, and impaired emotion regulation in depressed patients with a history of suicide attempts.

263 Forty-five depressed patients with a suicide attempt history, 47 no

264 map cortical gray matter deficits in elderly depressed patients with an illness onset after age 60 (l

265 No difference was found between depressed patients with and without ADM treatment (HR: 0

266 kelihood of probable depressive disorders in depressed patients with and without comorbid substance m

267 self-reported work productivity improved in depressed patients with antidepressant treatment even af

268 reduced fractional anisotropy compared with depressed patients with at least one copy of the G allel

269 series of a priori hypotheses regarding how depressed patients with atypical features (n = 130) woul

270 ntal magnetic resonance imaging procedure in depressed patients with bipolar disorder (BPD).

271 Depressed patients with bipolar disorder and comorbid an

272 ivided between the 2 sites were 58 currently depressed patients with bipolar I disorder, 58 age- and

273 authors compared the acute outcome of ECT in depressed patients with borderline personality disorder,

274 thin cancer groupings, and the proportion of depressed patients with cancer receiving potentially eff

275 Depressed patients with comorbid medical disorders tend

276 n and specialty counseling were similar, for depressed patients with comorbid medical disorders than

277 Among the depressed patients with comorbid medical disorders, the

278 s and improving cardiovascular biomarkers in depressed patients with coronary heart disease.

279 ts without generalized anxiety disorder, the depressed patients with DSM-IV and modified generalized

280 f LFMS in a large group of stably medicated, depressed patients with either BPD (n = 41) or major dep

281 Depressed patients with greater baseline suicidal ideati

282 Depressed patients with heart disease have poorer medica

283 ceptor availability characterizes a group of depressed patients with high levels of dysfunctional att

284 nin 5-HT(2A) receptor binding in unmedicated depressed patients with high scores on the Dysfunctional

285 glutamate may be preferentially effective in depressed patients with increased inflammation as measur

286 , brain activity was compared in unmedicated depressed patients with increased or decreased appetite

287 ring the neural responses to food stimuli of depressed patients with increased versus decreased appet

288 depression may improve the poor prognosis of depressed patients with ischemic heart disease.

289 kg(-1) intravenously) was administered to 11 depressed patients with MDD.

290 der, and total brain volume were controlled, depressed patients with psychosis had a significantly sm

291 Under usual care conditions, depressed patients with substance misuse had an increase

292 oughts, within 1 day and for up to 1 week in depressed patients with suicidal ideation.

293 eable, better informed, and less anxious and depressed patients, with a better mental well-being.

294 significantly smaller medial frontal pole in depressed patients, with a negative correlation of disea

295 clinically significant suicidal ideation in depressed patients within 24 hours compared with midazol

296 treatment but worse depression outcomes than depressed patients without comorbid medical illness.

297 Compared to the depressed patients without generalized anxiety disorder,

298 There were no differences between depressed patients without psychosis and healthy compari

299 tly smaller mean amygdala volume relative to depressed patients without psychosis and healthy compari

300 Approximately one-sixth of the 346 depressed patients would have been excluded from an effi