ライフサイエンスコーパス: depressed patient

1 ent response were measured in 72 unmedicated depressed patients.

2 frontal cortex, is dramatically increased in depressed patients.

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

4 owing treatment with citalopram in currently depressed patients.

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

6 epression (recurrent depressive episodes) in depressed patients.

7 versive sight and taste stimuli in recovered depressed patients.

8 on were partially abolished in more severely depressed patients.

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

10 te measures of recurrence risk in previously depressed patients.

11 m structural abnormalities commonly found in depressed patients.

12 f the dysregulated inflammatory responses in depressed patients.

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

14 not recruit representative treatment-seeking depressed patients.

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

16 ircadian rhythms in the postmortem brains of depressed patients.

17 pportunities for restoring energy balance in depressed patients.

18 vitamins in the clinical evaluation of older depressed patients.

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

20 pitalization and emergency room visits among depressed patients.

21 sociated with the expression of psychosis in depressed patients.

22 in at-risk populations or its recurrence in depressed patients.

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

24 may be related to affective dysregulation in depressed patients.

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

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

27 se of treatment and determining remission in depressed patients.

28 es and complaints of nonrestorative sleep in depressed patients.

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

30 tivity and network function in the brains of depressed patients.

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

32 Actors can effectively portray depressed patients.

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

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

35 Orexins are altered in anxious and depressed patients.

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

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

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

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

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

41 clinical and cognitive outcomes, in elderly depressed patients.

42 that occurs between healthy participants and depressed patients.

43 ntidepressant actions in treatment-resistant depressed patients.

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

45 Twenty-three depressed patients (14 females, age: 50.17 +/- 12.72 yea

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

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

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

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

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

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

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

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

54 While both healthy and depressed patients activated anterior paralimbic structu

55 apid and sustained antidepressant actions in depressed patients, addressing a major unmet need for th

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

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

58 Depressed patients also exhibited significant bilateral

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

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

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

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

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

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

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

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

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

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

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

70 c abnormalities have been widely reported in depressed patients and animal models.

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

72 Depressed patients and comparison subjects did not diffe

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

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

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

76 everal studies reporting differences between depressed patients and controls.

77 eased during the admission in this sample of depressed patients and early patterns of actigraphically

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

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

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

81 line causal connectivity differences between depressed patients and healthy controls were also evalua

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

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

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

85 innate and adaptive immune systems occur in depressed patients and hinder favorable prognosis, inclu

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

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

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

89 -13 produces rapid antidepressant actions in depressed patients and in preclinical rodent models.

90 ted disorders remain unclear, but studies in depressed patients and rodent models are beginning to yi

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

92 ck gene expression, corticoptropin levels in depressed patients and the temporal light intensity patt

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

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

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

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

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

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

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

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

101 we first discuss sex differences observed in depressed patients, as well as animal models that reveal

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

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

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

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

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

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

108 In severely depressed patients before and after electroconvulsive th

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

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

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

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

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

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

115 In depressed patients but not comparison subjects, volumes

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

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

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

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

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

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

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

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

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

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

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

127 Depressed patients demonstrated higher cortisol secretio

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

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

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

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

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

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

134 Depressed patients, even after remission, might also ben

135 Therefore, depressed patients faced an even higher ICD risk when re

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

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

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

139 Depressed patients had markedly lower baseline KCCQ summ

140 Severely depressed patients had significant increases in mean aro

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

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

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

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

145 heral and central markers of inflammation in depressed patients has not been established.

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

147 Depressed patients have been found to have higher levels

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

149 Depressed patients have diminished VZV-CMI responses to

150 Depressed patients have lower beta2*-nAChR availability

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

152 Depressed patients homozygous for the A allele of NTRK2

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

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

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

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

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

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

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

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

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

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

163 gested that posterior hippocampal volumes in depressed patients may be associated with antidepressant

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

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

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

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

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

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

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

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

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

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

174 Depressed patients performed significantly worse than co

175 Depressed patients performed worse than healthy subjects

176 Depressed patients performed worse than healthy subjects

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

178 Most depressed patients prefer psychotherapy over antidepress

179 Depressed patients present with motor activity abnormali

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

181 Among depressed patients, rates of achieving the primary outco

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

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

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

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

186 take months to take full effect, and ~30% of depressed patients remain treatment resistant.

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

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

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

190 Depressed patients report alleviation of core symptoms w

191 Depressed patients report the alleviation of major depre

192 pharmacological therapies, only the half of depressed patients respond to currently available treatm

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

194 Depressed patients scored significantly worse than non-d

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

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

197 Depressed patients show abnormalities in brain connectiv

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

199 However, depressed patients show impairments in this system.

200 Depressed patients show preferential processing of negat

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

202 Additionally, depressed patients showed greater activation in bilatera

203 Depressed patients showed greater REM sleep percentages.

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

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

206 Depressed patients showed larger decreases than healthy

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

208 Depressed patients showed smaller decreases than healthy

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

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

211 regulated homeostatic biological pathways in depressed patients, such as increased inflammation and d

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

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

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

215 Among depressed patients, superiority assessment of the compos

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

217 Depressed patients tended to be younger than non-depress

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

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

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

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

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

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

224 Depressed patients treated in mental health settings com

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

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

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

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

229 Actors portrayed depressed patients using scripts derived from HDRS asses

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

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

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

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

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

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

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

237 Depressed patients were more likely to have sex for mone

238 To test this hypothesis, depressed patients were pretreated with rapamycin, an mT

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

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

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

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

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

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

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

246 Depressed patients who did not improve clinically showed

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

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

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

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

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

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

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

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

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

256 Depressed patients who received placebo showed reduced r

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

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

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

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

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

262 Depressed patients with a history of suicide attempt sho

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

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

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

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

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

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

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

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

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

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

278 Depressed patients with greater baseline suicidal ideati

279 Depressed patients with heart disease have poorer medica

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

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

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

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

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

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

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

287 eutics can produce antidepressant effects in depressed patients with primary inflammatory disorders t

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

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

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

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

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

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

294 s rapid and robust antidepressant effects in depressed patients within hours of administration, often

295 action in depressed and treatment-resistant depressed patients within hours.

296 ed changes in HDAC1 expression in the NAc of depressed patients without antidepressant treatment in l

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