ライフサイエンスコーパス: depressive symptom

1 between subclinical thyroid dysfunction and depressive symptoms.

2 mechanistic role in inflammation-associated depressive symptoms.

3 othyroidism to reduce the risk of developing depressive symptoms.

4 s surveyed reported experiencing burnout and depressive symptoms.

5 ntal areas were associated with worsening of depressive symptoms.

6 decisional conflict and perceived stress or depressive symptoms.

7 n, and are associated with the trajectory of depressive symptoms.

8 rgets effective for two discrete clusters of depressive symptoms.

9 sruptive work environment and 35.4% reported depressive symptoms.

10 e nap duration would reduce the incidence of depressive symptoms.

11 between-area difference in the prevalence of depressive symptoms.

12 thyroidism in particular, is associated with depressive symptoms.

13 r QOL was significantly correlated with more depressive symptoms.

14 criteria based on diagnosis and severity of depressive symptoms.

15 ore volunteer activities, and possibly fewer depressive symptoms.

16 ation between arterial stiffness and risk of depressive symptoms.

17 structural connectivity explaining change in depressive symptoms.

18 kers mediated the association between PA and depressive symptoms.

19 linking volumetric reductions with worsening depressive symptoms.

20 lnerability for adversities such as maternal depressive symptoms.

21 ART initiation, 30% of participants reported depressive symptoms.

22 s, which may be a mechanism linking ELA with depressive symptoms.

23 f concentration of individuals reporting new depressive symptoms.

24 ncreased processing/gait speed, and relieved depressive symptoms.

25 % (n = 484) of the participants had incident depressive symptoms.

26 ayed significant negative relationships with depressive symptoms.

27 should be avoided to maximize improvement of depressive symptoms.

28 ity, course, and intrasubject variability of depressive symptoms.

29 sleep difficulties were associated with more depressive symptoms.

30 ose in life, optimism, resilient coping, and depressive symptoms.

31 sleep, nighttime sleep and daytime nap, and depressive symptoms.

32 brainstem volume mediates the seasonality of depressive symptoms.

33 focused on transient rather than persistent depressive symptoms.

34 ant confounders, including prenatal maternal depressive symptoms.

35 us edema, poorer physical function, and more depressive symptoms.

36 modestly worse health regarding obesity and depressive symptoms.

37 young children exposed to maternal prenatal depressive symptoms.

38 sed anxiety (-3.61%; P = 0.008) and possibly depressive symptoms (-1.14%; P = 0.05) increased mortali

39 vel >8%), obesity (body mass index >30), and depressive symptoms (2-item Patient Health Questionnaire

40 No associations were seen with postpartum depressive symptoms (7% of women) or with any of the per

41 osed to persistently high levels of maternal depressive symptoms across the perinatal period had smal

42 ere significantly associated with persistent depressive symptoms across the study period.

43 Seasonal differences in mood and depressive symptoms affect a large percentage of the gen

44 n significantly correlated with reduction in depressive symptoms after 8 weeks of treatment.

45 d neighborhood disorder, social cohesion and depressive symptoms among 50-year-olds in 16 different c

46 are mildly effective interventions to reduce depressive symptoms among adolescents.

47 thors examined the prevalence of burnout and depressive symptoms among North American psychiatrists,

48 paredness resource to mitigate post-disaster depressive symptoms among older survivors of the 2011 Gr

49 ighborhood disorder and social cohesion with depressive symptoms among persons aged 50 years or more

50 e nap was associated with lower incidence of depressive symptoms among the elderly after adjusting al

51 dinal association between sleep duration and depressive symptoms among the elderly in China.

52 89-0.97) was also negatively associated with depressive symptoms among the elderly.

53 Stool samples from 10 people with current depressive symptoms and 10 matched healthy control subje

54 abolites and inflammatory markers along with depressive symptoms and antidepressant treatment respons

55 icant improvements in a composite measure of depressive symptoms and cardiometabolic indices at 24 mo

56 derated the association between care partner depressive symptoms and care partner physical (B=0.05, P

57 d the association between postnatal maternal depressive symptoms and child attention problems.

58 ates relationships between prenatal maternal depressive symptoms and child behavior.

59 ted the relationship between third trimester depressive symptoms and child externalizing behavior in

60 469 mother-child pairs with data on maternal depressive symptoms and child neuroimaging at age 10.

61 Depressive symptoms and cognition were assessed prior to

62 We estimated the relationship between depressive symptoms and cumulative HIV incidence using a

63 We estimated the relationship between depressive symptoms and cumulative HIV incidence using a

64 x mediated the relationship between maternal depressive symptoms and externalizing behavior in boys,

65 velopment explained associations of ELA with depressive symptoms and externalizing problems.

66 ions to estimate associations between recent depressive symptoms and having a detectable viral load (

67 95% CI: 0.2, 4.5) of the association between depressive symptoms and HIV incidence.

68 Depressive symptoms and impaired physical functioning ar

69 A measures were associated with decreases in depressive symptoms and improvements in mental and physi

70 ificant associations between the severity of depressive symptoms and increased myeloid and CD4(+) T-c

71 wort (SJW) is used in the treatment of mild depressive symptoms and is known for its drug-drug inter

72 The association between depressive symptoms and missing an HIV visit (RR, 1.20;

73 icipants had information about self-reported depressive symptoms and no CVD history at baseline.

74 00 IU/d vitamin D for 12 mo had no effect on depressive symptoms and physical functioning in older pe

75 on; (2) Relative to the combined Z values of depressive symptoms and processing speed, sleep quality

76 e of spirituality on the association between depressive symptoms and QOL within survivor-care partner

77 ) receptor antagonist, can rapidly alleviate depressive symptoms and reduce suicidality, possibly by

78 Secondary outcomes at 2, 6 and 12 weeks were depressive symptoms and remission (PHQ-9 and Beck Depres

79 erstand these abnormalities in patients with depressive symptoms and syndromes.

80 e that glial hypofunction is associated with depressive symptoms and that antidepressants may normali

81 with the relation between sleep quality and depressive symptoms and the further moderation of gender

82 es of psychological distress (anxiety and/or depressive symptoms) and normalized characteristic path

83 emotional well-being (enjoyment of life and depressive symptoms), and social function (organizationa

84 ntial association between early exposure and depressive symptoms, and 3) the contributions of other k

85 Older DNAm age was related to greater depressive symptoms, and a significant indirect effect o

86 likelihood of poor blood pressure control or depressive symptoms, and a smaller percentage of the cha

87 s were considered (sociodemographic factors, depressive symptoms, and health behaviors).

88 subjects showed significant improvements in depressive symptoms, and healthy control subjects exhibi

89 Higher CRP/IL-6 were associated with future depressive symptoms, and higher depressive symptoms were

90 prospective cohort, we assessed disability, depressive symptoms, and HRQL before and at 3- to 6-mont

91 mated the magnitude of change in disability, depressive symptoms, and HRQL with hierarchical segmente

92 Disability, depressive symptoms, and impaired health-related quality

93 sive therapy, chronic GVHD and its symptoms, depressive symptoms, and improved overall survival.

94 nd between PD and major depressive disorder, depressive symptoms, and neuroticism.

95 ly low vitamin D status, clinically relevant depressive symptoms, and poor physical functioning.

96 individual differences in pain sensitivity, depressive symptoms, and reward processing.

97 somnia symptoms and coronary artery disease, depressive symptoms, and subjective well-being.

98 ycline may be an effective treatment of core depressive symptoms, and that further investigation of m

99 egiving status was significant in predicting depressive symptoms, and the interactions examining glob

100 tive impairment without dementia (CIND), and depressive symptoms, and we estimated the mediating effe

101 Validated items on burnout, depressive symptoms, and well being were included in the

102 ned as having any of the following: elevated depressive symptoms, antidepressant use, or depression h

103 1.02-1.06); existing comorbidities, such as depressive symptoms (AOR = 1.05, 95% CI 1.04-1.09); and

104 Recent depressive symptoms are a risk factor for unsuppressed v

105 Depressive symptoms are dynamic, however, and understand

106 It is uncertain whether depressive symptoms are independently associated with su

107 rlying the association of hyperglycemia with depressive symptoms are unknown.

108 past-year substance use and women's reported depressive symptoms as measured at the individual level.

109 of substances (alcohol and khat) and women's depressive symptoms as measured by the Patient Health Qu

110 fusivity and analyzed with maternal prenatal depressive symptoms as well as child behavior.

111 atment for adolescents with mild or moderate depressive symptoms as well as for at-risk adolescents t

112 ticipants had improvements in disability and depressive symptoms, as well as generic-physical, generi

113 fractional anisotropy (FA), whereas maternal depressive symptoms assessed prenatally or in childhood

114 The primary outcomes were the severity of depressive symptoms (assessed by PHQ-9 score) and the pr

115 ically significant reductions in anxiety and depressive symptoms at 3 months, and might be a feasible

116 Incident depression was defined as minimal depressive symptoms at baseline and clinically significa

117 ohort study of 123,045 men and women free of depressive symptoms at baseline who attended regular scr

118 hyroidism versus euthyroidism, adjusting for depressive symptoms at baseline, age, sex, education, an

119 0 years or older without clinically relevant depressive symptoms at baseline, treatment with vitamin

120 age 59.7 +/- 6.3 years; 35.8% women) free of depressive symptoms at baseline.

121 gle-time-point analyses showed that maternal depressive symptoms at child age 2 months were associate

122 licited a significantly greater reduction in depressive symptoms at the primary efficacy endpoint (24

123 al disinhibition, major depressive disorder, depressive symptoms, autism spectrum disorder, psychosis

124 d assessed anxiety [Beck Anxiety Inventory], depressive symptoms [Beck Depression Inventory-II], and

125 Depressive symptoms before and after STN-DBS surgery wer

126 ohort, the depression PRS predicted baseline depressive symptoms (beta=0.557, SE=0.200) and prospecti

127 re followed up with repeated measurements of depressive symptoms between 1992 and 2012 (n = 2,788) an

128 As outcomes, we explored depressive symptoms, bipolar disorder, neuroticism, lone

129 ELS is positively correlated with depressive symptoms both in major depression disorder pa

130 Identify distinct trajectories of change in depressive symptoms by mid-treatment during psychotherap

131 structure is a mechanism via which prenatal depressive symptoms can impact child behavior, highlight

132 Structural connectivity was linked to depressive symptom change under STN-DBS.

133 ologne data served as the test-set for which depressive symptom change was predicted.

134 ntal and physical health (self-rated health, depressive symptoms, chronic disease), less chronic pain

135 symptoms measured by the Quick Inventory of Depressive Symptoms-Clinician-Rated (QIDS-C) at 12 weeks

136 isfaction, positive affect, neuroticism, and depressive symptoms, collectively referred to as the wel

137 spectrum disorder genetic load, the less the depressive symptoms decreased over time.

138 Depressive symptoms decreased significantly on the Hamil

139 Anxiety and depressive symptoms decreased significantly, with reduct

140 ding status, mothers experiencing antepartum depressive symptoms delivered offspring who exhibited lo

141 Depressive symptoms differed significantly from those re

142 with data on thyroid status at baseline and depressive symptoms during follow-up.

143 clinical thyroid dysfunction at baseline and depressive symptoms during follow-up.

144 ositively associated with incident "elevated depressive symptoms" (EDS: CES-D(total) >= 16) among AA

145 bjective cognitive complaints are related to depressive symptoms, emphasizing the importance of recog

146 depression (CES-D score >= 7), and number of depressive symptoms endorsed.

147 little to no effect on physical functioning, depressive symptoms, energy and vitality, or cognition.

148 recall, delayed recall, verbal fluency) and depressive symptoms (EURO-D scale) were conducted at 2-y

149 group (609 depression or clinically relevant depressive symptom events; 12.9/1000 person-years) and t

150 group (625 depression or clinically relevant depressive symptom events; 13.3/1000 person-years) (haza

151 rie intake, body mass index, sleep duration, depressive symptoms, family history of diabetes, history

152 Presence of depressive symptoms, female gender, inability to control

153 cingulate cortex (ACC) predicts reduction of depressive symptoms following open-label celecoxib admin

154 ciated structural connectivity on changes in depressive symptoms following STN-DBS, which have been r

155 psychosis and remission or near-remission of depressive symptoms for 8 weeks before entering the clin

156 xhibited modest but significant increases in depressive symptoms for up to 1 day after ketamine admin

157 e the effect of vitamin D supplementation on depressive symptoms, functional limitations, and physica

158 chronic pain), emotional wellbeing (e.g. few depressive symptoms, good sleep), greater physical activ

159 nts aged 60-80 y who had clinically relevant depressive symptoms, >=1 functional limitations, and ser

160 ile those with constantly low and decreasing depressive symptoms had fluctuating cognition.

161 AGYW with depressive symptoms had higher cumulative incidence of H

162 AGYW with depressive symptoms had higher cumulative incidence of H

163 Participants with increasing depressive symptoms had the fastest decline, while those

164 Children of mothers with worse depressive symptoms had weaker white matter connectivity

165 tively predicted onset of moderate to severe depressive symptoms (hazard ratio=1.202, 95% CI=1.045-1.

166 Conversely, anti-TNF significantly improved depressive symptoms (Hospital Anxiety and Depression Rat

167 scence was associated with a higher level of depressive symptoms in adulthood during all follow-up pe

168 oeconomic disadvantage and increased risk of depressive symptoms in adulthood is well established.

169 l tolerated, and relatively safe in reducing depressive symptoms in adults with bipolar I depression.

170 We assessed whether depressive symptoms in AGYW were longitudinally associat

171 between subclinical thyroid dysfunction and depressive symptoms in all prospective cohorts with rele

172 Deep brain stimulation (DBS) reduces depressive symptoms in approximately 40%-60% of patients

173 nificantly associated with 9% higher odds of depressive symptoms in HIV+ participants (odds ratio = 1

174 We characterized the network structure of depressive symptoms in late-life and used indices of "st

175 analysis focused on the network structure of depressive symptoms in late-life because of their distin

176 mism constitute the "backbone" that sustains depressive symptoms in late-life.

177 t (OCI), subjective cognitive complaints and depressive symptoms in men and women with classical and

178 e decline across distinctive trajectories of depressive symptoms in older adults.

179 Depressive symptoms in patients also predicted greater p

180 ST led to clinically meaningful reduction in depressive symptoms in patients with MDD and produced mi

181 antidepressant drugs, could help to relieve depressive symptoms in patients with metabolic comorbidi

182 n the Berlin cohort could predict changes in depressive symptoms in Queensland patients and vice vers

183 We compared trajectories of depressive symptoms in sexual-minority adolescents and h

184 hronic hyperglycemia, cortical thinning, and depressive symptoms in T1D.

185 joint training-set map predicted changes in depressive symptoms in the independent test-set.

186 at antidepressants were also efficacious for depressive symptoms in those without diagnosis of MDD.

187 ween plasma and CSF inflammatory markers and depressive symptoms including anhedonia and reduced moti

188 me of the core affective and neurovegetative depressive symptoms, including social withdrawal, anhedo

189 e decline is present in individuals, in whom depressive symptoms increase late in life.

190 In multivariable analysis, recent depressive symptoms increased the risk of having a detec

191 larly) and characteristics (eg, younger age, depressive symptoms) independently associated with great

192 ndividuals presenting clinically significant depressive symptoms (indicating >=15 on the PHQ-9) and 5

193 subclinical hypothyroidism, the presence of depressive symptoms is often a reason for starting levot

194 Psychological interventions reduced depressive symptoms (k = 31; n = 2,075; SMD = -0.87, 95%

195 2.6 years) showed significant improvement in depressive symptoms (k = 7, Hedges' g = 0.44, 95% confid

196 linear multilevel models with growth curves (depressive symptoms), logistic multilevel models (self-h

197 Core depressive symptoms (low mood, anhedonia) were measured

198 reater offspring emotional well-being, fewer depressive symptoms, lower risk of overeating and certai

199 tic correlations between adoption status and depressive symptoms, major depression, and schizophrenia

200 t functional connectivity changes related to depressive symptoms may be highly heterogenous.

201 Symptoms central to the network of depressive symptoms may be used as targets for novel, fo

202 ant associations across all four measures of depressive symptoms (MD: betas = .020-.029, p(corr) < .0

203 The primary outcome was depressive symptoms measured at first available follow-u

204 For phase 2, the primary outcome was depressive symptoms measured by the Quick Inventory of D

205 ale (range 0-63, higher values indicate more depressive symptoms, minimal clinically important differ

206 ubjects exhibited a significant reduction of depressive symptoms (Montgomery-Asberg Depression Rating

207 overweight or obese adults with subsyndromal depressive symptoms, multinutrient supplementation compa

208 Covariates included age, sex, education, depressive symptoms, nonmilitary trauma, alcohol use, an

209 lescents were more likely to experience high depressive symptoms (odds ratio [OR] 5.43, 95% CI 4.32-6

210 ighest tertile had a higher risk of incident depressive symptoms (odds ratio: 1.43; 95% confidence in

211 ncluded patients aged 18 to 74 years who had depressive symptoms of any severity or duration in the p

212 4 years, 59% females) endorsing at least one depressive symptom on the EURO-D scale for depression (N

213 onal migrants showed above average levels of depressive symptoms on a 12-item standardized short-form

214 The effect of depressive symptoms on progression through the human imm

215 white matter hyperintensities in those with depressive symptoms only compared to those without.

216 urrence of depression or clinically relevant depressive symptoms or for change in mood scores over a

217 ghttime sleep was negatively associated with depressive symptoms (OR=0.88, 95% CI: 0.84 to 0.92), whi

218 me nap displayed a positive association with depressive symptoms (OR=0.88, 95% CI: 0.84 to 0.92).

219 appers had significantly higher incidence of depressive symptoms (OR=1.32, 95% CI: 1.19 to 1.45).

220 not driven by factors such as prosperity or depressive symptoms, or by outcome levels before the mea

221 Women with a history of depression, current depressive symptoms, or certain socioeconomic risk facto

222 ions (cognitive-affective versus somatic) of depressive symptoms over a 14-year period using Trait-St

223 nflammation was directly linked to increased depressive symptoms over time and at baseline, different

224 c inflammation may influence trajectories of depressive symptoms over time, perhaps differentially by

225 -occurs with specific patterns of changes in depressive symptoms over time.

226 re analysis was from the genetic loading for depressive symptoms (p = 0.001, standardized coefficient

227 After relapse of depressive symptoms, participants received a course of s

228 dults (body mass index, 25-40) with elevated depressive symptoms (Patient Health Questionnaire-9 [PHQ

229 eletions, duplications might protect against depressive symptoms, possibly via higher STS expression/

230 oimaging and clinically for combat exposure, depressive symptoms, prior head injury, and posttraumati

231 lites may mediate an inflammation-associated depressive symptom profile via CNS KP metabolites that c

232 eye care providers should ask patients about depressive symptoms, provide reassurance when appropriat

233 Finally, depressive symptoms, quality and frequency of social int

234 vated neurodevelopmental, externalizing, and depressive symptoms (R(2) = 0.26-1.69%), but not with an

235 Finally, depressive symptoms reduce happiness more in volatile th

236 tly more effective than placebo in improving depressive symptoms (reducing MADRS total score); the le

237 Distinct clusters of depressive symptoms responded better to different TMS ta

238 n the olfactory function and the severity of depressive symptoms, response inhibition, and emotional

239 ard deviation increase in polygenic risk for depressive symptoms, schizophrenia, and neuroticism was

240 ore regression and polygenic risk scores for depressive symptoms, schizophrenia, neuroticism, and sub

241 ex to striatum was associated with increased depressive symptom severity in 165 participants.

242 sive disorder that is not fully reflected in depressive symptom severity measures.

243 Increased depressive symptom severity was related to decreased rew

244 t produced a clinically meaningful change in depressive symptom severity, this did not differ from sh

245 Primary outcome was change in depressive symptom severity, while secondary outcomes we

246 igh plasma CRP (>3 mg/L) and correlated with depressive symptom severity.

247 Current depressive symptom showed strong or moderate direct rela

248 ividuals with increasing and constantly high depressive symptoms showed linear cognitive decline, whi

249 mediating effects and mediating pathways of depressive symptoms, sleep quality and processing speed

250 Mediating variables include depressive symptoms, sleep quality and processing speed.

251 <0.01); (3) Processing speed was affected by depressive symptoms, sleep quality, and in turn, yieldin

252 cognitive function was partially mediated by depressive symptoms, sleep quality, and processing speed

253 Measures of depressive symptoms, sleep quality, processing speed, an

254 y attenuated the average treatment effect on depressive symptoms (SMD = 0.20, 95% CI: 0.06-0.35), but

255 howed modest but significant effects on core depressive symptoms (SMD = 0.29, 95% CI [0.12-0.45]) and

256 ociations between inflammatory processes and depressive symptoms stratified by HIV serostatus.

257 eatment effects were also noted for the DRSP depressive symptom subscale (42% [SD=22] compared with 2

258 neficial to the decrease of the incidence of depressive symptoms than daytime nap.

259 8, 95% CI [0.26-0.70]) had larger effects on depressive symptoms than other drug classes.

260 Immunomodulatory drugs may have efficacy for depressive symptoms that are co-morbidly associated with

261 tive memory specificity was related to lower depressive symptoms through fewer negative self-cognitio

262 her IFN-alpha and anti-TNF enhance/attenuate depressive symptoms through modulation of amygdala emoti

263 hborhood socioeconomic disadvantage to later depressive symptoms throughout life, 2) the persistence

264 he risk of depression or clinically relevant depressive symptoms (total of incident and recurrent cas

265 exposure or other covariates, the antepartum depressive symptom trajectory was associated with reduce

266 complaints using a structured interview and depressive symptoms using a depression scale (CESD).

267 onflict using the Decisional Conflict Scale, depressive symptoms using the Patient Health Questionnai

268 The risk of the onset of depressive symptoms was 1.34 (95% CI: 1.03-1.74) among t

269 the change after moving in the prevalence of depressive symptoms was 15.2% (95% CI, 13.1%-17.2%) of t

270 Worsening of depressive symptoms was associated with left prefrontal

271 Therefore, the relation of sleep on depressive symptoms was dependent on grandparent caregiv

272 Presence of depressive symptoms was determined at baseline and at 4

273 The severity of depressive symptoms was inversely correlated with SV2A d

274 Risk of depression or clinically relevant depressive symptoms was not significantly different betw

275 ficant indirect effect of threat exposure on depressive symptoms was observed through DNAm age.

276 ment in positive (weight = 0.62) and anxious/depressive symptoms (weight = 0.49).

277 rated health, chronic health conditions, and depressive symptoms were assessed between July, 2010, an

278 Depressive symptoms were assessed from wave 1 (2002-03)

279 Emotional processing and depressive symptoms were assessed using emotional tasks

280 Depressive symptoms were assessed using the Arabic Edinb

281 Depressive symptoms were assessed using the GDS with a c

282 563 255 participants in 22 cohorts, baseline depressive symptoms were associated with CVD incidence,

283 with future depressive symptoms, and higher depressive symptoms were associated with higher future C

284 At age 10 years, depressive symptoms were higher in sexual minorities (me

285 Four distinct trajectories of depressive symptoms were identified: constantly low (n =

286 Reductions in depressive symptoms were maintained among responders thr

287 Recent depressive symptoms were measured using the Patient Heal

288 Depressive symptoms were more prominent in the standard

289 The trajectories of depressive symptoms were obtained using latent growth mi

290 Depressive symptoms were recorded using validated instru

291 We observed weak evidence that depressive symptoms were reduced by sertraline at 12 wee

292 Greater patient depressive symptoms were related to greater patient deci

293 The associations with depressive symptoms were replicated in the second epidem

294 nce or modulate neuroplasticity often reduce depressive symptoms when applied as stand-alone treatmen

295 y whether poor sleep quality results in more depressive symptoms when older individuals are also cari

296 ystems in somatic versus cognitive-affective depressive symptoms which remains largely unexplored.

297 The association of maternal depressive symptoms with child brain development at each

298 ociations only among white participants with depressive symptoms with presence of white matter hyperi

299 Sertraline is unlikely to reduce depressive symptoms within 6 weeks in primary care but w

300 whether individuals experiencing significant depressive symptoms would differ from non-depressed cont