ライフサイエンスコーパス: mood

1 nitude characteristic of depression-like low mood.

2 to central functional resistance) may affect mood.

3 or medical conditions with known effects on mood.

4 e release, and are known to affect momentary mood.

5 e- and stress-induced changes in craving and mood.

6 isspeptin administration attenuated negative mood.

7 gical regulation of addictive states, and of mood.

8 dy temperature, respiration, aggression, and mood.

9 treatment goal, coping strategies, QOL, and mood.

10 impulsivity, willingness to take risks, and mood.

11 comitant disruption in circadian rhythms and mood.

12 s, and between patients' clinical status and mood.

13 to rhythms, and their effects on arousal and mood.

14 oping strategies in order to enhance QOL and mood.

15 omatology, IBUD attenuated the stimulant and mood-altering effects of alcohol as compared with placeb

16 were partially independent of its effects on mood, although subsequent trials in transdiagnostic samp

17 wareness and worse quality of life (QOL) and mood among patients with advanced cancer.

18 rsistently elevated, expansive, or irritable mood and abnormally and persistently increased activity

19 dies provide fairly consistent evidence that mood and activation represent distinct dimensions of bip

20 Serotonin is implicated in mood and affective disorders.

21 tress or external threats is a key factor in mood and anxiety disorder aetiology.

22 o develop therapies for those suffering from mood and anxiety disorders and provide insight into addi

23 opment of eCB-based treatment approaches for mood and anxiety disorders and suggest a potentially wid

24 01 healthy participants and individuals with mood and anxiety disorders completed an approach-avoidan

25 lable repertoire of effective treatments for mood and anxiety disorders represents a critical unmet n

26 bust antidepressant effects in patients with mood and anxiety disorders that were previously resistan

27 ications for the treatment and prevention of mood and anxiety disorders.

28 plays a critical role in the neurobiology of mood and anxiety disorders.

29 plays a critical role in the neurobiology of mood and anxiety disorders.

30 We show an increased reliance in the mood and anxiety group on a parameter of our reinforceme

31 This was particularly the case when the mood and anxiety group was under stress.

32 on and Anhedonic Depression subscales of the Mood and Anxiety Symptoms Questionnaire-short form.

33 a time-to-event model, including measures of mood and anxiety, general psychosocial functioning, age

34 ssant treatment when tested in paradigms for mood and anxiety.

35 is safe and associated with improvements in mood and anxiety.

36 ehaviors, hyperarousal, as well as depressed mood and anxiety.

37 o significant association between post-natal mood and atopic eczema was seen after taking account of

38 Clinical evidence suggests that mood and behavioral symptoms in premenstrual dysphoric d

39 their function as it relates specifically to mood and biological rhythms.

40 ll excitatory input) and behavioral control (mood and cognition).

41 hysiology, including brain functions such as mood and cognition, and influence many neurological and

42 enologically rich descriptions of changes in mood and cognition, loss of interest and anhedonia and e

43 ergic dysfunction of the mPFC and associated mood and cognitive behaviors.SIGNIFICANCE STATEMENT Chro

44 innervation of the mPFC was associated with mood and cognitive changes that persisted long after the

45 E STATEMENT Chronic stress causes persistent mood and cognitive changes typically associated with dys

46 cated in the pathophysiology of a variety of mood and cognitive disorders.

47 exploring the relationship between depressed mood and cognitive ToM, specifically visual perspective-

48 s behavior in humans is characterized by low mood and fatigue, which have been suggested to reflect c

49 , and 86, as measured with the self-reported Mood and Feelings Questionnaire (MFQ).

50 essive symptoms were measured with the Short Mood and Feelings Questionnaire (SMFQ) at age 13 years i

51 olescents self-reported depressive symptoms (Mood and Feelings Questionnaire [MFQ]) at each timepoint

52 relevance to the influence of ketamine upon mood and its other functional actions in vivo.

53 night sweats, increased weight, and altered mood and libido-are recognised, but are generally mild.

54 Serotonin (5-HT) is associated with mood and motivation but the function of endogenous 5-HT

55 se of ketamine as an off-label treatment for mood and other psychiatric disorders.

56 follow-up visit, TRS score was measured, and mood and psychological batteries were administered under

57 n, more severe non-motor symptoms (including mood and sexual function), depressive symptoms, sleep im

58 with eating disorders that is comorbid with mood and substance use disorders.

59 strate that indices associated with positive mood and surprise are both associated with network flexi

60 with HCs, are less stable in their negative mood and these dynamics are related to differences in in

61 ne provided self-reports of stress, craving, mood, and behavior on electronic diaries for up to 16 we

62 , clinical presentation, including behavior, mood, and cognitive symptoms and dementia.

63 ical responses, such as feeding behavior and mood, and has been implicated in the development of fatt

64 They contribute to cognition, reward, mood, and nociception and are implicated in a range of n

65 group had serious adverse events of altered mood, and one patient in the topiramate group had a suic

66 have beneficial effects on disease activity, mood, and quality of life in patients with inflammatory

67 questionnaires focusing on quality of life, mood, and relationship, were conducted at inclusion and

68 with psychometric measures of reward, drive, mood, and sexual aversion, providing functional signific

69 (efferent) vagus in regulation of appetite, mood, and the immune system, as well as the pathophysiol

70 olar disorder and demonstrably distinct from mood, and to identify any significant between- and withi

71 e results suggest that the effects of TNP on mood- and smoking-related outcomes may vary depending on

72 Participants included mothers with depressed mood, anhedonia, or depression history but who were not

73 condary outcomes were body-mass index (BMI), mood, anxiety, affective regulation, and anorexia nervos

74 g dimensions measured by the EPDS: depressed mood, anxiety, and anhedonia.

75 We also assessed 14 lifetime DSM-IV mood, anxiety, disruptive behavior and substance disorde

76 implicated in the pathophysiology of FND and mood/anxiety disorders.

77 contribute to human neurological diseases of mood, appetite, and movement.

78 der (rMDD) often report more fluctuations in mood as residual symptomatology.

79 Clinical, neurocognitive and mood assessments using the PRIME-MD and BDI instruments

80 Mood-associated circadian effects between rapid (D1) res

81 lar clock regularly render mice with altered mood-associated phenotypes.

82 upplement reduces vulnerability to depressed mood at postpartum day 5, the typical peak of PPB.

83 ive behavior (beta = -0.08, P = .14) and low mood (beta = -0.03, P = .65) were not.

84 Low maternal mood between delivery and 6 months post-partum was assoc

85 mes such as sleepiness, quality of life, and mood but also intermediate cardiovascular end points suc

86 However, it could improve mood by increasing alert scores [SMD: 0.71 (95% CI; 0.01

87 potential mechanism for how PER3 influences mood by utilizing a comprehensive circadian clock model

88 tudy groups reported improvements in QOL and mood by week 12.

89 Digit-Substitution Test, Word Fluency Test), mood (Center for Epidemiological Studies-Depression Scal

90 c symptoms, and emphasizing core features of mood change and alterations in cognitive content and psy

91 Increased activity and energy alongside mood change are identified in the DSM-5 as cardinal symp

92 hat mediators of continuing ketamine-induced mood changes include altered timing and amplitude of the

93 oinflammatory signaling in the brain affects mood, cognition, and behavior and is linked with the eti

94 e instability was increased in most negative mood/cognition variables and that the DMS had less conne

95 d experience sampling methodology to monitor mood/cognitions (10 times a day for 6 days) and calculat

96 d four potential subtypes: high anxiety, low mood, combined and non-affective (psychotic).

97 r nicotine use, early dysphoric or anhedonic mood, conduct disorder, and childhood sexual abuse.

98 series analyses detected synchronies between mood cycles and three lunar cycles that modulate the amp

99 1:2, 1:3, 2:3 and other modes of coupling of mood cycles to the two bi-weekly lunar cycles.

100 eover, the ClockDelta19 mouse exhibits rapid mood cycling (a manic-like phenotype during the day foll

101 of lithium for prophylaxis of the recurrent mood disorder and encouraged its greater use.

102 The probability of suffering the mood disorder depression is up to 30% in women and 15% i

103 Post-partum depression is a serious mood disorder in women that might be triggered by peripa

104 ty, general psychosocial functioning, age at mood disorder onset in the bipolar parent, and age at ea

105 odents, they experience a 2-fold increase in mood disorder prevalence vs. males.

106 unction with the core behavioral features of mood disorder remain poorly understood.

107 ve, randomized, cross-over study in a French mood disorder unit for inpatients.

108 chizophrenia, schizoaffective disorder, or a mood disorder who had moderate or severe tardive dyskine

109 the concept of depression as an independent mood disorder with characteristic symptoms/signs and a g

110 lifetime psychopathology and 25 had a non-BD mood disorder), and 80 unrelated healthy individuals.

111 jor depressive disorder (MDD) is a disabling mood disorder, and despite a known heritable component,

112 isorder (MDD) is a complex and heterogeneous mood disorder, making it difficult to develop a generali

113 terozygosity for the wild-type P2X7R and its mood disorder-associated variant P2X7R-Gln460Arg represe

114 HCM females vs. controls and correlated with mood disorder-related symptoms.

115 sychosocial functioning; and parental age at mood disorder.

116 schizophrenia, schizoaffective disorder, or mood disorder.

117 se disorders (aOR, 1.34; 95% CI, 1.05-1.72), mood disorders (aOR, 1.15; 95% CI, 1.01-1.30), anxiety (

118 s aids to psychotherapy for the treatment of mood disorders and alcohol dependence, drugs such as LSD

119 normalities in NRG3 transcriptomics occur in mood disorders and are genetically determined.

120 a variety of behaviors, including models of mood disorders and behavioral responses to nicotine.

121 cancer survivors are more likely to develop mood disorders and cognitive deficits than women in the

122 eas 24a and 24b) appears to be important for mood disorders and constitutes a neuroanatomical substra

123 on the use of ketamine for the treatment of mood disorders and highlights the limitations of the exi

124 for the understanding of sex differences in mood disorders and of the side effects of cytochrome P45

125 are targets of existing drugs used to treat mood disorders and suicidality (lithium, clozapine and o

126 al studies report strong association between mood disorders and tobacco addiction.

127 Treatment options for these mood disorders are currently suboptimal for many patient

128 el mechanism underlying learning deficits in mood disorders as well as a potential target - altering

129 Mood disorders can be debilitating, and are often correl

130 s10748842 risk genotype and are increased in mood disorders further implicates a molecular mechanism

131 ers had impaired trajectories, and more with mood disorders had better functioning trajectories.

132 Recent evidence suggests that some mood disorders have a circadian component, and disruptio

133 ural and functional brain changes, and thus, mood disorders in patients with heart disease should not

134 Diagnostic criteria for mood disorders including major depressive disorder (MDD)

135 cal mechanism of a novel risk gene for major mood disorders involved in synaptic function and related

136 Finding robust brain substrates of mood disorders is an important target for research.

137 lar and molecular mechanisms associated with mood disorders may be localized to specific hippocampal

138 Major depressive disorder (MDD) and other mood disorders remain difficult to effectively treat, an

139 Lithium use for the treatment of mood disorders remains quite low, particularly in the Un

140 sity is associated with a high prevalence of mood disorders such as anxiety and depression.

141 These results indicated that among the mood disorders the hippocampal subfields were more affec

142 cts of inflammation on glia and glutamate in mood disorders will be discussed along with their transl

143 and GRM7 (which potentially affects risk for mood disorders).

144 such as Parkinson's disease, schizophrenia, mood disorders, and addiction.

145 rs10748842 was genotyped in individuals with mood disorders, and association with NRG3 isoform expres

146 hizophrenia spectrum disorders and psychotic mood disorders, and associations of the empirically deri

147 agus nerve dysfunction resulting in obesity, mood disorders, and inflammation.

148 and 14 (88%) of the 16 patients had comorbid mood disorders, anxiety disorders, or both.

149 eline dyspnea index), quality of life (QoL), mood disorders, exacerbations, comorbidities, lung funct

150 ncluded age, sex, race/ethnicity, anxiety or mood disorders, family history of drug, alcohol, and beh

151 reference in arousal and activity) and sleep/mood disorders, including seasonal affective disorder (S

152 mine may be beneficial to some patients with mood disorders, it is important to consider the limitati

153 including schizophrenia-spectrum disorders, mood disorders, neurotic stress-related and somatoform d

154 between obesity, stress, gut microbiota and mood disorders, obesity was induced in mice using a high

155 short attention spans, aggressive behaviors, mood disorders, or schizophrenia.

156 stemic HCM stress can lead to development of mood disorders, possibly through inducing structural and

157 vascular dysfunction is highly comorbid with mood disorders, such as anxiety and depression.

158 vo hippocampal subfield volumes and specific mood disorders, such as bipolar disorder (BD) and major

159 Controversy exists whether mood disorders, such as depression, are associated with

160 between glutamate-related genes and risk for mood disorders, suicide, and treatment response, particu

161 ement of glutamate-related genes in risk for mood disorders, treatment response, and phenotypic chara

162 etamine are effective in treatment-resistant mood disorders, underscoring the potential importance of

163 nergic (DA) neurons, known to be affected in mood disorders, using a novel, translational strategy th

164 Major mood disorders, which primarily include bipolar disorder

165 ed with impairment of cognitive function and mood disorders.

166 (PUFAs) is a hallmark of poor nutrition and mood disorders.

167 in the susceptibility and drug treatment of mood disorders.

168 pharmacological targets for the treatment of mood disorders.

169 (P2X7R) has repeatedly been associated with mood disorders.

170 lated isoforms in the brain of patients with mood disorders.

171 s stress sensitivity, a major risk factor in mood disorders.

172 of the hippocampus have been associated with mood disorders.

173 andidate for the treatment of stress-related mood disorders.

174 adian function have strong associations with mood disorders.

175 oral functions, or on addictive diseases and mood disorders.

176 (PCDH17) as a susceptibility gene for major mood disorders.

177 ln460Arg has repeatedly been associated with mood disorders.

178 roof of concept studies for the treatment of mood disorders.

179 cal response (SVR) on cognitive function and mood disorders.

180 ion and bipolar disorder are the most common mood disorders.

181 spines in the brains of patients with major mood disorders.

182 t role in the pathology of anxiety and other mood disorders.

183 masome-dependent signaling may contribute to mood disorders.

184 p and might increase the risk for developing mood disorders.

185 cadian timekeeping (amplitude and timing) in mood disorders.

186 utflow; all of these have been implicated in mood disorders.

187 uence susceptibility for substance abuse and mood disorders.

188 eficit/hyperactivity, substance-related, and mood disorders.

189 he role of gut microbiota in obesity-related mood disorders.

190 are two novel pathways to pathophysiology in mood disorders.

191 m to the pathophysiology and therapeutics of mood disorders.

192 potentially able to convey susceptibility to mood disorders.SIGNIFICANCE STATEMENT Depression and bip

193 flammation increase the risk and severity of mood disorders; however, only recently have the importan

194 gion are significantly associated with major mood disorders; subjects carrying the risk allele showed

195 otor functions, and affected self-reports of mood/drug effects in both groups.

196 ssion showed that alcohol-induced changes in mood/drug effects were associated with changes in thalam

197 nalyses to examine whether symptom burden or mood during HCT mediated the effect of the intervention

198 -reported symptoms, lower sustained positive mood during the induction, and higher negative bias on a

199 tivity eliminates vulnerability to depressed mood during the peak of PPB.

200 piness in a computational model of momentary mood dynamics (z = 4.55; P < .001) that was not attenuat

201 der is a heritable disorder characterized by mood dysregulation associated with brain functional dysc

202 17 years, 93 youths with anxiety, disruptive mood dysregulation, and/or attention-deficit/hyperactivi

203 feelings of social exclusion, beyond general mood effects.

204 energy stores and also to the analgesic and mood-elevating effects of exercise.

205 ositive effects of physical exercise such as mood elevation and stress reduction.

206 test associations between iron exposures and mood, emotion, cognition, and memory; animal studies to

207 of asenapine in preventing recurrence of any mood episode in adults with bipolar I disorder.

208 Time to recurrence of any mood episode was statistically significantly longer for

209 icacy endpoint was time to recurrence of any mood event during the double-blind period.

210 ive than placebo in preventing recurrence of mood events in adults with bipolar I disorder and was ge

211 baseline performance, hand use, lesion size, mood, fatigue, or whether distraction was tested during

212 difference for classifying 16-year-olds with mood fluctuation and psychotic symptoms relative to the

213 ence of psychotic symptoms in the context of mood fluctuation at age 16, assessed in the full sample.

214 s relative to the control groups (those with mood fluctuations but no psychotic symptoms and those wi

215 association between depression and momentary mood fluctuations during cognitive tasks.

216 t step to gain a better understanding of how mood fluctuations in real life are represented in the br

217 re (EIPC) improves quality of life (QOL) and mood for patients with advanced cancer.

218 ductions in areas that control cognition and mood functions, even if such losses are apparently indep

219 Perinatal maternal stress and low mood have been linked to offspring atopic eczema.

220 ed to be the mediators of light's effects on mood, here we present an alternative model that dispense

221 l Assessment of Cancer Therapy-General), and mood (Hospital Anxiety and Depression Scale) within 8 we

222 IBUD was associated with mood improvements on the secondary measures of stress ex

223 among prognostic awareness, coping, QOL, and mood in patients with newly diagnosed, incurable cancer.

224 nostic awareness is related to worse QOL and mood in patients with newly diagnosed, incurable cancer;

225 P, there was a robust induction of depressed mood in the control group, but no effect in the suppleme

226 Compared with either placebo or baseline, a mood-independent decrease of the central circadian value

227 rol subjects) completed a sustained positive mood induction during functional magnetic resonance imag

228 d on a visual analog scale following the sad mood induction procedure (MIP).

229 One such feature is persistent mood instability, and efforts are underway to understand

230 arch are fatigue, disorders of behaviour and mood, interventions for the needs of caregivers, and tim

231 measures of mania, depression, anxiety, and mood lability; psychosocial functioning; and parental ag

232 We further show that mood, measured independently on Twitter, contains distin

233 nxiety scores, supporting a role for PER3 in mood modulation.

234 fcMRI) and the distinctive paradigm of rapid mood normalization following ketamine treatment, the cur

235 as quantitated by the elevation in depressed mood on a visual analog scale following the sad mood ind

236 the role of reverse causation (influence of mood on intake) as potential explanation for the observe

237 potential target - altering an individual's mood or task novelty - to improve learning.

238 Symptom severity correlated with baseline mood parameters in laboratory (rho = -0.54; P < 1 x 10-6

239 lation between symptom severity and baseline mood parameters supports an association between depressi

240 ective effects that include: marked positive mood, pleasant/unusual bodily sensations and pro-social,

241 rate, depression symptom level, and rate of mood polarity switch, as well as to explore sleep qualit

242 No mood polarity switches were observed.

243 sociated with network flexibility - positive mood portends a more flexible brain while increased leve

244 We assessed patients' mood, post-traumatic stress disorder (PTSD) symptoms, an

245 Mental disorders (any disorder, mood, posttraumatic stress disorder, anxiety, alcohol us

246 ne and 6 months post-transplant, we assessed mood, PTSD symptoms, and QOL with the Hospital Anxiety a

247 ference, sleep quality/timing and sleepiness/mood questionnaires.

248 56.3%), and Met/Met (N=19, 26.8%)) received mood ratings before infusion, after infusion, and for th

249 ality between the two phenomena and explains mood regulation by light via another ipRGC-dependent mec

250 rning, social and communication, emotion and mood regulation, and behaviour (n=5100-6952).

251 adrenal gland hypertrophy, reduced volume in mood-related brain regions, and reduced hippocampal sign

252 poxide, pharmacological agents used to treat mood-related disorders in the clinical population, would

253 widely implicated in the pathophysiology of mood-related disorders such as anxiety and major depress

254 adopted to examine vicarious stress-induced mood-related disorders, as well as pharmacological antid

255 Stress is a prevailing risk factor for mood-related illnesses, wherein women represent the majo

256 r levels in this brain region that regulates mood-related phenotypes.

257 e circadian activity patterns indicate rapid mood response to ketamine, and that mediators of continu

258 striatum (nucleus accumbens) and its role in mood, reward, and motivation has been the focus of signi

259 reatment of uncertainty-related disorders of mood.Rewards or punishments elicit diverse behavioral re

260 rmation for Suicidality) and for anxiety and mood (SASS, Simplified Affective State Scale)) by themse

261 Subjective mood, satiety, and circulating hormone levels were measu

262 al symptoms using the Anxiety Depression and Mood Scale (ADAMS) total score.

263 e anxiety and depressive symptoms and Global Mood Scale negative and positive affect), and personalit

264 sked if they had experienced symptoms of low mood since childbirth and completed the Edinburgh Postna

265 Lithium (Li) is a potent mood stabilizer and displays neuroprotective and neuroge

266 kin to the antipsychotic haloperidol and the mood stabilizer lithium carbonate.

267 ith infants exposed to another commonly used mood stabilizer, lamotrigine.

268 ng older patients with bipolar disorder with mood stabilizers need evidence from age-specific randomi

269 tonin reuptake inhibitors, by 98% for use of mood stabilizers, by 171% for use of antipsychotics, and

270 tonin reuptake inhibitors, by 63% for use of mood stabilizers, by 60% for use of antipsychotics, and

271 te initiation in bipolar patients not taking mood stabilizers, careful assessment to rule out bipolar

272 By contrast, for patients taking mood stabilizers, the risk of mania was lower after star

273 ion of lithium, a drug with well established mood-stabilizing effect in humans with BD, reverses the

274 e, used in monotherapy or with a concomitant mood-stabilizing medication, in patients with bipolar di

275 disorder who were concomitantly receiving a mood-stabilizing medication.

276 ps: those with and those without concomitant mood-stabilizing treatment.

277 how the ClockDelta19 mouse responds to other mood-stabilizing treatments of BD such as valproate, lam

278 istory of psychosis but no associations with mood state at the time of scanning.

279 preferences, in large part because positive mood states act as a protective buffer against otherwise

280 In particular, changing mood states are likely to shape artistic preferences, in

281 Improvement in the Profile of Mood States depression subscale was greater at day 1 for

282 the comprehensive measure and the Profile of Mood States-Brief, Fatigue subscale for the short measur

283 eatments may aid in both depressed and manic mood states.

284 that addicts use drugs to alleviate negative mood states.

285 disorder characterized by episodes of severe mood swings.

286 The authors compared medication-induced mood switch risk (primary outcome), as well as treatment

287 t can be dissociated from its effects on the mood symptoms of depression.

288 ld CTE pathology, 26 (96%) had behavioral or mood symptoms or both, 23 (85%) had cognitive symptoms,

289 re CTE pathology, 75 (89%) had behavioral or mood symptoms or both, 80 (95%) had cognitive symptoms,

290 f Functioning (GAF), psychotic symptoms, and mood symptoms were rated at each assessment.

291 but no psychotic symptoms and those with no mood symptoms) was hyperactivation of the hippocampus/am

292 er have recurrent major depression, residual mood symptoms, and limited treatment options.

293 assessed functional impairments relating to mood symptoms.

294 ssessed using food frequency questionnaires, mood using validated questionnaires.

295 happiness ratings as a measure of momentary mood was also tested in the laboratory in 74 participant

296 At each visit, mood was assessed using standardized rating scales.

297 Momentary mood was measured during risky decision making.

298 Mood was measured repeatedly throughout the experiment.

299 Cognitive function and mood were not adversely affected by deferiprone therapy.

300 To examine the relation of maternal stress/mood with atopic eczema in the offspring, focusing parti