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1 ing the sensitivity to stressful stimuli and dysphoria.
2 ased signaling may produce analgesia without dysphoria.
3 depressive-like states such as anhedonia and dysphoria.
4 rbance and co-occurring anxiety disorders or dysphoria.
5 se without a history of anxiety disorders or dysphoria.
6 high rates of anxiety disorders and chronic dysphoria.
7 d is consistent with a link between CREB and dysphoria.
8 2 because of vernacular changes referring to dysphoria.
9 s anhedonia, craving, fatigue, insomnia, and dysphoria.
10 ren and may be prodromal markers of risk for dysphoria.
11 More than 1 in 4 patients had moderate dysphoria.
12 rapeutic options for women with premenstrual dysphoria.
14 ects of diagnosis and treatment condition on dysphoria after quitting smoking and the effects of dysp
18 profile suggests that it will be without the dysphoria and other adverse effects promoted by arrestin
19 pression in patients with CVD improves their dysphoria and other signs and symptoms of depression, im
20 ole of ovarian steroids in both premenstrual dysphoria and perimenopausal depression has led to the s
24 or without surgery, to improve their gender dysphoria and to better align their physical and psychol
25 d, implicates dynorphin as a key mediator of dysphoria, and emphasizes kappa-receptor antagonists as
26 ed by some KOR agonists, including sedation, dysphoria, and hallucinations, have limited their clinic
28 icolimbic system; the ensuing kappa-mediated dysphoria appears to contribute to addiction and withdra
29 experience reward (anhedonia) and aversion (dysphoria) are in high demand because many psychiatric c
30 r than placebo for treatment of premenstrual dysphoria as reflected by symptomatic improvement and ch
33 ain the rapid alleviation of the anxiety and dysphoria associated with late luteal phase dysphoria di
34 ld contribute to alleviating the anxiety and dysphoria associated with the symptomatology of major un
35 with analgesia being G protein-mediated and dysphoria being mediated through betaarrestin2 recruitme
37 tinue the study, and have increased rates of dysphoria, depressive symptoms, and extrapyramidal sympt
39 dysphoria associated with late luteal phase dysphoria disorder and major unipolar depression by thes
41 Transgender women experience lifelong gender dysphoria due to a gender assignment at birth that is in
42 fective symptoms reflecting areas of chronic dysphoria (e.g., anger and loneliness/emptiness) and int
43 h mania, and the bimodal distribution of the dysphoria factor is consistent with the possibility that
47 olecular mechanisms mediating stress-induced dysphoria in humans and conditioned place aversion in ro
48 The first and strongest factor represented dysphoria in mania, with strong positive loadings for de
49 different forms of stress presumed to evoke dysphoria in mice, we found that repeated forced swim an
50 ms responsible for cognitive dysfunction and dysphoria in nondemented patients with Parkinson's disea
53 eported more pain than those without current dysphoria, irrespective of whether they had a history of
55 Understanding how KOR activation produces dysphoria is key to the development of better analgesics
57 tors (KORs) in monoamine circuits results in dysphoria-like behaviors and stress-induced reinstatemen
58 ng in different stress responses: analgesia, dysphoria-like behaviors, anxiety-like responses, and in
59 roadly consistent with Simms and colleagues' Dysphoria Model of PTSD symptoms) which provided a bette
60 ed by neuroendocrine dysregulation, fatigue, dysphoria, myalgia, and impaired mental and physical per
61 e disorders, anhedonia (lack of pleasure) or dysphoria (negative affect) can result from breakdowns o
62 with lifetime anxiety disorders and lifetime dysphoria (odds ratio=3.82, 95% CI=1.56-9.38, and odds r
66 patial and mnemonic functioning but not with dysphoria; pattern 2 correlated with dysphoria but not w
67 itoral enlargement, and reductions in gender dysphoria, perceived stress, anxiety, and depression.
68 aused by treatments that cause anhedonia and dysphoria (prodepressive effects) in rats and humans (e.
69 ith general depression (R = -.523, P = .01), dysphoria (R = -.455, P = .05), and lassitude (R = -.449
72 ssive symptoms at the time of the interview (dysphoria) reported more pain than those without current
73 tility, narcissism, emotional dysregulation, dysphoria, schizoid orientation, obsessionality, thought
75 epressed women met criteria for premenstrual dysphoria (symptom cyclicity and at least moderate sever
76 ms; this association was most pronounced for dysphoria symptoms (r = -0.45; 95% CI, -0.10 to -0.70).
77 ing and hyperarousal symptoms, and loss (ie, dysphoria) symptoms, such as emotional numbing and depre
80 Compared with respondents with no history of dysphoria, the odds ratio for MI associated with a histo
82 n-releasing factor (CRF) in the induction of dysphoria, the potentiation of drug seeking, and stress-
83 bic pathway has been proposed to mediate the dysphoria underlying this response, we tested dopamine-d
84 ds ratio for MI associated with a history of dysphoria was 2.07 (95% CI, 1.16 to 3.71), and the odds
85 s-related symptom cyclicity nor premenstrual dysphoria was an invariant accompaniment of perimenopaus
88 s-related symptom cyclicity and premenstrual dysphoria was observed in perimenopausal depressed women
90 al syndrome and postpartum or postmenopausal dysphoria, when increased emotional lability and BDZ ins
91 ve emotional symptoms, such as anhedonia and dysphoria, which may be due in part, to dysfunction of t
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