コーパス検索結果 (１語後でソート)
通し番号をクリックするとPubMedの該当ページを表示します
1 ry effect on a major medical complication of depressive illness.
2 tical thinning poses for developing familial depressive illness.
3 arker of a more severe, chronic, and complex depressive illness.
4 of both acute and chronic manifestations of depressive illness.
5 ue to neuroticism, genetic risk, or previous depressive illness.
6 ines are at greater risk of developing major depressive illness.
7 is associated with cognitive impairments and depressive illness.
8 port a direct role for adult neurogenesis in depressive illness.
9 enefit in individuals without a diagnosis of depressive illness.
10 in turn may increase the risk of developing depressive illness.
11 ased vulnerability to co-morbidities such as depressive illness.
12 m the monoamine systems, is dysfunctional in depressive illness.
13 suggest that they are part of a spectrum of depressive illness.
14 anity" similar to dementia praecox and manic depressive illness.
15 uence of the AC7 gene on a heritable form of depressive illness.
16 use neuroticism indexes the genetic risk for depressive illness.
17 bout how they interrelate in the etiology of depressive illness.
18 morphometric deficits associated with manic-depressive illness.
19 d in 1996-1997 for their lifetime history of depressive illness.
20 ile dysfunction in men with mild-to-moderate depressive illness.
21 malignant course and character of subsequent depressive illness.
22 le dysfunction and mild-to-moderate comorbid depressive illness.
23 m serotonergic nuclei merit further study in depressive illness.
24 he right frontal lobe of patients with manic-depressive illness.
25 benefits because of illness, and 75.5% had a depressive illness.
26 MD that reflect a high familial liability to depressive illness.
27 probably reflect a high genetic liability to depressive illness.
28 ly in 12 adult depressed patients with manic-depressive illness.
29 ssociated with a familial risk of developing depressive illness.
30 r the therapeutic action of lithium in manic-depressive illness.
31 ommonly used drug for the treatment of manic depressive illness.
32 the proposed targets of Li+ therapy in manic-depressive illness.
33 who were selected via syndromal criteria for depressive illness.
34 clinical efficacy in the treatment for manic depressive illness.
35 d genetically complex disorder such as manic depressive illness.
36 nd a particularly high familial liability to depressive illness.
37 lunitrazepam is not altered in subjects with depressive illnesses.
38 may underlie both antidepressant therapy and depressive illnesses.
40 and extended to patients with nonrefractory depressive illness a pilot study indicating that patient
43 gonadal men showed an increased incidence of depressive illness and a shorter time to diagnosis of de
45 vated basal cortisol levels are a feature of depressive illness and cause deficits in learning and me
46 ortisol-DHEA ratios may be a state marker of depressive illness and may contribute to the associated
48 g a series of animal model investigations of depressive illness and serotonergic function, Deakin and
51 l morphology during medication treatment for depressive illness and the first to provide within an RC
53 psychiatric diseases as schizophrenia, manic depressive illness, and borderline personality disorder.
54 dulation, molecular pathophysiology of manic-depressive illness, and therapeutic mechanism of mood st
55 life are known risk factors for anxiety and depressive illnesses, and they inhibit hippocampal neuro
57 eatures of bipolar affective disorder (manic-depressive illness) are episodes of mania (bipolar I, BP
58 ying lithium's therapeutic efficacy in manic-depressive illness (bipolar affective disorder) is the i
60 t of n-3 PUFAs in individuals with diagnosed depressive illness but no evidence of any benefit in ind
62 impairment of quality of life and associated depressive illness, cardiovascular disease, and a serone
63 Unlike healthy controls, if patients with a depressive illness commit an error, they can be at incre
64 eover, clinical characteristics of subjects' depressive illness, demographic variables, and psychosoc
67 bnormalities of the medial frontal cortex in depressive illness; however, the mechanism by which anti
70 may confer resilience to the development of depressive illness in individuals at high familial risk
74 sion is common in patients with delirium and depressive illness is a recognised sequelae of delirium.
75 onic social stressors, and hence, that major depressive illness is associated with a parainflammatory
76 has received considerable attention, is that depressive illness is associated with a specific underly
78 re consistent with the view that early-onset depressive illness is distinguished from late-onset majo
83 e disorders, and there is some evidence that depressive illness itself may be a risk factor in the ae
84 nucleus (DRN) may be dysfunctional in major depressive illness, making it important to understand th
85 efinement of the definition of chronicity in depressive illness may increase the power of such studie
86 ition to its use in the treatment of bipolar depressive illness, may have an expanded use in the inte
87 ich our major diagnostic categories of manic-depressive illness (MDI) and dementia praecox were devel
90 havioral and physiological manifestations of depressive illness produce a significant decrease in lif
91 mood stabilizers for the treatment of manic-depressive illness, stimulated the ERK pathway in the ra
94 of polymorphisms in the AC7 gene with major depressive illness (unipolar depression) based on Diagno
96 matched controls to test the hypothesis that depressive illness was associated with a blunted behavio
99 ic social isolation, a known risk factor for depressive illness, we show that 5-HT neurons in the dor
100 compares the health and disability costs of depressive illness with those of four other chronic cond
WebLSDに未収録の専門用語（用法）は "新規対訳" から投稿できます。