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1 m serotonergic nuclei merit further study in depressive illness.
2 ponsiveness in obese subjects with co-morbid depressive illness.
3 rability pathways from social experiences to depressive illness.
4 udy reward learning deficits associated with depressive illness.
5 ssociated with a familial risk of developing depressive illness.
6 tical thinning poses for developing familial depressive illness.
7 arker of a more severe, chronic, and complex depressive illness.
8  of both acute and chronic manifestations of depressive illness.
9 ue to neuroticism, genetic risk, or previous depressive illness.
10 ines are at greater risk of developing major depressive illness.
11 is associated with cognitive impairments and depressive illness.
12 port a direct role for adult neurogenesis in depressive illness.
13 enefit in individuals without a diagnosis of depressive illness.
14  in turn may increase the risk of developing depressive illness.
15 ry effect on a major medical complication of depressive illness.
16 ased vulnerability to co-morbidities such as depressive illness.
17 m the monoamine systems, is dysfunctional in depressive illness.
18  suggest that they are part of a spectrum of depressive illness.
19 uence of the AC7 gene on a heritable form of depressive illness.
20 use neuroticism indexes the genetic risk for depressive illness.
21 bout how they interrelate in the etiology of depressive illness.
22  morphometric deficits associated with manic-depressive illness.
23 d in 1996-1997 for their lifetime history of depressive illness.
24 ile dysfunction in men with mild-to-moderate depressive illness.
25 malignant course and character of subsequent depressive illness.
26 le dysfunction and mild-to-moderate comorbid depressive illness.
27 anity" similar to dementia praecox and manic depressive illness.
28 he right frontal lobe of patients with manic-depressive illness.
29 benefits because of illness, and 75.5% had a depressive illness.
30 MD that reflect a high familial liability to depressive illness.
31 probably reflect a high genetic liability to depressive illness.
32 ly in 12 adult depressed patients with manic-depressive illness.
33 r the therapeutic action of lithium in manic-depressive illness.
34 ommonly used drug for the treatment of manic depressive illness.
35 the proposed targets of Li+ therapy in manic-depressive illness.
36 who were selected via syndromal criteria for depressive illness.
37 clinical efficacy in the treatment for manic depressive illness.
38 d genetically complex disorder such as manic depressive illness.
39 nd a particularly high familial liability to depressive illness.
40 lunitrazepam is not altered in subjects with depressive illnesses.
41 may underlie both antidepressant therapy and depressive illnesses.
42        We investigated the lifetime rates of depressive illness 50 years after closed head injury.
43  and extended to patients with nonrefractory depressive illness a pilot study indicating that patient
44 or treatment decisions and for understanding depressive illness across the life span.
45                                        Manic-depressive illness afflicts about one percent of the pop
46 gonadal men showed an increased incidence of depressive illness and a shorter time to diagnosis of de
47 e, Alzheimer's disease, schizophrenia, major depressive illness and bipolar disorder.
48 vated basal cortisol levels are a feature of depressive illness and cause deficits in learning and me
49 ortisol-DHEA ratios may be a state marker of depressive illness and may contribute to the associated
50 s in the etiology of such disorders as manic depressive illness and schizophrenia.
51 g a series of animal model investigations of depressive illness and serotonergic function, Deakin and
52               The strong association between depressive illness and sick days in younger workers sugg
53 uals--and it is a risk factor for subsequent depressive illness and substance abuse.
54 ve an increased risk of developing co-morbid depressive illness and that these patients have reduced
55 l morphology during medication treatment for depressive illness and the first to provide within an RC
56 ights into the detrimental role of stress in depressive illness and the general population.
57 liability of QEEG for response prediction in depressive illness and to identify methodological limita
58 psychiatric diseases as schizophrenia, manic depressive illness, and borderline personality disorder.
59 dulation, molecular pathophysiology of manic-depressive illness, and therapeutic mechanism of mood st
60 ay play a causal role in decreasing risk for depressive illness, and these findings support efforts t
61  life are known risk factors for anxiety and depressive illnesses, and they inhibit hippocampal neuro
62 ysiology and therapeutic mechanisms of manic-depressive illness are unknown.
63 eatures of bipolar affective disorder (manic-depressive illness) are episodes of mania (bipolar I, BP
64 -analysis of diagnostic accuracy for QEEG in depressive illness, based on articles published between
65 ying lithium's therapeutic efficacy in manic-depressive illness (bipolar affective disorder) is the i
66 nd associated with increased comorbidity and depressive illness burden.
67 t of n-3 PUFAs in individuals with diagnosed depressive illness but no evidence of any benefit in ind
68 y be optimal in studies of the triggering of depressive illness by childbirth.
69 impairment of quality of life and associated depressive illness, cardiovascular disease, and a serone
70  Unlike healthy controls, if patients with a depressive illness commit an error, they can be at incre
71 eover, clinical characteristics of subjects' depressive illness, demographic variables, and psychosoc
72 esented a quantitatively more severe form of depressive illness fitted the data well.
73                                        Manic-depressive illness has been conceptualized as a neuroche
74 bnormalities of the medial frontal cortex in depressive illness; however, the mechanism by which anti
75 ssociated with a more severe presentation of depressive illness in elderly subjects.
76 improve our understanding of the etiology of depressive illness in general.
77  may confer resilience to the development of depressive illness in individuals at high familial risk
78 the role of testosterone in the treatment of depressive illness in older men.
79                                        Manic depressive illness is a common and frequently debilitati
80                    Bipolar disorder or manic depressive illness is a major psychiatric disorder that
81 sion is common in patients with delirium and depressive illness is a recognised sequelae of delirium.
82 onic social stressors, and hence, that major depressive illness is associated with a parainflammatory
83 has received considerable attention, is that depressive illness is associated with a specific underly
84 s accumulated from case-control studies that depressive illness is associated with blunted reward act
85                                              Depressive illness is associated with sustained widespre
86 re consistent with the view that early-onset depressive illness is distinguished from late-onset majo
87  action of lithium in the treatment of manic-depressive illness is still unknown.
88 city as a subtype in the genetic analysis of depressive illness is warranted.
89            Bipolar affective disorder (manic-depressive illness) is a chronic, severe, debilitating i
90      Bipolar affective disorder (BPAD; manic-depressive illness) is characterized by episodes of mani
91 e disorders, and there is some evidence that depressive illness itself may be a risk factor in the ae
92  nucleus (DRN) may be dysfunctional in major depressive illness, making it important to understand th
93 efinement of the definition of chronicity in depressive illness may increase the power of such studie
94 ition to its use in the treatment of bipolar depressive illness, may have an expanded use in the inte
95 ich our major diagnostic categories of manic-depressive illness (MDI) and dementia praecox were devel
96  on this region as a potential biomarker for depressive illness, noting meanwhile that differences at
97                                        Manic depressive illness, or bipolar disorder (BP), is charact
98                               Employees with depressive illness plus any of the other conditions cost
99 havioral and physiological manifestations of depressive illness produce a significant decrease in lif
100 ll hypothesis that both unipolar and bipolar depressive illnesses show similarly blunted reward learn
101  mood stabilizers for the treatment of manic-depressive illness, stimulated the ERK pathway in the ra
102       Despite the indications of more severe depressive illness, those who received higher levels of
103         Using such methods, linkage of manic depressive illness to loci on chromosome 18 has been rep
104  of polymorphisms in the AC7 gene with major depressive illness (unipolar depression) based on Diagno
105            The 2-year incidence of diagnosed depressive illness was 21.7% in hypogonadal men vs 7.1%
106 matched controls to test the hypothesis that depressive illness was associated with a blunted behavio
107                                              Depressive illness was associated with a mean of 9.86 an
108                                            A depressive illness was present in 13.9% of the traumatic
109 ic social isolation, a known risk factor for depressive illness, we show that 5-HT neurons in the dor
110  compares the health and disability costs of depressive illness with those of four other chronic cond

 
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