Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Treatment of L cells with 3 to 10 mM 3':5'-cyclic adenosine monophosphate (cAMP) in the presence of interferon was found to potentiate the development of antiviral activity. The dose response of interferon activity at various time periods in the presence and absence of cAMP indicated that potentiation of interferon activity by cAMP occurred at an early stage in the development of antiviral activity. Among the analogues of cAMP tested for interferon-potentiating activity, only the acylated derivatives were found to be active. Combined L-epinephrine and theophylline treatment of cells elevated cellular cAMP levels and also potentiated interferon-mediated antiviral activity. Interferon was also found to elevate cAMP levels in L cells. This activity was limited to biologically active interferon and antagonized the depression of cAMP associated with vesicular stomatitis virus (VSV) infection of L cells. These observations suggest that some aspects of interferon's biological activity is associated with an alteration in cellular levels of cAMP.
J Gen Virol 1975 Sep
PMID:Cyclic AMP potentiation of interferon antiviral activity and effect of interferon on cellular cyclic AMP levels. 17 Mar 77

The electroencephalographic sleep patterns of 12 patients with a final diagnosis of primary depression and those of 12 patients admitted to the Clinical Research Unit with this diagnosis, but subsequently also found to be suffering from severe medical disease, were compared. Patients with depression concurrent with severe medical disease have significantly less phasic conjugate rapid eye movement (REM) activity during REM sleep than subjects with the diagnosis of a primary depression. These findings suggest that quantification of REM density may be used clinically to distinguish between medical-depressive syndromes and primary affective disorders.
Arch Gen Psychiatry 1976 Sep
PMID:Rapid eye movement sleep density. An objective indicator in severe medical-depressive syndromes. 18 22

Studies of severely depressed hospitalized patients suggest a shortened rapid eye movement (REM) latency as a specific biological marker for primary affective disease. To assess the validity of these findings, 40 outpatients referred to our Electroencephalographic Sleep Center for evaluation of depressive symptoms were studied. Concurrent with the all night EEG sleep studies, all patients received a brief clinical interview and a battery of self-rating scales. The entire sample was then subdivided into primary and secondary depressives on the basis of follow-up diagnoses. While there were no significant differences between groups on self-ratings of depressive symptoms, the group of primary depressives had significantly shorter REM latencies and higher measures of phasic REM than the secondary depressives. Furthermore, in this patient group, the delineation of primary vs secondary depression was greater than 80% on the basis of only two nights of EEG sleep. Such objective biological measures, if replicated, could provide a method for increasing the accuracy of differential diagnosis among depressed populations in clinical research.
Arch Gen Psychiatry 1976 Sep
PMID:Electroencephalographic sleep diagnosis of primary depression. 18 23

In the treatment of endogenous depression by rapid eye movement (REM) sleep deprivation, depression improvement, measured on Hamilton and Global scales, correlated positively and significantly (P less than .05) with REM pressure (increase of REM sleep stimulated by REM sleep deprivation). This dose-response relationship suggests that (1) REM pressure was an indicator of a process that mediated the antidepressant effects of REM sleep deprivation, and (2) since improvement varied with stimulation of REM sleep, an unknown stimulus of REM sleep is a naturally occurring, endogenous antidepressant.
Arch Gen Psychiatry 1977 Jan
PMID:Endogenous depression improvement and REM pressure. 18 25

Biochemical and electrophysiological factors were studied longitudinally in a rapidly cycling manic-depressive patient. Slow changes in mood, motor activity, sleep, and urinary norepinephrine levels during the course of each depressed and manic episode are reported, as well as rapid alterations in many variables at the time of mood switch. Urinary concentrations of norepinephrine and its metabolite, 3-methoxy-4-hydroxyphenyl glycol (MHPG) were significantly lower in depression than in mania; norepinephrine but not MHPG excretion increased prior to the switch. We postulate that the slow behavioral and biological changes preceding switches in this patient are an important manifestation of the cyclic process in manic-depressive illness.
Arch Gen Psychiatry 1977 Apr
PMID:Alterations in motor activity, sleep, and biochemistry in a cycling manic-depressive patient. 19 69

When retinas from dark-adapted C57BL/6 mice were incubated in the dark for 5 min at 37 degrees C in Earle's medium, they contained 80-120 pmol/mg protein of cGMP and about 13 pmol/mg protein of cAMP. When the incubation in darkness was in calcium-deficient Earle's medium with 3 mM EGTA, a 10-20 fold increase occurred in the cGMP level, peaking at 2-3 min, but no change occurred in cAMP. This elevated level fell in 3 min to normal dark levels on return to normal Earle's medium, but was still about three times that of control levels after 15 min in EGTA-containing solution. Bright light after 2 min of dark incubation of dark-adapted retinas resulted in a 40-50% fall in cGMP, and bright light sharply reduced the elevated dark cGMP level of retinas in calcium-deficient media with 3 mM EDTA. However, no depression of normal dark levels of cGMP has thus far been obtained by increasing external calcium levels, even in the presence of the ionophore A23187. All the above phenomena involving dark cGMP levels and calcium are similar in Earle's medium with 100 mM of K+ substituted for Na+. Congenic rodless (rd/rd) mouse retinas have less than 5% of control cGMP and show only traces of calcium sensitivity. Thus, the above phenomena in controls are likely to be largely occurring in rods. The data suggest a dependency of the dark cGMP level on the calcium level, but that the light-induced fall in cGMP may largely be calcium insensitive.
J Gen Physiol 1978 May
PMID:Calcium and cyclic nucleotide regulation in incubated mouse retinas. 20 16

Nocturnal sleep was recorded from ten unrestrained, group-living Macaca nemestrina (pigtail) monkey infants, using implantable multichannel biotelemetry systems, during the agitation-depression behavioral reaction that follows maternal separation. Sleep disturbances during the four nights of separation were characterized by decreases in rapid eye movement (REM) time and in the number of REM periods, and increases in REM latency. Time awake and number of arousals were increased. Slow-wave sleep was not significantly affected. Sleep pattern changes were most pronounced the first separation night, and tended to decrease as separation continued, whereas behavioral measures of depression tended to increase as separation continued (up to four days). Sleep patterns returned to normal following reunion with the mother. Those infants who had the most severe sleep disturbances the first separation night (more time awake, less total sleep, less REM) also tended to become most depressed behaviorally later in the separation period.
Arch Gen Psychiatry 1978 Oct
PMID:Nocturnal sleep in separated monkey infants. 21 85

Piribedil, a compound that stimulates dopamine receptors in a relatively specific fashion, was administered to 11 hospitalized depressed patients. The dopamine agonist significantly decreased rapid eye movement (REM) sleep and percent REM sleep and increased REM latency. Piribedil decreased the probenecid-induced accumulation of the dopamine metabolite homovanillic acid (HVA) in CSF. A range of mild to moderate antidepressant effects was noted; one patient worsened and one developed recurrent manic episodes. The degree of improvement in depression was negatively correlated with pretreatment values of HVA in CSF (r = -.66, P less than .05). These data suggest that the heterogeneity of clinical response may be related to biological differences in depressed patients and that those with low initial dopaminergic function respond best to increased dopamine receptor stimulation.
Arch Gen Psychiatry 1978 May
PMID:Effects of a dopamine agonist piribedil in depressed patients: relationship of pretreatment homovanillic acid to antidepressant response. 21 97

The effectiveness of estrogen therapy for alleviating severe depressions was investigated in a double blind study in which large doses of estrogen were administered to 15 premenopausal and 8 postmenopausal women and placebos were administered to 12 premenopausal and 5 postmenopausal women. The estrogens and placebos were administered over a three month period, and the women were blind rated each week by psychologists and psychiatrists using Hamilton rating scales for depression. There was a significant decline in the depression scores for the group treated with estrogens when compared to the placebo treated group. Considerable variation in the degree of improvement for the women in the estrogen treated group was observed. These variations were not related to age or to menstrual status but were significantly related to depression duration. Women with shorter histories of depression were more likely to show improvement than women with longer illness durations. Efforts were also made to understand the physiological mechanisms through which estrogen treatment contributed toward reducing depression. Previous studies revealed that decreased availability of norepinephrine at the central adrenegic receptor sites in the brain was related to the manifestation of depression while increased availability of norepinephrine at these sites was ralated to a manifestation of elation. Increased availability of norepinephrine has been shown to be related to an inhibition of monoamine oxidase activity (MAO), and estrogen, in turn, has been demonstrated to inhibit MAO activity. During the 3 month study period, 2 blood samples were obtained from the women every week and analyzed for MAO activity. All patients had elevated levels of plasma MAO activity prior to treatment. In estrogen treated patients, MAO levels declined significantly; MAO levels unexplicably increased for the placebo treated group. Reduced MAO activity was not, however, significantly correlated with lower depression ratings. In determining the risk/benefit ratio of estrogen therapy both the risk of developing endometrial cancer and the risks of life long disability and suicide stemming from severe depression should be considered. Tables show 1) mean depression ratings and average MAO activity levels before and after treatment for the estrogen and placebo treated groups and 2) degree of change in depression ratings before and after treatment for both groups of women.
Arch Gen Psychiatry 1979 May
PMID:Estrogen therapy for severe persistent depressions in women. 21 2

We attempted to validate the DSM-II diagnosis of hysterical personality and the depression often experienced by such patients by comparing mean Minnesota Multiphasic Personality inventory (MMP) scores of hysterical personality patients with those of paranoid schizophrenic patients and a group with mixed psychiatric diagnoses. Index patients had significantly higher scores than either control group and could be distinguished on individual scales from the paranoid schizophrenics. However, the mean MMPl profile of hysterical personalities was similar to that of depressed controls. Therefore, the MMPl alone could not differentiate these two groups nor could it confirm or refute the validity of the diagnostic concept of hysterical personality, but it did support the clinical observation that depression is a major risk for individuals given this diagnosis and that the experience of depression by these patients is genuine.
Arch Gen Psychiatry 1975 Feb
PMID:The hysterical personality. An attempt at validation with the MMPI. 23 26


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