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)

With a highly sensitive time-resolved fluorometric immunoassay (TR-FIA), serum thyrotropin (TSH) levels were determined in various conditions in healthy subjects. In addition, we compared the thyroid function in 10 depressed female patients with that in 27 female controls. 1) We evaluated a highly sensitive time-resolved fluorometric immunoassay kit for serum TSH. The lower limit of detection of TSH in serum was 0.008 less than U/ml. The intraassay and interassay variances were 3.0 greater than 3.6% and 3.4 greater than 5.1%, respectively. There was a significant correlation between basal TSH levels and maximum TSH values after TRH administration (r = 0.797, p less than 0.01). 2) The mean TSH levels in 31 healthy controls of both sexes was 1.26 +/- 0.96 less than U/ml, but TSH levels in women were significantly higher than in men (p less than 0.01). A large intra-individual variation of serum TSH levels determined on different days was found equally in both men and women. The nyctohemeral elevation of TSH levels was not clearly seen prior to the onset of normal sleep, but the nocturnal rise of TSH levels was remarkably accentuated by sleep deprivation. 3) The serum TSH levels in depressed female patients were significantly lower than those in healthy female controls when the post-menopausal subjects were excluded. For the serum thyroid hormone concentrations, serum T4 levels were normal. Serum free T3 levels tended to be lower, although the reduction was not significant. The serum levels of these 3 thyroid hormones were not related to serum TSH values. The present study demonstrated a large variation of TSH levels in various conditions, even in the same individuals, indicating the necessity of strictly controlled conditions in the study of TSH secretion. A significant reduction in TSH levels was observed in the depressed female patients when the post-menopausal subjects were excluded. Our results suggest that the dysfunction of the regulating mechanism of the pituitary-thyroid axis in depression may occur at a pituitary or a suprapituitary level.
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PMID:[Studies on the factors affecting serum thyrotropin levels in healthy controls and on the thyroid function in depressed patients using a highly sensitive immunoassay]. 228 57

Prostaglandin E2 (PGE2) has been known to modulate immune responses by inhibiting T-cell activation following hemorrhagic and traumatic injury. Recently, we documented a sepsis-related depression in concanavalin A (ConA)-induced T-cell proliferation and intracellular Ca2+ (Ca2+i) mobilization. The present study evaluated the potential role of PGE2 in the sepsis-related attenuation in Ca2+ signaling and proliferation in T cells. Sepsis was induced in rats by implanting into their abdomen fecal pellets containing Escherichia coli (150 CFU) and Bacteroides fragilis (10(4) CFU). A group of rats implanted with septic pellets were treated with indomethacin at three consecutive time points. Levels of PGE2 in blood were measured with a radioimmunoassay kit. ConA-induced [Ca2+]i mobilization in T cells obtained from indomethacin-treated and untreated rats was measured with Fura-2 and microfluorometry. We observed a 10-fold increase in PGE2 levels in the circulation of septic rats compared with levels in rats implanted with bacterium-free sterilized pellets. The proliferative response and Ca2+i mobilization were significantly depressed in T cells obtained from septic rats 48 h after implantations compared with those in rats implanted with sterile pellets. However, treatment of rats with the cyclooxygenase inhibitor indomethacin prevented the sepsis-related depression in ConA-induced T-cell Ca2+i mobilization as well as proliferation. Further, incubation of T cells from nonimplanted control rats with PGE2 resulted in a substantial depression in both T-cell proliferation and Ca2+i mobilization. The restoration of T-cell proliferation and Ca2+ signaling after indomethacin treatment of septic rats and the depression in the mitogen responsiveness in T cells previously exposed to PGE2 suggest that the PGE2 does play a significant role in the modulation of T-cell responses in septic rats and that such PGE2-induced suppression in T-cell activation is likely due to an attenuation in Ca2+ signaling.
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PMID:Role of Ca2+ in prostaglandin E2-induced T-lymphocyte proliferative suppression in sepsis. 762 37

It has been reported that fasting plasma ghrelin levels may play a role in the pathophysiology of eating disorders. In this study, the authors examined whether serum levels of ghrelin were altered in the patients with bulimia nervosa (BN). We enrolled 18 female patients with BN, and 21 age-matched female controls for this study. Eating-related psychopathology, depressive symptoms were evaluated by using the Bulimic Investigatory Test, Edinburgh (BITE) and the 17-item Hamilton Depression Rating Scale (HDRS). Serum levels of ghrelin were measured by Ghrelin enzyme immunoassay kit. There were no significant differences in serum ghrelin levels between the patients with BN and normal controls. Furthermore, the authors did not found correlation between serum ghrelin levels and clinical parameters in the patients with BN. Our study suggests that serum ghrelin levels in the patients with BN were indistinguishable from normal controls. Therefore, it is unlikely that ghrelin plays a role in the pathophysiology of BN.
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PMID:No changes in serum ghrelin levels in female patients with bulimia nervosa. 1561 Sep 31

Psychological depression is an independent risk factor for coronary artery disease. C-reactive protein has been implicated as a mediator of the effect of psychological depression. Several studies have found that individuals, especially men, who report higher levels of psychological depression also have higher levels of C-reactive protein. The current study was undertaken to replicate these results in a Brazilian population, in which there is a much wider range of variation in both background characteristics (such as socioeconomic status) and coronary artery disease risk factors. A sample of 271 individuals was interviewed using the Center for Epidemiological Studies Depression Scale. Fasting blood samples were obtained and evaluated for C-reactive protein (assessed by a turbidimetric immunoassay using a Dade Behring kit) analysis in a subsample (N = 258) of individuals. The mean +/- SD C-reactive protein for the entire sample was 0.43 +/- 0.44, with 0.42 +/- 0.48 for men and 0.43 +/- 0.42 mg/L for women. Data were analyzed using multiple regression analysis, controlling for age, sex, body mass index, socioeconomic status, tobacco use, and both total cholesterol and low-density lipoprotein cholesterol. Higher reported depressive symptoms were correlated with higher C-reactive protein for men (partial r = 0.298, P = 0.004) and with lower C-reactive protein for women (partial r = -0.154, P = 0.059). The differences in the associations for men and women could be a result of differential effects of sex hormones on stress reactivity and immune response. On the other hand, this difference in the associations may be related to gender differences in the disclosure of emotion and the effect that self-disclosure has on physical health and immune response.
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PMID:Depressive symptoms and C-reactive protein in a Brazilian urban community. 1690 75

A 65-year-old woman had a history of deep vein thrombosis and depression. Psoriasis was diagnosed in 1986 and various topical and systemic therapies, singly or in combination, were prescribed: tar, topical corticosteroids, cyclosporine, etretinate, and methotrexate. Two courses of oral and one course of bath psoralen plus UVA (PUVA) therapy (cumulative dose, 467 J/cm(2)) and UVB (2.96 J/cm(2)) had been given. In January 1999, she developed a flare of generalized psoriasis. In May 1999, therapy with PUVA (8-methoxypsoralen) plus topical acetonide triamcinolone 0.1% was initiated. At the time, she was taking acenocoumarol, lorazepam, and hydroxyzine chlorhydrate. In August 1999, at session 30, when the dose of UVA was 9 J/cm(2), and the total dose was 205 J/cm(2), a bulla appeared on the dorsum of the toe and was controlled with topical antibiotics. Five further sessions of PUVA were given and a generalized itching bullous eruption appeared all over the body. PUVA was stopped and the patient was hospitalized. On physical examination, extensive psoriatic plaques plus vesicles and bullae on the normal skin and on psoriatic lesions were observed all over the body (Fig. 1). Histopathologic study of a lesion showed a subepidermal vesicle containing fibrin, neutrophils, and a few eosinophils. No sunburn cells were observed (Fig. 2). The direct immunofluorescence (DIF) test of perilesional uninvolved skin revealed immunoglobulin G (IgG) (Fig. 3) and C3 at the dermal-epidermal junction. The DIF study using the patient's skin, previously treated with 1 m NaCl, localized the IgG at both the epidermal and dermal sides of the basement membrane zone (Fig. 4). Bullous pemphigoid (BP) was diagnosed and therapy with prednisone (60 mg/day) was started. The disease was well controlled in 3 weeks. The dose of prednisone was tapered and stopped 20 months later, without any recurrence. Study of the antibodies by the indirect immunofluorescence (IIF) test, using monkey esophagus and guinea pig as substrate, was positive at a titer of 1/160 in September 1999. The titer decreased to 1/10 in January 2000, and was negative in July 2000. An enzyme-linked immunosorbent assay (ELISA) test, performed using the commercial kit MBL, which identifies antibodies directed against epitopes of the extracellular fragment NC16 of antigen 2 of BP, was positive at 15 U/mL (normal value, < 9 U/mL) in September 1999, and negative in July 2000 (Table 1).
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PMID:Bullous pemphigoid in a patient with psoriasis during the course of PUVA therapy: study by ELISA test. 1696 18

The aim of the present study was to investigate the role of mitochondrial nitric oxide synthase (mtNOS) in the septic shock and analyze its relationship to ventricular contractility. Two models of septic shock [lipopolysaccharide (LPS)-induced and cecal ligation and puncture (CLP)-induced] were used. There was a significant depression of ventricular contractile parameters recorded in the late stage of the septic shock. After measurement of ventricular-dynamic parameters, mitochondrial and cytoplasmic fractions were isolated and their nitric oxide synthase (NOS) activity was assessed using a NOS activity assay kit. Both models showed a larger increase in mitochondrial NOS activity than that in cytosol. However, the increase in mtNOS activity in the LPS-induced shock model was less pronounced than in the CLP-induced model. Regression analysis shows that mitochondrial nitric oxide synthase (mtNOS) activity is negatively correlative to the left ventricular developed pressure in CLP model. The results suggest that mitochondrial NOS may mainly contribute to the ventricular depression in the septic shock.
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PMID:The relationship of ventricular dynamics and mitochondrial nitric oxide synthase activity in septic shock models. 1728 88

In this present work, it is aimed to demonstrate BDNF serum concentrations in patients with dysthymia and to compare them with BDNF serum concentrations in patients with major depressive disorder and healthy subjects. The study was carried out in Celal Bayar University Hospital, Manisa, Turkey. Seventeen patients with dysthymia, 24 patients with major depressive disorder and 26 subjects without any psychiatric diagnosis and any psychiatric treatment were included in the study. The severity of depression was assessed with 17-item HAM-D. All subjects were asked to give their written consent. Blood samples were collected at baseline. Serum BDNF was kept at -70 degrees C before testing, and assayed with an ELISA Kit (Promega; Madison, WI, USA), after dilution with the Block and Sample solution provided with the kit. The data were subjected to the analysis of variance. The BDNF serum concentrations of the dysthymia group (mean=28.9+/-9.2 ng/ml) were significantly higher than that of the major depressive disorder group (21.2+/-11.3 ng/ml) (p=0.002), and it was not different from the level of the control group (31.4+/-8.8 ng/ml). BDNF serum concentrations and HAM-D score did not have any significant correlation in the dysthymia and major depression groups (r=-0.276, p=0.086). The low level of BDNF in patients with dysthymic disorder seems to point out that BDNF changes in mood disorders are state-dependent and vary according to the severity of depressive episodes.
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PMID:Serum brain-derived neurotrophic factor level in dysthymia: a comparative study with major depressive disorder. 1743 17

This study tried to investigate the relationships between serum brain-derived neurotrophic factor (BDNF) protein levels and major depressive patients and discuss the effects of antidepressants on the serum BDNF protein levels. A total of 218 participants, including 111 patients with major depression (91 women) and 107 healthy controls (65 women), were recruited in this study. Serum BDNF protein levels were measured using an ELISA kit. Psychiatric diagnoses were made according to DSM-IV criteria. Severity of major depression was assessed by the 17-item Hamilton Depression Rating Scale. Using analysis of covariance with age adjustment, there were significantly low serum BDNF protein levels in depressive patients than healthy controls in women (F=7.530, p=0.007), but not in men. Additionally, changes in serum BDNF protein levels were significantly increased in 79 patients taking antidepressants during a period of 4 weeks (t=2.116, p=0.038), especially in 61 women (t=2.542, p=0.014). Age-adjusted ANCOVA revealed no significant differences in serum BDNF protein levels between 58 responders and 21 non-responders (F=0.008, P=0.928). In responders, there were significantly increased changes in serum BDNF protein levels in 44 women (t=2.501, p=0.016), but not in 14 men (t=-0.767, p=0.457). These analytical results suggest that low serum BDNF may play an important role in depressive women and antidepressant treatment significantly increase serum BDNF. However, further studies of larger populations are necessary to confirm these results and further elucidate the effects of different classes of antidepressants on serum BDNF protein levels.
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PMID:Serum brain-derived neurotrophic factor levels in patients with major depression: effects of antidepressants. 1758 40

The objectives of the present study were to evaluate the presence of antipolymer antibody (APA) seropositivity in 285 Italian patients affected by primary fibromyalgia (FM) and to verify whether APA levels correlate with disease severity and with cytokine levels.APA levels were determined on serum samples by an indirect ELISA kit that detects IgG APA. Cytokines (IL-1, IL-6, IL-8, IL-10 and TNFalpha) were measured by ELISA in plasma. The impact of FM on the quality of life was estimated using the Fibromyalgia Impact Questionnaire, while pain severity was evaluated using a visual analogic scale. Patients were also characterized by the presence of tiredness, stiffness, nonrestorative sleep, anxiety, depression, tension headache, irritable bowel syndrome, temporomandibular dysfunction and Raynaud's phenomena. Using a cut-off value of 30 U, APA-positive values were detected in 60 FM patients (21.05%) and in 15 healthy control individuals (15.00%) without significant differences among their levels or the percentage of seropositivity. FM patients with moderate and severe symptoms had slightly higher APA levels with respect to patients with mild symptoms. APA-seropositive patients exhibited significant correlations between APA levels and the Fibromyalgia Impact Questionnaire estimate (P = 0.042), tiredness (P = 0.003) and IL-1 levels (P = 0.0072). In conclusion, APA cannot be considered a marker of disease in Italian FM patients. The presence of APA, however, might permit the identification of a subset of FM patients with more severe symptoms and of patients who may respond differently to different therapeutic strategies.
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PMID:Antipolymer antibody in Italian fibromyalgic patients. 1782 28

Posttraumatic stress disorder (PTSD) is a severely debilitating anxiety disorder. Over 80% of patients with PTSD also exhibit other psychiatric condition, such as bipolar disorder (BP) or major depression (MDD). Previously, it has been found that p11 mRNA expression was significantly changed in post mortem cortex of patients with PTSD and depression. We hypothesize that p11 mRNA levels in the peripheral blood cells will be a potential biomarker for PTSD with heterogeneity in terms of type of trauma, time since trauma and duration of illness. We examined the peripheral blood mononuclear cell (PBMC) P11 mRNA of patients with PTSD (n=13), major depressive disorder (MDD, n=16), bipolar disorder (BP, n=24), and schizophrenia (SCZ, n=12) or controls (n=14) using quantitative real-time PCR and the circulating levels of cortisol in blood plasma and saliva of PTSD using radioimmunoassay kit CORT-CT2. The Hamilton Rating Scale for Depression (HAMD) and Anxiety (HARS), the Chinese version of the Davidson Trauma Scale-Frequency (CDTS-F) and the Chinese version of the Davidson Trauma Scale-Severity (CDTS-S), and Impact of Event Scale-Revised (IES-R) were administered. We found that patients with PTSD had lower levels of p11 mRNA than control subjects, while those with MDD, BP and SCZ had significantly higher p11 levels than the controls. P11 mRNA levels were positively correlated with the scores of HAMD (r=0.62, p<0.05), CDTS-F (r=0.71, p<0.05) and CDTS-S (r=0.62, p<0.05), while they did not correlate with scores of HARS and IES-R. Basal levels of plasma and salivary cortisol of PTSD patients were not statistically different from those of controls. Our findings suggest that PBMC p11 mRNA expression levels may serve as a potential biomarker to distinguish PTSD from BP, MDD and SCZ.
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PMID:Levels of the potential biomarker p11 in peripheral blood cells distinguish patients with PTSD from those with other major psychiatric disorders. 1938 Jan 52


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