1,293 publications from this institution
Viral diseases are one of the main problems and risk factors in aquaculture. At present diseases are diagnosed by detection of pathogens and clinical symptoms. Identification of genes involved in early responses to viruses is important for better knowledge of antiviral defence and development of diagnostic tools. The aim of this study was to search for gene markers common for viral infections in Atlantic salmon based on microarray analyses of a wide range of samples. Gene expression profiles from fish and cell cultures infected with different viruses and treated with the synthetic double-stranded RNA poly(I:C) were compared in order to identify virus responsive genes (VRG). The list of VRG defined in this study contained 117 genes with known or unidentified functions. Several genes, including the most highly ranked one (receptor transporting protein), had not been previously reported to be involved in antiviral defence. VRG were characterized by a rapid induction and low tissue specificity, and their expression levels were related to the viral load. Immunofluorescence analyses of proteins encoded by VRG in cardiac tissue of salmon with the viral disease cardiomyopathy syndrome (CMS) revealed a common expression pattern. In head kidney leukocytes VRG showed comparable or equal responses to CpG and poly(I:C), which mimic respectively bacterial DNA and viral RNA. Most VRG showed highly correlated expression with interferon-a (IFNa). Sequence comparison of salmon VRG with those from other species gave an understanding of the evolution of these genes, which showed a remarkably rapid sequence divergence in comparison with the entire proteome. VRG emerged both before and after separation of teleosts and tetrapods, and among genes found exclusively in fish species there were members of several multigene families: tripartite motif proteins, gig1- and gig2-like proteins. Several VRG, including genes with unknown functions and orthologs to mammalian RNA helicase RIG-I and chemokine C-X-C type 10, were present in cyprinid and salmonid fish but not in the phylogenetically advanced orders, suggesting that they have been lost in the evolution of Teleostei. Apparently, a number of genes involved in antiviral responses in salmon have acquired different functional roles in higher vertebrates.
Abstract There is some evidence that major depression is accompanied by activation of the inflammatory‐response system (IRS). It has been hypothesized that increased production of proinflammatory cytokines may play a role in the etiology of major depression. If increased production of proinflammatory cytokines is at all involved in the etiology of depression, one would expect antidepressive treatments to have negative immunoregulatory effects. This paper reviews the effects of antidepressants, such as tricyclic antidepressants (TCAs), selective serotonin reuptake inhibitors (SSRIs), heterocyclic antidepressants (HCAs), serotonin‐noradrenaline reuptake inhibitors (SNRIs), lithium, l ‐5‐hydroxytroptophan (L‐5‐HTP), reversible inhibitors of MAO‐A (RIMA) on the production of proinflammatory cytokines, e.g. interferon‐γ (IFNγ), and negative immunoregulatory cytokines and agents, e.g. interleukin‐10 (IL‐10). In depressed patients, prolonged treatment with antidepressants and mood stabilizers normalizes signs of activation of the IRS, such as increased serum IL‐6 and acute phase protein concentrations. In vitro, it has been shown that various types of antidepressive drugs, including TCAs (imipramine; clomipramine); SSRIs (citalopram, fluoxetine, sertraline); lithium; SNRIs (venlafaxine); HCAs (trazodone); RIMAs (moclobemide) and L‐5‐HTP significantly suppress the ratio of IFNγ/IL‐10 production by peripheral blood immunocytes. These antidepressant drugs appear to have a common effect on the IRS, i.e. in vitro they increase the production of IL‐10 by peripheral blood leukocytes. Thus, the results suggest that antidepressants have negative immunoregulatory effects. It may be speculated that antidepressants exert some of their antidepressant effects through their negative immunoregulatory capacities. Copyright © 2001 John Wiley & Sons, Ltd.
There is now evidence that the availability of plasma tryptophan is decreased during pregnancy and the puerperium and also in patients with major depression and inflammation. The aims of the present study were to examine: (i) the effects of pregnancy and delivery on plasma tryptophan and the amino acids known to compete for the same cerebral uptake mechanism (CAAs), valine, leucine, tyrosine, phenylalanine and isoleucine; (ii) the relationships between the availability of plasma tryptophan and postpartum depression or anxiety; and (iii) the relationships between the availability of plasma tryptophan to the brain and inflammatory markers, such as serum interleukin-6 (IL-6), interleukin-1 receptor-antagonist (IL-1RA) and the leukaemia inhibitory factor receptor (LIF-R).The above variables were measured in 13 healthy non-pregnant and in 98 pregnant women 3 to 6 days before delivery and 1 and 3 days after delivery. On each occasion the parturient women completed the state version of Spielberger State-Trait Anxiety Inventory (STAI) and the Zung Depression Rating Scale (ZDS).Plasma tryptophan and the tryptophan/CAA ratio were significantly lower at the end of term and after delivery than in the plasma of non-pregnant, healthy women. The tryptophan/CAA ratio was significantly lower in the early puerperium than at the end of term. There were no significant relationships between the availability of plasma tryptophan and either post-partum depression or changes in the STAI or ZDS scores in the early puerperium. The changes in the tryptophan/CAA ratio from the end of term to the early puerperium were significantly and inversely related to serum IL-6, IL-IRA and LIF-R.The results show that the reduction in the availability of plasma tryptophan from the end of term to the early puerperium is related to immune activation; and that the lowered availability of plasma tryptophan is not related either to depressive or anxiety symptoms in the early puerperium or to post-partum depression ensuing some months later.
SYNOPSIS Several authors have reported attenuated adrenocorticotropin hormone (ACTH) responses to corticotropin releasing factor (CRF) administration in melancholic patients as compared with healthy controls. In order to explore the integrity of the hypothalamic–pituitary–adrenal (HPA)-axis in melancholics, we examined the following parameters in 98 subjects: the ACTH; β-endorphin; and cortisol responses to ovine CRF (oCRF) (100 μg/i.v.); and the postdexamethasone cortisol values. We found significant lower CRF-induced ACTH responses in melancholic patients as opposed to healthy controls and minor depressives, while major depressives occupied an intermediate position. The psychopathological correlates of the blunted CRF-induced ACTH responses were feelings of worthlessness, self-reproach, or excessive guilt. The CRF-stimulated β-endorphin and cortisol response did not differ between the study samples. Higher baseline plasma cortisol was associated with attenuated CRF-induced ACTH responses, but these effects were not pertinent to melancholia. There were no relationships between the disordered oCRF test results, and postdexamethasone cortisol values, age, body size, sex and severity of illness. The diagnostic power of the oCRF and the dexamethasone suppression test for melancholia is enhanced when both test results are combined.
Recently, analysis of partial variance (APV) was proposed as a technique to control for day-to-day variance in mitogen-induced lymphoproliferative responses whereby data obtained from controls, run in the laboratory on the same day, are used as covariates in regression analysis. In order to check the utility of the APV method in the interpretation of functional immune tests, we have reanalyzed lymphoproliferative responses in experimental subjects with depression (n = 38) stimulated by phytohemagglutinin (PHA), pokeweed mitogen (PWM) and concanavalin A (Con A) in relation to responses obtained in laboratory controls. There were no significant relationships between the depressed patients' and laboratory controls' lymphoproliferative responses to PHA, PWM or Con A. Controlling for day-to-day variation by means of regression analysis did not significantly alter the significant relationships between the patients' lymphoproliferative responses and clinical variables, such as depressive classification and severity of illness. It is argued that the APV method may not be used to adjust for an inappropriately high day-to-day variability in immune assays.
Abstract Xanthurenic acid (XA) is a secondary product of the biosynthesis of nicotinamide from L ‐tryptophan. Disturbances in this pathway have been observed in depression. An enhanced glucocorticoid secretion is considered to induce this pathway. This could result in reduced levels of L ‐tryptophan (L‐TRP) in the plasma. The present study investigates whether the synthesis of XA from L‐TRP is distrubed in depression, and also whether the synthesis of XA is intercorrelated with L‐TRP or measures of glucocorticoid secretion. To this end the XA excretion in 24 hour urine following L‐TRP loading was determined in 166 psychiatric inpatients. There were no significant differences in XA excretion between non‐depressed psychiatric controls, minor depression and major depression. Among the depressed patients there was a significant ( p <0·01) negative correlation between the excretion of XA and total L‐TRP levels in plasma, with abnormally decreased ( p <0·0006) L‐TRP levels occurring in the depressed patients with a disturbed XA excretion (≥ 106·8 m̈mol/24 hour).
The aim of the present study was to examine the relationships between suicidal ideation or suicidal attempts and severity of depression, presence of personality disorders, and sociodemographic factors in a population of depressed in‐patients. A total of 338 adult depressed psychiatric in‐patients were examined and classified according to DSM‐III criteria as having major depression with or without melancholic or psychotic features, adjustment disorder with depressed mood or dysthymic disorder. Scores on the Hamilton Depression Rating Scale (HDRS), Beck Depression Inventory (BDI) and Zung Self‐Rating Depression and Anxiety Scales (SDS and SAS) were measured. We found that suicidal ideation was significantly related to severity of depression (according to the HDRS and all self‐rating scales), a lower global assessment of functioning the year before hospitalization, and previous psychiatric hospitalizations. The items with the strongest predictive value for suicidal ideation were hopelessness, depressed mood, feelings of guilt, loss of interest and low self‐esteem. These symptoms predicted 43% of the variance in suicidal ideation. None of the above predictors of suicidal ideation was related to suicidal attempts. Depressed patients with a personality disorder attempted significantly more suicidal attempts and showed more suicidal ideation than depressed patients without personality disorder. No significant correlations were found between suicidal ideation or suicide attempts and gender, marital status, employment status or psychosocial stressors during the previous 6 months.
