UMLS:C0011570 - FACTA Search

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Query: UMLS:C0011570 (depression)
172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Self-injurious behavior involving deliberate self-harm and suicide attempts by inmates while under custodial authority is a major problem for prisons and jails (prevalence, legal obligation for suicide prevention, and stress for officers). The differentiation of "serious" vs. "non-serious" and often manipulative suicide attempts as distinct phenomena, each with its own clinical features, is controversially discussed in current literature and a challenge for every diagnostician. If distinct clinical presentations and histories can be observed, an estimation of the seriousness of each act of self-injurious behavior can be simplified, whereby appropriate treatment of the individual case becomes possible. The aim of the study was to find differences between self-injurious behavior of "low seriousness" (i.e. low lethality and low suicidal intent) and of "high seriousness". Therefore, inmates showing self-injurious behavior were divided into subgroups of deliberate self-harm and suicide attempters on the basis of the act's intent and lethality. This was followed by a comparison of the clinical presentations of the individual inmates constituting the subgroups. Hence, 49 inmates showing self-injurious behavior were interviewed and tested with a variety of instruments (SCID-I and II, PCL-R, BDI-II, BHS, BSS, SIS, etc.), and their prison and health files were examined. The results indicate significant correlations between seriousness and some demographic, prison-related variables as well as different measures of depression. Negative, but nonsignificant correlations could be observed with regard to cluster B personality disorders. The PCL-R total score as well as PCL-R factor 1 showed a statistical trend for negative correlations with measures of seriousness. Inmates showing deliberate self-harm and suicide attempters seem to differ in a number of ways. Implications on how the individual prisoner should be treated are discussed.
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PMID:Deliberate self-harm and suicide attempt in custody: distinguishing features in male inmates' self-injurious behavior. 1678

This study aimed at the identification of acute and post-traumatic stress responses, and comorbid mental disorders in breast cancer patients. Structured clinical interviews for DSM-IV (SCID) were conducted post-surgery with 127 patients (t1). Screening measures were used to assess post-traumatic stress responses, anxiety, and depression at t1 and at 6 months follow-up (t2). Based on the SCID, prevalence rates were 2.4% for both, cancer-related ASD and PTSD. Experiences most frequently described as traumatic were the cancer diagnosis itself and subsequent feelings of uncertainty. Patients with lifetime PTSD (8.7%) were more likely to meet the criteria for cancer-related ASD or PTSD (OR=14.1). Prevalence estimates were 7.1% for Adjustment Disorder, 4.7% for Major Depression, 3.1% for Dysthymic Disorder and 6.3% for Generalized Anxiety Disorder. Using the screening instruments, IES-R, PCL-C and HADS, we found PTSD in 18.5% at t1 and 11.2-16.3% at t2. The estimates of anxiety and depression reveal rates of 39.6% (t1) and 32.7% (t2) for anxiety, as well as 16.0% (t1) and 13.3% (t2) for depression (t1) (cut-off> or =8). The diagnosis of a life-threatening illness has been included as a potential trauma in the DSM-IV. However, it has to be critically evaluated whether subjective feelings of uncertainty like fears of treatment count among traumatic stressors, and thus, whether the diagnosis of PTSD is appropriate in this group of cancer patients. However, a large number of women with emotional distress illustrate the need for psychosocial counseling and support in this early treatment phase.
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PMID:Prevalence of acute and post-traumatic stress disorder and comorbid mental disorders in breast cancer patients during primary cancer care: a prospective study. 1685 47

Long-term depression (LTD) is one of the paradigms used in vivo or ex vivo for studying memory formation. In order to identify genes with potential relevance for memory formation we used mouse organotypic hippocampal slice cultures in which chemical LTD was induced by applications of 3,5-dihydroxyphenylglycine (DHPG). The induction of chemical LTD was robust, as monitored electrophysiologically. Gene expression analysis after chemical LTD induction was performed using cDNA microarrays containing >7,000 probes. The DHPG-induced expression of immediate early genes (c-fos, junB, egr1 and nr4a1) was subsequently verified by TaqMan polymerase chain reaction. Bioinformatic analysis suggested a common regulator element [serum response factor (SRF)/Elk-1 binding sites] within the promoter region of these genes. Indeed, here we could show a DHPG-dependent binding of SRF at the SRF response element (SRE) site within the promoter region of c-fos and junB. However, SRF binding to egr1 promoter sites was constitutive. The phosphorylation of the ternary complex factor Elk-1 and its localization in the nucleus of hippocampal neurones after DHPG treatment was shown by immunofluorescence using a phosphospecific antibody. We suggest that LTD leads to SRF/Elk-1-regulated gene expression of immediate early transcription factors, which could in turn promote a second broader wave of gene expression.
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PMID:Long-term depression activates transcription of immediate early transcription factor genes: involvement of serum response factor/Elk-1. 1690 57

This study investigated the signaling pathways responsible for ketamine-induced cardiac depression in guinea pigs. The left ventricular development pressure (LVDP), velocity of the change in pressure (dP/dt), and heart rate (HR) accompanied with the total magnesium efflux ([Mg]e) were measured simultaneously in perfused hearts. The level of activation of the extracellular signal-regulated kinases 1/2 (ERK 1/2) and p38 mitogen-activated protein (MAP) kinase. The intracellular ionized magnesium concentration ([Mg2+]i) was measured using Mag-fura 2 AM in a single cardiomyocyte. Ketamine produced reversible decreases in the LVDP, dP/dt, and HR accompanied by increases in the [Mg]e. Ketamine also produced significant activation of p38 MAP kinase and ERK 1/2, and produced a dose-dependent increase in the [Mg2+]i, which was inhibited SB203580 and PD98059. These results suggest that ketamine-induced cardiac depression can be partly responsible for the increase in [Mg2+]i and [Mg]e, accompanied by the activation of p38 MAP kinase and ERK 1/2 in guinea pigs.
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PMID:Ketamine-induced cardiac depression is associated with increase in [Mg2+]i and activation of p38 MAP kinase and ERK 1/2 in guinea pig. 1694 37

Cognitive dysfunction in patients with rheumatic disease encompasses a range of impairment. Their prevalence, co-occurrence, and impact on symptom severity were assessed in 57 patients with fibromyalgia (FMS) and 57 patients with rheumatic disease without FMS. Information pertaining to memory decline, mental confusion, and speech difficulty was extracted from questions embedded in a health questionnaire and a blind retrospective chart review. Pain, morning stiffness, fatigue, and sleep difficulty were established on a 0- to 100-mm visual analog scale. Variables of mental confusion, fatigue, tension, depression, anger, and vigor were assessed using the Profile of Mood States.Compared with the non-FMS sample, patients with FMS complained more often of memory decline (70.2-24.6%), mental confusion (56.1-12.3%), and speech difficulty (40.4-3.5%). Memory decline and mental confusion were coupled more often in patients with FMS (50.9-8.8%). Patients with FMS with this combination of cognitive problems reported more pain (76.0-45.4%), stiffness (79.7-43.7%), fatigue (79.6-52.6%), and disturbed sleep (59.2-36.6%) compared with patients with FMS with memory problems alone. Patients with rheumatic disease substantially differ in cognitive vulnerability, with patients with FMS at considerably higher risk for cognitive difficulty. More importantly, the prevalence of a combined disturbance in memory and mental clarity is high and closely associated with the perception of increased illness severity and diminished mental health in FMS. That this linkage has the possibility of having a great deal to do with an important clinical variant of FMS underscores the need for greater clinical recognition of this underrecognized pattern and for further research.Patients with fibromyalgia frequently report memory and concentration problems, especially if asked about them. Clinicians could judge these complaints as similar to adult attention deficit syndrome and reassure the patient. Trying medication to improve attention and concentration is sensible but untested in fibromyalgia.
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PMID:The prevalence and clinical impact of reported cognitive difficulties (fibrofog) in patients with rheumatic disease with and without fibromyalgia. 1704 64

This study documents the prevalence of male childhood sexual abuse (CSA) and psychological sequelae in a sample of disaster workers deployed to the World Trade Center (WTC) site following the September 11, 2001 terrorist attack. There are limited data on male CSA and its psychological impact, especially on a large non-treatment seeking sample. As part of a mandatory medical screening program, workers were assessed with well-validated and widely used clinician interview and self-report measures following their involvement in the restoration of services to Ground Zero and surrounding areas of lower Manhattan. Frequency of CSA measured by the Traumatic Events Interview (TEI) was 4.3% (n = 92). Clinician interview and self-report data were analyzed using t-tests, revealing statistically significant relationships (but not clinically meaningful scores) between CSA and scores on the CAPS, PCL, BDI, STAXI, and SDS. Further analyses revealed that individuals endorsing CSA were three-times more likely to score high (vs. low) on the BDI and CAPS. Since disaster workers traditionally summon images of strength and mastery, professionals may overlook CSA and symptoms of depression and PTSD in this population.
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PMID:Incidence of male childhood sexual abuse and psychological sequelae in disaster workers exposed to a terrorist attack. 1713 72

Adenosine is arguably the most potent and widespread presynaptic modulator in the CNS, yet adenosine receptor signal transduction pathways remain unresolved. Here, we demonstrate a novel mechanism in which adenosine A1 receptor stimulation leads to p38 mitogen-activated protein kinase (MAPK) activation and contributes to the inhibition of synaptic transmission. Western blot analysis indicated that selective A1 receptor activation [with N6-cyclopentyladenosine (CPA)] resulted in rapid increases in phosphorylated p38 (phospho-p38) MAPK immunoreactivity in membrane fractions, and decreases in phospho-p38 MAPK in cytosolic fractions. Immunoprecipitation with a phospho-p38 MAPK antibody revealed constitutive association of this phosphoprotein with adenosine A1 receptors. Phospho-p38 MAPK activation by A1 receptor stimulation induced translocation of PP2a (protein phosphatase 2a) to the membrane. We then examined the actions of p38 MAPK activation in A1 receptor-mediated synaptic inhibition. Excitatory postsynaptic field potentials evoked in area CA1 of the rat hippocampus markedly decreased in response to adenosine (10 microM), the A1 receptor agonist CPA (40 nM), or a 5 min exposure to hypoxia. These inhibitory responses were mediated by A1 receptor activation because the selective antagonist DPCPX (8-cyclopentyl-1,3-dipropylxanthine) (100 nM) prevented them. In agreement with the biochemical analysis, the selective p38 MAPK inhibitor SB203580 [4-(4-fluorophenyl)-2-(4-methylsulfinylphenyl)-5-(4-pyridyl)-1H-imidazole] (25 microM) blocked the inhibitory actions of A1 receptor activation, whereas both the inactive analog SB202474 [4-ethyl-2-(p-methoxyphenyl)-5-(4'-pyridyl)-1H-imidazole] (25 microM) and the ERK 1/2 (extracellular signal-regulated kinase 1/2) MAPK inhibitor PD98059 [2'-amino-3'-methoxyflavone] (50 microM) were ineffective. In contrast, the p38 MAPK inhibitors did not inhibit GABA(B)-mediated synaptic depression. These data suggest A1 receptor-mediated p38 MAPK activation is a crucial step underlying the presynaptic inhibitory effect of adenosine on CA3-CA1 synaptic transmission.
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PMID:p38 mitogen-activated protein kinase contributes to adenosine A1 receptor-mediated synaptic depression in area CA1 of the rat hippocampus. 1713 4

Most previous studies on RET and p53 proteins have focused on thyroid papillary carcinoma. We investigated the role of RET and p53 protein expressions using immunohistochemistry on 52 cases of thyroid follicular adenomas and studied the follow-up records of these patients. The range of follow-up period was 3 to 14 years. The patients were between 15 and 71 years of age with a median age of 34.5 years. There were 46 females and 6 males. Except for 3 cases, all patients were Malays. The minimum volume of the tumour was 1000 mm3 and the maximum was 512,000 mm3 with a median of 270,000 mm3. Eleven (21.2%) cases showed RET expression. RET expression was not statistically significant when cross-tabulated against sex (p = 0.322), ethnicity (p = 0.518), age (p = 0.466) and symptom duration (p = 0.144). Six (11.5%) of 52 cases showed p53 immunopositivity. p53 expressions were also not significantly correlated to the clinical parameters above. There was no correlation between RET and p53 protein expressions. The only statistically significant finding was the association of tumour volume with duration of symptoms (p = 0.05). All patients are alive at the time of writing. 3 had recurrent goitre, 2 of these were diagnosed as colloid goitre while the third was a follicular lesion. One patient suffered from depression requiring anti-depressant treatment. In conclusion, unlike papillary carcinoma in which the roles of ret and p53 oncogenes are known, their roles in influencing the behaviour of follicular adenoma has not been ascertained.
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PMID:RET and p53 expression in thyroid follicular adenoma: a study of 52 cases with 14 years follow-up. 1719 91

Pathological immunoactivation is thought to play an important role in the etiology of depression; however, the effect of novel antidepressant drugs on immunity has been poorly recognized. Mirtazapine, an antidepressant drug, enhances noradrenergic and serotonergic neurotransmissions, which are crucially involved in the regulation of immune system activity. In the present study we examined the effect of acute and seven-day repeated administration of mirtazapine (20 mg/kg, i.p.) on immunoreactivity in noradrenaline transporter knockout (NET-KO) and wild-type male C57BL/6J mice subjected to the forced swimming test (FST). Mirtazapine decreased immobility time in the FST after acute, but not seven-day repeated, administration to C57BL/6J mice. Lack of the antidepressant effect of mirtazapine was observed, after acute and repeated administration to NET-KO mice, although those mice showed a significantly shorter immobility time in the FST than did wild-type animals. Seven-day repeated mirtazapine administration to wild-type mice suppressed the proliferative activity of splenocytes and their ability to produce pro-inflammatory cytokines, whereas production of IL-4 was stimulated. Acute mirtazapine administration did not change immune parameters in C57BL/6J mice. In NET-KO mice, acute and seven-day repeated mirtazapine administration reduced the proliferative activity of splenocytes and their ability to produce pro-inflammatory cytokines. This study indicates that, in comparison with wild-type C57BL/6J mice, NET-KO mice show enhanced mobility, which is not further potentiated by mirtazapine treatment. Furthermore, the NET-KO mice display higher susceptibility to the immunosuppressive effects of mirtazapine than do the wild-type animals. The present paper postulates an essential role of noradrenergic system in the immunological and behavioral effects of mirtazapine.
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PMID:Effect of acute and repeated treatment with mirtazapine on the immunity of noradrenaline transporter knockout C57BL/6J mice. 1719 39

The advance of functional genomics revealed the superfamily of G-protein coupled receptors (GPCRs). Hundreds of GPCRs have been cloned but many of them are orphan GPCRs with unidentified ligands. The first identified orphan GPCR is the opioid receptor like orphan receptor, ORL1. It was cloned in 1994 during the identification of opioid receptor subtypes and was de-orphanized in 1995 by the discovery of its endogenous ligand, nociceptin or orphanin FQ (N/OFQ). This receptor was renamed as N/OFQ peptide (NOP) receptor. Several selective ligands acting at NOP receptors or other anti-N/OFQ agents have been reported. These include N/OFQ-derived peptides acting as agonists (cyclo[Cys(10),Cys(14)]N/OFQ, [Arg(14), Lys(15)]N/OFQ, [pX]Phe(4)N/OFQ(1-13)-NH(2), UFP-102, [(pF)Phe(4),Aib(7), Aib(11),Arg(14),Lys(15)]N/OFQ-NH(2)) or antagonists (Phe(1)psi(CH(2)-NH)Gly(2)]N/OFQ(1-13)-NH(2), [Nphe(1)]N/OFQ(1-13)-NH(2), UFP-101, [Nphe(1), (pF)Phe(4),Aib(7),Aib(11),Arg(14),Lys(15)]N/OFQ-NH(2)), hexapeptides, other peptide derivatives (peptide III-BTD, ZP-120, OS-461, OS-462, OS-500), non-peptide agonists (NNC 63-0532, Ro 64-6198, (+)-5a compound, W-212393, 3-(4-piperidinyl)indoles, 3-(4-piperidinyl) pyrrolo[2,3-b]pyridines) and antagonists (TRK-820, J-113397, JTC-801, octahydrobenzimidazol-2-ones, 2-(1,2,4-oxadiazol-5-yl)-1 H-indole, N-benzyl-D-prolines, SB-612111), biostable RNA Spiegelmers specific against N/OFQ, and a functional antagonist, nocistatin. Buprenorphine and naloxone benzoylhydrazone are two opioid receptor ligands showing high affinity for NOP receptors. NOP receptor agonists might be beneficial in the treatment of pain, anxiety, stress-induced anorexia, cough, neurogenic bladder, edema, drug dependence, and, less promising, in cerebral ischemia and epilepsy, while antagonists might be of help in the management of pain, depression, dementia and Parkinsonism. N/OFQ is also involved in cardiovascular, gastrointestinal and immune regulation. Altered plasma levels of N/OFQ have been reported in patients with various pain states, depression and liver diseases. This review summarizes the pharmacological characteristics of, and studies with, the available NOP receptor ligands and their possible clinical implications.
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PMID:Nociceptin/orphanin FQ peptide receptors: pharmacology and clinical implications. 1726 36

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