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)

Bradykinin and beta-endorphin increases during acute pancreatitis are thought to contribute to the development of hypotension and myocardial depression in acute pancreatitis. beta-Endorphin release is mediated by trypsin-like enzymes and bradykinin from the pituitary gland. This study was undertaken to investigate the effect of a long-acting bradykinin receptor antagonist on bradykinin and beta-endorphin release and on hemodynamic changes during acute pancreatitis. Pancreatitis was induced by the injection of autologous bile mixed with trypsin into the main pancreatic duct after ligation of the accessory duct. Serum bradykinin and plasma beta-endorphin levels and cardiovascular function were measured. Twelve dogs (control group) were given 10 ml/kg/h of lactate Ringer's solution intravenously beginning 1 h before the induction of pancreatitis and continuing throughout the experiments. Six dogs received an intravenous infusion of 0.6 mg/kg/h of a new bradykinin receptor antagonist, HOE 140, D-Arg-[Hyp3, Thi5, D-Tic, Oic8]-bradykinin, in lactate Ringer's solution soon after the induction of pancreatitis. Six of twelve dogs in the control group, and none of the six dogs in the bradykinin receptor antagonist group, died during the experiments. Serum bradykinin levels in both groups increased until 1 h after the induction of pancreatitis, but thereafter the levels in the bradykinin receptor antagonist group decreased gradually until 5 h after induction, and levels were significantly lower than those in the control group (p < 0.05). Plasma beta-endorphin levels in the control group increased significantly, to 291.8 pg/ml (+/- 6.6 SEM) 5 h after the induction of pancreatitis, from the mean levels of 47.8 pg/ml before the induction of pancreatitis, while the mean beta-endorphin level in the bradykinin receptor antagonist group did not increase after the induction of pancreatitis. Infusion of the bradykinin receptor antagonist improved survival rates, hypotension, myocardial depression, and plasma lactate, suggesting that the bradykinin receptor antagonist inhibited the release of bradykinin and beta-endorphin, which contributed to the clinical improvement.
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PMID:Effects of bradykinin receptor antagonist on the release of beta-endorphin and bradykinin and on hemodynamic changes in a canine model of experimental acute pancreatitis. 892 25

Evidence suggests both opioid mu and delta receptors may participate in the regulation of respiration at different central nervous system sites. In the past, the overlapping receptor specificity of various opioid drugs has made it difficult to dissect the receptor subtype-specific activities involved in respiratory regulation. The new family of delta receptor selective agents such as cyclic[D-Pen2, 5]enkephalin, deltorphins, (+)-4-((alpha-R)-alpha-((2S,5R)-4-allyl-2, 5-dimethyl-1-piperazinyl)-3-hydroxybenzyl)-N,N-diethylbenzamide, naltrindole and H-Tyr-Tic(psi)[CH2NH]Phe-Phe-OH have now made it feasible to more clearly define the role of delta receptors in respiratory control. In a series of experiments we observed that systemic infusion of rats with the highly mu receptor-specific opioid alfentanil induced antinociception and hypercapnia, and both of these effects were antagonized by the mu antagonist D-Phe-Cys-Tyr-Orn-Thr-Pen-Thr-NH2. However, peripheral administration of the delta receptor antagonist naltrindole reverses the hypercapnia but not the antinociceptive activity of alfentanil. This differential effect of naltrindole on antinociception and hypercapnia could also be produced with the delta agonist (+)-4-((alpha-R)-alpha-((2S,5R)-4-allyl-2, 5-dimethyl-1-piperazinyl)-3-hydroxybenzyl)-N,N-diethylbenzamide. In addition, intracerebroventricular delivery of a number of peptide delta ligands cyclic[D-Pen2,5]enkephalin, deltorpnin II and H-Tyr-Tic(psi)[CH2NH]Phe-Phe-OH also produced the same differential reversal of hypercapnia without affecting antinociception. Thus, both the traditional delta agonists and antagonists are able to reverse the alfentanil-induced hypercapnia without affecting antinociception. The reversal of alfentanil-induced hypercapnia by these delta ligands was antagonized by a novel synthetic delta antagonist cis-4-(alpha-(4-((Z)-2-butenyl)-3, 5-dimethyl-1-piperazinyl)-3-hydroxybenzyl)-N,N-diethylbenzamide. We propose that in this experimental respiration model, the delta antagonists naltrindole and H-Tyr-Tic(psi)[CH2NH]Phe-Phe-OH behave like delta agonists with low but sufficient intrinsic activities to reverse alfentanil-induced hypercapnia in rats. The results suggest that a function of the delta receptor is to modulate or counteract the respiratory depression induced by the mu receptor.
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PMID:Delta-opioid ligands reverse alfentanil-induced respiratory depression but not antinociception. 986 59

The B(1) receptor for kinins, stimulated by kinin metabolites without the C-terminal Arg residue (e.g., des-Arg(9)-bradykinin (BK) and Lys-des-Arg(9)-BK), is an increasingly recognized molecular target for the development of analgesic and anti-inflammatory drugs. Recently developed antagonists of this receptor were compared to a conventional antagonist, Ac-Lys-[Leu(8)]-des-Arg(9)-BK, in pharmacological assays based on the rabbit B(1) receptor. B-9858 (Lys-Lys-[Hyp(3), Igl(5), D-Igl(7), Oic(8)]des-Arg(9)-BK) and three other analogues possessing the alpha-2-indanylglycine(5) (Igl(5)) residue (order of potency B-9858 approximately B-10146>B-10148>B-10050) were partially insurmountable antagonists of des-Arg(9)-BK in the contractility assay based on rabbit aortic rings. B-9858-induced depression of the maximal effect was more pronounced in tissues treated with the protein synthesis inhibitor cycloheximide to block the spontaneous increase of response attributed to the post-isolation formation of B(1) receptors, and only partly reversible on washing. By comparison, Ac-Lys-[Leu(8)]des-Arg(9)-BK was a surmountable antagonist (pA(2) 7. 5), even in cycloheximide-treated tissues. B-9958 (Lys-[Hyp(3), CpG(5), D-Tic(7), CpG(8)]des-Arg(9)-BK) was also surmountable (pA(2) 8.5). The binding of [(3)H]-Lys-des-Arg(9)-BK to recombinant rabbit B(1) receptors expressed in COS-1 cells was influenced by two of the antagonists: while Ac-Lys-[Leu(8)]des-Arg(9)-BK competed for the radioligand binding without affecting the B(max), B-9858 decreased the B(max) in a time-dependent and washout-resistant manner. B-9858 and analogues possessing Igl(5) are the first reported non-competitive, non-equilibrium antagonists of the kinin B(1) receptor.
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PMID:Non-competitive pharmacological antagonism at the rabbit B(1) receptor. 1105 7

We report about a five year-old patient suffering from tics and ADHD (attention deficit hyperkinetic disorder), aggressions, depression and emotional disorder. Furthermore, an epileptic focus and perinatal encephalopathy were diagnosed. Lofexidine (Britlofex) medication did not reduce Tic symptomatology, but showed remarkable sedative effects. Family therapy and Clonidine (Catapressan) medication reduced symptomatology significantly.
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PMID:[Therapy of tic disorders apparently of organic origin in a multi-morbid 5-year-old patient with lofexidine (Britlofex) and clonidine (Catapressan)]. 1158 98

There is evidence that abnormalities in the dopaminergic system involving the dopamine transporter (DAT) are involved in the pathophysiology of Tourette's disorder (TD) from previous studies using [(123)I]2beta-carbomethoxy-3-(4-iodophenyl)tropane ([(123)I]beta-CIT) and single photon emission tomography (SPECT). However, because those studies were performed in medicated adult patients with TD, we decided to compare DAT densities in nine drug-naive children with TD and eight normal children. The children with TD did not suffer from associated psychiatric problems such as obsessive-compulsive symptoms, attention deficit hyperactivity disorder, anxiety, depression and developmental difficulties. We performed brain SPECT 2 h after the intravenous administration of I-123N-(3-iodopropen-2-yl)-2beta-carbomethoxy-3beta-(4-chlorophenyl)tropane ([(123)I]IPT) and carried out both quantitative and qualitative analyses using the obtained SPECT data, which were reconstructed for the assessment of the specific/non-specific DAT binding ratio in the basal ganglia. We then investigated the correlation between the severity of tics in children with TD assessed with the Yale Global Tic Severity Scale (YGTSS) and the specific/non-specific DAT binding ratio of the basal ganglia. Drug-naive children with TD showed a significantly increased specific/non-specific DAT binding ratio in the basal ganglia compared with normal children that did not correlate significantly with the severity of tics. Our results with drug-naive children with TD between the ages of 6 and 12 may help to clarify previous findings concerning DAT binding in adult patients with TD and suggest that DAT densities may be associated directly with the pathophysiology of TD, regardless of disease progress or drug effect.
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PMID:Dopamine transporter density of the basal ganglia assessed with [123I]IPT SPECT in drug-naive children with Tourette's disorder. 1497 71

Although motor tics and/or vocal tics are the defining features of chronic tic disorder (CTD) and Tourette syndrome (TS), older youths and adults often report their tics to be preceded by an unpleasant sensation or "premonitory urge." While premonitory urge phenomena may play an important role in behavioral interventions for CTD/TS, standardized assessments for premonitory urges do not exist. The current study of 42 youths with TS or CTD presents initial psychometric data for a new, brief self-report scale designed to measure tic-related premonitory urges. Results showed that the Premonitory Urge for Tics Scale (PUTS) was internally consistent (alpha = .81) and temporally stable at 1 (r = 0.79, p < .01) and 2 (r = 0.86, p < .01) weeks. PUTS scores were also correlated with overall tic severity as measured by the Yale Global Tic Severity Scale (YGTSS; r = 0.31, p < .05) and the YGTSS number (r = 0.35, p < .05), complexity (r = 0.49, p < .01), and interference (r = 0.36, p < .05) subscales. Finally, an examination of the psychiatric correlates of the premonitory urge phenomenon yielded significant correlations between the PUTS and the Child Behavior Checklist (CBCL) anxiety/depression (r = 0.33, p < .05), and withdrawal (r = 0.38, p < .05) subscales as well as the Children's Yale-Brown Obsessive Compulsive Scale (CYBOCS; r = 0.31, p < .05). However, a cross-sectional examination of the data showed that the psychometric properties of the PUTS were not acceptable for youths 10 years of age and younger. Likewise, significant correlations found between the YGTSS subscales, CBCL subscales, CYBOCS, and the PUTS did not emerge in this younger age group. The clinical and theoretical implications of these findings are discussed.
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PMID:Premonitory Urge for Tics Scale (PUTS): initial psychometric results and examination of the premonitory urge phenomenon in youths with Tic disorders. 1634 54

To investigate the reliability and validity of the Yale Global Tic Severity Scale (YGTSS), 28 youth aged 6 to 17 years with Tourette's syndrome (TS) participated in the study. Data included clinician reports of tics and obsessive-compulsive disorder (OCD) severity, parent reports of tics, internalizing and externalizing problems, and child reports of depression and anxiety. All children participated in a 2nd YGTSS administration by the same rater 48 days later. Good internal consistency and stability were found for the YGTSS scores. YGTSS scores demonstrated strong correlations with parent-rated tic severity (r = .58-.68). YGTSS scores were not significantly related to measures of clinician ratings of OCD severity (r = .01-.15), parent ratings of externalizing and internalizing behavior (r = -.07-.20), and child ratings of depression (r = .02-.26) and anxiety (r = -.06 -.28). Findings suggest that the YGTSS is a reliable and valid instrument for the assessment of pediatric TS.
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PMID:Reliability and validity of the Yale Global Tic Severity Scale. 1639 16

This study determined the prevalence of and factors associated with comorbid major depressive disorder (MDD) in patients with Gilles de la Tourette syndrome (GTS). How a simple self-report instrument, the Beck Depression Inventory (BDI), correlates with clinical assessment of comorbid MDD in this population was assessed. In a continuous sample of 114 adult patients with GTS, assessed clinically using the Diagnostic and Statistical Manual of Mental Disorders-IV criteria, 26 (23%) patients met criteria for MDD; more severe tics as measured with the Yale Global Tic Severity Scale, conduct disorder in childhood or higher age at the time of assessment were associated with MDD. The BDI score had a high negative predictive value for diagnosis of MDD, but a low positive predictive value. Using the BDI as a screening tool for comorbid MDD in patients with GTS is suggested.
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PMID:Beck Depression Inventory is a useful screening tool for major depressive disorder in Gilles de la Tourette syndrome. 1650 Sep 43

Despite wide use, relatively little is known about sociodemographic and clinical characteristics that predict early fluoxetine response. What research has been conducted has produced inconsistent findings, which may be due to the statistical procedures used, and no studies to date have examined predictors of early fluoxetine treatment response. Sixty adults with obsessive-compulsive disorder (OCD) completed an open-label fluoxetine trial for 8 weeks (up to 40 mg) after a 1-week, single-blind, placebo run-in before baseline assessment. The baseline and posttreatment assessment battery included the Yale-Brown Obsessive Compulsive Scale, the Hamilton Rating Scale for Depression, and the Yale Global Tic Severity Scale. Patient characteristics included illness duration, age, age of onset, gender, and pharmacological treatment history. Independent t-tests and multiple logistic regression analysis showed that longer illness duration, older age, and greater symptom severity were associated with nonresponse. Our findings highlight the impact of functional psychiatric impairment on determining those who may respond to treatment. Furthermore, findings suggest early predictors of patients with certain characteristics who may ultimately need adjunctive care to facilitate response.
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PMID:Clinical predictors of early fluoxetine treatment response in obsessive-compulsive disorder. 1684 43

The aim of our study was to assess the role of gender in OCD symptom dimensions with a multivariate analysis while controlling for history of tic disorders and age at onset of OCD. One hundred and eighty-six consecutive outpatients with a DSM-IV diagnosis of OCD were interviewed. Yale-Brown Obsessive-Compulsive Scale (YBOC-S), YBOC-S Symptom Checklist, and Hamilton Depression and Anxiety Scales were administered to all patients. Lifetime history of tic disorders was assessed with the tic inventory section of the Yale Global Tic Severity Scale. Age at onset of OCD was assessed by direct interview. Statistical analysis was carried out through logistic regression to calculate adjusted female:male odds ratios (OR) for each dimension. A relationship was found between gender and two main OCD dimensions: contamination/cleaning (higher in females; female:male OR=2.02, P=0.03) and sexual/religious (lower in females; female:male OR=0.41, P=0.03). We did not find gender differences in the aggressive/checking, symmetry/ordering, or hoarding dimensions. We also found a greater history of tic disorders in those patients with symptoms from the symmetry/ordering, dimension (P<0.01). Both symmetry/ordering and sexual/religious dimensions were associated with an earlier age at onset of OCD (P<0.05). Gender is a variable that plays a role in the expression of OCD, particularly the contamination/cleaning and sexual/religious dimensions. Our results underscore the need to examine the relationship between OCD dimensions and clinical variables such as gender, tics, age at onset and severity of the disorder to improve the identification of OCD subtypes.
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PMID:Gender differences in obsessive-compulsive symptom dimensions. 1743 12


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