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1.
J Psychiatr Res ; 46(9): 1243-8, 2012 Sep.
Article in English | MEDLINE | ID: mdl-22770507

ABSTRACT

Despite its popularity in clinical research, the emotional Stroop task's reliability in patient groups is unknown. Given the low reliability of interference scores in healthy subjects, correlations with other variables pose a problem, especially as reliability in clinical samples is unknown. To assess reliability in panic disorder for the first time, we used the spilt-half method in two independent samples of patients and controls. As expected, only patients showed the behavioral interference effect. Reliability of interference scores (i.e. mean response latency emotional minus neutral words) was insufficiently low for patient and control samples; however, reliability scores derived from the conditions' response latencies (i.e. mean response latency emotional or neutral words) were much higher. The assumption that reliability scores in patients might differ from controls was not supported. This finding questions the use of correlations with external variables and suggests the use of response latencies instead of interference scores.


Subject(s)
Emotions/physiology , Panic Disorder/physiopathology , Panic Disorder/psychology , Adult , Humans , Middle Aged , Neuropsychological Tests , Photic Stimulation , Reaction Time , Reproducibility of Results
2.
Pharmacopsychiatry ; 45(1): 30-4, 2012 Jan.
Article in English | MEDLINE | ID: mdl-21993870

ABSTRACT

Citalopram (CIT) is a widely used antidepressant which acts by a selective serotonin reuptake inhibition. It is considered to be safer than tricyclic antidepressants at therapeutic levels, but also with respect to intoxications. We report the case of a 46-year-old woman, who ingested in suicidal intention 1400 mg CIT. During the following inpatient treatment repeatedly ECGs and determinations of the serum level of CIT were performed. Initially the patient's serum level of CIT was 1231 ng/mL and QTc interval was 541.60 ms. It took 12 days until the serum level of CIT fell below the upper threshold of the recommended therapeutic range (130 ng/mL). The QTc interval on the sixth day after the intoxication for the first time was below 500 ms. The QTc interval correlated significantly with the serum level of CIT after intoxication (r=0.943; p<0.005). Although CIT is estimated as a safe antidepressant regarding serious adverse effects, toxic doses can lead to potentially hazardous ECG changes which according to our findings correlate strongly with the serum level of the drug.


Subject(s)
Antidepressive Agents/blood , Citalopram/blood , Citalopram/poisoning , Depressive Disorder, Major/blood , Depressive Disorder, Major/drug therapy , Long QT Syndrome/chemically induced , Selective Serotonin Reuptake Inhibitors/blood , Antidepressive Agents/pharmacokinetics , Antidepressive Agents/poisoning , Citalopram/pharmacokinetics , Depressive Disorder, Major/metabolism , Depressive Disorder, Major/psychology , Female , Humans , Middle Aged , Selective Serotonin Reuptake Inhibitors/pharmacokinetics , Selective Serotonin Reuptake Inhibitors/poisoning , Suicide, Attempted , Treatment Outcome
3.
Expert Rev Neurother ; 10(8): 1273-84, 2010 Aug.
Article in English | MEDLINE | ID: mdl-20662753

ABSTRACT

There is evidence for either genetic heterogeneity or complex inheritance with an interaction of environmental factors and multiple single genes in the etiology of panic disorder. Although linkage analyses of panic disorder have implicated several chromosomal regions including 1q, 2q, 4q, 7p, 9q, 12q, 13q, 15q and 22q, they so far have not been able to identify a major gene responsible for panic disorder. Several genes of classical candidate neurotransmitter systems have been reported to be associated with panic disorder. Genetic variation in genes of monoamine oxidase A, catechol-O-methyltransferase, adenosine receptor (ADORA2A) and cholecystokinin B receptor have been inconsistently replicated. There are multiple lines of evidence for highly relevant effects of gender and ethnicity. Future research strategies might focus on broad phenotypes defined by comorbidity or intermediate phenotypes and include the use of animal models for identifying candidate genes, such as the regulator of G-protein signaling (RGS2) gene, genome-wide association studies in large samples, studies of gene-gene and gene-environment interactions and pharmacogenetic studies. The identification of novel pathophysiological pathways may provide the basis for the development of novel therapeutic interventions.


Subject(s)
Neurotransmitter Agents/genetics , Panic Disorder/genetics , Panic Disorder/therapy , Catechol O-Methyltransferase/genetics , GTP-Binding Protein Regulators/genetics , Genetic Association Studies , Genetic Predisposition to Disease , Humans , Monoamine Oxidase/genetics , Receptor, Cholecystokinin B/genetics , Receptors, Purinergic P1/genetics , Risk Factors
4.
Histochemistry ; 102(4): 255-63, 1994 Oct.
Article in English | MEDLINE | ID: mdl-7843988

ABSTRACT

Basolateral uptake of chloride by the HCl-secreting parietal cells of the gastric (oxyntic) glands is most likely mediated by a HCO3-/Cl- anion exchange mechanism. Circumstantial evidence indicates that in rodents the anion exchange proceeds through an anion exchanger 2(AE2)-like membrane protein. In the present study, we raised antibodies against a bacterial fusion protein expressing a approximately 26-kDa portion of the human AE2 sequence. These antibodies were used to identify and localize AE2 in the human stomach. Here we report that the mucosa of the human stomach expresses an approximately 160-kDa immunoreactive form of AE2 containing the AE2-specific exoplasmic domain (Z-loop) as identified by polymerase chain reaction. Immunostaining specific for AE2 was restricted to the basolateral membrane domain of parietal cells and was also detected in small epithelial cells localized in the glandular isthmus region. The latter cells most likely represent pre-parietal cells. Parietal cells were identified by simultaneous and sequential labelling with antibodies against the gastric H+,K(+)-ATPase and actin, respectively. Both actin and the H+,K(+)-ATPase were localized along the apical membrane of parietal cells and the membrane of their secretory intracellular canaliculi. In addition, actin was shown to be colocalized with AE2 along the basolateral cell surface. Discontinuous staining for AE2 coincided with infoldings of the basolateral plasma membrane labelled by the actin antibody. These observations indicate that AE2 might be placed at specialized (folded) microdomains of the basolateral cell surface by linkage to the actin-based cytoskeleton.


Subject(s)
Antiporters/analysis , Parietal Cells, Gastric/chemistry , Actins/analysis , Animals , Antibodies , Base Sequence , Fluorescent Antibody Technique , Humans , Molecular Sequence Data , Polymerase Chain Reaction , Rabbits , Rats , Swine
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