Bacs Kiskun County Hospital

Kecskemét, Hungary

Bacs Kiskun County Hospital

Kecskemét, Hungary
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Kelemen O.,Bacs Kiskun County Hospital | Kiss I.,Gyula Nyiro Hospital | Benedek G.,University of Szeged | Keri S.,Gyula Nyiro Hospital | And 2 more authors.
Progress in Neuro-Psychopharmacology and Biological Psychiatry | Year: 2013

Schizophrenia is characterized by anomalous perceptual experiences (e.g., sensory irritation, inundation, and flooding) and specific alterations in visual perception. We aimed to investigate the effects of short-term antipsychotic medication on these perceptual alterations. We assessed 28 drug-naïve first episode patients with schizophrenia and 20 matched healthy controls at baseline and follow-up 8. weeks later. Contrast sensitivity was measured with steady- and pulsed-pedestal tests. Participants also received a motion coherence task, the Structured Interview for Assessing Perceptual Anomalies (SIAPA), and the Repeatable Battery for the Assessment of Neuropsychological Status (RBANS). Proton magnetic resonance spectroscopy was used to measure gamma-aminobutyric acid (GABA) levels in the occipital cortex (GABA/total creatine [Cr] ratio). Results revealed that, comparing baseline and follow-up values, patients with schizophrenia exhibited a marked sensitivity reduction on the steady-pedestal test at low spatial frequency. Anomalous perceptual experiences were also significantly ameliorated. Antipsychotic medications had no effect on motion perception. RBANS scores showed mild improvements. At baseline, but not at follow-up, patients with schizophrenia outperformed controls on the steady-pedestal test at low spatial frequency. The dysfunction of motion perception (higher coherence threshold in patients relative to controls) was similar at both assessments. There were reduced GABA levels in schizophrenia at both assessments, which were not related to perceptual functions. These results suggest that antipsychotics dominantly affect visual contrast sensitivity and anomalous perceptual experiences. The prominent dampening effect on low spatial frequency in the steady-pedestal test might indicate the normalization of putatively overactive magnocellular retino-geniculo-cortical pathways. © 2013 Elsevier Inc.

Kelemen O.,Bacs Kiskun County Hospital | Kovacs T.,Gyula Nyirodouble acute Hospital National Institute of Psychiatry and Addictions | Keri S.,Gyula Nyirodouble acute Hospital National Institute of Psychiatry and Addictions | Keri S.,University of Szeged | Keri S.,Budapest University of Technology and Economics
Progress in Neuro-Psychopharmacology and Biological Psychiatry | Year: 2013

Recent studies demonstrated a reduced expression of Fragile X Mental Retardation Protein (FMRP), an RNA binding protein and translation regulator, in the brain and peripheral lymphocytes of patients with schizophrenia. Low FMRP levels may be related to impaired neurodevelopmental processes and synaptic plasticity. Here, we studied the relationship between peripheral FMRP level, visual perception (contrast sensitivity, perceptual integration, motion/form perception), and neuropsychological functions in schizophrenia as measured with the Repeatable Battery for the Assessment of Neuropsychological Status (RBANS). Results revealed that patients with schizophrenia displayed lower FMRP levels in peripheral lymphocytes as compared to control individuals. We found significant correlations between FMRP levels and contrast sensitivity at low spatial and high temporal frequencies, perceptual integration, and motion perception. The relationship between FMRP level and neuropsychological functions was less pronounced than that seen in the case of visual perception, with the greatest effect for RBANS attention. FMRP level was not related to contrast sensitivity at high spatial and low temporal frequencies and form perception. This pattern of data is reminiscent to that observed in patients with Fragile X Syndrome (FXS). These results suggest that FMRP may be implicated in the pathogenesis of schizophrenia, possibly via the regulation of neurodevelopment, plasticity, GABA-ergic, and glutamatergic neurotransmission. © 2013 Elsevier Inc.

Levy-Gigi E.,National Psychiatry Center | Levy-Gigi E.,Haifa University | Szabo C.,National Psychiatry Center | Kelemen O.,Bacs Kiskun County Hospital | And 3 more authors.
Biological Psychiatry | Year: 2013

Background Posttraumatic stress disorder (PTSD) is characterized by a reduced expression of FKBP5, a key modulator of the glucocorticoid receptor. Smaller hippocampal volume has also been documented in PTSD. We explored possible changes in FKBP5 gene expression and brain structure in patients with PTSD after cognitive behavioral therapy (CBT). Methods We measured peripheral FKBP5 RNA and volumes of the hippocampus, amygdala, and medial orbitofrontal cortex in 39 patients with PTSD before and after CBT. The control subjects were 31 trauma-exposed individuals without PTSD who were also assessed twice. Gene expression changes were screened with a microarray toolkit, which was followed by quantitative polymerase chain reaction for FKBP5 RNA. Brain volumes were measured using FreeSurfer. Results At baseline, patients with PTSD showed lower FKBP5 gene expression and smaller hippocampal and medial orbitofrontal cortex, but not amygdala, volumes relative to control subjects. At follow-up, we found significantly increased FKBP5 expression and increased hippocampal volume in patients with PTSD. At follow-up, patients did not differ from control subjects in hippocampal volume. Improvement in PTSD symptoms was predicted by increased FKBP5 expression and increased hippocampal volume, but the primary predictor was FKBP5 expression. The most significantly altered gene expression in patients with PTSD relative to control subjects was found for ribosomal protein S6 kinase, which did not change after CBT and did not correlate with hippocampal volume. Conclusions Clinical improvement in individuals with PTSD was associated with increased expression of FKBP5 and increased hippocampal volume, which were positively correlated. © 2013 Published by Elsevier Inc.

Keri S.,National Psychiatry Center | Keri S.,University of Szeged | Szamosi A.,National Psychiatry Center | Benedek G.,University of Szeged | Kelemen O.,Bacs Kiskun County Hospital
Neuropsychologia | Year: 2012

Paired associates learning is impaired in both schizophrenia and amnestic mild cognitive impairment (aMCI), which may reflect hippocampal pathology. In addition, schizophrenia is characterized by the dysfunction of the retino-geniculo-striatal magnocellular (M) visual pathway. The purpose of this study was to investigate the interaction between visual perceptual and memory dysfunctions. We administered a modified version of the CANTAB paired associates learning task to patients with schizophrenia (n=20), aMCI (n=20), and two groups of matched healthy controls (n=20 for each patient group). The stimuli in the paired associates learning task biased information processing toward the M pathways (low contrast, low spatial frequency) and parvocellular (P) pathways (high contrast, high spatial frequency). Results revealed that patients with schizophrenia exhibited a more pronounced learning deficit for M-biased relative to P-biased stimuli. In aMCI, there were similar memory deficits for both types of stimuli. Orientation discrimination for M- and P-biased stimuli was intact in both groups of patients. The number of errors in the M-biased memory condition significantly and inversely correlated with the volume of the right hippocampus in schizophrenia. These results suggest an interaction between M-biased perceptual processing and short-term relational memory in schizophrenia, which may be associated with the structural alteration of the right hippocampus. © 2012 Elsevier Ltd.

Keri S.,Budapest University of Technology and Economics | Keri S.,Nyiro Gyula Hospital National Institute of Psychiatry and Addictions | Keri S.,University of Szeged | Szabo C.,Nyiro Gyula Hospital National Institute of Psychiatry and Addictions | Kelemen O.,Bacs Kiskun County Hospital
Brain, Behavior, and Immunity | Year: 2014

In recent years, increased attention has been paid to the inflammatory mechanisms of major depressive disorder (MDD). The aim of the present study was to investigate pro-inflammatory pathways related to the "leaky gut" hypothesis of MDD, which is based on the putative intestinal translocation of Gram-negative bacteria and a subsequent abnormal immune response mediated by the Toll-Like Receptor-4 (TLR-4) pathway. 50 patients with first-episode MDD and 30 healthy control subjects participated in the study. Real-time quantitative PCR was used to measure TLR-4 and TLR-2 RNA from peripheral mononuclear blood cells, as well as the expression of NF-κβ, a key transcription factor of the pro-inflammatory response. TLR-4 protein expression was determined by using flow cytometry. TLR-2 served as a control molecule. Low-grade inflammation was characterized by the measurement of interleukin-6 (IL-6) and C-reactive protein (CRP). Bacterial translocation was investigated by the measurement of the 16S rRNA subunit (16S rDNA) of intestinal microbiota in the blood plasma of the participants. We performed these analyses before (t1) and after (t2) cognitive-behavioral therapy (CBT) in MDD. The healthy control subjects were also assessed two times. We found significantly elevated expressions of all three markers (TLR-4 RNA and protein, NF-κβ RNA) and 16S rDNA in MDD at t1 relative to healthy control subjects. These markers showed a significant decrease during CBT (t1 > t2 in MDD). We observed no between-group differences and changes in the case of TLR-2. Greater reduction of pro-inflammatory markers during CBT was associated with more pronounced clinical improvement. IL-6 and CRP displayed a moderately elevated level in MDD and did not change during CBT. In conclusion, TLR-4 signaling is up-regulated in newly diagnosed patients with MDD, which may be related to bacterial translocation or to the presence of various damage-associated molecular patterns. Clinical improvement during psychotherapy is associated with decreased expression of pro-inflammatory markers. © 2014 Elsevier Inc.

Keri S.,University of Szeged | Keri S.,Nyiro Gyula Hospital | Keri S.,Budapest University of Technology and Economics | Szabo C.,Nyiro Gyula Hospital | Kelemen O.,Bacs Kiskun County Hospital
Journal of Affective Disorders | Year: 2014

Background Results from convergent genomics indicated new peripheral biomarkers for mood states. We sought to investigate the clinical utility of the BioM-10 Mood Panel, a peripheral biomarker set of low vs. high mood states, in the diagnosis of major depressive episode and to monitor the effectiveness of cognitive-behavioral therapy (CBT). Method 44 patients with a first episode of major depression and 30 healthy control subjects participated in the study. The BioM-10 panel's gene expression profile was measured from whole peripheral blood with the Affymetrix Human Genome U133 Plus 2.0 Gene Chips, focusing on 10 top genes related to high mood states (MBP, EDG2, FZD3, ATXN1, and EDNRB) and low mood states (FGFR1, MAG, PMP22, UGT8, and ERBB3). We studied gene expression before and after CBT. Results The BioM-10 prediction score discriminated patients and controls with high sensitivity (84%) and specificity (90%). There was an increase in the BioM-10 prediction score after CBT relative to the pretreatment value. Clinical improvement was associated with higher prediction scores reflecting a greater ratio of high mood markers relative to low mood markers. Limitations Sample size was small for a genome-wide microarray study. Convergent genomic studies have not been conducted in major depressive disorder. More evidence is needed from patients with severe, recurrent, and chronic forms of depression. Conclusions The BioM-10 panel is a promising tool as a biomarker setup for the evaluation of low and high mood states across diagnostic categories. The panel includes genes related to growth factor pathways and myelination, which may provide new insights into the pathophysiology of mood dysregulation. © 2014 Elsevier B.V.

Kovacs T.,National Psychiatry Center | Kelemen O.,Bacs Kiskun County Hospital | Keri S.,National Psychiatry Center | Keri S.,University of Szeged
Psychiatry Research | Year: 2013

The purpose of this study was to investigate Fragile X Syndrome (FXS)-related mechanisms in schizophrenia, including CGG triplet expansion, FMR1 mRNA, and fragile X mental retardation protein (FMRP) levels in lymphocytes. We investigated 36 patients with schizophrenia and 30 healthy controls using Southern blot analysis, mRNA assay, and enzyme-linked immunosorbent assay (ELISA). General intellectual functions were assessed with the Wechsler Adult Intelligence Scale-III, and the clinical symptoms were evaluated with the Positive and Negative Syndrome Scale. Results revealed that, relative to healthy controls, CGG triplet size and FMR1 mRNA were unaltered in patients with schizophrenia. However, the FMRP level was significantly reduced in patients compared with controls. We found an association between lower FMRP levels, reduced IQ, and earlier illness onset in schizophrenia. Chlorpromazine-equivalent antipsychotic dose did not correlate with FMRP levels. These results raise the possibility of impaired translation of FMR1 mRNA, altered epigenetic regulation, or increased degradation of FMRP in schizophrenia, which may play a role in dysfunctional neurodevelopmental processes and impaired neuroplasticity. © 2012 Elsevier Ireland Ltd.

Keri S.,Semmelweis University | Seres I.,Semmelweis University | Kelemen O.,Bacs Kiskun County Hospital | Benedek G.,University of Szeged
Schizophrenia Bulletin | Year: 2011

Background: Previous studies reported an association between weak habituation of skin conductance orienting response and psychosis proneness. The aim of this study was to investigate the relationship among neuregulin 1 (NRG1)-stimulated AKT phosphorylation (a putative marker of psychosis), orienting response habituation, delusional ideas, anxiety, and depression in nonclinical individuals. Methods: One hundred twenty individuals participated in the skin conductance measurements. Weak and strong habituators were compared on measures of NRG1-stimulated AKT phosphorylation in B lymphoblasts, delusional ideas, anxiety, and depression. The predictors of delusional ideas were determined by multiple regression analysis. Results: Weak habituators displayed higher levels of delusional ideas/anxiety and a lower ratio of phosphorylated AKT as compared with strong habituators. There were 3 significant predictors of delusional ideas: decreased habituation, NRG1-induced AKT phosphorylation, and anxiety. Age, gender, education, IQ, and depression did not predict delusional ideas. Conclusions: These results suggest that decreased habituation of arousal, NRG1-induced AKT phosphorylation, and anxiety are related to delusional ideation in the general population. © 2010 The Author.

Ruzsa Z.,Bacs Kiskun County Hospital | Pinter L.,Augusta Hospital | Kolvenbach R.,Augusta Hospital
Catheterization and Cardiovascular Interventions | Year: 2012

Management of critical limb ischemia (CLI) requires a combined treatment approach: optimal medical therapy and revascularization procedures are both essential for favorable outcome. With the development of endovascular interventions these new modalities took the primary role in limb revascularization, especially in CLI patients, where the culprit lesion is often located below the knee (BTK) level, making the surgical procedure unfeasible. In our present case report, we demonstrate a successful percutaneous recanalization of a surgically non-treatable tibioperoneal trunk occlusion. The procedure was performed with dual access from anterograde and retrograde transpedal approach, and modified "V stenting" technique was used. We describe feasibility of bail out stenting using retrograde posterior tibial artery access after failed retrograde guidewire externalization. Our report discusses the feasibility, safety, and efficacy of the retrograde approach applying 4F compatible devices. Copyright © 2012 Wiley Periodicals, Inc.

Szamosi A.,National Psychiatry Center | Kelemen O.,Bacs Kiskun County Hospital | Keri S.,National Psychiatry Center | Keri S.,University of Szeged
Journal of Psychiatric Research | Year: 2012

Objective: The phosphoinositide 3'-kinase (PI3K) - protein kinase B (AKT1) - glycogen synthase kinase (GSK)-3β system is modulated by several factors implicated in the pathophysiology of schizophrenia. Evidence suggests that neuregulin 1 (NRG1) induces decreased AKT phosphorylation in schizophrenia relative to healthy controls, which may be related to dysfunctional neurodevelopment and neuroplasticity. The aim of this study was to investigate the relationship between NRG1 - induced AKT phosphorylation and hippocampal volume in schizophrenia. Methods: Participants were 20 first-episode patients with schizophrenia who did not receive psychotropic medications and 20 matched healthy controls. We measured the phosphorylated AKT - total AKT and phosphorylated ERK (extracellular signal-regulated kinase) - total ERK ratios in peripheral lymphoblasts before and after NRG1 administration. Whole-brain, left, and right hippocampal volumes were quantified using FreeSurfer software. Results: Patients with schizophrenia displayed decreased AKT but normal ERK ratio compared with controls. Patients also had a reduction in left hippocampal volume. There was no significant difference between patients and controls in whole-brain and right hippocampal volume. Decreased AKT ratio was associated with reduced hippocampal volume. There was no significant relationship between ERK ratio and brain structure. Conclusion: Activation of the AKT system is specifically associated with hippocampal volume in first-episode schizophrenia, which provides further evidence for the pivotal role of this messenger system in the pathophysiology of psychotic disorders. © 2011 Elsevier Ltd.

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