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Purpose: Bipolar affective disorder (BP) causes major functional impairment and reduced quality of life not only for patients, but also for many close relatives. We aimed to investigate mRNA levels in BP patients to find differentially expressed genes linked to specific clinical course variants; assuming that several gene expression alterations might indicate vulnerability pathways for specific course and severity of the disease., Materials: We searched for up- and down-regulated genes comparing patients with diagnosis of BP type I (BPI) vs type II (BPII), history of suicide attempts, psychotic symptoms, predominance of manic/hypomanic episodes, and history of numerous episodes and comorbidity of substance use disorders or anxiety disorders. RNA was extracted from peripheral blood mononuclear cells and analyzed with use of microarray slides., Results: Differentially expressed genes (DEGs) were found in all disease characteristics compared. The lowest number of DEGs were revealed when comparing BPI and BPII patients (18 genes), and the highest number when comparing patients with and without psychotic symptoms (3223 genes). Down-regulated genes identified here with the use of the DAVID database were among others linked to cell migration, defense response, and inflammatory response., Conclusions: The most specific transcriptome profile was revealed in BP with psychotic symptoms. Differentially expressed genes in this variant include, among others, genes involved in inflammatory and immune processes. It might suggest the overlap of biological background between BP with a history of psychotic features and schizophrenia., Competing Interests: Declaration of competing interest The authors declare no conflict of interest. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript; or in the decision to publish the results., (Copyright © 2024 Medical University of Bialystok. Published by Elsevier B.V. All rights reserved.)

Background: Conflicting data regarding the efficacy of antidepressants of different mechanism of action on unexplained painful physical symptoms (UPPS) in depression have been published so far., Objective: The aim of this study was to compare the impact of escitalopram (ESC), nortriptyline (NOR), and venlafaxine (VEN) on UPPS in patients with major depression., Materials and Methods: Sixty patients, participants in the GENDEP study, with a diagnosis of depression according to the ICD-10 criteria were randomly assigned to treatment with ESC (10-30 mg, mean dose 15.2, standard deviation [SD]±9.2) or NOR (50-150 mg, mean dose 106.2, SD±8.2). Additionally, 30 patients who were treated with VEN (75-225 mg, mean dose 181.3, SD±8.8) were included. Before inclusion (day 0) and throughout the study (days 14, 28, 42, 56), the severity of pain was monitored using the visual analog scale., Results: The patients treated with ESC, NOR, and VEN did not differ in the intensity of pain at days 0, 14, 28, 42, and 56., Conclusion: Our results do not support the hypothesis suggesting the superiority of VEN over ESC and NOR in the management of UPPS in major depression., Competing Interests: The authors Jan Jaracz, Karolina Gattner, Krystyna Jaracz, Krystyna Górna, Jerzy Moczko, and Joanna Hauser declare that they have no conflicts of interest concerning this article., (© Georg Thieme Verlag KG Stuttgart · New York.)

Patients with major depression often report pain. In this article, we review the current literature regarding the prevalence and consequences, as well as the pathophysiology, of unexplained painful physical symptoms (UPPS) in patients with major depressive disorder (MDD). UPPS are experienced by approximately two-thirds of depressed patients. The presence of UPPS makes a correct diagnosis of depression more difficult. Moreover, UPPS are a predictor of a poor response to treatment and a more chronic course of depression. Pain, in the course of depression, also has a negative impact on functioning and quality of life. Frequent comorbidity of depression and UPPS has inspired the formulation of an hypothesis regarding a shared neurobiological mechanism of both conditions. Evidence from neuroimaging studies has shown that frontal-limbic dysfunction in depression may explain abnormal pain processing, leading to the presence of UPPS. Increased levels of proinflamatory cytokines and substance P in patients with MDD may also clarify the pathophysiology of UPPS. Finally, dysfunction of the descending serotonergic and noradrenergic pathways that normally suppress ascending sensations has been proposed as a core mechanism of UPPS. Psychological factors such as catastrophizing also play a role in both depression and chronic pain. Therefore, pharmacological treatment and/or cognitive therapy are recommended in the treatment of depression with UPPS. Some data suggest that serotonin and noradrenaline reuptake inhibitors (SNRIs) are more effective than selective serotonin reuptake inhibitors (SSRIs) in the alleviation of depression and UPPS. However, the pooled analysis of eight randomised clinical trials showed similar efficacy of duloxetine (an SNRI) and paroxetine (an SSRI) in reducing UPPS in depression. Further integrative studies examining genetic factors (e.g. polymorphisms of genes for interleukins, serotonin transporter and receptors), molecular factors (e.g. cytokines, substance P) and neuroimaging findings (e.g. functional studies during painful stimulation) might provide further explanation of the pathophysiology of UPPS in MDD and therefore facilitate the development of more effective methods of treatment.

Objective: Unexplained painful physical symptoms are commonly reported by depressed patients. The evidence suggests that dual-action antidepressants are potent in relieving pain in depression. However, a direct comparison of the effects of selective serotonergic and selective noradrenergic antidepressants on painful symptoms has not been investigated so far., Method: Sixty patients who participated in the Genome-based Therapeutic Drugs for Depression study with a diagnosis of moderate or severe episodes of depression according to the International Classification of Diseases, 10th Revision, and the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, criteria were involved. All the participants were randomly allocated to receive nortriptyline or escitalopram. The severity of depression was measured using the Montgomery-Åsberg Depression Rating Scale, the Hamilton Depression Rating Scale and the Beck Depression Inventory at weeks 0, 2, 4, 6 and 8. The intensity of pain was measured on the Visual Analog Scale at the same points of the study., Results: At "week 0," 83.3% of the patients later randomized to treatment with escitalopram and 86.7% of those treated with nortriptyline reported at least one painful symptom. A significant decrease of pain intensity was observed after 2 weeks of treatment. The two groups did not differ in degree of pain reduction at weeks 2, 4, 6 and 8 in comparison to baseline values. A 50% reduction in pain intensity preceded the 50% reduction of depression severity. The intensity of pain at "week 0" did not differ in remitted or nonremitted patients at week 8., Conclusion: Both selective serotonergic and selective noradrenergic antidepressants are equally effective in alleviations of painful physical symptoms of depression. The presence of painful symptoms before the onset of treatment did not determine the final response., (Copyright © 2015 Elsevier Inc. All rights reserved.)

Aim: The authors analyzed the association between polymorphism of serotonin transporter gene and schizophrenia. This polymorphism is characterised by a 44-bp insertion or deletion in the promoter region of the gene which influences its transcriptional activity., Method: 349 not related patients with paranoid schizophrenia were included in this study. Using the SCID (Structured Clinical Interview for DSM-IV Axis I Disorders) a consensus diagnosis, according to the DSM-IV criteria was made by two independent psychiatrists for each patient. The control group consisted of 372 persons who have not been examined by psychiatrists. Genomic DNA was extracted from whole blood leukocytes using a salting out method. The polymorphism was amplified by the polymerase chain reaction (PCR). We received two products of PCR: 406 base pairs (short allele) and 450 base pairs (long allele)., Results: We analyzed genotypes and alleles of the 5-HTTLPR polymorphism in the group of patients and in the control group. We also divided our sample according to their gender and early onset of schizophrenia. The analysis did not show any significant differences between the studied groups., Conclusions: In the present study no association between 5-HTTLPR polymorphism and schizophrenia was found.

Polycystic kidney disease 1 (PKD1) is the major locus of the common genetic disorder autosomal dominant polycystic kidney disease. We have studied PKD1 mRNA, with an RNase protection assay, and found widespread expression in adult tissue, with high levels in brain and moderate signal in kidney. Expression of the PKD1 protein, polycystin, was assessed in kidney using monoclonal antibodies to a recombinant protein containing the C terminus of the molecule. In fetal and adult kidney, staining is restricted to epithelial cells. Expression in the developing nephron is most prominent in mature tubules, with lesser staining in Bowman's capsule and the proximal ureteric bud. In the nephrogenic zone, detectable signal was observed in comma- and S-shaped bodies as well as the distal branches of the ureteric bud. By contrast, uninduced mesenchyme and glomerular tufts showed no staining. In later fetal (>20 weeks) and adult kidney, strong staining persists in cortical tubules with moderate staining detected in the loops of Henle and collecting ducts. These results suggest that polycystin's major role is in the maintenance of renal epithelial differentiation and organization from early fetal life. Interestingly, polycystin expression, monitored at the mRNA level and by immunohistochemistry, appears higher in cystic epithelia, indicating that the disease does not result from complete loss of the protein.