32 research outputs found

    DESIGNING OF AN ELEMENTARY TRANSMITTER BASED ON SURFACE

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    Co adatoms on the Cu(111) surface are known to exhibit strong ferromagnetic character of the exchange interaction, if coupled directly, and explicit antiferromagnetic one, if separated by two Cu atoms [1]. Our calculations, carried out in terms of Heisenberg model, re-vealed a possibility to design an elementary transmitting unit by adjusting geometry of the system. The transmittance of the unit was found stable up to ≈100 Å (100 bonds of FM chain) in small magnetic fields (~1 meV) at room temperature

    Гельминтофауна горбуши Oncorhynchus gorbuscha (Walbaum, 1792) юго-восточного Сахалина по результатам многолетних исследований

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    The purpose of the research is to describe and analyze the qualitative and quantitative composition of pink salmon helminths of southeastern Sakhalin.Materials and methods. Standard parasitological methods of collecting material were used. At the autopsy, the ureters, eyeballs, gill petals and arches, and the brain of fish were not examined. The method of collecting salmon parasites in the laboratory has been unchanged since 1992. Collections of representatives of monogenetic suckers were not carried out. Parasitological studies of pink salmon of southeastern Sakhalin were carried out from 1992 to 2022, a total of 4163 fish specimens were examined. The fish is caught in the estuaries of rivers and the sea coast.Results and discussion. According to the results of their own research and literature data, the pink salmon helminth fauna of southeastern Sakhalin is represented by 23 species: Dibothriocephalus nihonkaiensis pl., Eubothrium salvelini, Eu. crassum, Nybelinia surmenicola pl., Pelichnibothrium speciosum pl., Tetraphyllidea gen. sp., Brachyphallus crenatus, Cryptocotyle sp. mtc., Hemiurus levinseni, Lecithaster gibbosus, Prosorhynchoides gracilescens, Parahemiurus merus, Derogenes varicus, Capiatestes thyrsitae, Corynosoma strumosum l., Echinorhynchus gadi, Bolbosoma caenoforme juv., B. bobrovoi juv., Rhadinorhynchus trachuri, Anisakis simplex l., Ascarophis pacifica, Ascarophis skrjabini, Hysterothylacium aduncum. The qualitative composition of the helminth fauna is currently undergoing minor changes, while the quantitative characteristics of some helminths are significantly reduced. Thus, the infection of pink salmon with Bolbosoma sp. juv scrapers. decreased to 0.61±0.18.Цель исследований – описать и проанализировать качественно-количественный состав гельминтов горбуши юговосточного Сахалина.Материалы и методы. Сбор материала проводили с использованием стандартных паразитологических методов. При вскрытии не исследовали мочеточники, глазные яблоки, жаберные лепестки и дуги, мозг рыб. Методика сбора паразитов лососей в лаборатории была неизменной с 1992 г. Сборы представителей моногенетических сосальщиков не проводили. Паразитологические исследования горбуши юго-восточного Сахалина осуществляли с 1992 по 2022 гг. Всего обследовано 4163 экз. рыб. Рыба выловлена в устьях рек и морском прибрежье.Результаты и обсуждение. Гельминтофауна горбуши юго-восточного Сахалина по результатам собственных исследований и литературным данным представлена 23 видами: Dibothriocephalus nihonkaiensis pl., Eubothrium salvelini, Eu. crassum, Nybelinia surmenicola pl., Pelichnibothrium speciosum pl., Tetraphyllidea gen. sp., Brachyphallus crenatus, Cryptocotyle sp. mtс., Hemiurus levinseni, Lecithaster gibbosus, Prosorhynchoides gracilescens, Parahemiurus merus, Derogenes varicus, Capiatestes thyrsitae, Corynosoma strumosum l., Echinorhynchus gadi, Bolbosoma caenoforme juv., B. bobrovoi juv., Rhadinorhynchus trachuri, Anisakis simplex l., Ascarophis pacifica, A. skrjabini, Hysterothylacium aduncum. Качественный состав гельминтофауны в настоящее время претерпевает незначительные изменения, в то время как количественные характеристики некоторых гельминтов существенно снижаются. Так, зараженность горбуши скребнями Bolbosoma spp. juv. снизилась до 0,61±0,18

    Preliminary pharmacogenetic study to explore putative dopaminergic mechanisms of antidepressant action

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    Background: There is sufficient evidence that interference of dopaminergic neurotransmission contributes to the therapeutic effects of antidepressants in unipolar and bipolar depression. Methods: Hamilton depression rating scale (HAMD 17) scores of 163 at least moderately ill patients with major depressive disorders were used to establish treatment response. HAMD 17 score status was measured before initiation, after two weeks, and after four weeks of treatment with various antidepressants. The possible association between response and genotype in a total of 14 variants of dopamine neurotransmission-related proteins was investigated. Results: DRD4 rs11246226 CA heterozygous patients were found with a greater improvement of HAMD 17 score when compared to homozygous C patients during 0–2 weeks and 0–4 weeks. Patients with MAOB rs1799836 heterozygous GA and homozygous A also demonstrated improved scores during 2–4 weeks and 0–4 weeks. Conclusions: The results are preliminary due to the limited population size and the small number of variants. Further research into the involvement of habenular dopamine D4 receptors in the antidepressant response is desirable

    Polymorphisms in the adrenergic neurotransmission pathway impact antidepressant response in depressed patients

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    Mood disorders are a prevalent mental health disorder. The adrenergic neurotransmission pathway presents an opportunity to determine whether genetic mutations impact antidepressant response. For this study, 163 patients with major depressive disorders were enrolled to measure treatment response using the Hamilton Depression Rating Scale (HAMD-17). More than half of the patients had never been treated with antidepressants previously. Patients were genotyped for 14 SNPs within ADRA1A, SLC6A2, ADRβ1, MAOA and COMT to determine the impact of adrenergic neurotransmission polymorphisms related in antidepressant response. Patients were treated mainly with SSRIs and TCAs. The difference in HAMD-17 scores between the measurement periods were defined as the outcome measure. Multiple linear regression was conducted to determine the association between the genotypes and difference in HAMD-17 across the study period. Covariates of age, sex, antidepressant medication and depression diagnoses were included in the regression. Throughout the study HAMD-17 scores were measured at initiation, at two weeks and at four weeks for each patient. The difference in HAMD-17 scores was found to be 11.2 ​± ​4.4 between initiation and two weeks, 7.8 ​± ​5.3 between two week and four week, and 19.0 ​± ​5.3 throughout the entire study. SLC6A2 rs1532701 homozygous G/G Patients were associated with improved ΔHAMD-17 across week 2–4 and the entire study (B ​= ​7.1, p ​= ​0.002; B ​= ​6.7, p ​= ​0.013) compared to homozygous A/A patients. SLC6A2 rs1532701 homozygous A/G patients were further associated with improved ΔHAMD-17 compared to homozygous A/A patients at week 2–4 (B ​= ​2.8, p ​= ​0.023). Through our investigation, we were able to determine the genes within the adrenergic pathway to investigate further. To further elucidate these findings, replication and combination with other neurotransmitter pathways to better map the mechanism of actions of antidepressant for tailored treatment would be suggested

    Limited Associations Between 5-HT Receptor Gene Polymorphisms and Treatment Response in Antidepressant Treatment-Free Patients With Depression

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    Major depressive disorder has become a prominent cause of disability, as lifetime prevalence has increased to similar to 15% in the Western world. Pharmacological effects of serotonin (5-hydroxytryptamine, 5-HT) are mediated through 5-hydroxytryptamine receptor (5-HTR) binding. Serotonin regulation of amygdala activity is attained through activation of three 5-HT2 family receptor subtypes, 5-HT2A, 5-HT2B, and 5-HT2C. Specifically, HT2A and the HT2C receptors have similar gross cerebral distribution and function, with higher constitutive activity found in HT2C than in HT2A. We investigated the possible association of 5-HTR gene polymorphisms to specific and non-specific antidepressant treatment responses in treatment-free patients in Siberia. 156 patients, aged between 18-70 years and clinically diagnosed with depressive disorders, were treated with antidepressants for 4 weeks. Patients were genotyped for a subset of 29 SNPs from the following 5-HT Receptor genes: HTR1A, HTR1B, HTR2A, HTR2C, HTR3A, HTR3B and HTR6. Primary outcome was measured by differences in Hamilton Depression Rating Scale (Delta HAM-D 17) scores between baseline/week two, week two/week four and baseline/week four. Univariate linear regression was initially conducted to determine the 5-HTR SNPs to be studied within the multiple linear regression. Multiple linear regression analyses over the three time periods were conducted for Delta HAM-D 17 with independent factors including: age, gender, depression diagnosis, antidepressant treatment and selected 5-HTR SNPs. We found improved increment HAM-D 17 in patients taking tricyclic antidepressants (0-4 weeks: B = 4.85, p = 0.0002; 0-2 weeks: B = 3.58, p = 0.002) compared to patients taking SSRIs. Over the course of study, significant associations between 5-HT receptors SNPs and antidepressant response were not identified

    Association Between BDNF Gene Variant Rs6265 and the Severity of Depression in Antidepressant Treatment-Free Depressed Patients

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    Background: Brain-derived neurotrophic factor (BDNF) plays an important role in neuronal plasticity, and its dysregulation has been associated with the pathogenesis of mood and anxiety disorders. Prolactin (PRL) is a pituitary hormone which is also produced as a cytokine by immune cells and could be a neurotrophic factor regulating the functional activity of stress-related mechanisms. Aim: To investigate the possible relationship between depressive state and BDNF and PRL genotypes or levels with special reference to severity of depression. Methods: Participants of 18–70 years with a clinical diagnosis of depressive disorder of at least moderate severity were included. These patients had not been treated with antidepressant drugs before admission to hospital during the preceding period of the last 6 months, and 54.5% had never been treated with antidepressant drugs during their entire life. The DNA was genotyped for rs1341239 within the prolactin and for rs6265, rs7124442, and rs11030104 within the BDNF gene. Rs11030104 violated the Hardy-Weinberg equilibrium distribution and was excluded from further analyses. BDNF and prolactin concentration was measured in serum by MAGPIX multiplex analyzer (Luminex, USA) using MILLIPLEX® MAP kit (Merck, Germany). Genetic associations were determined by sequentially regressing prolactin, BDNF, 17-items Hamilton's Depression (HAMD-17) and Clinical Global Impression scale, Severity (CGI-S) ratings, and depression (absent/present) on the available SNPs. Genetic associations were evaluated assuming an additive model. Results: A total of 186 depressed patients (of which 169 were women) and 94 healthy controls (67 women) were genotyped. After excluding subjects without genetic information on all three study SNPs, 217 remained of whom 138 suffered from depression. Within depressed patients we observed an association of rs6265 with HAMD-17: mean difference (MD) 2.33 (95%CI 0.49; 4.16; p = 0.014) and CGI-S: MD 0.38 (95%CI 0.09; 0.66; p = 0.011). No significant association was observed between the prolactin SNP rs1341239 and prolactin levels. Similarly the mean differences of BDNF SNPs did not show an association with BDNF: rs6265 −0.042 ln(pg/ml) (95%CI −0.198; 0.113), and rs7124442 0.006 ln(pg/ml) (95%CI −0.117; 0.130). No other association reached statistical significance. Conclusion: We observed a significant association between BDNF gene variant rs6265 and the severity of depression in newly admitted, antidepressant treatment-free, depressed patients. Actual PRL and BDNF levels were not elevated sufficiently in depressed patients to reach statistical significance and were not associated with the studied genotypes

    Investigating the potential role of BDNF and PRL genotypes on antidepressant response in depression patients:A prospective inception cohort study in treatment-free patients

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    Background: Brain-derived neurotrophic factor (BDNF) is associated with response to antidepressant drugs in mood and anxiety disorders. Prolactin (PRL) is a pituitary hormone with behavioural effects, acting as a neurotrophic factor within the brain and may be involved in antidepressant response. Objectives: To investigate the relationship between BDNF and PRL genotypes with antidepressant drug response. Methods: Prospective inception cohort of 186 Russian treatment-free participants (28 men and 158 women) between 18 and 70 years clinically diagnosed with depressive disorder who initiated antidepressant medication. DNA polymorphisms were genotyped for PRL rs1341239, BDNF rs6265 and rs7124442. Primary outcome was measured by differences in Hamilton Depression Rating Scale (Delta HAM-D) scores between baseline/week two, week two/week four, and baseline/week four. Linear regression and independent t-test determined the significance between polymorphisms and Delta HAM-D. Results: Comparisons between genotypes did not reveal any significant differences in scores during the first two weeks of treatment. In the latter two weeks, BDNF rs7124442 homozygous C patients responded significantly worse in comparison to homozygous T patients during this period. Further analysis within women and in postmenopausal women found a similar comparison between alleles. Limitations: Study lasted four weeks, which may be considered short to associate genuine antidepressant effects. Conclusions: Patients taking tricylic antidepressants were noted to have a significant improvement in Delta HAM-D compared to patients taking SSRIs. Homozygous C BDNF rs712442 patients were found to respond significantly worse in the last two weeks of treatment

    Influence of eight ABCB1 polymorphisms on antidepressant response in a prospective cohort of treatment-free Russian patients with moderate or severe depression:An explorative psychopharmacological study with naturalistic design

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    BACKGROUND: Many antidepressants are substrates of P-glycoprotein, an efflux transporter in the blood-brain-barrier encoded by the ABCB1 gene. Genetic variations might influence the transport rate of antidepressants and hence their pharmacological effects. This study investigates the influence of eight polymorphisms in the ABCB1 gene on antidepressant treatment response. METHOD: 152 patients were included from psychiatric departments of the Mental Health Research Institute in Tomsk. The difference in Hamilton-Depression-Rating-Scale (HAMD-17)-scores between baseline and week two, week two and four, and baseline and week four was used to estimate timing of improvement of depression. Associations between the ABCB1 gene-polymorphisms and reduction in HAMD-17 score were assessed using independent t-test and multiple linear regression. RESULTS: Tricyclic antidepressants were associated with a higher reduction of HAMD-17 score when compared to SSRIs. The SNP rs2235040 A-allele had a significant positive influence on the ΔHAMD-17(0→2W) score but a significant negative influence on the ΔHAMD-17(2→4W) score. The rs4148739 G-allele had a significant negative influence on the ΔHAMD-17(0→2W) score but a significant positive influence on the ΔHAMD-17(2→4W) score. The SNP rs2235015 T-allele is significant negatively related to the ΔHAMD-17(2→4W) score. CONCLUSION: ABCB1 Genetic variations appear to affect speed but not magnitude of antidepressant drug response
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