IMPACT OF ANXIETY AND DEPRESSIVE DISORDERS ON THE NEUROPEPTIDE-CYTOKINE STATUS OF IMMUNE SYSTEM IN VARIOUS VARIANTS OF THE CLINICAL COURSE OF CHRONIC ISCHEMIC HEART DISEASE

Occurrence of coronary artery disease in combination with anxiety-depressive disorders is common in clinical practice. In such patients, affective disorders significantly may cause progression of atherosclerotic processes, thus complicating the course of cardiac pathology and prognosis. Distinct markers of immune inflammation, first of all, cytokines are of particular importance for the pro-atherogenic effects in atherosclerotic foci. Endogenous opiate peptides are considered the main regulators of these processes at the neuroimmune level. Their role for stabilization of cytokine levels in evolving inflammation in atherosclerotic plaque, and during adaptation of heart muscle to stressful effects was previously shown. Despite reliable data on the role of immune inflammatory markers in atherogenesis, the validity of the regulatory role of opiate peptides in this process, questions still exist about the effects of affective disorders upon neuropeptide-cytokine status of the immune system in the patients with chronic ischemic heart disease (IHD). Another issue concerns the ranges of these changes in painful and painless forms of myocardial ischemia.Therefore, the purpose of our study was to assess the impact of severity of anxiety-depressive disorders upon the neuropeptide-cytokine status of immune system in patients with various clinical variants of chronic IHD, as well as comparisons of these changes expressed in painlul and painless myocardial ischemia.Appropriate groups were formed, then being divided into subgroups, according to the percentage of painful and painless episodes of angina pectoris: Group 1 (n = 36) included patients with chronic coronary artery disease occurring and moderate-grade anxiety/depression; Group 2 (n = 34) consisted of patients with chronic coronary artery disease and mild anxiety-depressive disorders; Group 3 (n = 20) included patients with chronic coronary artery disease without anxiety and depressive disorders; Group 4 (n = 22) represented controls (healthy persons). As based on presence of painful and painless episodes of stenocardia, the following subgroups were specified: in the 1 st group of patients, painful form of IHD was detected in 44% of cases (n = 17); painless form of IHD was detected in 56% of patients (n = 19); in the 2 nd group of patients, painful form of IHD is in 52% of the examined persons (n = 18), painless form of IHD was revealed in 48% of cases (n = 16); in the 3 rd group, the painful form of IHD was confirmed in 37% of patients (n = 8), painless form of IHD was observed in 63% of patients (n = 12). In all these groups, the following parameters were evaluated: the state of psychophysiological status determined by psychological testing, the levels of vegetative regulation (β-endorphin), the function of cardiovascular system (SMECG), and the levels of peripheral blood TNFα, IL-1β, IL-6 and IL-4, IL-10 were also measured.As based on the data of clinical and laboratory examination, we have suggested that, in the patients with chronic IHD, anxiety and depressive disorders exert a direct pathological effect on the neuropeptide-cytokine status of immune system expressed as suppression of β-endorphin, increased level of pro-inflammatory cytokines and a decrease in anti-inflammatory factors. Meanwhile, these changes are especially pronounced in the patients with painless myocardial ischemia

Efficiency validation for application of medical and psychological rehabilitation and digitalpsychophysiological therapy in regulation of atherosclerosis development at the level of neuropeptide-cytokine links of immune system in polymorbid cardiovascular pathology in presence of affective spectrum disorders in marine specialists in the Far North

Scientific medical literature has accumulated a lot of data suggesting most important components of coronary heart disease pathogenesis and hypertension to be complex triggering processes of neuro-immune and neuro-endocrine interactions. Risk factors for cardiovascular diseases at the initial stages of atherosclerosis formation cause endothelial dysfunction and trigger a cascade of immune inflammation in coronary vessels, which is based on shifting immune response towards activation of lymphocytes, with predominance of cellular immune reactions. As a rule, it results in remodeling of the vascular wall under participation of proinflammatory cytokines, shifting blood lipid balance towards atherogenicity, destabilization of atherosclerotic plaque, development of thrombosis and acute coronary syndrome. In this respect, the aim of our work was to develop treatment methods that allow, under participation of endogenous immune regulators, to change the structure of pro-atherogenic links via their interactions at the initial stages of the atherosclerotic lesion formation in chronic coronary heart disease and hypertension.To achieve this goal, 80 patients (men) were selected among the marine specialists of the ship crews serving in the Arctic latitudes and the Far North, with ischemic heart disease, stage 1 hypertension and astheno-neurotic disorders with anxiety and depressive manifestations. The groups of patients were formed as follows: Group 1 (n = 31, patients who received standard therapy with cardiotropic drugs; Group 2 (n = 29), subjects who underwent drug correction with weak tranquilizers as a part of standard cardiotropic therapy; Group 3 (n = 34), standard therapy accompanied by medical and psychological rehabilitation and digital psychophysiological therapy. Effectiveness of the treatment was studied by assessing the dynamics of parameters characterizing the neuropeptide-cytokine immune status, the markers used in the diagnostics of atherosclerosis, as well as paired relationships between them. The laboratory part of the work was represented by a set of diagnostic kits, including markers of atherosclerotic process, and test systems for determination of β-endorphin, proinflammatory cytokines (TNF α, IL-1 β, IL-6), and anti-inflammatory (IL-4, IL-10) spectrum.We have found that the use of medical and psychological rehabilitation, along with digital psychophysiological therapy contributes to optimization of neuropeptide-cytokine interactions, thus showing efficiency of cardiotropic drugs usage. It seems to correct the relationships within proatherogenic structures of immune system and pathogenetic links involved in development of atherosclerotic process in polymorbid cardiovascular pathology from marine specialists with intense workloads

Anyui Volcano in Chukotka: Age, structure, pecularities of rocks' composition and eruptions

The study of lavas and pyroclastics from Anyui Volcano made it possible to reconstruct succession of its eruption events. The age of the eruption is estimated by isotopic methods to be 0.248 ± 0.030 Ma. It is established that the last episode of volcanic activity in northeastern Russia occurred 0.2‒0.5 Ma ago (in its continental part, 0.2‒0.3 Ma ago). This episode is chronologically close to the last peak in activation of volcanism in the Arctic and Subarctic regions. The absence of features indicating glacial influence on lavas from Anyui Volcano provides grounds for an assumption that no significant glaciations took place in the continental areas of western Chukotka during the last 250 ka

Fungal infection possible pathogenic role in Parkinsonian disease and parkinsonism

The critical review of scientific data and own statement concerning a fungal infection possible pathogenetic role in Parkinsonian disease and parkinsonism is given. Authors are based on the numerous clinical observation results which confirm that the fungal infection (mainly of the Candida species) is considered in aspect of its pathogenetic importance in the abovementioned pathology. The data about both fungal-induced striatal damage and dopaminergic striato-nigral neurotransmission failure are interesting that represents the main link of Parkinsonian disease and parkinsonism pathogenesis. Comparing data of clinical works authors emphasize a community of candidosis and parkinsonian clinical manifestations that confirms additionally by these diseases clinical manifestation improvement after antifungal preparations and levadopa treatment. Authors conclude that revealed interrelation between a fungal infection and Parkinsonian disease and parkinsonism allows to consider confidently about the functional pallido-striato-nigral system failure additional pathogenetic link in the form of fungal infection and fungal-induced nervous system intoxication.Представлен критический обзор данных научной литературы, а также собственные положения, касающиеся возможной патогенетической роли грибковой инфекции при болезни Паркинсона и паркинсонизме. Авторы основываются на результатах многочисленных клинических исследований, которые свидетельствуют в пользу того, что грибковая инфекция (преимущественно грибы роды Candida) рассматривается в аспекте её патогенетического значения при вышеуказанной патологии. В этом отношении интересны данные о фунгальноиндуцированном поражении стриатума, дофаминергической стриато-нигральной нейропередачи, что представляет собой основное звено патогенеза болезни Паркинсона и паркинсонизма. Сопоставляя данные клинических работ, авторы подчеркивают общность клинических проявлений кандидоза и паркинсонизма, что дополнительно подтверждается улучшением клинического течения этих заболеваний вследствие назначения противогрибковых препаратов и левадопы. Авторы заключают, что продемонстрированная взаимосвязь между грибковой инфекцией и наличием болезни Паркинсона и паркинсонизмом позволяет с уверенностью полагать наличие дополнительного патогенетического звена функционального поражения паллидо-стриато-нигральной системы в виде наличия грибковой инфекции и развития фунгальной интоксикации нервной системы.Подано критичний огляд даних наукової літератури, а також власні положення, що стосуються можливої патогенетичної ролі грибкової інфекції при хворобі Паркінсона та паркінсонізмі. Автори грунтуються на результатах численних клінічних досліджень, які свідчать на користь того, що грибкова інфекція (переважно гриби роду Candida) розглядається в аспекті її патогенетичного значення за умов вищевказаної патології. У цьому відношенні цікавими постають дані про фунгально-індуковане ураження стріатуму, дофамінергічної стріатонігральної нейропередачі, що є провідною ланкою патогенезу хвороби Паркінсона і паркінсонізму. Зіставляючи дані клінічних робіт, автори підкреслюють спільність клінічних проявів кандидозу і паркінсонізму, що додатково підтверджується покращенням клінічного перебігу цих захворювань внаслідок призначення протигрибкових препаратів і левадопи. Автори висловлюють, що висвітлений взаємозв'язок між грибковою інфекцією і наявністю хвороби Паркінсона і паркінсонізмом дозволяє з упевненістю вважати наявність додаткової патогенетичної ланки функціонального ураження палідо-стріато-нігральної системи у вигляді наявності грибкової інфекції і розвитку фунгальної інтоксикації нервової системи

CHARACTERISTIC INFLUENCE OF PULSE ELECTROTHERAPY (ELECTRICAL SLEEP) AT A NEUROPEPTIDE-CYTOKINE LINKS IN ARTERIAL HYPERTENSION ACCOMPANIED BY A ASTHENONEUROTIC DISTURBANCES IN YOUNG MEN EMPLOYED IN STRESSFUL PROFESSIONS

Disorders in functioning of major regulatory systems in patients with somatic diseases required development of new and effective integrated approaches to their treatment and prevention. Effective electrotherapy (electrical sleep) is among these methods. Despite existence of studies proving high efficiency of electrical sleep results in therapeutic practice, some open questions remain concerning impact of this treatment upon neuropeptide-cytokine links of immune system, which is one of the most important effector of pathogenesis in cardiovascular diseases in young persons with hypertension from the group occupied with stressful jobs. In this connection, the aim of our study was to investigate the influence on electrical sleep upon neuropeptide-cytokine profile in arterial hypertension conditions accomplished by asthenic-neurotic disorders in young men from the group of stressful activities. The following treatment groups were formed: 1st (n = 12), antihypertensive therapy; 2nd (n = 10), complex therapeutic measures added to antihypertensive therapy plus minor tranquilizers; in the 3rd group (n = 12), electric sleep was performed. Neuropeptide-cytokine profile was investigated as serum contents of β-endorphin, proinflammatory (TNFα, IL-1β, IL-6) and anti-inflammatory (IL-4, IL-10) cytokines. In the course of the clinical and laboratory examination, the authors have found that electric sleep applied in a complex primary schedule, with antihypertensive drug treatment in patients with hypertension and asthenic-neurotic disorders proved to exert optimizing effect upon functioning of neuropeptide-cytokine pool of immune system, which manifested by stimulation of beta-endorphin production, a decrease via regulation of proinflammatory effectors (TNFα, IL-1β, IL-6), and increased anti-inflammatory cytokines (IL-4, IL-10)

CHARACTERISTICS OF NEUROPEPTIDE-CYTOKINE IMMUNITY LINKS IN PATIENTS WITH COMBINED CARDIOVASCULAR PATHOLOGY, PROCEEDING WITH ANXIETY/DEPRESSION DISORDER

To date, pathogenetic events underlying coronary heart disease and hypertensive syndrome should be regarded as complex reactions of neuroimmune interactions characterized by activation of proinflammatory cytokines, opiate receptors and endogenous opioid peptides. These changes are mediated by high activity of basic regulatory systems that increase myocardial resistance to acute and chronic ischemic damage. However, there is lack of data concerning severity of these changes in the course of complicated coronary heart disease and hypertension, which occur in the background of anxiety-depressive disorders.The aim of present study was to assess regulatory disturbances at the level of neuropeptide-cytokine pool in the patients with polymorbid cardiovascular disease accomplished by anxiety and depressive conditions. Clinical examination of 85 patients (males) aged 35 to 45 years, with complicated cardiovascular disease (coronary heart disease combined with essential hypertension stage II) associated with anxiety and depressive disorders. To address these issues, we have formed a group of patients with anxiety and depressive disorders (group 1, n = 40), patients with coronary artery disease and stage II hypertension; group 2 (n = 20) included patients with coronary artery disease; group 3 (n = 25) included patients with hypertension stage II; group 4 (n = 30) represented controls (healthy person). In order to study dysfunction of regulatory neuropeptides at the level of cytokine-mediated immunity in these groups, we have studied diagnostic markers of the suprasegmentary autonomous nervous condition, and cytokine pool of immune system. Immune testing was used to determine β-endorphin, cytokines of pro-inflammatory (TNFα, IL-1β, IL-6) and anti-inflammatory (IL-4, IL-10) spectra in blood serum of patients.In the course of clinical and laboratory examination, the authors found that the patients with polymorbid cardiovascular pathology exhibit regulatory dysfunctions at the level of neuropeptide-cytokine links of immunity characterized by 1.5-2-fold decrease of β-endorphin levels, increase in pro-inflammatory cytokines (TNFα, IL-1β, IL-6) and decrease in anti-inflammatory (IL-4, IL-10) cytokines

INDICATORS OF CYTOKINE ACTIVITY AND BETA-ENDORPHIN PRODUCTION LEVEL IN ARTERIAL HYPERTENSION ASSOCIATED WITH ASTHENIC/NEUROTIC DISORDERS IN YOUNG MEN EMPLOYED IN STRESSFUL PROFESSIONS

At the present time, arterial hypertension is the most common somatic pathology among young and able-bodied persons. Development and progression of hypertension in young people occupied with stressful jobs presents a particular problem. Anxiety and depression arise quite commonly in such persons subjected to chronic stress. Direct pathophysiological effects of anxiety and depressive disorders upon cardiovascular system leads to development of disturbances of basic regulatory processes and life-threatening clinical forms of ischemic heart disease and hypertension. However, despite sufficient data about the impact of anxiety and depressive disorders on the course of cardiac pathology, some open questions remain concerning the degree of changes in neuropeptide-cytokine pool of immune system in young, intensively working hypertensive patients.Moreover, there is lack of knowledge concerning interdependence in functioning of the major regulatory systems (autonomic nervous and immune) in such patients.In this connection, the aim of this work was to study cytokines of the immune system, and the levels of betaendorphin production in hypertension, proceeding with astheno-neurotic disorders in young men of intensive specialties, as well as study of interactions between the indices of autonomic nervous system functioning, and immunity parameters in these patients. The following groups were under study: 1st (n = 34) included patients with hypertension and astheno-neurotic problems; 2nd (n = 20), patients with hypertension without psychological disorders, with acute or chronic stress in previous history (controls). Neuropeptide-cytokine profile of the immune system was evaluated by levels of proinflammatory cytokines (TNFα, IL-1β, IL-6), antiinflammatory cytokines (IL-4, IL-10), and β-endorphin.In the course of clinical and laboratory examination, we have found that, in the patients with hypertension and astheno-neurotic disorders, activation of proinflammatory cytokines (TNFα, IL-1β, IL-6), suppression of anti-inflammatory cytokines (IL-4, IL-10), and reduced β-endorphin in the blood are registered. Moreover, the disturbances detected showed the mutual interactions between autonomic nervous and immune systems in these patients

Возможная патогенетическая роль грибковой инфекции при болезни Паркинсона и паркинсонизме = Fungal infection possible pathogenic role in Parkinson disease and parkinsonism

Gertsev V. V., Muratova T. N., Vastyanov R. S., Stoyanov A. N. Возможная патогенетическая роль грибковой инфекции при болезни Паркинсона и паркинсонизме = Fungal infection possible pathogenic role in Parkinson disease and parkinsonism. Journal of Education, Health and Sport. 2015;5(3):68-78. ISSN 2391-8306. DOI: 10.5281/zenodo.16247 http://ojs.ukw.edu.pl/index.php/johs/article/view/2015%3B5%283%29%3A68-78 https://pbn.nauka.gov.pl/works/547948 http://dx.doi.org/10.5281/zenodo.16247 Formerly Journal of Health Sciences. ISSN 1429-9623 / 2300-665X. Archives 2011 – 2014 http://journal.rsw.edu.pl/index.php/JHS/issue/archive   Deklaracja. Specyfika i zawartość merytoryczna czasopisma nie ulega zmianie. Zgodnie z informacją MNiSW z dnia 2 czerwca 2014 r., że w roku 2014 nie będzie przeprowadzana ocena czasopism naukowych; czasopismo o zmienionym tytule otrzymuje tyle samo punktów co na wykazie czasopism naukowych z dnia 31 grudnia 2014 r. The journal has had 5 points in Ministry of Science and Higher Education of Poland parametric evaluation. Part B item 1089. (31.12.2014). © The Author (s) 2015; This article is published with open access at Licensee Open Journal Systems of Kazimierz Wielki University in Bydgoszcz, Poland and Radom University in Radom, Poland Open Access. This article is distributed under the terms of the Creative Commons Attribution Noncommercial License which permits any noncommercial use, distribution, and reproduction in any medium, provided the original author(s) and source are credited. This is an open access article licensed under the terms of the Creative Commons Attribution Non Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted, non commercial use, distribution and reproduction in any medium, provided the work is properly cited. This is an open access article licensed under the terms of the Creative Commons Attribution Non Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted, non commercial use, distribution and reproduction in any medium, provided the work is properly cited. The authors declare that there is no conflict of interests regarding the publication of this paper. Received: 20.01.2014. Revised 27.02.2015. Accepted: 12.03.2015.   УДК 616/617.7 + 612.017.1: 616-056.3   ВОЗМОЖНАЯ ПАТОГЕНЕТИЧЕСКАЯ РОЛЬ ГРИБКОВОЙ ИНФЕКЦИИ ПРИ БОЛЕЗНИ ПАРКИНСОНА И ПАРКИНСОНИЗМЕ   FUNGAL INFECTION POSSIBLE PATHOGENIC ROLE IN PARKINSONIAN DISEASE AND PARKINSONISM   В. В. Герцев, Т. Н. Муратова, Р. С. Вастьянов, А. Н. Стоянов V. V. Gertsev, T. N. Muratova, R. S. Vastyanov, A. N. Stoyanov   Одесский национальный медицинский университет   Odessa National Medical University   Abstract   The critical review of scientific data and own statement concerning a fungal infection possible pathogenetic role in Parkinsonian disease and parkinsonism is given. Authors are based on the numerous clinical observation results which confirm that the fungal infection (mainly of the Candida species) is considered in aspect of its pathogenetic importance in the abovementioned pathology. The data about both fungal-induced striatal damage and dopaminergic striato-nigral neurotransmission failure are interesting that represents the main link of Parkinsonian disease and parkinsonism pathogenesis. Comparing data of clinical works authors emphasize a community of candidosis and parkinsonian clinical manifestations that confirms additionally by these diseases clinical manifestation improvement after antifungal preparations and levadopa treatment. Authors conclude that revealed interrelation between a fungal infection and Parkinsonian disease and parkinsonism allows to consider confidently about the functional pallido-striato-nigral system failure additional pathogenetic link in the form of fungal infection and fungal-induced nervous system intoxication.   Key words: fungal infection, candidosis, Parkinsonian disease, pathogenetic mechanisms.   Резюме   Представлен критический обзор данных научной литературы, а также собственные положения, касающиеся возможной патогенетической роли грибковой инфекции при болезни Паркинсона и паркинсонизме. Авторы основываются на результатах многочисленных клинических исследований, которые свидетельствуют в пользу того, что грибковая инфекция (преимущественно грибы роды Candida) рассматривается в аспекте её патогенетического значения при вышеуказанной патологии. В этом отношении интересны данные о фунгально-индуцированном поражении стриатума, дофаминергической стриато-нигральной нейропередачи, что представляет собой основное звено патогенеза болезни Паркинсона и паркинсонизма. Сопоставляя данные клинических работ, авторы подчеркивают общность клинических проявлений кандидоза и паркинсонизма, что дополнительно подтверждается улучшением клинического течения этих заболеваний вследствие назначения противогрибковых препаратов и левадопы. Авторы заключают, что продемонстрированная взаимосвязь между грибковой инфекцией и наличием болезни Паркинсона и паркинсонизмом позволяет с уверенностью полагать наличие дополнительного патогенетического звена функционального поражения паллидо-стриато-нигральной системы в виде наличия грибковой инфекции и развития фунгальной интоксикации нервной системы.   Ключевые слова: грибковая инфекция, кандидоз, болезнь Паркинсона, патогенетические механизмы.   Резюме   Подано критичний огляд даних наукової літератури, а також власні положення, що стосуються можливої  патогенетичної ролі грибкової інфекції при хворобі Паркінсона та паркінсонізмі. Автори грунтуються на результатах численних клінічних досліджень, які свідчать на користь того, що грибкова інфекція (переважно гриби роду Candida) розглядається в аспекті її патогенетичного значення за умов вищевказаної патології. У цьому відношенні цікавими постають дані про фунгально-індуковане ураження стріатуму, дофамінергічної стріато-нігральної нейропередачі, що є провідною ланкою патогенезу хвороби Паркінсона і паркінсонізму. Зіставляючи дані клінічних робіт, автори підкреслюють спільність клінічних проявів кандидозу і паркінсонізму, що додатково підтверджується покращенням клінічного перебігу цих захворювань внаслідок призначення протигрибкових препаратів і левадопи. Автори висловлюють, що висвітлений взаємозв'язок між грибковою інфекцією і наявністю хвороби Паркінсона і паркінсонізмом дозволяє з упевненістю вважати наявність додаткової патогенетичної ланки функціонального ураження палідо-стріато-нігральної системи у вигляді наявності грибкової інфекції і розвитку фунгальної інтоксикації нервової системи.   Ключові слова: грибкова інфекція, кандидоз, хвороба Паркінсона, патогенетичні механізми