18 research outputs found

    Early Coaching to Increase Water Intake in CKD.

    Get PDF
    Introduction: In observational studies, increased water intake improves kidney function but not in adults with CKD stage 3 and more. CKD WIT trial has shown a nonsignificant gradual decline in kidney function after 1 year of coaching to increase water intake (CIWI) [1]. We propose that CIWI may benefit in CKD stage 1–2 (G1 and G2) and depends on functional renal functional reserve (RFR) [2, 3]. Objective: Parallel-group randomized trial was aimed to determinate the effectiveness of CIWI dependence of estimated glomerular filtration rate (eGFR) stage and RFR in adults with CKD 1–2 stages. Methods: CKD WIT trial was taken as the basis for prospective multicenter randomized trial named "Early Coaching to Increase Water Intake in CKD (ECIWIC)." The primary outcome was the change in kidney function by eGFR from baseline to 12 months. Secondary outcomes included 1-year change in urine albumin/Cr ratio, and patient-reported overall quality of health (QH) ranged from 0 (worst possible) to 10 (best possible). CIWI aimed to have the diuresis being 1.7–2 L. There were 4 groups with nondiet sodium restriction which consisted of 31 patients each: 2 groups with CKD G1 and CKD G2, undergoing CIWI and 2 others with CKD G1 and CKD G2 without CIWI (Fig. 1a). Overall checks were made at 0, 6, and 12 months. RFR evaluation was performed using 0.45% sodium chloride oral solution. Results: Of our randomized 124 patients (mean age 53.2 years; men 83 [67%], 0 died), mean change in 24-h urine volume was 0.6 L per day in G1 with CIWI group and 0.5 L in G2. No statistically significant data on eGFR depending CIWI were obtained (Fig. 1b). However, the trend suggests that CIWI improves eGFR in CKD G1 (from 95 to 96 mL/min/1.73 m2) and preserves eGFR decline in CKD G2 (78–78). The QH values were also preserved (from 7 to 7 in G1 and G2 groups). Although coaching to maintain the same water intake did not preserve physiological and pathological eGFR decreasing in CKD G1-2 (G1 from 96 to 93, G2 from 76 to 73; t = 0.6, p = 0.29, and p ≤ 0.05 in all groups) and the QH was declined (from 7 to 6 in both groups). An individual analysis of the RFR has shown that patients with RFR more than 50% (G1 19 patients, 61%, and G2 13 patients, 42%) had reliable preservation of eGFR with its increase of 1.5 mL/min on CIWI, while patients with low functional renal reserve had a drop of eGFR at 1.1 mL/min/m2 within 12 months. Patients with low normal serum sodium levels have shown worse results on CIWI. Conclusions: With CKD G1, the CIWI leads to the preservation of the renal function with its increase of GFR per 1 mL/min/m2/per year in comparison with the same water intake. In CKD G2, the CIWI prevents physiological and pathological loss of renal function, and RFR above 50% aids restoration of eGFR both in CKD G1-2. ECIWIC trial demonstrates benefit of CIWI in patients with CKD 1–2 and preserved RFR

    Modulating Neuro-Endocrine Effects Of Bioactive Water Naftussya From Layers Truskavets’ And Pomyarky At Humans With Dysfunction Of Neuro-Endocrine-Immune Complex

    Get PDF
    Background. Previously we have been carry out comparative investigation long-term effects of Bioactive Water Naftussya from layers Truskavets’, Pomyarky and Skhidnyts’a on some metabolic and biophysical parameters at men with dysfunction of neuro-endocrine-immune complex. The aim of this study is the investigation long-term effects on neuro-endocrine regulation at similar patients. Materials and methods. The object of observation were 20 volunteers: ten women and ten men aged 33-76 years without clinical diagnose but with dysfunction of neuro-endocrine-immune complex and metabolism. We evaluated the trait and reactive anxiety, recorded EEG, HRV and blood pressure, determined levels of Cortisol, Aldosterone, Testosterone, Triiodothyronine and Calcitonin. After examination volunteers within 7 days used bioactive water Naftussya (250 mL three times a day) from Truskavets’ or Pomyarky layer, then repeated the tests listed. Results. Weekly drinking of Bioactive Water Naftussya normalizes initially elevated levels of testosterone in women and reduces initially normal its level in men, in both sexes normalizes initially elevated levels of triiodothyronine and activity of the autonomic regulatory systems as the parasympathetic, so sympathetic, combined with a slight increase in the normal levels of aldosterone and trend to increase (under low) reactive anxiety as well as post occlusive reactivity of vascular tone. Among the 164 registered parameters quantitative EEG revealed noticeable changes only 8. This is, above all, normalizing increase initially reduced spectral power density (SPD) α-rhythm in loci T6 by 93%, P4 by 33%, F7 by 29%, increase by 10% in the normal range modal frequency of β-rhythm and further enhance SPD θ-rhythm in locus T5 by 42%. On the other hand, showed a reduction by 28% initially normal PSD of β-rhythm in locus in O2 and further reduction its by 20% in locus P4. Moreover, there was left-sided lateralization initially symmetric α-rhythm. No significant differences between the effects of Naftussya both deposits were found. Conclusion. Bioactive water Naftussya both Truskavets’ and Pomyarky layers causes favorable normalizing effects on abnormalities neuro-endocrine parameters, which is a manifestation of its adaptogenic properties

    Cluster analysis of uric acid exchange parameters in female rats

    Get PDF
    Background. Uric acid is traditionally considered as the final product of human and primate DNA/RNA degradation, devoid ofuseful physiological activity. However, there is an opinion that theuric acid molecule, by analogy with methylxanthines (caffeine, theophylin, theobromine) has physiological activity. The acquired experience allows us to offer a topic for future research: “Neurotropic and immunotropic activity of endogenous uric acid”. Working hypothesis. Uric acid, interacting with A1 and A2a adenosine receptors as well as phosphodiesterase and Na,K-ATPase of neurons, modulates the activity of nerve centers, which in turn modulate immunocytes. Perhaps the direct effect of uric acid on immunocytes, since the existence oftheophylline-resistant and theophylline-sensitive subpopulations of T-lymphocytes has long been known. The proposed article is the first swallow of the announced project.Material and Methods. Experiment was performed on 58 healthy female Wistar rats 220-300 g. Among them 10 animals remained intact, using tap water from drinking ad libitum. The rats of others groups for 6 days administered through the tube various fluids at a dose of 1,5 mL/100 g of body mass.The day after the completion of the drinking course the plasma and urine levels of the uric acid (uricase method) were determined. Results. We obtained a wide range of uric acid metabolism parameters, divided into four clusters, quantitatively and qualitatively different from each other. On the basis of the accepted criteria, 29,3% of animals state normouricemia in combination with normal or slightly increased excretion of uric acid. In 24,1% of rats, hypouricemia is combined with normal or slightly reduced uricosuria. In 31,0% of animals normal or slightly elevated levels of plasma uric acid are accompanied by a very marked dispersion of uricosuria. The remaining 15,5% of rats expressed hyperuricemia combined with normal or slightly increased uricosuria. In the following articles, functional relationships of uricemia and uricosuria with the parameters of autonomic regulation, immunity and metabolism will be analyzed

    Interrelations between changes in parameters of HRV, EEG and phagocytosis at patients with chronic pyelonephritis and cholecystitis

    Get PDF
    Background. Previously we have shown within the immunological homunculus conception that take place causal relationships between induced by balneotherapy changes in parameters of EEG and HRV, on the one hand, and the parameters of humoral and cellular immunity, on the other hand. The purpose of this study is to find out the relationships between induced by balneotherapy changes in parameters of EEG and HRV, on the one hand, and the parameters of phagocytosis , on the other hand. Material and methods. In basal conditions in 33 men and 10 women with chronic pyelonephritis and cholecystitis in remission, we recorded twice, before and after balneotherapy at the spa Truskavets’, EEG (“NeuroCom Standard”) and HRV (“Cardiolab+VSR”). In blood estimated parameters of phagocytic function of neutrophils against Staphylococcus aureus and Escherichia coli. Results. Judging by the coefficients of canonical correlation, the maximal subordinate nervous regulation is the completeness of phagocytosis of E. coli (R=0,944), whereas the influence of the nervous system on the completeness of phagocytosis Staph. aur. is minimal (R=0,607). With regard to the intensity of phagocytosis, the differences in the strength of nerve influence are expressed less (0,893 vs 0,744), and in relation to the activity of phagocytosis as well as the bactericidal ability of neutrophils, there are no differences between R (0,858 vs 0,857 and 0,831 vs 0,834, respectively). However, significant differences were found between profiles of correlation coefficients between EEG and HRV parameters, on the one hand, and phagocytosis parameters, on the other hand, for representatives of Gram-negative and Gram-positive microbes. Conclusion. In the nervous regulation of phagocytosis by neutrophils of the Gram-negative and Gram-positive microbes are involved the structures that are localized in different parts of the CNS

    Individual Immune Responses to Chronic Stress and their Neuro-Endocrine Accompaniment, 200 s.

    Get PDF
    The monograph presents the literature data and the results of its own study of interindividual differences in the immune responses of rats of both sexes to chronic restraint stress and their neuro-endocrine accompaniment. The neuroendocrine-immune interrelations and sexual dimorphism are analyzed in detail. For physiologists, endocrinologists, immunologists

    Mineral waters, metabolism, neuro-endocrine-immune complex, s. 252.

    Get PDF
    Dedicated to the 75th anniversary of Volodymyr Illich Kozyavkin with gratitude for the support of the Truskavetsian Scientific School of BalneologyThe monograph systematizes these writers and highlights the results of their own priority experimental and clinical-physiological studies of the impact of drinking mineral waters of Ukraine on neuroendocrine regulation, metabolism and immunity of healthy rats and patients in the process of rehabilitation of chronic pyelonephritis and cholecystitis in remission. In line with the concepts of functional-metabolic continuum and neuroendocrine-immune complex using the methods of factor, discriminant and canonical correlation analysis, it is demonstrated that mineral waters have both similar and specific physiologically favorable modulating effects on the parameters of the studied body systems. For specialists in medical rehabilitation, endocrinologists, immunologists, biochemists, pathophysiologists

    Gas Discharge Visualization (Electrophotonic Imaging, Kirlianography). Theoretical and Applied Aspects, 189 s.

    Get PDF
    The monograph highlights the results of priority clinical-physiological studies of the relationships between gas discharge visualization (electrophotonic imaging, kirlianography) parameters, on the one hand, and electroencephalograms, heart rate variability, immunograms, phagocytosis, the content of the main adaptation hormones (cortisol, aldosterone, testosterone, triiodothyronine, calcitonin) in the blood as well as acupuncture points - on the other hand. It is shown that the GDV/EPI method reliably reflects the state of the body's neuro-endocrine-immune complex as well as others parameters and has the right to take its place in the arsenal of physiological/biophysical methods. For biophysicists, physiologists, psychophysiologists, endocrinologists, immunologists, medical rehabilitation specialists. INTRODUCTION Advances in biophysics, biology, functional genomics, neuroscience, psychology, psychoneuroimmunology, and other fields suggest the existence of a subtle system of “biofield” interactions that organize biological processes from the subatomic, atomic, molecular, cellular, and organismic to the interpersonal and cosmic levels. Biofield interactions may bring about regulation of biochemical, cellular, and neurological processes through means related to electromagnetism, quantum fields, and perhaps other means of modulating biological activity and information flow. The biofield paradigm, in contrast to a reductionist, chemistry-centered viewpoint, emphasizes the informational content of biological processes; biofield interactions are thought to operate in part via low-energy or “subtle” processes such as weak, nonthermal electromagnetic fields (EMFs) or processes potentially related to consciousness and nonlocality. Biofield interactions may also operate through or be reflected in more well-understood informational processes found in EEG and ECG data. Recent advances have led to the development of a wide variety of therapeutic and diagnostic biofield devices, defined as physical instruments best understood from the viewpoint of a biofield paradigm [Muehsam D et al, 2015]. Biofield devices comprise physical instruments that may be most clearly understood from the viewpoint of a biofield paradigm, and a large and diverse number of devices have been developed to measure or manipulate biofield interactions. These include both diagnostic devices (to measure biofield properties) and therapeutic devices (to manipulate biofield interactions). The study of biofield devices is at a nascent stage of development, and much further research is needed to determine clinical efficacy and elucidate the underlying mechanisms of action for many of the devices mentioned here. The biofield devices operate through a variety of modalities rather than a single mechanism. Some biofield devices function through well-understood mechanisms and are already widely used in clinical settings: for example, electroencephalography (EEG)- and electrocardiography (ECG)-based heart rate variability (HRV). Other devices appear to operate through mechanisms that are novel or incompletely understood. However, all of these devices share a common property: rather than functioning primarily in a reductionist, chemistry-centered manner, biofield devices function via the informational content of biological processes and can interact via low-energy or “subtle” processes, including those potentially related to consciousness and nonlocality [Muehsam D et al, 2015]. Here Muehsam D et al [2015] provide a brief overview of the broad categories of biofield devices, with the goal being to stimulate further discussion and research. Authors describe those devices for which thay deemed that sufficient evidence exists to warrant mention. They chose to focus upon devices for which peer-reviewed scientific reports suggesting efficacy are available rather than conference proceedings or manufacturers' white papers. However, in the few cases that specific devices with sufficient promise and relevance lacked a peer-reviewed basis, authors have presented whatever evidence was available. Here, devices are organized according to mode of operation and these modalities include electromagnetic field (EMF)-light, EMF-heat, EMF-nonthermal, electrical current, vibration and sound, physical and mechanical, intentionality and nonlocality, gas and plasma, and other (mode of operation not well understood). Muehsam D et al [2015] deemed that gas discharge visualization (GDV) is an important example of the use of plasma in biofield science. Back in 1880 Nikola Tesla demonstrated that when placing the man in the high-frequency field around the body there is a bright glow [cit. by Korotkov KG, 2001]. In 1892 Nardkevych-Yodko YO recorded glow human hands on photographic plate [cit. by Ciesielska I, 2009]. However, a well-known method of "high-frequency photography" was due to spouses Kirlian SD&VH who in 1939 independently discovered this phenomenon [Kirlian SD & Kirlian VKh, 1961], later called "Kirlian’s effect". This technique has been called corona discharge photography [Boyers DG & Tiller WA, 1973], electrophotography [Earle L, 1975], electrography [Konikiewicz LW, 1979], GDV [Bankovskii NG et al, 1986]. In 1996 Korotkov KG created a new scientific approach, based on the digital videotechnics, modern electronics and computer processing quantitative data, called as method gas discharge visualization (GDV bioelectrography). Parallel uses the terms Kirlianography and Electrophotonic imaging (EPI) [Korotkov KG, 2001; 2007; 2014; Korotkov KG et al, 2002; Wisneski LA & Anderson L, 2009; Jakovleva E & Korotkov K, 2013]. Method of GDV, essence of which consists in registration of photoelectronic emission of skin, induced by high-frequency electromagnetic impulses, allows to estimate integrated psycho-somatic state of organism. The first base parameter of GDV is Area of Gas Discharge Image (GDI) in Right, Frontal and Left projections registered both with and without polyethylene filter. The second base parameter is a coefficient of form/shape (ratio of square of length of external contour of GDI toward his area), which characterizes the measure of serration/fractality of external contour. The third base parameter of GDI is Entropy, id est measure of chaos. It is considered that GDI, taken off without filter, characterizes the functional changes of organism, and with a filter characterizes organic changes. Program estimates also Energy and Asymmetry of virtual Chakras [Korotkov KG, 2001; 2007; 2014]. Nearly 1000 papers have been published (mostly in Russian) on GDV research and a few hundred more in the West. These intriguing data suggest that informatics based upon biofield measurement devices such as the GDV may be useful for gaining deeper understanding of disease states and guiding practitioners and their patients towards states of greater wellness [Muehsam D et al, 2015]. Without regard to the wideuse enough of method in medicine, psychology, valeology and others like that, he yields to the just criticizing for an insufficient physiology ground. There fore we put before itself sweep to analyse relationships between the parameters of GDV - from one side, and by the row of neurodynamics, endocrine, immune. psychophysiological, and other parameters - on the other hand

    Similarity Of Effects On EEG Parameters Of Aramaic, Greek Catholic And Krishnaic Prayers

    Get PDF
    The neurotropic effects of Prayer are manifested in two inhibitory and three activating patterns. The first inhibitory pattern reflects the decrease in elevated and upper limit levels of SPD of θ-and δ-rhythm in frontal loci and the second - decrease in normal SPD levels of β-and θ-rhythm in the frontal, central, temporal and parietal loci. The first activating pattern reflects a small increase in normal levels of β-rhythm index and asymmetry and SPD entropy in locus C3, as well as a further increase in elevated δ-rhythm SPD levels in loci P3 and T3. The second pattern reflects the slight increase in normal SPD levels of θ-rhythm in loci T3, T5, T6, O2 and α-rhythm in locus T5, as well as their indices and entropy SPD in locus O2. The third pattern reflects a slight increase in amplitude and SPD of α-rhythm in central, frontal, temporal and occipital loci

    Uric acid, metabolism, neuro-endocrine-immune complex, 258 s.

    Get PDF
    LITERATURE 1. Avtandylov H.G. Medical morphometry. Moscow. Medicine; 1990: 384 p. 2. Baevsky R.M., Kirillov O.I., Kletskin S.Z. Mathematical analysis of heart rate changes during stress. Moscow. Science; 1984: 221 p. 3. Baevsky R.M., Ivanov H.G. Variability of the heart rhythm: theoretical aspects and opportunities for clinical application. Ultrasound and functional diagnostics. 2001; 3: 106-127. 4. Bazarnova M.A. Cytological examination of punctate spleen. Guide to practical classes in clinical laboratory diagnostics. K.: Higher school; 1988: 263-264. 5. Balanovsky V.P., Popovych I.L., Karpynets SV. About the ambivalent-equilibrator nature of the influence of Naftusya medicinal water on the human body. ANU reports. Mat., prop., tech. science 1993; 3: 154-158. 6. Belousova OI, Fedotova MY. Comparative data on changes in the number of lymphocytes of the spleen, goiter and bone marrow in the early stages after irradiation in a wide range of doses. Radiobiology-radiotherapy. 1968; 9(3): 309-313. 7. Bilas V.R., Popovych I.L. The role of microflora and organic substances of Naftusya water in its modulating effect on the neuroendocrine-immune complex and metabolism. Medical hydrology and rehabilitation. 2009; 7(1): 68-102. 8. Biloshitsky P.V. Temperature, information, water, anabiosis, immortality. Health and longevity. Kyiv; 2007: 46-47. 9. Harkavy L.H., Kvakina E.B., Kuzmenko T.S. Antistress reactions and activating therapy. Moscow. Imedis; 1998: 654 p. 10. Harkavy L.H., Kvakina E.B., Ukolova M.A. Adaptation reactions and resistance of the body. Rostov-on-Don. Rostov University Publishing House, 3rd ed.; 1990: 224 p. 11. Harkavy L.H., Romasyuk S.I., Barantsev F.G., Kuzmenko T.S., Otkydach S.A., Tattsov O.V., Barantseva L.P. Activation therapy in the sanatorium-resort stage of rehabilitation of patients with internal organ diseases. Sochi; 2000: 94 p. 12. Gozhenko A.I. Theory of disease. Odesa. Phoenix; 2018: 236 p. 13. Gozhenko A.I. Dysregulation as the basis of the pathophysiology of homeostasis. Clinical and experimental pathology. 2004; 3 (2): 191-193. 14. Gozhenko A.I. Functional-metabolic continuum. The National Academy of Sciences of Ukraine. 2016; 22(1): 3-8. 15. Gozhenko A.I., Korda M.M., Popadynets O.O., Popovych I.L. Entropy, harmony, synchronization and their neuro-endocrine-immune correlates. Odesa. Phoenix; 2021: 232 p. 16. Horyachkovsky A.M. Clinical biochemistry. Odesa: Astroprint; 1998: 608 p. 17. Datsko O.R., Bubnyak A.B., Ivasivka S.V. The organic component of Naftusya mineral water. Development of an idea about its composition and origin. Medical hydrology and rehabilitation. 2008; 6(1): 168-174. 18. Ivasivka S.V., Popovych I.L., Aksentiychuk B.I., Flunt I.S. Physiological activity of uric acid and its role in the mechanism of action of Naftusya water. K. Computer Press; 2004: 163 p. 19. Lapovets L.Y., Lutsik B.D. Laboratory immunology. Kyiv. 2004. 173 p. 20. Perederiy V.G., Zemskov A.M., Bychkova N.G., Zemskov V.M. Immune status, principles of its evaluation and correction of immune disorders. K. Health; 1995: 211 p. 21. Popovych I.L. Informational effects of Naftusya bioactive water in rats: modulation of entropy, reversal of desynchronizing and limitation of disharmonizing effect of water-immersion stress on informational components of the neuro-endocrine-immune system and metabolism, which correlates with a gastroprotective effect. Medical hydrology and rehabilitation. 2007; 5(3): 50-70. 22. I.L. Popovych Concept of neuro-endocrine-immune complex. Medical hydrology and rehabilitation. 2009; 7(2): 9-18. 23. I.L. Popovych Stress-limiting adaptogenic mechanism of biological and therapeutic activity of Naftusya water. Kyiv. Computer press; 2011: 300 c. 24. Popovich I.L., Flunt I.S., Alekseev O.I. etc. Sanogenetic principles of rehabilitation at the Truskavets resort of urological patients of the Chernobyl contingent. Kyiv. Computer press; 2003: 192 p. 25. Popovich I.L., Flunt I.S., Nischeta I.V., Loboda M.V., Aksentiychuk B.I., Pryima B.G., Tserkovnyuk R.G. General adaptation reactions and resistance of the organism of liquidators of the Chernobyl accident. Kyiv. Computer press; 2000: 117 p. 26. Portnychenko A.G. Ukrainian balneology: scientific trends of the last decade (scientometric analysis). Medical hydrology and rehabilitation. 2015; 13(4): 41-52. 27. Smagliy V.S., Gozhenko A.I., Badyuk N.S., Popovych I.L. Variants of uric acid metabolism and their immune and microbial accompaniments in patients with complex neuro-endocrine-immune dysfunction. In: VIII National Congress of Pathophysiologists of Ukraine "Pathological Physiology - Health Care of Ukraine" (Odesa, May 13-15, 2020). Odesa; 2020: 314-315. 28. Khaitov R.M., Pinegin B.V., Istamov K.I. Ecological immunology. Moscow. INWARD; 1995: 219 p. 29. Khmelevsky Yu.V., Usatenko O.K. Basic biochemical constants of a person in normal and pathological conditions. Kyiv. Health; 1987: 160 p. 30. Efroimson V.P. Some biological factors of mental activity. VIET. 1987; 4: 74-84. 31. Yushkovska O.H. The use of information theory to study the adaptive reactions of athletes' bodies. Medical rehabilitation Spa therapy Physiotherapy. 2001; 1 (25): 40-43. 32. Abdel Aziz N., Tallima H., Hafez E.A., El Ridi R. Papain-based vaccination modulates Schistosoma mansoni infection-induced cytokine signals. Scand J Immunol. 2016;83(2):128–138. 33. Ahbap E., Sakaci T., Kara E., Sahutoglu T., Koc Y., Basturk T. Serum uric acid levels and inflammatory markers with respect to dipping status: a retrospective analysis of hypertensive patients with or without chronic kidney disease . Clin Exp Hypertens. 2016;38(6):555–563. 34. Akbar S.R., Long D.M., Hussain K., Alhajhusain A., Ahmed U.S., Iqbal H.I. Hyperuricemia: an early marker for severity of illness in sepsis. Int J Nephrol. 2015; 301021. 35. Alberti K.G., Eckel R.H., Grundy S.M., Zimmet P.Z., Cleeman J.I., Donato K.A. Harmonizing the metabolic syndrome: a joint interim statement of the international diabetes federation task force on epidemiology and prevention; national heart, lung, and blood institute; american heart association; world heart federation; international atherosclerosis society; and international association for the study of obesity. Circulation. 2009;120(16):1640–1645. 36. Aldenderfer M.S., Blashfield R.K. Cluster analysis (Second printing, 1985) [transl. from English in Russian]. In: Factor, Discriminant and Cluster Analysis. Moscow. Finance and Statistics; 1989: 139-214. 37. Alvarez-Lario B., Macarrón-Vicente J. Is there anything good in uric acid? QJM. 2011;104(12):1015–1024.] 38. Alvarez-Lario B., Macarron-Vicente J. Uric acid and evolution. Rheumatology. 2010;49(11):2010–2015. 39. Amaral F.A., Costa V.V., Tavares L.D., Sachs D., Coelho F.M., Fagundes C.T. NLRP3 inflammasome-mediated neutrophil recruitment and hypernociception depend on leukotriene B(4) in a murine model of gout. Arthritis Rheum. 2012;64(2):474–484. 40. Amaral K.B., Silva T.P., Malta K.K., Carmo L.A.S., Dias F.F., Almeida M.R. Natural Schistosoma mansoni infection in the wild reservoir Nectomys squamipes leads to excessive lipid droplet accumulation in hepatocytes in the absence of liver functional impairment. Plos One. 2016;11(11):e0166979. 41. Amaral L.M., Cunningham M.W., Jr, Cornelius D.C., LaMarca B. Preeclampsia: long-term consequences for vascular health. Vasc Health Risk Manage. 2015; 11: 403–415. 42. Ames B.N., Cathcart R., Schwiers E., Hochstein P. Uric acid provides an antioxidant defense in humans against oxidant- and radical-caused aging and cancer: a hypothesis. Proc Natl Acad Sci U S A. 1981;78(11):6858–6862. 43. Amsellem V., Abid S., Poupel L., Parpaleix A., Rodero M., Gary-Bobo G., Latiri M., Dubois-Rande J.L., Lipskaia L., Combadiere C., et al. Roles for the CX3CL1/CX3CR1 and CCL2/CCR2 Chemokine Systems in Hypoxic Pulmonary Hypertension. Am. J. Respir. Cell. Mol. Biol. 2017; 56:597–608. 44. Ando K., Takahashi H., Watanabe T., Daidoji H., Otaki Y., Nishiyama S. Impact of serum uric acid levels on coronary plaque stability evaluated using integrated backscatter intravascular ultrasound in patients with coronary artery disease. J Atheroscler Thromb. 2016;23(8):932–939. 45. Andreadou E., Nikolaou C., Gournaras F., Rentzos M., Boufidou F., Tsoutsou A. Serum uric acid levels in patients with Parkinson's disease: their relationship to treatment and disease duration. Clin Neurol Neurosurg. 2009;111(9):724–728. 46. Annanmaki T., Muuronen A., Murros K. Low plasma uric acid level in Parkinson's disease. Mov Disord. 2007;22(8):1133–1137. 47. Anthony R.M., Rutitzky L.I., Urban J.F., Jr., Stadecker M.J., Gause W.C. Protective immune mechanisms in helminth infection. Nat Rev Immunol. 2007;7(12):975–987. Review. 48. Anzai N., Ichida K., Jutabha P., Kimura T., Babu E., Jin C.J. Plasma urate level is directly regulated by a voltage-driven urate efflux transporter URATv1 (SLC2A9) in humans. J Biol Chem. 2008;283(40):26834–26838. 49. Apasov S, Chen JF, Smith P, Sitkovsky M. A2A receptor dependent and A2A receptor independent effects of extracellular adenosine on murine thymocytes in the condition of adenosine deaminase deficiency. Blood. 2000; 95(12): 3859-3867. 50. Araya J., Rodrigo R., Videla L.A., Thielemann L., Orellana M., Pettinelli P. Increase in long-chain polyunsaturated fatty acid n - 6/n - 3 ratio in relation to hepatic steatosis in patients with non- alcoholic fatty liver disease. Clin Sci (Lond) 2004;106(6):635–643. 51. Aribas A., Kayrak M., Ulucan S., Keser A., Demir K., Alibasic H. The relationship between uric acid and erectile dysfunction in hypertensive subjects. Blood Press. 2014;23: 370–376. 52. Arvola L, Bertelsen G, Hassaf D, Ytrehus K. Positive inotropic and sustained anti-beta-adrenergic effect of diadenosine pentaphosphate in human and guinea pig hearts. Role of dinucleotide receptors and adenosine receptors. Acta Physiol Scand. 2004;182(3):277-285. 53. Arnold I.C., Mathisen S., Schulthess J., Danne C., Hegazy A.N., Powrie F. CD11c(+) monocyte/macrophages promote chronic Helicobacter hepaticus-induced intestinal inflammation through the production of IL-23. Mucosal Immunol. 2016; 9:352–363. 54. Auerbach A. Dose-ResponseAnalysis When There Is a Correlation between Affinity and Efficacy. Mol. Pharmacol. 2016; 89:297–302. 55. Babio N., Martínez-González M.A., Estruch R., Wärnberg J., Recondo J., Ortega-Calvo M. Associations between serum uric acid concentrations and metabolic syndrome and its components in the PREDIMED study. Nutr Metab Cardiovasc Dis. 2015;25(2):173–180. 56. Bakhtiari S., Toosi P., Samadi S., Bakhshi M. Assessment of uric acid level in the saliva of patients with oral lichen planus. Med Princ Pract. 2017;26(1):57–60. 57. Barabé F, Gilbert C, Liao N, Bourgoin SG, Naccache PH. Crystal-induced neutrophil activationVI. Involvement of FcgammaRIIIB (CD16) and CD11b in response to inflammatory microcrystals. FASEB J. 1998;12(2):209-220. doi:10.1096/fasebj.12.2.209 58. Barakat R., Abou El-Ela N.E., Sharaf S., El Sagheer O., Selim S., Tallima H. Efficacy and safety of arachidonic acid for treatment of school-age children in Schistosoma mansoni high-endemic regions. Am J Trop Med Hyg. 2015;92(4):797–804. 59. Bardin T., Richette P. Definition of hyperuricemia and gouty conditions. Curr. Opin. Rheumatol. 2014;26: 186–191. 60. Barikbin B., Yousefi M., Rahimi H., Hedayati M., Razavi S.M., Lotfi S. Antioxidant status in patients with lichen planus. Clin Exp Dermatol. 2011;36(8):851–854. 61. Bartáková V., Kuricová K., Pácal L., Nová Z., Dvořáková V., Švrčková M. Hyperuricemia contributes to the faster progression of diabetic kidney disease in type 2 diabetes mellitus. J Diabetes Complications. 2016;30(7):1300–1307. 62. Barylyak L.G., Malyuchkova R.V., Tolstanov O.B., Tymochko O.B., Hryvnak R.F., Uhryn M.R. Comparative estimation of informativeness of leukocytary index of adaptation by Garkavi and by Popovych. Medical Hydrology and Rehabilitation. 2013; 11(1): 5-20. 63. Basseville A., Bates S. Gout, genetics and ABC transporters. F1000 Biology Reports. 2011;3: 23. 64. Beck L.H. Requiem for gouty nephropathy. Kidney Int. 1986;30(2):280–287. 65. Becker B.F. Towards the physiological function of uric acid. Free Radical Biol Med. 1993;14(6):615–631. 66. Bellomo G., Venanzi S., Verdura C., Saronio P., Esposito A., Timio M. Association of uric acid with changes in kidney function in healthy normotensive individuals. Am J Kidney Dis. 2010;56(2):264–272. 67. Berntson GG, Bigger JT jr, Eckberg DL, Grossman P, Kaufman PG, Malik M, Nagaraja HN, Porges SW, Saul JP, Stone PH, Van der Molen MW. Heart Rate Variability: Origins, methods, and interpretive caveats. Psychophysiology. 1997; 34: 623-648. 68. Bianco C. Population of lymphocytes bearing a membrane receptor for antigen-antibody complex. J Exp Med. 1970; 134(4): 702-720. 69. Bjorkander S., Heidari-Hamedani G., Bremme K., Gunnarsson I., Holmlund U. Peripheral monocyte expression of the chemokine receptors CCR2, CCR5 and CXCR3 is altered at parturition in healthy women and in women with systemic lupus erythematosus. Scand. J. Immunol. 2013;77: 200–212. 70. Birch RE, Rosenthal AK, Polmer SH. Pharmacological modification of immunoregulatory T lymphocytes. II. Modulation of T lymphocyte cell surface characteristics. Clin Exp Immunol. 1982; 48(1): 231-238. 71. Bjornstad P., Lanaspa M.A., Ishimoto T., Kosugi T., Kume S., Jalal D. Fructose and uric acid in diabetic nephropathy. Diabetology. 2015;58(9):1993–2002. 72. Bjornstad P., Maahs D.M., Johnson R.J., Rewers M., Snell-Bergeon J.K. Estimated insulin sensitivity predicts regression of albuminuria in Type 1 diabetes. Diabetes Med. 2015;32(2):257–261. 73. Bjornstad P., Roncal C., Milagres T., Pyle L., Lanaspa M.A., Bishop F.K. Hyperfiltration and uricosuria in adolescents with type 1 diabetes. Pediatr Nephrol. 2016;(5):787–793. 74. Bjornstad P., Snell-Bergeon J.K., McFann K., Wadwa R.P., Rewers M., Rivard C.J. Serum uric acid and insulin sensitivity in adolescents and adults with and without type 1 diabetes. J Diabetes Complications. 2014;28(3):298–304. 75. Bobulescu I.A., Moe O.W. Renal transport of uric acid: evolving concepts and uncertainties. Adv Chronic Kidney Dis. 2012;19(6):358–371. 76. Bocarsly M.E., Powell E.S., Avena N.M., Hoebel B.G. High-fructose corn syrup causes characteristics of obesity in rats: increased body weight, body fat and triglyceride levels. Pharmacol Biochem Behav. 2010;97: 101–106. 77. Broz P., Dixit V.M. Inflammasomes: mechanism of assembly, regulation and signaling. Nat Rev Immunol. 2016;16(7):407–420. 78. Bruno C.M., Pricoco G., Cantone D., Elisa Marino E., Bruno F. Tubular handling of uric acid and factors influencing its renal excretion: a short review. EMJ Nephrol. 2016;4(1):92–97. 79. Busso N., Ea H.K. The mechanisms of inflammation in gout and pseudogout (CPP-induced arthritis) Rheumatismo. 2012;63(4):230–237. 80. Busso N., So A. Mechanisms of inflammation in gout. Arthritis Res Ther. 2010;12(2):206. 81. Busso N., So A. Microcrystals as DAMPs and their role in joint inflammation. Rheumatology (Oxford) 2012;51(7):1154–1160. 82. Cammalleri L., Malaguarnera M. Rasburicase represents a new tool for hyperuricemia in tumor lysis syndrome and in gout. International Journal of Medical Sciences. 2007;4(2):83–93. doi: 10.7150/ijms.4.83. 83. Campion E.W., Glynn R.J., DeLabry L.O. Asymptomatic hyperuricemia. Risks and consequences in the Normative Aging Study. Am J Med. 1987; 82:421. 84. Carito V., Ceccanti M., Tarani L., Ferraguti G., Chaldakov G. N., Fiore M. Neurotrophins' modulation by olive polyphenols. Current Medicinal Chemistry. 2016;23(28):3189–3197. 85. Carvalho LAC, Lopes JPPB, Kaihami GH, Silva RP, Bruni-Cordoso A, Baldini RL, Meotti FC. Uric acid disrupts hypochlorous acid production and bactericidal activity of HL-60 cells. Redox Biology. 2018; 16: 179-188. 86. Chakraborti G., Biswas R., Chakraborti S., Sen P.K. Altered serum uric acid level in lichen planus patients. Indian J Dermatol. 2014;59(6):558–561. 87. Chang B.S. Ancient insights into uric acid metabolism in primates. Proc Natl Acad Sci USA. 2014;111(10):3657–3658. 88. Chaudhary K., Malhotra K., Sowers J., Aroor A. Uric Acid - key ingredient in the recipe for cardiorenal metabolic syndrome. Cardiorenal Med. 2013;3(3):208–220. 89. Chen CJ, Shi Y, Hearn A, et al. MyD88-dependent IL-1 receptor signaling is essential for gouty inflammation stimulated by monosodium urate crystals. J Clin Invest. 2006;116(8):2262-2271. 90. Chen H., Cao G., Chen D. Q., et al. Metabolomics insights into activated redox signaling and lipid metabolism dysfunction in chronic kidney disease progression. Redox Biology. 2016; 10:168–178. 91. Chen Y., Xu B., Sun W., Sun J., Wang T., Xu Y. Impact of the serum uric acid level on subclinical atherosclerosis in middle-aged and elderly Chinese. J Atheroscler Thromb. 2015;22(8):823–832. 92. Chen-Xu M., Yokose C., Rai S.K., Pillinger M.H., Choi H.K. Contemporary Prevalence of Gout and Hyperuricemia in the United States and Decadal Trends: The National Health and Nutrition Examination Survey, 2007–2016. Arthritis Rheumatol. 2019; 71:991–999. 93. Cheung K.J., Tzameli I., Pissios P., Rovira I., Gavrilova O., Ohtsubo T. Xanthine oxidoreductase is a regulator of adipogenesis and PPARγ activity. Cell Metab. 2007; 5:115–128. 94. Cheungpasitporn W., Thongprayoon C., Harrison A.M., Erickson S.B. Admission hyperuricemia increases the risk of acute kidney injury in hospitalized patients. Clin Kidney J. 2016;9(1):51–56. 95. Chiquete E., Ruiz-Sandoval J.L., Murillo-Bonilla L.M., Arauz A., Orozco-Valera D.R., Ochoa-Guzmán A. Serum uric acid and outcome after acute ischemic stroke: PREMIER study. Cerebrovasc Dis. 2013;35(2):168–174. 96. Cho J., Kim C., Kang D.R., Park J. Hyperuricemia and uncontrolled hypertension in treated hypertensive patients: K-MetS study. Medicine (Baltimore) 2016;95(28): e4177. 97. Choi H.K., Curhan G. Independent impact of gout on mortality and risk for coronary heart disease. Circulation. 2007;116(8):894–900. 98. Choi H.K., Ford E.S. Prevalence of the metabolic syndrome in individuals with hyperuricemia. Am J Med. 2007;120(5):442–447. 99.Choi Y.J., Shin H.S., Choi H.S., Park J.W., Jo I., Oh E.S. Uric acid induces fat accumulation via generation of endoplasmic reticulum stress and SREBP-1c activation in hepatocytes. Lab Invest. 2014;94(10):1114–1125. 100.Chou Y.C., Kuan J.C., Yang T., Chou W.Y., Hsieh P.C., Bai C.H. Elevated uric acid level as a significant predictor of chronic kidney disease: a cohort study with repeated measurements. J Nephrol. 2015;28(4):457–462. 101. Cicerchi C., Li N., Kratzer J., Garcia G., Roncal-Jimenez C.A., Tanabe K. Uric acid-dependent inhibition of AMP kinase induces hepatic glucose production in diabetes and starvation: evolutionary implications of the uricase loss in hominids FASEB J. 2014;(8):3339–3350. 102. Cicero A., Rosticci M., Tartagni E., Parini A., Grandi E., D'Addato S. Serum uric acid level, but not renal function or arterial stiffness, is associated to worse blood pressure control in general practice : data from the brisighella heart study. J Hypertens. 2015;33(Suppl 1):e22. 103. Cicero A.F., Rosticci M., Fogacci F., Grandi E., D'Addato S., Borghi C. High serum uric acid is associated with poorly controlled blood pressure and higher arterial stiffness in hypertensive subjects. Eur J Intern Med. 2017;37: 38–42. 104. Cinel I, Gür S. Direct inotropic effects of propofol and adenosine on rat atrial muscle: possible mechanisms. Pharmacol Res. 2000;42(2):123-128. 105. Clarson L.E., Chandratre P., Hider S.L., Belcher J., Heneghan C., Roddy E. Increased cardiovascular mortality associated with gout: a systematic review and meta-analysis. Eur J Prev Cardiol. 2015;22(3):335–343. 106. Clémençon B., Lüscher B.P., Fine M., Baumann M.U., Surbek D.V., Bonny O. Expression, purification, and structural insights for the human uric acid transporter, GLUT9, using the Xenopus laevis oocytes system. PLoS ONE. 2014;9(10):e108852. 107. Cleophas M. C., Joosten L. A., Stamp L. K., Dalbeth N., Woodward O. M., Merriman T. R. ABCG2 polymorphisms in gout: insights into disease susceptibility and treatment approaches. Ph. DArmacogenomics and Personalized Medicine. 2017; 10:129–142. 108. Conen D, Wietlisbach V, Bovet P, Shamlaye C, Riesen W, Paccaud F, et al. Prevalence of hyperuricemia and relationship of serum uric acid with cardiovascular risk factors in a developing country. BMC public health. 2004; 4:9. 109. Convento M.S., Pessoa E., Dalboni M.A., Borges F.T., Schor N. Pro-inflammatory and oxidative effects of noncrystalline uric acid in human mesangial cells: contribution to hyperuricemic glomerular damage. Urol Res. 2011;39(1):21–27. 110.Cristóbal-García M., García-Arroyo F.E., Tapia E., Osorio H., Arellano-Buendía A.S., Madero M. Renal oxidative stress induced by long-term hyperuricemia alters mitochondrial function and maintains systemic hypertension. Oxid Med Cell Longev. 2015; 535686. 111. Culleton B.F., Larson M.G., Kannel W.B., Levy D. Serum uric acid and risk for cardiovascular disease and death: the Framingham Heart Study. Ann Intern Med. 1999;131(1):7–13. 112. Dalbeth N., Merriman T. Crystal ball gazing: new therapeutic targets for hyperuricemia and gout. Rheumatology (Oxford). 2009;48(3):222–226. 113. De Cosmo S., Viazzi F., Pacilli A., Giorda C., Ceriello A., Gentile S. Serum uric acid and risk of CKD in Type 2 diabetes. Clin J Am Soc Nephrol. 2015;10(11):1921–1929. 114. De Duve C, Wattiaux R. Functions of lysosomes. Annu Rev Physiol. 1966; 28:435–492. 115. De Vera M., Rahman M.M., Rankin J., Kopec J., Gao X., Choi H. Gout and the risk of Parkinson's disease: a cohort study. Art

    Метаболические и аутоиммунные корреляты структурных изменений головного мозга больных с рассеянным склерозом = Metabolic and autoimmune correlates of brain’s structural changes in disseminated sclerosis patients

    Get PDF
    Gozhenko A I, Naumenko O Y. Метаболические и аутоиммунные корреляты структурных изменений головного мозга больных с рассеянным склерозом = Metabolic and autoimmune correlates of brain’s structural changes in disseminated sclerosis patients. Journal of Education, Health and Sport. 2015;5(1):163-170. ISSN 2391-8306. DOI: 10.5281/zenodo.14792 http://ojs.ukw.edu.pl/index.php/johs/article/view/2015%3B5%281%29%3A163-170 https://pbn.nauka.gov.pl/works/533080 http://dx.doi.org/10.5281/zenodo.14792 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: 20.10.2014. Revised 18.01.2015. Accepted: 25.01.2015.     Метаболические и аутоиммунные корреляты структурных изменений головного мозга больных с рассеянным склерозом   METABOLIC AND AUTOIMMUNE CORRELATES OF BRAIN’S STRUCTURAL CHANGES IN DISSEMINATED SCLEROSIS PATIENTS   А.И. Гоженко, О.Ю. Науменко AI Gozhenko, OY Naumenko   Украинский НИИ медицины транспорта, г.Одесса, Украина Ukrainian Research Institute of Medical Transport, Odessa, Ukraine [email protected]   Резюме Авторы на основании данных комплексного обследования 64 больных, у которых, на основании клинико-неврологического исследования, диагностирован рассеянный склероз, изучали связь между структурными изменениями головного мозга и состоянием цикла мочевой кислоты и интенсивностью аутоиммунного процесса. Выявлено, что структурные изменения головного мозга не связаны с половозрастными особенностями больных, но всегда сопровождаются сниженным содержанием мочевой кислоты и наличием миелинассоциированного гликопротеида. Авторы указывают, что величина двух последних показателей коррелирует с длительностью процесса. Авторы полагают, что изменения в активности цикла мочевой кислоты способствуют возникновению аутоиммунного процесса, который обеспечивает структурное повреждение мозга. Нарастание биохимических и аутоиммунных нарушений в динамике заболевания, по мнению автора, способствуют сохранению повреждений мозга и нивелируют компенсаторные изменения в нем.   Ключевые слова: рассеянный склероз, мочевая кислота, структурные повреждения мозга.       Abstract Clinical-and-neurological examination of 64 patients proved the diagnosis of disseminated sclerosis (DS). The relation between brain’s structural changes (BSC), uric acid cycle and autoimmune process intensity has been studied in the group under observation. It has been revealed that BSC have no connection with sexual and age peculiarities  of the patients and are always followed by the decreased content of uric acid and the presence of myelin-associated glycoprotein. The amount of the two latter in indexes correlates with the process time duration. The Authors suppose that  uric acid cycle changes promote the appearance of autoimmune process which in its turn confers BSC. Aggravation of biochemical and autoimmune disturbances in the dynamics of the disease leads to brain’s disorders preservation and levels its compensatory changes.   Key words: disseminated sclerosis, uric acid, structural changes of brain
    corecore