Ramaniuk V.P.,National Academy of Sciences of Belarus |
Nikitchenko N.V.,National Academy of Sciences of Belarus |
Savina N.V.,National Academy of Sciences of Belarus |
Kuzhir T.D.,National Academy of Sciences of Belarus |
And 4 more authors.
Biomarkers | Year: 2014
Context: The study of DNA base and nucleotide excision repair gene polymorphisms in bladder cancer seems to have a predictive value because of the evident relationship between the DNA damage response induced by environmental mutagens and cancer predisposition. Objective: The objective was to determine OGG1 Ser326Cys, XRCC1 Arg399Gln, XPD Asp312Asn, and ERCC6 Met1097Val polymorphisms in bladder cancer patients as compared to controls. Methods: Both groups were predominantly represented by Belarusians and Eastern Slavs. DNA samples from 336 patients and 370 controls were genotyped using a PCR-RFLP method. Results: The genotype distributions were in agreement with the Hardy-Weinberg equilibrium. The minor allele frequencies in the control population were in the range of those in Caucasians in contrast to Asians. The OGG1 326 Ser/Cys and XPD 312 Asp/Asn heterozygous genotypes were inversely associated with cancer risk (OR [95% CI]=0.69 [0.50-0.95] and 1.35 [1.0-1.82], respectively). The contrasting effects of these genotypes were potentiated due to their interactions with smoking habit or age. Conclusions: Among four DNA repair gene polymorphisms, the OGG1 326 Ser/Cys and XPD 312 Asp/Asn heterozygous genotypes might be recognized as potential genetic markers modifying susceptibility to bladder cancer in Belarus. © 2014 Informa UK Ltd. All rights reserved: reproduction in whole or part not permitted.
Cherniavsky E.A.,Belarusian State University |
Strakha I.S.,Belarusian State University |
Adzerikho I.E.,Belarusian Medical Academy of Postgraduate Education |
Shkumatov V.M.,Belarusian State University
BMC Biochemistry | Year: 2011
Background: Pharmacological thrombolysis with streptokinase, urokinase or tissue activator of plasminogen (t-PA), and mechanical interventions are frequently used in the treatment of both arterial and venous thrombotic diseases. It has been previously reported that application of ultrasound as an adjunct to thrombolytic therapy offers unique potential to improve effectiveness. However, little is known about effects of the ultrasound on proteins of blood coagulation and fibrinolysis. Here, we investigated the effects of the ultrasound on fibrinogen on processes of coagulation and fibrinogenolysis in an in vitro system. Results: Our study demonstrated that low frequency high intensity pulse ultrasound (25.1 kHz, 48.4 W/cm2, duty 50%) induced denaturation of plasminogen and t-PA and fibrinogen aggregates formation in vitro. The aggregates were characterized by the loss of clotting ability and a greater rate of plasminolysis than native fibrinogen. We investigated the effect of the ultrasound on individual proteins. In case of plasminogen and t-PA, ultrasound led to a decrease of the fibrinogenolysis rate, while it increased the fibrinogenolysis rate in case of fibrinogen. It has been shown that upon ultrasound treatment of mixture fibrinogen or fibrin with plasminogen, t-PA, or both, the rate of proteolytic digestion of fibrin(ogen) increases too. It has been shown that summary effect on the fibrin(ogen) proteolytic degradation under the conditions for combined ultrasound treatment is determined exclusively by effect on fibrin(ogen). Conclusions: The data presented here suggest that among proteins of fibrinolytic systems, the fibrinogen is one of the most sensitive proteins to the action of ultrasound. It has been shown in vitro that ultrasound induced fibrinogen aggregates formation, characterized by the loss of clotting ability and a greater rate of plasminolysis than native fibrinogen in different model systems and under different mode of ultrasound treatment. Under ultrasound treatment of plasminogen and/or t-PA in the presence of fibrin(ogen) the stabilizing effect fibrin(ogen) on given proteins was shown. On the other hand, an increase in the rate of fibrin(ogen) lysis was observed due to both the change in the substrate structure and promoting of the protein-protein complexes formation. © 2011 Cherniavsky et al; licensee BioMed Central Ltd.
Krupchanka D.,Social Republic |
Krupchanka D.,Kings College London |
Krupchanka D.,Belarusian Medical Academy of Postgraduate Education |
Katliar M.,Max Planck Institute for Biological Cybernetics
Schizophrenia Bulletin | Year: 2016
Background: There is evidence of a positive association between insight and depression among patients with schizophrenia. Self-stigma was shown to play a mediating role in this association. We attempted to broaden this concept by investigating insight as a potential moderator of the association between depressive symptoms amongst people with schizophrenia and stigmatizing views towards people with mental disorders in their close social environment. Method: In the initial sample of 120 pairs, data were gathered from 96 patients with a diagnosis of "paranoid schizophrenia" and 96 of their nearest relatives (80% response rate). In this cross-sectional study data were collected by clinical interview using the following questionnaires: "The Scale to Assess Unawareness of Mental Disorder," "Calgary Depression Scale for Schizophrenia," and "Brief Psychiatric Rating Scale." The stigmatizing views of patients' nearest relatives towards people with mental disorders were assessed with the "Mental Health in Public Conscience" scale. Results: Among patients with schizophrenia depressive symptom severity was positively associated with the intensity of nearest relatives' stigmatizing beliefs ("Nonbiological vision of mental illness," τ = 0.24; P <. 001). The association was moderated by the level of patients' awareness of presence of mental disorder while controlling for age, sex, duration of illness and psychopathological symptoms. Conclusions: The results support the hypothesis that the positive association between patients' depression and their nearest relatives' stigmatizing views is moderated by patients' insight. Directions for further research and practical implications are discussed. © The Author 2016. Published by Oxford University Press on behalf of the Maryland Psychiatric Research Center.
Fedorovich S.V.,National Academy of Sciences of Belarus |
Alekseenko A.V.,National Academy of Sciences of Belarus |
Alekseenko A.V.,Belarusian Medical Academy of Postgraduate Education |
Waseem T.V.,National Academy of Sciences of Belarus
Biochemical Society Transactions | Year: 2010
The last few years have been marked by real breakthroughs in the field of nanotechnology. Application of nanoparticles was proposed for diagnosis and treatment of different central nervous system diseases. Exposure to nanoparticles in vivo increases the risk of onset of neurodegenerative diseases and nanoparticles are apparently able to kill neurons in vitro. We suggested that presynaptic terminals of neurons are another target for nanoparticles, beyond the already established microglial cells. Ferritin was chosen as a prototypic nanoparticle model. We found that even a high concentration of ferritin, 800 μg/ml, was not able to induce spontaneous release of [ 14C]glutamate. In contrast, [14C]glutamate uptake was inhibited by ferritin in a dose-dependent fashion. As a next step, the influence of ferritin on the formation of reactive oxygen species was monitored using the fluorescent dye DCFH-DA (2′,7′-dichlorofluorescein diacetate). It was shown that ferritin leads to a dose-dependent formation of free radicals. We found that the ferritin-mediated changes in glutamatergic neurotransmission at presynaptic endings can result in neuronal damage and finally neurodegeneration. ©The Authors.
Volkovich T.K.,Belarusian Medical Academy of Postgraduate Education
Novosti Khirurgii | Year: 2015
The article presents a scientific literature review devoted to studying the features of epidemiology, pathogenesis, diagnosis and treatment of ocular surface squamous neoplasia (OSSN). In different countries morbidity rate varies significantly from 0,03 to 3,5 cases per 100 000 population. The most important and studied causes of ocular surface neoplasia development are considered to be solar insolation, human papilloma virus, human immunodeficiency virus. Variability of the clinical picture requires the proper differential diagnostics, since OSSN often masks as degenerative diseases of the conjunctiva (pinguecula, pterygium), vascularized corneal opacity, and can also manifest itself as melanoma or nevus. Difficulties in the differential diagnostics based on clinical examination data necessitate the usage of high-tech research methods (optical coherence tomography of the ocular anterior segment) and the obligatory morphological diagnostics (cytological and histological diagnosis). Treatment of OSSN includes various medical and surgical approaches, more often their combination - surgical removal of tumors or usage of cytostatics or the medication interferon without taking into consideration the etiology. The high recurrence rate of OSSN is still remained - 10- 56% of cases depending on the growth type, volume of surgery and duration of postoperative care of patients. It is relevant to further studying the etiology and pathogenesis of ocular surface squamous neoplasia, as well as the development of integrated approaches in diagnosis and treatment taking into account the etiology of disease.