Get Adobe Flash player

LUSTER AND POVERTY OF HIV-INFECTION ANTIRETROVIRAL THERAPY

Аuthors: Dyachenko A. G.,  Dyachenko P. A., Gorobchenko K. M.

Pages: 372-384

Аbstract

   

          Advances in antiretroviral therapy (ART) have drastically improved the quality of life for people with HIV infection. However, complex therapy leads to suppression of plasma viral loads in HIV-1 patients. Despite this therapy, a low level of viremia in plasma can be frequently detected by sensitive clinical assays. Additionally, many patients experience transient episodes of viremia above the detection limit, even if they have been undergoing highly suppressive therapy for many years. Failure of HAART to eradicate HIV associates with the existence of persistent infection in certain cellular and anatomical reservoirs. The latent reservoir considers being the major hurdle in HIV eradication. In addition, deep suppression of viral replication does not restore the immune status fully that was effected by HIV infection. This is a consequence of chronic immune activation, caused by the increased permeability of the intestinal barrier and translocation of bacteria and products of their decay. Progress in the infection eradication requires new approaches in the fight against latency and immunodeficiency.

        Key words: human immunodeficiency virus (HIV), HIV-infection, latency, antiretroviral therapy (ART), microbial translocation (MT), immune activation.

            This email address is being protected from spambots. You need JavaScript enabled to view it.">*This email address is being protected from spambots. You need JavaScript enabled to view it.

  

The full text

To viev the full text

References

1. Maraviroc for previously treated patients with R5 HIV-1 infection / R. M. Gulick, J. Lalezari, J. Goodrich [et al.] // N. Engl. J. Med. – 2008. – Vol. 359. – P. 1429–41.
2. Raltegravir with optimized background therapy for resistant HIV-1 infection / R. T. Steigbigel, D. A. Cooper, P. N. Kumar [et al.] // N. Engl. J. Med. – 2008. – Vol. 359. – P. 339–354.
3. Timing of initiation of antiretroviral therapy in AIDS-free HIV-1-infected patients: a collaborative analysis of 18 HIV cohort studies/ J. A. Sterne, M. May, D. Costagliola [et al.] // Lancet. – 2009. – Vol. 373. –P. 1352–1363.
4. Effect of early versus deferred antiretroviral therapy for HIV on survival / M. M. Kitahata, S. J. Gange, A. G. Abraham [et al.] // N. Engl. J. Med. – 2009. – Vol. 360. – P. 1815–1826.
5. Major clinical outcomes in antiretroviral therapy (ART)-naive participants and in those not receiving ART at baseline in the SMART study / S. Emery, J. A. Neuhaus, A. N. Phillips [et al.] // J. Infect. Dis. – 2008. – Vol. 197. – P. 1133–1144.
6. UNAIDS. Report on the global AIDS epidemic: Joint United Nations Programme on HIV/AIDS (UNAIDS) and World Health Organization (WHO). – 2008. – P. 1–36.
7. Continued improvement in survival among HIV-infected individuals with newer forms of highly active antiretroviral therapy / V. D. Lima, R. S. Hogg, P. R. Harrigan [et al.] // Aids. – 2007. – Vol. 21. – P. 685–692.
8. Collaboration TATC. Life expectancy of individuals on combination antiretroviral therapy in high-income countries: a collaborative analysis of 14 cohort studies // The Lancet. – 2008. – Vol. 372. – P. 293–299.
9. Changes in the risk of death after HIV seroconversion compared with mortality in the general population / K. Bhaskaran, O. Hamouda, M. Sannes [et al.] // JАМА. – 2008. – Vol. 300. – P. 51.
10. Deeks S. G. HIV infection, antiretroviral treatment, ageing, and non-AIDS related morbidity / S. G. Deeks, A. N. Phillips // BМJ. – 2009. – Vol. 338. – P. 3172.
11. Changes in causes of death among adults infected by HIV between 2000 and 2005: The “Mortalite 2000 and 2005” surveys (ANRS EN19 and Mortavic) / C. Lewden, T. May, E. Rosenthal [et al.] // J. Acquir. Immune Defic. Syndr. – 2008. – Vol. 48. – P. 590–598.
12. Increased acute myocardial infarction rates and cardiovascular risk factors among patients with human immunodeficiency virus disease / V. A. Triant, H. Lee, C. Hadigan, S. K. Grinspoon // J. Clin. Endocrinol. Metab. – 2007. – Vol. 92. – P. 2506–2512.
13. Serum immune activation markers are persistently increased in patients with HIV infection after 6 years of antiretroviral therapy despite suppression of viral replication and reconstitution of CD4 + T cells / M. A. French, M. S. King, J. M. Tschampa [et al.] // J. Infect. Dis. – 2009. – Vol. 200. – P. 1212–1215.
14. Inflammatory and coagulation biomarkers and mortality in patients with HIV infection / L. H. Kuller, R. Tracy, W. Belloso [et al.] // PLoS Med. – 2008. – Vol. 5:e203.
15. United Nations General Assembly. Political declaration on HIV/AIDS: intensifying our efforts to eliminate HIV/AIDS. United Nations General Assembly Resolution 65/277. – New York, United Nations, 2011.
16. WHO, UNICEF, UNAIDS. Progress report 2011. Global HIV/AIDS response Epidemic update and health sector progress towards universal access. WHO, UNICEF, UNAIDS. Geneva, Switzerland. – December, 2011.
17. US Food and Drugs Administration. Antiretroviral drugs used in the treatment of HIV infection, 2012.
18. Viral blip dynamics during highly active antiretroviral therapy / M. Di Mascio, M. Markowitz, M. Louie [et al.] // J. Virol. – 2003. – Vol. 77. – Р. 12165–12172.
19. Preferred antiretroviral drugs for the next decade of scale up / I. Andrieux-Meyer, A. Calmy, P. Cahn [et al.] // J. Int. AIDS Soc. – 2012. – Vol. 15. – Р. 17986.
20. Bartlett J. G. Guidelines for the use of antiretroviral agents in HIV-1-infected adults and adolescents / J. G. Bartlett, H. C. Lane. – 2007. Available at: http://aidsinfo.nih.gov/contentfiles/AdultandAdolescentGL.pdf.
21. Shen L. Viral reservoirs, residual viremia, and the potential of highly active antiretroviral therapy to eradicate HIV infection / L. Shen, R. F. Siliciano // J. Allergy Clin. Immunol. – 2008. – Vol. 122 (1). – P. 22–28.
22. Douek D. HIV Disease Progression: Immune Activation, Microbes, and a Leaky Gut / D. Douek // Top. HIV Med. – 2007. – Vol. 15 (4). – P. 114–117.
23. HIV-1 dynamics in vivo: virion clearance rate, infected cell life-span, and viral generation time / A. S. Perelson, A. U. Neumann, M. Markowitz [et al.] // Science. – 1996. – Vol. 271. – P. 1582–1586.
24. Decay characteristics of HIV-1-infected compartments during combination therapy / A. S. Perelson, P. Essunger, Y. Cao [et al.] // Nature. – 1997. – Vol. 387. – P. 188–91.
25. Finzi D. Viral dynamics in HIV-1 infection / D. Finzi, R. Siliciano // Cell. – 1998. – Vol. 93. – Р. 665–671.
26. Rong L. Modeling Latently Infected Cell Activation: Viral and Latent Reservoir Persistence, and Viral Blips in HIV-infected Patients on Potent Therapy / L. Rong, A. S. Perelson // PLoS Comput Biol. – 2009. – Vol. 5 (10): e1000533. doi:10.1371/journal.pcbi.1000533.
27. Low-level viremia persists for at least 7 years in patients on suppressive antiretroviral therapy / S. Palmer, F. Maldarelli, A. Wiegand [et al.] // Proc. Natl. Acad. Sci. USA. – 2008. – Vol. 105. – Р. 3879–3884.
28. Residual HIV-1 RNA in blood plasma of patients taking suppressive highly active antiretroviral therapy / G. Dornadula, H. Zhang, B. VanUitert [et al.] // JAMA. – 1999. – Vol. 282. – Р. 1627–1632.
29. The decay of the latent reservoir of replication-competent HIV-1 is inversely correlated with the extent of residual viral replication during prolonged anti-retroviral therapy / B. Ramratnam, J. E. Mittler, L. Zhang [et al.] // Nat. Med. – 2000. – Vol. 6. – Р. 82–85.
30. Duration of an intermittent episode of viremia / M. Di Mascio, J. K. Percus, O. E. Percus [et al.] // Bull. Math. Biol. – 2005. – Vol. 67. – Р. 885–900.
31. Long-term persistence of transmitted HIV drug resistance in male genital tract secretions: implications for secondary transmission / D. M. Smith, J. K. Wong, H. Shao [et al.] // J. Infect. Dis. – 2007. – Vol. 196. – Р. 356–360.
32. Induction of HIV-1 replication in latently infected CD4 + T cells using a combination of cytokines / T. W. Chun, D. Engel, S. B. Mizell [et al.] // J. Exp. Med. – 1998. – Vol. 188. – Р. 83–91.
33. Quantification of latent tissue reservoirs and total body viral load in HIV-1 infection / T. W. Chun, L. Carruth, D. Finzi [et al.] // Nature. – 1997. – Vol. 387. – Р. 183–188.
34. Long-term follow-up studies confirm the stability of the latent reservoir for HIV-1 in resting CD4 + T cells / J. D. Siliciano, J. Kajdas, D. Finzi [et al.] // Nat. Med. – 2003. – Vol. 9. – Р. 727–728.
35. Continued production of drug-sensitive human immunodeficiency virus type 1 in children on combination antiretroviral therapy who have undetectable viral loads / D. Persaud, G. K. Siberry, A. Ahonkhai [et al.] // J. Virol. – 2004. – Vol. 78. – Р. 968–979.
36. Residual human immunodeficiency virus type 1 viremia in some patients on antiretroviral therapy is dominated by a small number of invariant clones rarely found in circulating CD4 + T cells / J. R. Bailey, A. R. Sedaghat, T. Kieffer [et al.] // J. Virol. – 2006. – Vol. 80. – Р. 6441–6457.
37. Intermittent HIV-1 viremia (blips) and drug resistance in patients receiving HAART / R. E. Nettles, T. L. Kieffer, P. Kwon [et al.] // JAMA. – 2005. – Vol. 293. – Р. 817–1829.
38. Low-level viremia persists for at least 7 years in patients on suppressive antiretroviral therapy / S. Palmer, F. Maldarelli, A. Wiegand [et al.] // Proc. Natl. Acad. Sci. USA. – 2008. – Vol. 105. – Р. 3879–3884.
39. Douek D. HIV Disease Progression: Immune Activation, Microbes, and a Leaky Gut / D. Douek // Top. HIV Med. – 2007. – Vol. 15(4). – P. 114–117.
40. Weight loss, the gut and the inflammatory response in aids patients / T. P. Stein, B. Koerner, M. D. Schluter [et al.] // Cytokine. – 1997. –Vol. 9. – P. 143–147.
41. Pathogenesis of HIV infection: What the virus spares is as important as what it destroys / Z. Grossman, M. Meier-Schellersheim, W. E. Paul , L. J. Picker // Nat. Med. – 2006. – Vol. 12. – P. 289–295.
42. Severe CD4 + T-cell depletion in gut lymphoid tissue during primary human immunodeficiency virus type 1 infection and substantial delay in restoration following highly active antiretroviral therapy / M. Guadalupe, E. Reay, S. Sankaran [et al.] // J. Virol. – 2003. – Vol. 77. – P. 11708–11717.
43. Massive infection and loss of memory CD4 + T cells in multiple tissues during acute SIV infection / J. J. Mattapallil, D. C. Douek, B. Hill [et al.] // Nature. – 2005. – Vol. 434. – P. 1093–1097.
44. Biology of CCR5 and its role in HIV infection and treatment / M. M. Lederman, A. Penn-Nicholson, M. Cho, D. Mosier // JAMA. – 2006. – Vol. 296. – P. 815–826.
45. CD+4 T cell depletion during all stages of HIV disease occurs predominantly in the gastrointestinal tract / J. M. Brenchley, T. W. Schacker, L. E. Ruff [et al.] // J. Exp. Med. – 2004. – Vol. 200. – P. 749–759.
46. Microbial translocation is a cause of systemic immune activation in chronic HIV infection / J. M. Brenchley, D. A. Price, T. W. Schacker [et al.] // Nat. Med. – 2006. – Vol. 12. – P. 1365–1371.
47. Shorter survival in advanced human immunodeficiency virus type 1 infection is more closely associated with T lymphocyte activation than with plasma virus burden or virus chemokine coreceptor usage / J. V. Giorgi, L. E. Hultin, J. A. McKeating [et al.] // J. Infect. Dis. – 1999. – Vol. 179. – P. 859–870.
48. Antiretroviral therapy corrects HIV-1-induced expansion of CD8 + CD45RA+ CD27− CD11a(bright) activated T cells / L. Yin, C. A. Rodriguez, W. Hou [et al.] // J. Allergy Clin. Immunol. – 2008. – Vol. 122. – P. 166–172.
49. Damaged Intestinal Epithelial Integrity Linked to Microbial Translocation in Pathogenic SIV Infections / J. D. Estes, L. D. Harris, N. R Klatt. [et al.] // PLoS Pathog. – 2010. – Vol. 6 (8): e1001052. doi:10.1371/journal.ppat.1001052.
50. Microbial translocation is associated with increased monocyte activation and dementia in AIDS patients / P. Ancuta, A. Kamat, K. J. Kunstman [et al.] // PLoS ONE. – 2008. – 3: e2516.
51. Cell-cycle dysregulation in the immunopathogenesis of AIDS / M. Paiardini, B. Cervasi, R. Dunham [et al.] // Immunol. Res. – 2004. – Vol. 29. – P. 253–268.
52. Perturbations of cell cycle control in T cells contribute to the different outcomes of simian immunodeficiency virus infection in rhesus macaques and sooty mangabeys / M. Paiardini, B. Cervasi, B. Sumpter [et al.] // J. Virol. – 2006. – Vol. 80. – P. 634–642.
53. Inadequate clearance of translocated bacterial products in HIV-infected humanized mice / U. Hofer, E. Schlaepfer, S. Baenziger [et al.] // PLoS Pathog. 2010;6 doi: 10.1371/journal.ppat.1000867.
54. Biological determinants of immune reconstitution in HIV-infected patients receiving antiretroviral therapy: The role of interleukin 7 and interleukin 7 receptor alpha and microbial translocation / R. Rajasuriar, D. Booth, A. Solomon [et al.] // J. Infect. Dis. – 2010. – Vol. 202. – P. 1254–1264. doi: 10.1086/656369.
55. Immune activation, apoptosis, and Treg activity are associated with persistently reduced CD4+ T-cell counts during antiretroviral therapy / S. Piconi, D. Trabattoni, A. Gori [et al.] // AIDS. – 2010. – Vol. 24. – P. 1991–2000.doi: 10.1097 /QAD. 0b013e32833c93ce.
56. Simian immunodeficiency virus-induced intestinal cell apoptosis is the underlying mechanism of the regenerative enteropathy of early infection / Q. Li, J. D. Estes, L. Duan [et al.] // J. Infect. Dis. – 2008. – Vol. 197. – P. 420–429.
57. Brenchley J. M. Differential Th17 CD4 T-cell depletion in pathogenic and nonpathogenic lentiviral infections / J. M. Brenchley, M. Paiardini, K. S. Knox // Blood. – 2008. – Vol. 112. – P. 2826–2835.
58. Critical loss of the balance between Th17 and T regulatory cell populations in pathogenic SIV infection / D. Favre, S. Lederer, B. Kanwar [et al.] // PLoS Pathog 2009;5:e1000295.
59. Early impairment of gut function and gut flora supporting a role for alteration of gastrointestinal mucosa in human immunodeficiency virus pathogenesis / A. Gori, C. Tincati, G. Rizzardini [et al.] // J. Clin. Microbiol. – 2008. – Vol. 46. – P. 757–758.
60. Plasma Levels of Bacterial DNA Correlate with Immune Activation and the Magnitude of Immune Restoration in Persons with Antiretroviral-Treated HIV Infection / W. Jiang, M. M. Lederman, P. Hunt [et al.] // J. Infect. Dis. – 2009. – Vol. 199. – P. 1177–1185.

THE FREQUENCY OF METHYLENETETRAHYDROFOLATEREDUCTASE GENE C677T SINGLE NUCLEOTIDE POLYMORPHISM IN INDIVIDUALS OF DIFFERENT SEX

Аuthors: Sukhareva V. A., GarbuzovaV. Yu., AtamanA. V.

Pages: 385-389

Аbstract

   

      C677T polymorphism (rs 1801133) of methylenetetrahydrofolatereductase gene (MTHFR) in 124 healthy individuals was determined. It was shown that the ratio of major homozygous allele (C/C), heterozygotes (C/T) and homozygotes for the minor allele (T/T) was 46 %, 48.4 % and 5.6 %. Frequency of individuals-carriers of the minor allele (C/T+T/T) among men was higher than among women (P = 0.061). Female carriers minor allele (C/T+T/T) growth was significantly lower, and BMI was higher compared with women who were homozygous for major allele (C/C) (P < 0.001, P = 0.034 respectively).

            Key words: gene polymorphism, methylenetetrahydrofolate reductase, sex, body mass index.

            This email address is being protected from spambots. You need JavaScript enabled to view it.">*This email address is being protected from spambots. You need JavaScript enabled to view it.

 

  

The full text

To viev the full text

References

1. Фетисова И. Н. Полиморфизм генов фолатного обмена и болезни человека / И. Н. Фетисова, М. А. Липин, А. В. Поляков // Вестник новых медицинских технологий. – 2007. – Т. 10, № 1. – C. 7–12.
2. Gene structure of human and mouse methylenetetrahydrofolate reductase (MTHFR) / P. Goyette, A. Pai, R. Milos [et al.] // Mamm Genome. – 1998. – Vol. 9. – P. 652-665.
3. Genetic Polymorphism of Methylenetetrahydrofolate Reductase (MTHFR) and Coronary Artery Disease / F. Rassoul, V. Richte, T. Kuntze [et al.] // International Journal of Angiology. – 2000. – Vol. 9. – P. 205-207.
4. Analysis of the MTHFR Gene Linkage Disequilibrium Structure and Association Polymorphic Gene Variants with Coronary Atherosclerosis / E. A. Trifonova, M. G. Spiridonova, T. V. Gabidulina [et al.] // Russian Journal of Genetics. – 2012. – Vol. 48, No. 10. – P. 1035–1047.
5. MTHFR polymorphisms, dietary folate intake, and breast cancer risk: results from the Shanghai Breast Cancer Study.Shrubsole / Y. T. Gao, Q. Cai, X. O. Shu [et al.] // Cancer Epidemiol Biomarkers Prev. – 2004. – Vol. 13 (2). – P. 190–196.
6. Трифонова Е. А. Генетическое разнообразие и неравновесие по сцеплению в локусе метилентетрагидрофолатредуктазы / Е. А. Трифонова, М. Г. Спиридонова, В. А. Степанов // Генетика. – 2008. – Т. 44 (10). – С. 1410–1419.
7. Спиридонова М. Г. О роли полиморфных вариантов гена 5,10-метилентетрагидро-фолатредуктазы в патогенезе сердечно-сосудистых заболеваний / М. Г. Спиридонова, В. А. Степанова, В. П. Пузырев // Клинич. Медицина. – 2001. – Т. 2. – С. 10–16.
8. Van der Put N. M. Is the common 677CT mutation in the methylenetetrahydrofolate reductase gene a risk factor for neural tube defects? A meta-analysis / N. M. van der Put, T. K. Eskes, H. J. Blom // Q J Med. – 1997. – Vol. 90. – P. 111–115.
9. Heterogeneity in world distribution of thermolabile C677T mutation in 5,10-methylenetetrahydrofolate reductase / G. Pepe, O. C. Venegas, B. Giusti [et al.] // Am J Hum Genet. – 1998. – Vol. 63. – P. 917–920.
10. Worldwide distribution of a common methylenetetrahydrofolate reductase mutation / J. A. Scheinder, D. C. Rees, Y. T. Liu [et al.] // Am J Hum Genet. – 1998. – Vol. 62. – P. 1258–1260.
11. The Frequent 5,10-Methylenetetrahydrofolate Reductase C677T Polymorphism Is Associated with a Common Haplotype in Whites, Japanese and Africans / N. Rosenberg, M. Murata, Y. Ikeda [et al.] // Am J Hum Genet. – 2002. – Vol. 70. – P. 758–762.
12. Low frequency of mutated methylenetetrahydrofolate reductase 677C–>T and 1298A–>C genetics single nucleotide polymorphisms (SNPs) in Sub-Saharan populations / C. E. Adjalla, E. K. Amouzou, A. Sanni [et al.] // Clin Chem Lab Med. – 2003. – Vol. 41. – P. 1028–1032.
13. Geographical and ethnic variation of the 677C>T allele of 5,10 methylenetetrahydrofolate reductase (MTHFR): findings from over 7000 newborns from 16 areas world wide / B. Wilcken, F. Bamforth, Z. Li [et al.] // J Med Genet. – 2003. – Vol. 40. – P. 619–625.
14. Prevalence of methylene tetrahydrofolate reductase polymorphism in South Indian population / A. Radha Rama Devi, V. Govindaiah, G. Ramakrishna [et al.] // Current science. – 2004. – Vol. 86. – P. 440–443.
15. Methylenetetrahydrofolate reductase C677T polymorphism is associated with central adiposity and increased androgenicity in healthy postmenopausal women / I. Lambrinoudaki, G. Kaparos, D. Papadimitriou [et al.] // European Journal of Endocrinology. –2008. – Vol. 159. – P. 233–240.
16. Serum folate, total homocysteine levels and methylenetetrahydrofolate reductase 677C>T polymorphism in young healthy female Japanese / T. Taguchi, H. Mori, A. Hamada [et al.] // Asia Pac J Clin Nutr. – 2012. –Vol. 21 (2). – P. 291–295.
17. Li P. Methylenetetrahydrofolate reductase (MTHFR) gene polymorphisms and susceptibility to ischemic stroke: A meta-analysis / P. Li, C. Qin // Gene. – 2013. – P. 378 – 388.
18. Association between the MTHFR C677T polymorphism and recurrent pregnancy loss: a meta-analysis / X. Wu, L. Zhao, H. Zhu // Genet Test Mol Biomarkers. – 2012. – P. 806-811.
19. Folate metabolism gene polymorphisms MTHFR C677T and A1298C and risk for Down syndrome offspring: a meta-analysis / X. Wu, X. Wang, Y. Chan, S. Jia // Eur J Obstet Gynecol Reprod Biol. – 2013. –Vol. 167 (2). – P. 154-159.
20. Folate Intake, MTHFR Polymorphisms, and the Risk of Colorectal Cancer: A Systematic Review and Meta-Analysis / D. A. Kennedy, S. J. Stern, I. Matok, M. E. Moretti // J Cancer Epidemiol. – 2012

PLANIMETRIC ANALYSES OF THE BURN AREAS AFTER CHITOSAN MEMBRANES APPLICATION

Аuthors: Kornienko V. V.

Pages: 390-397

Аbstract

   

       The article is devoted to evaluate dynamics of planimetric indexes of burns. I took rats of different age and applied innovative chitosan membranes on the burns. I modeled IIIb burns on the rats from both experimental and control groups; I used chitosan-based coatings for topical treatment. Planimetric analyses of the affected areas were performed by the “SEOImagelab 2.0” program (Sumy, Ukraine) considering the total affected area (sm2); the relative areas of dead tissue, granulation tissue and epithelization (%). I measured them on 1st, 3rd, 7th, 14th and 21st days after the burn modelling. These days showkey phases of skin healing. I determined the rate of burn healing according to certain criteria: average rate of affected area reduction (sm2) per day; reduction in burn area (%) per day. Natural chitosan coatings prevented from repeated infections protecting the burn areas from exogenous factors. Besides, it was applied easily on the affected areas to protect newly formed epithelium. Healing process speeded up during the inflammatory phase as both burn cleaning and granulation tissue formation enhanced. Moreover, gripping of the burn edges occurred during the proliferation and remodeling phases. Due to these results I may claim that period of healing process with rate of epithelization has decreased by 1.5 day.

                      Keywords: burns, treatment, medicines, chitosan, planimetria.

                      This email address is being protected from spambots. You need JavaScript enabled to view it.

 

 

  

The full text

To viev the full text

References

1. Григорьева Т. Г. Новые технологии хирургического лечения обширных глубоких ожогов и их последствий / Т. Г. Григорьева // Междунар. мед. журнал. – 2002. – Vol. 8 (1–2). – P. 116–118.
2. Midwood K. S. Tissue repair and the dynamics of the extracellular matrix. / K. S. Midwood L. V. Williams, J. E. Schwarzbauer // The International Journal of Biochemistry & Cell Biology. – 2004. – Vol. 36 (6). – P. 1031–1037.
3. The cellular, biochemical, and mechanical phases of wound healing / R. E. Pollock, F. C. Brunicardi, D. K. Andersen [et al.] // Schwartz's Principles of Surgery, Ninth Edition. – 2009. – McGraw-Hill Professional.
4. Будкевич Л. И. 10-летний опыт применения культивированных аллофибробластов человека при лечении детей с глубокими ожогами / Л. И. Будкевич // Матер. ХХ з’їзду хірургів України. – Тернопіль, 2002. – Т. 2. – С. 636–639.
5. The cell based dressing with living allogenic keratinocytes in the treatment of foot ulcers: a case study / Y. Bayram, M. Deveci, N. Imirzalioglu [et al.] // British journal of plastic surgery. – 2005 – Vol. 58 (7). – P. 988–96.
6. Кризина П. С. Особливості пербігу запального процесу в інфікованих ранах при застосуванні для покриття їх поверхні гідратцелюлозною плівкою та АВВМ – "Дніпро" – МП / П. С. Кризина // Бук. мед. вісник. – 2001. – Т. 5, № 1. – C. 173–176.
7. Парамонов Б. А. Ожоги: Руководство для врачей / Б. А. Парамонов, Я. О. Порембский, В. Г. Яблонский. – СПб. : СпецЛит, 2000. – 480 с.
8. Абаев Ю. К. Справочник хирурга. Раны и раневая инфекция / Ю. К. Абаев // Ростов-на-Дону : Феникс, 2006. – 427 с.
9. Bren L. Helping wounds heal / L. Bren // FDA Consumer magazine. – May–June. – 2002. – Vol. 23. – P. 34–41.
10. Yamaguchi Y. Cutaneous wound healing: an update / Y. Yamaguchi // J. Dermatol. – 2001. – Vol. 28. – P. 521–534.
11. Сравнительное изучение эффекти-вности различных биоактивных материалов при лечении гнойных ран / С. Х. Григорян, А. К. Григорян, А. С. Нанян, Э. С. Григорян // Материалы Международной конференции / под ред. В. Д. Федорова, А. А. Адамяна. – М., 2001. – C. 101–102.
12. Добыш С. В. Современные перевязочные средства для лечения ран во второй фазе раневого процесса / С. В. Добыш, А. В. Васильев, О. В. Шурупова // Материалы Международной конференции / под ред. В. Д. Федорова, А. А. Адамяна. – М., 2001. – С. 115.
13. The Role of Moisture Balance in Wound Healing / D. Okan, K. Woo, E. Ayello, G. Sibbald // Adv Skin Wound Care. – 2007. – Vol. 20 (1). – P. 39–53.
14. Ovington L. Hanging Wet-to-Dry Dressings Out to Dry / L. Ovington // Adv Skin Wound Care. – 2002. – Vol. 15 (2). – P. 79–86.
15. Studies on nerve aftinity of chitosan-derived materials / G. HaiPeng, Z. Yinghui, L. Jianchun [et al.] // Journal of Biomedical Material Research. – 2000. – Vol. 52 (2). – P. 285–295.
16. Photocrosslinkable chitosan as a dressing for wound occlusion and accelerator in healing process / Masayuki, Ishihara, Kuniaki [et al.] // Biomaterials. – 2002. – Vol. 23 (5). – P. 833–840
17. Preparation and characterization on mechanical and antibacterial properties of chitosan/cellulose blends / Yu-Bey, Wu, Shu-Huei [et al.] // Carbohydrate Polymers. – 2004. – Vol. 57 (7). – P. 435–440.
18. Чадаев А. П. Современные методики местного медикаментозного лечения инфицированных ран / А. П. Чадаев, А. Д. Климиашвили // Русский медицинский журнал. – 2002. – № 26.
19. Wound bed preparation: a systematic approach to wound management / G. S. Schultz, R. G. Sibbald, V. Falanga [et al.] // Wound Repair Regen. – 2003. – Vol. 11. – P. 23–28.
20. Автандилов Г. Г. Медицинская морфо-метрия. Руководство / Г. Г. Автандилов // Медицина. – М., 1990. – 384 с. : ил.
21. Jones A. M. Are modern wound dressings a clinical and cost-effective alternative to the use of gauze? / A. M. Jones, L. San Miguel // Wound Care. – 2006. – Vol. 15. – P. 65–69.
22. Adsorption effect of activated charcoal on enterohemorrhagic Escherichia coli / K. Naka, S. Watarai, K. Tana [et al.] // Vet Med Sci. – 2001. – Vol. 63. – P. 281–285.
23. The use of physical hydrogels of chitosan for skin regeneration following third-degree burns / N. Boucard, C. Vitona, D. Agayb [et al.] // Biomaterials. – 2007. – Vol. 28. – P. 3478–3488.
24. Ovington L. G. Overview of matrix metalloprotease modulation and growth factor protection in wound healing / L. G. Ovington // Part 1. Ostomy Wound Manage. – 2002. – Vol. 48 (6 Suppl). – P. 3–7.
25. Electrospun nano-fibre mats with antibacterial properties from quaternized chitosan and poly(vinyl alcohol) / M. Ignatova, K. Starbova, N. Markova [et al.] // Carbohydr Res. – 2006. – Vol. 341. – P. 2098–2107.

THE 3D-MODEL OF RAT’S HUMERI TESTING TOUGHNESS PROPERTIES FOR VARIOUS DEFORMATION

Аuthors: Bushtruk A. N., Tkach G. F., Pogorielov M. V., Sikora V. Z.

Pages: 398-407

Аbstract

   

           The article is devoted to study toughness of rat’s humeri testing them for stiffness, strength and stretching. Our aim is to create a 3D-model of the long bone for rats of different age. This model will allow conducting numerous toughness tests by changing the initial parameters. The portable experimental unit was used to test humeri stretching, with the measuring scale accurate to 0.25 kg. Evaluation of toughness was carried by Pro/Engineer software package (PTC, USA) and included Pro/Mechanica modulus. The minimal value of critical toughness was measured in the bones of sucking rats. Value of stretching showed almostdirectly proportional dependence between critical bone toughness and rats age. Having compared experimental data and calculations of crack load values, we pointed that value deviation is less than 7%. The 3-D image of the long bone for rats of different age can be frequently used for various deformation influences and with different initial parameters of the bone tissue.

      Key words: toughness, humerus, deformation, 3D-model.

      This email address is being protected from spambots. You need JavaScript enabled to view it.">*This email address is being protected from spambots. You need JavaScript enabled to view it.

  

The full text

To viev the full text

References

1. Currey J. D. Bones / J. D. Currey // Princeton: Princeton University Press. – 2002.
2. Turner C. H., Burr D. B. Basic biomechanical measurements of bone: a tutorial. / C. H. Turner, D. B. Burr // Bone. – 1993. – Vol. 14. ¬ P. 595–608.
3. Bone biomechanical properties in prostaglandin EP1 and EP2 knockout mice./ M. P. Akhter, D. M. Cullen, G. Gong [et al.] // Bone. – 2001. – Vol. 29. – P.121–5.
4. Currey J. D. Mechanical properties of bone tissues with greatly differing functions. / J. D. Currey // J Biomech. – 1979. – Vol. 12. – P. 313–9.
5. Behiri J. C., Bonfield W. Orientation dependence of the fracture mechanics of cortical bone. / J. C. Behiri, W. Bonfield // J Biomech. – 1989. – Vol. 22. – P. 863–7.
6. Vashishth D. Rising crack-growth-resistance behavior in cortical bone: implications for toughness measurements. / D. Vashishth // J Biomech. – 2004. – Vol. 37. – P. 943–6.
7. Mechanistic aspects of fracture and Rcurve behavior in human cortical bone./ R. K. Nalla, J. J. Kruzic, J. H. Kinney [et al.] // Biomaterials. – 2005. – Vol. 26. – P. 217–31.
8. Taylor D., Hazenberg J. G., Lee T. C. Living with cracks: damage and repair in human bone. / D. Taylor, J. G. Hazenberg, T. C. Lee // Nature Mater. – 2007. – Vol. 6. – P. 249–317.
9. The effect of calcium supplementation on bone density during lactation and after weaning. / H. J. Kalkwarf, B. L. Specker, D. C. Bianchi [et al.] // New Engl J Med. – 1997. – Vol. 337. – P. 523–8.
10. Zioupos P., Currey J. D. Changes in the stiffness, strength, and toughness of human cortical bone with age. / P. Zioupos, J. D. Currey // Bone. – 1998. – Vol. 22. –P. 57–66.
11. Alendronate versus calcitriol for the prevention of bone loss after cardiac transplantation. / E. Shane, V. Addesso, P. Namerow [et al.] // New Engl J Med. – 2004. – Vol. 350. – P. 767–76.
12. Roodman G. D. Mechanisms of bonemetastasis. / G. D. Roodman // New Engl J Med. – 2004. – Vol. 350. – P. 1655–64.
13. Glucocorticoidtreated mice have localized changes in trabecular bone material properties and osteocyte lacunar size that are not observed in placebo-treated or estrogendeficient mice. / N. E. Lane, W. Yao, M. Balooch [et al.] // J Bone Miner Res. – 2006. – Vol. 21. – P. 466–76.
14. Bone biomechanical properties in lrp5 mutant mice./ M. P. Akhter, D. J. Wells, S. J. Short [et al.] // Bone. – 2004. – Vol. 35. – P. 162–9.
15. Nanoindentation and whole-bone bending estimates of material properties in bones from the senescence accelerated mouse samp6. / M. J. Silva, M. D. Brodt, Z. Fan [et al.] // J Biomech. – 2004. – Vol. 37. – P. 1639–46.
16. 3D bone microarchitecture modeling and fracture risk prediction / H. Li, X. Li, L. Bone [et al.]// Conference on Bioinformatics, Computational Biology and Biomedicine, BCB. – 2012. – P. 361-368
17. Cristofolini L., Viceconti M. Mechanical validation of whole bone composite tibia models / L. Cristofolini, M. Viceconti // Journal of Biomechanics. – Vol. 33 (3). – P. 279-288.
18. Modelling the fibrous tissue layer in cemented hip replacements: Experimental and finite element methods / V. Waide, L. Cristofolini, J. Stolk [et al.] / Journal of Biomechanics. – 2004. – Vol. 37 (1). – P. 13-26.
19. Experimental validation of a finite element model of a human cadaveric tibia / H. A. Gray, F. Taddei, A. B. Zavatsky [et al.] //Journal of Biomechanical Engineering. – 2008. – Vol. 130 (3).
20. Computationally-optimized bone mechanical modeling from high-resolution structural images / J. F. Magland, N. Zhang, C. S. Rajapakse, [et al.]. – PloS one. – 2012. – Vol. 7 (4). – P. 35–25.
21. Harrison N. M. Failure modelling of trabecular bone using a non-linear combined damage and fracture voxel finite element approach / N. M. Harrison, P. McDonnell, L. Mullins // Biomechanics and Modeling in Mechanobiology. – 2012. – P. 1-17.
22. Chennimalai Kumar N. Modeling of cortical bone adaptation in a rat ulna: Effect of frequency (2012) / N. Chennimalai Kumar, J. A. Dantzig, I. M. Jasiuk // Bone. – Vol. 50 (3). – P. 792–797.
23. Finite element modelling of squirrel, guinea pig and rat skulls: Using geometric morphometrics to assess sensitivity (2011) / Cox P.G., Fagan M. J., Rayfield E. J. [et al.] // Journal of Anatomy. – Vol. 219 (6). – P. 696–709.
24. Bernard S. Accurate measurement of cortical bone elasticity tensor with resonant ultrasound spectroscopy /, Q. Grimal, P. Laugier // Journal of the Mechanical Behavior of Biomedical Materials. – 2013. – Vol. 18. – P. 12–19.
25. A computational method for determining tissue material properties in ovine fracture calluses using electronic speckle pattern interferometry and finite element analysis / M. Steiner, L. Claes, U. Simon [et al.] // Medical Engineering and Physics. – 2012. – Vol. 34 (10). – P. 1521–1525.
26. Sacco S. M. Phytonutrients for bone health during ageing / S. M. Sacco, M.-N. Horcajada, E. Offord // British Journal of Clinical Pharmacology. – 2013. – Vol. 75 (3). – P. 697–707.
27. Inactivation of Lrp5 in osteocytes reduces Young's modulus and responsiveness to the mechanical loading 2013 / L. Zhao, J. W. Shim, T. R. Dodge [et al.] // Bone. – Vol. 54 (1). – P. 35–43.

THE FREQUENCY OF ALLELIC VARIANTS OF THE VITAMIN K-EPOXIDOREDUCTASE GENE IN PATIENTS WITH ACUTE CORONARY SYNDROME

Аuthors: Dubovyk Ye. I., Garbuzova V. Yu., Prosol D. А., Shimko K. A.

Pages: 408-412

Аbstract

   

      T2255C polymorphism (rs2359612) of vitamin K-epoxidoreductase (VKORC1) gene in 118 patients with acute coronary syndrome (ACS) and in 234 healthy people was determined. It was shown that in patients with ACS interrelation of main homozygotes, heterozygotes and minor homozygotes were 27.1 %, 41.5 % and 31.4 % (in control – 37.2 %, 42.7 %, 20.1 %. P = 0,038 by χ2-test). Thus, there is an association between T2255C polymorphism and the development of ACS: the risk of ACS in homozygotes for the minor allele (C/C) is 2.1 times higher than in homozygous for the major allele.

               Key words: vitamin K-epoxidoreductase, allelic polymorphism, acute coronary syndrome.

               This email address is being protected from spambots. You need JavaScript enabled to view it.">*This email address is being protected from spambots. You need JavaScript enabled to view it.

  

The full text

To viev the full text

References

1. Vitamin K epoxidereductase complex subunit 1 (VKORC1): The key protein of the vitamin K cycle / J. Oldenburg, C. G. Bevans, C. R. Muller [et al.] // Antioxid. Redox Signal. – 2006. – Vol.8 – P. 347–353.
2. Vitamin K Epoxide Reductase Complex Subunit 1 (VKORC1) Polymorphism and Aortic Calcification / M. Teichert, L. E. Visser, R. H. N. van Schaik [et al.] // Arterioscler. Thromb. Vasc. Biol. – 2008. – Vol.28. – P. 771–776.
3. Common VKORC1 variants are not associated with arterial or venous thrombosis / A. Hindorff, S. R. Heckbert, N. Smith, K. D. Bennet [et al.] // Journal of Thrombosis and Haemostasis. – 2007. – Vol. 5. – P. 2025–2027.
4. VKORC1 Haplotypes Are Associated With Arterial Vascular Diseases (Stroke, Coronary Heart Disease, and Aortic Dissection / Y. Wang, Z. Weili, Y. Zhang [et al.] // Circulation. – 2006. – Vol. 113. – P. 1615–1621.
5. ACC/AHA guidelinesfor the management of patients with unstable angina and non ST-elevation myocardial infarction: executive summary and recommendations. A report of the american college of cardiology / E. Braunwald, E. M. Antman, N. H. Brooks [et al.]// American Heart Association task force on practice guidelines (committee on management of patients with unstable angina) // Circulation.–2000. – Vol. 102. – P. 1193–1209.
6. Management of acute coronary syndromes in patients presenting without persistent ST-segment elevation. The task force on the management of acute coronary syndromes of the European society of cardiology / M. E. Bertrand, M. L. Simoons, K. A. Fox [et al.] // Eur. Heart J. – 2002. – Vol. 23. – P. 1809–1840.
7. World Health Organization. Nomenclature and criteria for diagnosis of ischemic heart disease // Circulation. – 1979. – Vol. 59. – P. 607–609.
8. Regulatory polymorphism in vitamin K epoxide reductase complex subunit 1 (VKORC1) affects gene expression and warfarin dose requirement / D. Wang, H. Chen, K. M. Momary [et al.] // Blood. – 2008. – Vol. 112. – P. 1013–1021.
9. VKORC1 Haplotypes Are Associated With Arterial Vascular Diseases (Stroke, Coronary Heart Disease, and Aortic Dissection / Y. Wang, Z. Weili, Y. Zhang [et al.] // Circulation. – 2006. – Vol. 113. – P. 1615–1621.
10. Lack of association between variants in the VKORC1 gene and cerebrovascular or coronary heart disease / R. Lemmens, S. Abboud, L. Vanhees [et al.] // Thromb. Haemost. – 2008. – Vol. 12. – P. 2220–2223.
11. Common VKORC1 variants are not associated with arterial or venous thrombosis / A. Hindorff, S. R. Heckbert, N. Smith [et al.] // Journal of Thrombosis and Haemostasis. – 2007. – Vol. 5. – P. 2025–2027.
12. VKORC1 genetic polymorphism and risk of venous thromboembolism in postmenopausal women: new findings and meta–analysis / C. Verstuyft, M. Canonico, E. Bouazi [et al.] // J. Thromb. Haemost. – 2009.– Vol. 7. – P. 1034–1036.
13. No clear link between VKORC1 genetic polymorphism and the risk of venous thrombosis or peripheral arterial disease / M. D. Smadja, M. A. Loriot, L. A. Hindorff [et al.] // Thromb. Haemost. – 2008. – Vol. 99. – P. 970–972.
14. Vitamin K epoxide reductase genetic polymorphism is associated with venous thromboembolism: results from the EDITH Study / K. Lacut, C. Larramendy–Gozalo [et al.] // J. Thromb. Haemost. – 2007. – Vol. 5. – P. 2020–2024.

THE PROTOCOL OF PATHOMORPHOLOGICAL INVESTIGATION OF THE PERIPHERAL NERVE HAEMOCIRCULATORY BLOOD STREAM

Аuthors: Besedinska O. V., Davydenko I. S., Besedinskyi V. I., Andreev S. A.

Pages: 413-418

Аbstract

   

       Peripheral neuropathy is a clinical syndrome that develops as a result of various aetiological factors impacting peripheral nerves. It is distinguished by heterogeneous pathogenetic mechanisms. Polioneuropathies occupy the second place in the structure of diseases of the peripheral nerve system after vertebraginic pathology, but greatly exceed it in the complicated clinical manifestations and crippling consequences. Important role is played by the vessel factors of neuropathy development, which are connected with the involvement of vasa nervorum and combine a big group of diseases. To detect the pathological changes in the microcirculatory blood stream of peripheral nerves advanced pathohistological research of its components on various levels is needed; this research is carried out by pathologists with the use of the whole complex of techniques aimed at the elective detection of various elements of vessel wall. The issue of protocol development enabling the complex multi-factor analysis of great amounts of data is therefore in question. The objective of our research is the development of the systematic list of pathohistological changes in the microcirculatory blood stream of the peripheral nerve.

    The research protocol for the description of pathohistological changes of some components of the microcirculatory русла of the peripheral nerve was developed based on referenced data and our own observation experience. The systematic list of pathohistological changes was verified in the examination of 220 n. tibialis of diabetes patients and in the control group.

    The use of the suggested research protocol for the description of pathomorphological changes in vessels will enable objective diagnosis and correct interpretation of the obtained data.

     The prospects of our research lie in the development of the computer-based morphometric analysis of the haemocirculatory blood stream of peripheral nerves.

        Key words: vessel wall, arteriole, venula, capillary, peripheral neuropathy, microangiopathy.

         This email address is being protected from spambots. You need JavaScript enabled to view it.">*This email address is being protected from spambots. You need JavaScript enabled to view it.

  

The full text

To viev the full text

References

1. Балаболкин М. И. Диабетическая нейропатия / М. И. Балаболкин, Т. Е. Чернышова, В. В. Трусов, И. В. Гурьева. – М. : Медицина, 2003. – 440 с.
2. Багрій М. М. Протокол патогістологічного дослідження судинної стінки / М. М. Багрій // Вісник проблем біології і медицини. − 2007. − № 2.− С. 35–38.
3. Зербино Д. Д. Васкулиты и ангиопатии / Д. Д. Зербино. – К. : Здоров’я, 1977. – 101 с.
4. Салтыков Б. Б. Диабетическая микроангиопатия / Б. Б. Салтыков, В. С. Пауков. – М. : Медицина, 2002. – 240 с.
5. Струков А. И. Сравнительная патология микроциркуляторного русла / А. И. Струков, А. А. Воробьева // Кардиология. – 1976. – № 11. – С. 8–17.
6. Зербино Д. Д. Автоматизированное описание патогистологических изменений в сосудах: формирования массива исходных данных / Д. Д. Зербино, Д. Ф. Эрдманис, Ю. А. Поспишаль. // Архив патологии. – 1982. – № 12. – С.73–75.
7. Гаврилюк О. М. Еластичні волокна: особливості структури та патогістологічні зміни / О. М. Гаврилюк // Львівський медичний часопис. – 1997. – № 1–2. – С. 9–13.
8. Куприянов В. В. Микроциркуляторное русло / В. В. Куприянов, Я. Л. Караганов, В. И. Козлов. – М. : Медицина. – 350 с.
9. Геращенко С. Б. Периферійний нерв (нейро-судинно-десмальні взаємовідношення в нормі та при патології) / С. Б. Геращенко, О. І. Дєльцова, А. К. Коломійцев, Ю. Б. Чайковський. – Тернопіль: Укрмедкнига, 2005. – 342 с.

THE COMPARATIVE ANALYZES OF SURGICAL TREATMENT RESULTS OF RECURRENT PILONIDAL SINUS DISEASE

Аuthors: Tsema Ye.V.

Pages: 419-426

Аbstract

   

       The article is devoted to discuss the results of radical surgical treatment of 57 patients with recurrent pilonidal disease. Patients with pilonidal disease were divided into the control and main groups. Thus, 31 (54.4 %) patients composed the control group of patients who were treated by wide excision with wound closure, while 26 (45.6 %) patients composed the main group of patients who were treated by Bascom's procedure (cleft lift procedure). The results of treatment patients were following for 1–3 years. There were 23 (74.2 %) complications in patients of the control group: wound abscess (16.1 %), primary wound dehiscence (16.1 %), secondary wound dehiscence (19.4 %), wound hematoma (12.9 %) and repeat recurrent of disease (9.7 %). There were 3 (11.5 %) complications in patients of the main group: wound abscess (3.8 %), secondary wound dehiscence (3.8 %) and wound hematoma (3.8 %). There was no repeat recurrent of disease after Bascom's procedure. The using cleft lift procedure (Bascom's procedure) permits essentially decrease (χ2 = 22,4; Р=0,001) frequency of postoperative complications in patients with recurrent pilonidal disease.

                  Key words: pilonidal sinus disease, recurrent after operation, radical surgical treatment, Bascom's procedure, cleft lift procedure.

                  This email address is being protected from spambots. You need JavaScript enabled to view it.">*This email address is being protected from spambots. You need JavaScript enabled to view it.

  

The full text

To viev the full text

References

1. Даценко Б. М. Острое нагноение эпителиального копчикового хода / Б. М. Даценко. – Х. : Прапор, 2006. – 166 c.
2. Лурин И. А. Этиология и патогенез пилонидальной болезни / И. А. Лурин, Е. В. Цема // Колопроктология. – 2013. – № 3. – С. 35–50.
3. Маркевич С. В. Використання ультразвукової кавітації в комплексному лікуванні дермоїдних кіст крижово-куприкової ділянки / С. В. Маркевич, А. А. Кобірніченко // Вісник Вінницького національного медичного університету імені М. І. Пирогова. – 2010. – Т. 14, № 2. – C. 277–279.
4. Русак О. Б. Комплесне хірургічне лікування ускладнених форм епітеліальних куприкових ходів : автореф. дис. ... канд. мед. наук : 14.01.03 / О. Б. Русак ; Буковинський державний медичний університет, Тернопільський державний медичний університет імені І. Я. Горбачевського. – Т., 2010. – 20 c.
5. Ультрасонографія у діагностиці та виборі лікувальної тактики при епітеліальному куприковому ході / М. П. Захараш, О. В. Лишавський, В. А. Дубовий [та ін.] // Хірургія України. – 2010. – № 2. – C. 66–71.
6. Цема Є. В. Еволюція уявлень про етіопатогенез пілонідальної хвороби / Є. В. Цема // Хірургія України. – 2013. – № 2. – С. 9–22.
7. Bascom J. Failed pilonidal surgery: new paradigm and new operation leading to cures / J. Bascom, T. Bascom // Arch. Surg. – 2002. – №. 10. – P. 1146–1151.
8. Bascom J. Surgical treatment of pilonidal disease / J. Bascom // BMJ. – 2008. – Vol. 336. – P. 842–843.
9. Bascom J. Utility of the cleft lift procedure in refractory pilonidal disease / J. Bascom, T. Bascom // Am. J. Surg. – 2007. – №. 5. – P. 606–609.
10. Bertelsen C. A. Bascom's operation for pilonidal fistula / C. A. Bertelsen, L. N. Jorgensen // Ugeskr. Laeger. – 2008. – №. 26. – P. 2313–2317.
11. Nordon I. M. A prospective randomized controlled trial of simple Bascom's technique versus Bascom's cleft closure for the treatment of chronic pilonidal disease / I. M. Nordon, A. Senapati, N. P. Cripps // Am. J. Surg. – 2009. – №. 2. – P. 189–192.
12. Thompson M. R. Pilonidal Sinus Disease. Anorectal and Colonic Diseases. A Practical Guide to Their Management / M. R. Thompson, A. Senapati, R. B. Kitchen; Editors: Jean-Claude R. Givel, Neil Mortensen, Bruno Roche. – 3rd ed. – Springer, 2010. – P. 373–386.

EFFECT OF DRUG THERAPY SUBCLINICAL HYPERTHYROIDISM ON MARKERS OF CARDIOVASCULAR RISK IN PATIENTS WITH TYPE 2 DIABETES

Аuthors: Kasatkina S.G., Panova T.N., Kasatkin S.N.

Pages: 427-431

Аbstract

   

        We examined 56 patients (12 men and 44 women) aged 45 to 60 years (mean 51.13 ± 5.32 years) in order to study the dynamics of indicators of endothelial dysfunction in patients with type 2 diabetes with subclinical hyperthyroidism on the background of the natural course and treatment thyrostatics. All patients were divided into two subgroups: the first subgroup received treatment (20 patients) with tyrosol; a second subgroup of dynamic monitoring (36 patients) did not receive treatment duringfollow-tyrosol.The results indicate an increased risk of cardio-vascular diseases for patients with type 2 diabetes with subclinical hyperthyroidism and require timely active preventive measures.

          Key words: diabetes mellitus, subclinical hyperthyroidism, intima-media complex, adhesion molecules.

          This email address is being protected from spambots. You need JavaScript enabled to view it.">*This email address is being protected from spambots. You need JavaScript enabled to view it.

 

  

The full text

To viev the full text

References

1. Helfand M. Screening for subclinical thyroid dysfunction in non-pregnant adults: a summary of the evidence for the US Preventive Services Task Force / M. Helfand // Ann. Intern. Med. – 2004. – Vol. 140. – P. 128–141.
2. Соореr D. S. Subclinical thyroid disease: consensus or conundrum? / D. S. Соореr // Clin. Endocrinol. – 2004. – Vol. 60. – P. 410–2.
3. Surks M. I., Ortiz E., Daniels G. [et al.]. Subclinical Thyroid Disease / M. I. Surks, E. Ortiz, G. Daniels [et al.] //. – JAMA. – 2004. – Vol; 291: – P. 228–38.
4. Toft A. D. Subclinical hyperthyroidism. / A. D. Toft // New Engl. J. Med. – 2001. – Vol. 345. – P. 512–6.
5. Дедов И. И. Сахарный диабет. // И. И. Дедов, М. В. Шестакова. – М. : Универсум Паблишинг. – 2003. – 455 с.
6. Терещенко И. В. Тиреоидная патология у больных сахарным диабетом / И. В. Терещенко, Е. С. Трефилова // Сахарный диабет, 2001. – № 4. – С. 22–24
7. Дубов В. В. Особенности тиреоидного статуса при сахарном диабете типа 2: дис. канд.мед.наук. – Самара, 2002. – 102 с.
8. Никитина Ю. М. Ультразвуковая допплеровская диагностика в клинике / Ю. М. Никитина, А. И. Труханова. – Москва, Иваново : Издательство МИК, 2004. – С. 115–135; С. 241–255.
9. Ross R. Atherosclerosis – an inflammatory disease / R. Ross // N. Engl. J. Med. – 1999. – Vol. 340. – P. 115–26.
10. Tomiyasu H. Effect of anticholesterol therapy on soluble 1CAM-1 in chronic stroke patients with hyperlipidemia. / H. Tomiyasu, K. Ishikawa, M. Yamamoto // Tokai J. Exp. Clin. Med. – 2005. – Vol. 30 (1). – P. 63–69.
11. Влияние тиреотоксикоза на сердечно-сосудистую систему / Е. А. Трошина, Ф. М. Абдулхабирова, Г. А. Мельниченко [и др.] // Российские медицинские вести, 2005. – № 2. – C. 13–20.
12. Аметов А. С. Сердечно-сосудистая система при тиреотоксикозе / А. С. Аметов, М. Ю. Кониева, И. В. Лукьянова // Consilium medicum, 2003. – Т. 5, № 11. – С. 34–38.
13. Трошина Е. А. Состояние сердечно-сосудистой системы при субклиническом тиреотоксикозе / Е. А. Трошина, Ф. М. Абдулхабирова // Кардиолог, 2006. – № 1. – С. 68–73.
14. Субклинический тиреотоксикоз и сердечно-сосудистая система. / Е. А. Трошина, Ф. М. Абдулхабирова, Л. А. Панченкова [и др.] // Клиническая и экспериментальная тиреоидология, 2006. – № 2. – C. 38–42.

FEATURES OF FUNCTIONAL STATE OF THE CARDIOVASCULAR SYSTEM IN TEENAGERS DUE TO THE DOPPLEROGRAPHY RESULTS

Аuthors: PopovS. V., BokovaS. I., BugaenkoV. O., Romanova T. O.

Pages: 432-436

Аbstract

   

        The aim of the study was to research the cardiovascular system functional state in healthy teenagers as they had done certain exercise tests. We examined 68 children by the Doppler echocardiography method. The inadequate response of cardiovascular system had 25 % of teenagers. The main factors that had led to the state were: basic high blood pressure and general low level of physical activities. The systolic function of the heart enhanced during the lower dynamics of diastolic function.

             Key words: cardiovascular system, Doppler echocardiography.

             This email address is being protected from spambots. You need JavaScript enabled to view it.">*This email address is being protected from spambots. You need JavaScript enabled to view it.

 

  

The full text

To viev the full text

References

1. Белозеров Ю. М. Нормативы эхометрических показателей сердца у детей. Пособие для врачей. / Ю. М. Белозеров, С. Ф. Гнусаев. – М., 2006. – 24 с.
2. Казакова Л. М. Оцінка у школярів функціональних резервів серцево – судинної системи за допомогою індексу Руф'є/ Л. М. Казакова, О. А. Строй, М. М.Васюкова // Педіатрія, акушерство та гінекологія : наук.-практ. журн. – 2011. – Т. 73, №. 4. – С. 64–65 .
3. Няньковський С. Л. Стан здоров’я школярів в Україні/ С. Л. Няньковський, М. С. Яцула, М. І. Чикайло [та ін.] //Здоровье ребенка. – 2012. – Т. 40, № 5. – С. 109–114.
4. Положення про медико-педагогічний контроль за фізичним вихованням учнів у загальноосвітніх навчальних закладах. Затверджено Наказом Міністерства охорони здоров’я України та Міністерства освіти і науки України № 518/674 від 20.07.2009 р.
5. Пыков М. И. Детская ультразвуковая диагностика. / М. И. Пыков, К. В. Ватолина. – М.: Видар, 2001. – 680 с.
6. Самсыгина Г. А. Кардиология и ревматология детского возраста. / Г. А. Самсыгина, М. Ю. Щербакова. – М.: ИДМедпрактика-М, 2004. – 744 с.
7. Сенаторова Г. С. Стан серцево-судинної системи у хлопчиків спортсменів / Г. С. Сенаторова, Н. К. Мацієвська, О. Ю. Кізенко [та ін.] // Педіатрія, акушерство та гінекологія : наук.-практ. журн. – 2011. – Т. 73, №. 4. – С. 130–131.
8. Шарыкин А. С. Нагрузочные тесты с эхокардиографией: физиологические аспекты / А. С. Шарыкин, М. А. Колес-никова, Е. В. Шилыковская [и др.]// Педиатрия. – 2010. – № 3. – С. 111–115.
9. Шиллер Н. Клиническая эхокардиография. Руководство для врачей / Н. Шиллер, М. Осипов. – М.: Практика-М, 2005. – 344 с.
10. Blaes A., Baquet G., Fabre C., Van Praagh E., Berthoin S. Is there any relationship between physical activity level and patterns, and physical performance in children? / A. Blaes, G. Baquet, C. Fabre [et al.]// Int. J. Behav. Nutr. Phys. Act. – 2011. – Vol. 8. – P. 122.
11. Guyton A. C. Textbook of medical physiology / A. C. Guyton, J. E. Hall. – 11-th Ed. – Philadelphia : Elsevier Inc, 2006. – 1116 p.
12. High Blood Pressure in Children and Adolescents. The Fourth Report on the Diagnosis, Evaluation, and Treatment of/ National High Blood Pressure Education Program Working Group on High Blood Pressure in Children and Adolescents// Pediatrics. – 2004. – Vol. 114 (2). – P. 555–576.
13. Schultheiss H. P., Kühl U. Overview on chronic viral cardiomyopathy/chronic myocarditis / H. P. Schultheiss, U. Kühl //Ernst Schering Res. Found Workshop. – 2006. – Vol. 3(55). – P. 18.

INTERRELATION OF THE MICROELEMENT, IMMUNE HOMEOSTASIS AND INDICATORS OF THE CONDITION OF THE INTESTINE MICROBIOCENOSIS IN CHILDREN WITH BRONCHIAL ASTHMA

Аuthors: Smiyan O. I., Kurganska V. O., Sichnenko P. I., ByndaT. P., Gorbas V. A., Vasylieva O. G

Pages: 437-444

Аbstract

   

         The influence of quantitative and qualitative composition of intestinal microflora on the state of mineral metabolism and the immune system was study in the 128 children with asthma. The correlation between the number of representatives of the intestinal microbiota, bioelements and indicators of immune status were studied. The dependence of immune parameters, micronutrient content and quality of intestinal microflora detected in children with asthma that manifested significant imbalance of immune and microelement’s homeostasis. The results give reason to consider overgrowth in school age children with asthma as one of the factors that support secondary immunodeficiency, impaired microelement’s metabolism. The reducing of the number of lacto-and bifidobacterias, E. coli colonies and growth of opportunistic microorganisms, staphylococci and fungi have a significant impact on changes in the immune system and the microelement’s composition, supports allergic inflammation in the body of the child, even in remission, which is important and promising in terms of finding new ways of optimal treatment of childhood asthma.

              Key words: asthma, intestinal microbiocenosis, dysbiosis, immune system, microelements.

             This email address is being protected from spambots. You need JavaScript enabled to view it.">*This email address is being protected from spambots. You need JavaScript enabled to view it.

 

  

The full text

To viev the full text

References

1. Профілактика та лікування мікроекологічних порушень у дітей раннього віку : методичні рекомендації / упоряд. : Ю. Г. Антипкін, О. Г. Шадрін, О. М. Муквіч. – Київ, 2010. – 32 с.
2. Хавкин А. И. Микробиоценоз кишечника и иммунитет / А. И. Хавкин // Русский медицинский журнал. – 2003. – Т. 11. – № 3. – С. 122–126.
3. Bacterial biogeography of the human digestive tract / J. C. Stearns, M. D. Lynch, D. B. Senadheera [et al.] // Sci Rep. – 2011. – № 1. – Р. 170.
4. Frick J. S. The Gut Microflora and Its Variety of Roles in Health and Disease / J. S. Frick, I. B. Autenrieth // Curr Top Microbiol Immunol. – 2012. – № 5. – Р. 112–124.
5. Пілецький А. М. Корекція порушень кишкового мікробіоценозу у хворих на бронхіальну астму, поєднану із синдромом хронічної втоми / А. М. Пілецький // Буковинський медичний вісник. – 2010. – Т. 14. – № 3 (55). С. 42–44.
6. Стан мікробіоценозу кишечника та оцінка застосування Лактовіту Фортепри при гострих обструктивних бронхітах у дітей раннього віку / О. І. Сміян, В. В. Слива, О. П. Мощич [та ін.] // Здоровье ребенка. – 2011. – № 8 (35). – С. 37–43.
7. Вміст про- та протизапальних цитокінів у сироватці крові дітей, хворих на бронхіальну астму різних ступенів тяжкості / О. І. Сміян, В. О. Курганська, О. П. Мощич [та ін.] // Здоровье ребёнка. – 2012. – № 4 (39). – С.35–38.
8. Сміян О. І. Концентрація цинку, міді, магнію та кальцію в сироватці крові дітей, хворих на бронхіальну астму, та її залежність від ступеня тяжкості захворювання / О. І. Сміян, В. О. Курганська, О. П. Мощич // Педіатрія, акушерство, гінекологія . – 2011. – Т. 73. – № 5. – С. 7–12 .
9. Про затвердження Протоколів діагностики та лікування алергологічних хвороб у дітей : Наказ Міністерства охорони здоров’я України від 27.12.2005 р., № 767.
10. Эпштейн-Литвак Р. В. Бактериологическая диагностика кишечника : метод. Рекомендации. / Р. В. Эпштейн-Литвак, Ф. Л. Вильшанская. – М., 1977. – 23 с.
11. Mancini G. Immunochemical quantita of antigene by einyle radial immunodiffusion / G. Mancini, A. C. Carbonaza, J. F. Heremana // Immunochemistry. 1965. – Vol.2. – P. 235–254.
12. Serum copper and zinc levels in healthy greek children and their parents / I. Voskaki, V. Arvanitidou, H. Athanasopoulou [et al.] // Biological trace element research. – 2010. – Vol. 134 (2). – P. 136–145.
13. Zinc homeostasis in pediatric critical illness / N. Z. Cvijanovich, J. C. King, H. R. Flori [et al.] // Pediatric critical care medicine. – 2009. – Vol. 10 (1). – P. 29–34.

EFFECTIVENESS CRITERIA OF THE TREATMENT WITH METFORMIN FOR PATIENTS WITH POLYCYSTIC OVARY SYNDROME AND OBESITY

Аuthors: Arkhypkina T.L.

Pages: 445-451

Аbstract

   

      The study involved 35 patients with polycystic ovary syndrome and obesity. According to the basal secretion of аnti-Müllerian hormone, all patients were divided into two groups: the first group consisted of 20 women with index >10,3 ng / ml (14,1 ± 0,5 ng / ml) and the second – 15 women with index < 10,3 ng / ml (9,2 ± 0,2 ng / ml). I noticed similar changes in both groups after six month of therapy with metformin: weight loss, decrease of insulin, luteinizing hormone, testosterone and increase sex hormone-binding globulin, which was accompanied by reduction of free androgen index. Besides, the number of antral follicles and volume of ovarian reduced, menstrual cycle normalized. Perhaps, pregnancy occurred only among the representatives from the second group. It is assumed that the basal secretion of аnti-Müllerian hormone may be a predictor of clinical effectiveness of treatment with metformin

          Key words: polycystic ovary syndrome, antimulleran hormone, obesity, hyperinsulinemia, metformin.

          This email address is being protected from spambots. You need JavaScript enabled to view it.">*This email address is being protected from spambots. You need JavaScript enabled to view it.

 

  

The full text

To viev the full text

References

1. Consensus on Women’s Health Aspects of Polycystic Ovary Syndrome (PCOS) // Hum. Reprod. – 2012. – Vol. 27, № 1. – Р. 14–24.
2. Prevalence of Metabolic syndromein women with polycystic ovary syndrome / D. Panidis, D. Macut, K. Tziomalos [et al.] // Clinical Endocrinology. – 2013. – Vol. 78, № 4. – Р. 586–592.
3. Marshall J.C. Oll Women with PCOS should be treated for insulin resistance / J. C. Marshall, A. Dunaif // Fertil. Steril. – 2012. – Vol. 97, № 1. – Р. 18–22.
4. Чернуха Г. Е. Сравнительная эффективность применения инсулиносенситайзеров у больных с синдромом поликистозных яичников / Г. Е. Чернуха, В. Л. Шевцова, И. В. Блинова // Трудный пациент. – 2007. – № 1. – С. 27–33.
5. Cicero A. F. Metformin and its clinical use: new insights for an old drug in clinical pactice / A. F. Cicero, E. Tartaqni, S. Ertec // Arch. Med. Sci. – 2012. – Vol. 9, № 8. – Р. 907–917.
6. Effect of Metformin and rosiglitazone monotherapy on insulin-mediated hepatic glucose upkate and their relation to visceal fat in type 2 diabetes / P. Iozzo, K. Hallsten, V. Oikopen [et al.] // Diabetes Care. – 2003. – Vol. 26, № 7. – Р. 2069–2074.
7. Diamanti-Kandarakis E. Molecular mechanism of insulin resistance in polycystic ovary syndrome / E. Diamanti–Kandarakis, A. Papavasiliou // Trends in Molecular Medicine. – 2006. – Vol. 12, № 7. – Р. 324–332.
8. Dunaif A. Insulin Resistence and Polycystic Ovary Syndrome: Mechanism and Implications for Patogenesis / A. Dunaif // Endocrin. Reviews. – 1997. – Vol. 18, № 6. – Р. 774–800.
9. Nestler J. E. Metforminfor the treatment of the polycystic ovary syndrome / J. E. Nestler // New England Journal of Medicine. – 2008. – Vol. 358, № 1. – Р. 47–54.
10. Metformin therapy in polycystic ovary syndrome reduces hyperinsulinemia, insulin resistance, hyperandrogenemia, and systolic blood pressure,while facilitating normal menses and pregnancy / E. M. Velazquez, S. Mendoza, T. Hamer [et al.] // Metabolic. – 1994. – Vol. 43, № 5. – Р. 647–654.
11. Omran M. Metformin and Polycystic Ovary Syndrome / M. Omran // Int. J. of Healthy Sciences. – 2007. – Vol. 1, № 1. – Р. 75–80.
12. Should physicians prescribe metformin to women with polycystic overy syndrome (PCOS)? / L. Duranteau, P. Lefevre, N. Jeandidier [et al.] // Annales dendocrinologie. – 2010. – Vol. 74, № 1. – Р. 25–27.
13. Evidence-based and potential benefist of metformin in the polycystic ovary syndrome: a comprehensive review / S. Palomba, A. Falbo, F. Zullo, F. Orio // Endocr. Rev. – 2009. – Vol. 30, № 1. – Р. 1–50.
14. Neaqu H. Anti-Mullerian hormone- a prognostic marker for metformin therapy efficiency in the treatment of women with infertility and polycystic ovary syndrome / H. Neaqu, C. Cristescu // J. Med. Life. – 2012. – Vol. 5, № 4. – Р. 462–464.
15. Effect of metformin on serum insulin and anti mullerian hormone levels and on hyperandrogenism in patients with polycystic ovary syndrome / A. D. Nascimento, L. A. Silva Lara, A. C. Japur de Sa Rosa-e-Silva [et al.] // Gynecol. Endocrinology. – 2013. – Vol. 29, № 3. – Р. 246–249.
16. Criterial for Defining Polycystic Ovary Syndrome as a Predominantly Hyperandrogenic Syndrome: An Androgen Excess Society / R. Azziz, E. Carmini, D. Dewailly [et al.] // Guideline. – 2006. – Vol. 9, № 11. – Р. 4237–4245.
17. Khaodhiar L. Obesity and comorbid conditions / L. Khaodhiar, K. C. Mc Cowen, G. L. Blackburn // Clin. Cornerstone. – 1999. – Vol. 2, №1. – Р. 17–31.
18. Homeostasis model assessment: insulin resistance and β-cell function from fasting plasma glucose and insulin concentrations in man / D. R. Matthews, J. P. Hosker, A. S. Rudenski [et al.] // Diabetologia. – 1985. – Vol. 28, № 7. – Р. 412–419.
19. Morley J. E. Evaluating of assays available to measure free testosterone / J. E. Morley, P. Patrics, H. M. Perry // Metabolism Clinical Experimental. – 2002. – Vol. 51, № 5. – Р. 554–559.
20. Adams J. Brevalens of polycystic ovaries in women with anovulation and hirsutism / J. Adams, D. W. Polson, S. Franks // Br. Med. J. – 1986. – Vol. 293. – Р. 355–359.
21. Effect of Metformin on the clinical and metabolic assessment of women with polycystic ovary syndrome / L. F. Santana, M. F. de Sa´, R. A. Ferriani [et al.] // Gynecol. Endocrinol. – 2004. – Vol. 19, № 2. – Р. 88–96.
22. Effect of dose escalation of Metformin on clinical features insulin sensitivity and androgen profile in polycystic ovary syndrome / E. Jasmin, J. Glanvill, J. Barth, A. H. Balen // Eur. J. Obstet Gynecol Reprod. Biol. – 2011. – Vol. 156, № 1. – Р. 67–71.
23. Пат. 69387 Україна, МПК G01N 33/48, A61B 5/145. Спосіб діагностики синдрому полікістозних яєчників / Т. Л. Архипкіна, Л. П. Любимова, В. О. Бондаренко [та ін.] (UA) ; заявник і патентовласник Державна установа «Інститут проблем ендокринної патології ім. В. Я. Данілевського АМН України» (UA). – № u 201112514 ; заявл. 25.10.11; опубл. 25.04.12, Бюл. № 8. – 4 с.
24. Serum anti-Mullerian hormone as a predective marker of polycystic ovarian syndrome / S. Parco, C. Novelli, F. Vascotto, T. Princi // Int. J. Gen. Med. – 2011. – № 4. – Р. 759–763.
25. Systemic and local effect of metformin administration in patients with polycystic ovary syndrome(PCOS): relationship to the ovulatory response / S. Palomba, A. Falbo, T. Russo [et al.] // Hum. Reprod. – 2010. – Vol. 25, № 4. – Р. 1005–1013.

DIAGNOSTIC IMPORTANCE OF CYTOKINE EVALUATION IN BLOOD SERUM OF CHILDREN WITH IMPAIRED RENAL FUNCTION DUE TO ASPHYXIA AT BIRTH

Аuthors: Loboda A. M., Markevych V. E. 

Pages: 452-460

Аbstract

   

      The article examines the features of the balance of pro-and anti-inflammatory cytokines in full-term infants with impaired renal function due to asphyxia at birth. The study involved 252 full-term newborns with signs of kidney damage: 102 children who had severe asphyxia and 150 children with moderate asphyxia. The level of interleukin -1β, interleukin -6, tumor necrosis factor α and interleukin -10 in serum determined by on the 12nd , 78th  and 2530th days of life by ELISA.

     Interleukin-6 is the most informative cytokine; its level increased in the first days of life in case of impaired renal function and depended on the severity of asphyxia. Determination of interleukin-1β in serum is necessary for retrospective assess severity of the asphyxia in newborns at the end of neonatal period. Serum level of interleukin-10 is closely correlated with the levels of proinflammatory cytokines in the first days of life in children with impaired renal function due to asphyxia. Character of correlation depends on the prevalence of regulatory or suppressive processes.

         Key words: asphyxia, kidneys, newborn, interleukin, serum.

         This email address is being protected from spambots. You need JavaScript enabled to view it.">*This email address is being protected from spambots. You need JavaScript enabled to view it.

 

  

The full text

To viev the full text

References

1. Лебедева О. В. Цитокины как предикторы перинатальных осложнений у глибоко-недоношенных новорожденных / О. В. Лебедева // Вопросы практической педиатрии. – 2012. – № 2. – С. 9–13.
2. Струнин О. В. Цитокіновий профіль при корекції вроджених вад серця в умовах екстрокорпоральної перфузії у дітей до року життя / О. В. Струнин, С. В. Сеников, Л. Г. Князьков [та ін.] //Анестезіологія, реаніматологія та перфузіологія. – 2005. – № 1. – С. 49–52.
3. Александрова Ю. Н. Цитокины IL-1α, IL-2, IL-6, ФНО-α у новорожденных детей различного гестационного возраста с гипоксическим поражением ЦНС и менингитом: автореферат дис. канд. мед. наук: 14.01.08 / Ю. Н. Александрова; Российский государственный медицинский университет. – Москва, 2011. – 32 с.
4. Ємець І. М. Цитокіновий статус при складних вадах серця у новонароджених / І. М. Ємець, Г. М. Воробйова, Н. М. Руденко [та ін.] // Щорічник наукових праць Асоціації серцево-судинних хірургів України. – 2010. – Вип. 18. – С. 84–92.
5. Schmitz T. Interleukin-1beta, interleukin-18, and interferon-gamma expression in the cerebrospinal fluid of premature infants with posthemorrhagic hydrocephalus--markers of white matter damage? / T. Schmitz, A. Heep, F. Groenendaal [et al.] // Pediatr. Res. –2007. – Vol. 61. – P. 722–726.
6. Aly H. IL-1beta, IL-6 and TNF-alpha and outcomes of neonatal hypoxic ischemic encephalopathy / H. Aly, M. T. Khashaba, M. El-Ayouty [et al.] // Brain Dev. – 2006. – Vol. 28. – P. 178-182.
7. Nijboer C. Protecting the newborn brain: molecular mechanisms & therapeutic targets. – Rotterdam, 2008. – Р. 247.
8. Donnahoo K. K. Early renal ischemia with and without reperfusion activates NF-κB and increases TNF-α bioactivity in the kidney / K. K. Donnahoo, D. R. Meldrum, R. Shenkar [et al.] // J. Urol. – 2000. – Vol. 163, № 4. – Р. 1328–1332.
9. Ko G. J. Kidney-lung crosstalk in the critically ill patient / G. J. Ko, H. Rabb, H. T. Hassoun // Blood Purif. – 2009. – Vol. 28, № 2. – Р. 75–83.
10. Liu M. Acute kidney injury leads to inflammation and functional changes in the brain / M. Liu, Y. Liang, S. Chigurupati [et al.] // J. Am. Soc. Nephrol. –2008. – Vol. 19, № 7. – Р. 1360–1370.
11. Куликова Н. Ю. Клинико-функциональная характеристика ишемической нефропатии у доношенных новорожденных, находящихся в критическом состоянии (механизмы формирования, прогнозирование, ранняя диагностика, профилактика, коррекция). автореферат дис. доктора мед. наук: 14.01.08 / Н. Ю. Куликова; Ивановская гос. мед. академия. – Иваново, 2011. – 40 с.
12. Saliba E. Inflammatory mediators and neonatal brain damage / E. Saliba, A. Henrot // Biol. Neonate. – 2001. – Vol. 79, № 3–4. – P. 224–227.
13. Рябичева Т. Г. Новые наборы реагентов для определения интерлейкина-1бета и интерлейкина-6 / Т. Г. Рябичева, Н. А. Вараксин, Н. В. Тимофеева // Новости "Вектор-Бест" (информационный бюлле-тень). – 2007. – № 2 (44). – С. 13–15.
14. Вашурина Т. В. Гломерулярное воспаление и интерлейкин-10 [Електронний ресурс]/ Т. В. Вашурина, Т. В. Сергеева // Нефрология и диализ. – 2000. – № 3. Режим доступу: http://www.nephro.ru/magazine/article.php?id=5607 – Назва з екрану.
15. Таболин В. А. Актуальные вопросы перинатальной иммунологии / В. А. Таболин, Н. Н. Володин, М. В. Дегтярева [и др.] // Int. J. of Immunorehabilitation. –1997. – № 6. – С. 112–122.
16. Roos J. F. Diagnostic accuracy of cystatin C compared to serum creatinine for the estimation of renal dysfunction in adults and children – a meta-analysis. / J. F. Roos, J. Doust, S. E. Tett [et al.] // Clin. Biochem. – 2007. – Vol. 40, № 5–6. – Р. 383–391.
17. Vlassaks E. Fetal asphyctic preconditioning modulates the acute cytokine response thereby protecting against perinatal asphyxia in neonatal rats [Електронний ресурс]/ E. Vlassaks, E. Strackx, J. SH. Vles [et al.]// Journal of Neuroinflammation. – 2013. – Vol.10:14. Режим доступу: http://www.jneuroinflammation.com/content/10/1/14 –Назва з екрану.
18. Okazaki K. Elevation of cytokine concentrations in asphyxiated neonates / K. Okazaki, A. Nishida, M. Kato [et al.] – Neonatology. – 2006. – Vol. 89. – P. 183–189.

CLINICAL AND ANTI-INFLAMMATORY EFFECTIVENESS OF COMPLEX TREATMENT WITH ATORVASTATIN IN PATIENTS WITH CHRONIC OBSTRUCTIVE PULMONARY DISEASE

Аuthors: Prystupa L. N., Murenets N. A., Dominas V. M.,  Kyrychenko N. N., Shkandala A. Yu.

Pages: 461-465

Аbstract

   

      We determinated increase of C-reactive protein and proinflammatory cytokins (IL-6, IL-8, TNF-α) in patients with chronic obstructive pulmonary disease II and III stages. Application of atorvastatin in addition to basis therapy in patients with chronic obstructive pulmonary disease enhanced the level of anti-inflammatory treatment effectiveness by: faster decrease of C-reactive proteins and proinflammatory cytokins levels. With this data we can recommend statins to eliminate inflammation and slow the disease course.

      Key words: system inflammation, C-reactive protein, cytokines, chronic obstructive pulmonary disease, atorvastatin.

      This email address is being protected from spambots. You need JavaScript enabled to view it.">*This email address is being protected from spambots. You need JavaScript enabled to view it.

This email address is being protected from spambots. You need JavaScript enabled to view it.">

 

  

The full text

To viev the full text

References

1. Profiling serum biomarkers in patients with COPD: associations with clinical parameters / V. Pinto-Plata, J. Toso, K. Lee [et al.] // Thorax. – 2007. – Vol. 62, № 7. – P. 595–601.
2. Systemic inflammation and decline in lung function in a general population: a prospective study / A. W. Fogarty, S. Jones, J. R. Britton [et al.] // Thorax. – 2007. – Vol. 62. – P. 515–20.
3. Черняк Б. А. Воспаление при ХОБЛ: клиническое значение и возможности фармакотерапевтического контроля / Б. А. Черняк, Ф. И. Петровский // Атмосфера. Пульмонология и аллергология. – 2008. – № 1. – С. 23–28.
4. Vestbo J. Systemic inflammation and progression of COPD / J. Vestbo // Thorax. – 2007. – Vol. 62. – P. 469–470.
5. Wang C. Y. Pleiotropic effects of statin therapy: molecular mechanisms and clinical results / C. Y. Wang, P. Y. Liu, J. K. Liao // Trends Mol. Med. – 2008. – Vol. 14, № 1. – P. 37–44.
6. Pleiotropic effects of statins-clinical evidence / V. G. Athyros, A. I. Kakafika, K. Tziomalos [et al.] // Curr. Pharm. Des. – 2009. – Vol. 15, № 5. – P. 479–489.
7. Statin reduce all-cause mortality risk in COPD / Lies Lahousse, Daan W. Loth, Guy F. Joos [et al.] // Pulm Pharmacol Ther. – 2013. – Vol. 26, № 2. – P. 212–217.
8. Statins use in COPD parients is associated with a reduction in mortality: a national cohort study / C. M. M. Lawes, S. Thornley, R. Young [et al.] // Primary Care Respiratory Journal. – 2012. – Vol. 21, № 1. – P. 35–40.
9. Pearson Mike. Statins for COPD: a challenge to conventional beliefs? / M. Pearson // Primary Care Respiratory Journal. – 2012. – Vol. 21, № 1. – P. 5–7.
10. Statin use reduces decline in lung function / S. E. Alexeeff, A. A. Litonjua, D. Sparrow [et al.] // A. J. Respir. // Crit. Care Med. – 2007. – Vol. 176. – P. 742–747.
11. Statins may reduce episodes of exacerbation and the requirement for intubation in patients with COPD: evidence from a retrospective cohort study / A. I. Blamoun, G. N. Batty, V. A. DeBari [et al.] // Int. J. Clin. Pract. – 2008. – Vol. 62, № 9. – P. 1373–1378.
12. Simvastatin inhibits cigarette smoking-induced emphysema and pulmonary hypertension in rat lungs / J. H. Lee, D. S. Lee, E. K. Kim [et al.] // Am. J. Respir. Crit. Care Med. – 2005. – Vol. 172, № 8. – P. 987–993.
13. Usefulness of C-reactive protein and interleukin-6 as predictors of outcomes in patients with chronic obstructive pulmonary disease receiving pravastatin / T. M. Lee, M. S. Lin, N. C. Chang [et al.] // Am. J. Cardiol. – 2008. – Vol. 101, № 4. – P. 530–535.
14. The value of C-reactive protein as a marker of systemic inflammation in stable chronic obstructive pulmonary disease / F. Karadag, S. Kirdar, A. B. Karul [et al.] // Eur. J. Intern. Med. – 2008. – Vol. 19, № 2. – P. 104–108.
15. Reduction of morbidity and mortality by statins, angiotensin-converting enzyme inhibitors, and angiotensin receptor blockers in patients with chronic obstructive pulmonary disease / G. B. Mancini, M. Etminan, B. Zhang [et al.] // J. Am. Coll. Cardiol. – 2006. – Vol. 47, № 12. – P. 2554–2560.
16. Куницина Ю. Л. Противовоспалительная терапия при ХОБЛ / Ю. Л. Куницина, Б. И. Шмелев // Пульмонология. – 2003. – № 2. – С. 111–116.

FEATURES OF ECHOCARDIOGRAPHIC AND ELECTROCARDIOGRAPHIC PARAMETERS OF MЕСHANICAL DYSSYNCHRONY IN PATIENTS WITH HEART FAILURE COMBINED WITH TYPE 2 DIABETES

Аuthors: Vlasenko M.A., Rodionova Yu. V.

Pages: 466-473

Аbstract

   

      Myocardial dyssynchrony is important part of the etiopathogenesis of heart failure. Diagnostic criteria and methods for determining the dyssynchrony are not enough investigated. We analyzed various types of dyssynchrony and discussed modern parameters to diagnose them. The authors proposed a unified approach to identify dyssynchrony in patients with heart failure combined with diabetes mellitus type 2. There were determined the diagnostic sensitivity and specificity of the basic ECG and echocardiographic parameters in the diagnosis of dyssynchrony. We developed criteria to diagnose dyssynchrony using ECG and echocardiographic routine markers. The proposed diagnostic algorithm enables to diagnose dyssynchrony highly reliably.

         Key words: chronic heart failure, myocardial dyssynchrony, echocardiography, diabetes mellitus type 2.

        This email address is being protected from spambots. You need JavaScript enabled to view it.">*This email address is being protected from spambots. You need JavaScript enabled to view it.

 

  

The full text

To viev the full text

References

1. Foley P. W. X. What is treatment success in cardiac resynchronizaion therapy? / P. W. X. Foley, F. Leyva, M. P. Frenneaux // Europace. – 2009. № 11 (suppl. 5). – P. 58–65.
2. States Golberg R. J. B. Epidemiology of decompensated heart failure in a single community in the northeastern / R. J. B. States Golberg // United American J. Cardiology. 2009. – Vol. 104. – P. 377–382.
3. Cheng S. Advances in the epidemiology of heart failure and left ventricular remodeling / S. Cheng, R. S. Vasan // Circulation. – 2011. – Vol. 124. – P. 516–519.
4. Cohen-Solal A. Heart failure and diabetes mellitus: Epidemiology and management of an alarming association / A. Cohen-Solal, F. Beauvais, D. Logeart // Journal of Cardiac Failure. – 2008. – Vol. 14(7). – P. 615–625.
5. Kass D. A. An epidemic of dyssynchrony: but what does it mean? / D. A. Kass // Journal of the American College of Cardiology. – 2008. – Vol. 51. – P. 12–17.
6. Ревишвили А. Ш. Сердечная ресинхронизирующая терапия в лечении хронической сердечной недостаточности / А. Ш. Ревишвили, Н. М. Неминущий // Вестник аритмологии. – 2007. – № 48. – С. 45–46.
7. Left ventricular dyssynchrony predicts response to cardiac resynchronization therapy / D. Knappe, A. C. Pouleur, A. M. Shah [et al] // Circ. Heart Fail. – 2011. № 4. – P. 33–40.
8. Сердечная ресинхронизирующая терапия: некоторые аспекты патофизиологии диссинхронии и изменений гемодинамики / М. В. Киютина, И. Г. Гордеев, И. В. Самойленко [и др.] // Российский кардиологический журнал. – 2012. № 2 (94). – C. 79–84.
9. Национальные рекомендации ВНОК и ОССН по диагностике и лечению ХСН (третий пересмотр) // Сердечная недостаточность. – 2010. № 11. – С. 3–62.
10. Responders to cardiac resynchronization therapy with narrow or intermediate QRS complexes identified by simple echocardiographic indices of dyssynchrony: the DESIRE study / S. J. Cazeau, J. C. Paul Daubert [et al.] // European Journal of Heart Failure. – 2008. № 10. – P. 273–280.
11. Cardiac resynchronization therapy tailored by echocardiographic evaluation of ventricular asynchrony / M. V. Pitzaliz, M. Iacoviello, R. Romito [et al.] // J. Am. Coll. Cardiol. – 2002. № 40. – P. 1615¬1622.
12. Three-dimensional vectorcardiography to predict CRT-responder / W. Koglek, J. Brandl, A. Oberbichler [et al.] // Herzschrittmacherther Elektrophysiol. – 2006. – Vol. 17 (1). – P. 128–136.
13. Improvement of left ventricular function after cardiac resynchronization therapy is predicted by tissue Doppler imaging echocardiography / M. Penicka, J. Bartunek, B. De Bruyne [et al.] // Circulation. – 2004. – Vol. 109 (8). – P. 978–983.
14. Гублер Е. В. Вычислительные методы анализа и распознавания патологических процессов. / Е. В. Гублер. – М. : Медицина, 1978. – 296 с .
15. Зосимов А. М. Дисертаційні помилки : монографія, 4-те вид., допов. і випр. / А. М. Зосимов, В. П. Голік. – Х. : ІНЖЕК, 2009. – 264 с.
16. Генкин А. А. Применение последовательного статистического анализа для дифференциальной диагностики и использование этого метода для различения двух форм ожоговой болезни / А. А. Генкин, Е. В. Гублер // Применение математи-ческих методов в биологии. – 1964. – Вып. I. – С. 174–176.