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Conclusion terms of gestation 22-27 weeks, it should be possible to prolong
If you move to a common denominator of all mortality rates pregnancy, at least 8 days, since the only way to reduce the overall fetuses and newborns with premature rupture of membranes, in mortality rate from 83.3 to 19.2 %.
References:
1. Premature V. M. Birth/V. M. Sidelnikova//Materials of the V Russian forum "Mother and child". - M., 2003. - P. 320.
2. Caughey A. B. Contemprorary Diagnosis and Management of Preterm Premature Rupture of Membranes/A. B. Caughey, J. N. Robinson, E. R. Norwiz//Rev. Obstet. Gynecol. - 2008. - Vol. 1, № 1. - P. 11-12.
Israilov Radjab Israilovich, MD Professor, Tashkent Medical Academy E-mail: rpam89@mail.ru Tursunov Khasan Ziyaevich, MD Professor, Tashkent Medical Academy E-mail: tursunov.hasan@bk.ru Eshbaev Erkin Abdukhalimovich, Chair assistant, Tashkent Medical Academy
Morphological changes of newborns coronary vessels in preeclampsia in mothers
Abstract: In this work we made heart measuring, tissue measuring of coronary vessels and their walls in newborns born from mothers with preeclampsia. Heart weight is decreased when the edematous form of preeclampsia is present. Heart weight is increased with vessels number multiplication when the hypertensive form of preeclampsia is present. Walls of small arteries (SA) and arterioles (Ar) tunica media area is increased in 1.7 times, a major artery (MaA) in 1.2 times and a middle artery (MiA) in 1.3 times in comparison with the control values. The wall thickness and sectional area of the tunica media, the size of the lumen of the coronary arteries of all sizes have changed ambiguously. Thus in MaA and MiA the wall thickness and sectional area of the tunica media is increased, and in SA and Ar is decreased.
Keywords: preeclampsia, heart, newborn, coronary vessels, tissue measuring.
Relevance of the topic
Changes in a woman's body in pre-eclampsia, studied much better than the body of children born to mothers with a history of preeclampsia during pregnancy. The mother base body pathologies of the cardiovascular system of a spasm ofblood vessels, reduction in circulating blood volume, a change in blood clotting and flow, disturbance of microcirculation. The defeat of the inner lining of vessels — the endothelium leads to increase vascular permeability and exudation of fluid into the tissues, the yield change, viscosity and clotting, susceptibility to blood clots in the bloodstream. Furthermore, in preeclampsia there is a weakening of the heart and a reduction in the circulating blood. All this leads to a significant reduction ofblood supply to tissues with the development of degenerative changes in them up to tissue destruction. The organs most sensitive to the lack ofblood supply, are the heart, kidneys, liver and brain [1; 2; 5]. When preeclampsia pregnant structural and functional abnormalities in the internal organs: violation ofmicrocirculation, blood clots, degenerative changes in parenchymal cells, the development of punctate or small focal hemorrhage, increased intracranial pressure.
The placenta, mostly made up ofvessels that underwent characteristic for preeclampsia change, can not cope with its core function of ensuring the exchange of oxygen and nutrients between mother and fetus, causing the defeat of the cardiovascular system of the fetus and the intrauterine and the formation of a heart, and cardiovascular system of the fetus.
Objective. In order to identify pathological changes in coronary vessels by us laws hearts studied 27 infants died in the neonatal period born to mothers with preeclampsia.
Material and methods
They were measured and separately weighing the modified method [3; 4; 9]. Heart filmed as a whole, and after the division into departments. Pieces of myocardium was excised for histological examination in accordance with the existing guidelines Avtandilov G. G. The material was fixed in 10 % neutral formalin and embedded in paraffin. Histological sections stained with hematoxylin and eosin, by van Gieson. To determine the density of myocardial blood vessels counted in their number to 1.72 mm 2 cut area not less than 20 sites. Coronary artery divided major artery (MaA) (more than 115 microns), middle artery (MiA) (35-115 microns), small arteries (SA) (25-35 microns) and arterioles (Ar). Measurements were carried out screw ocular micrometer MOV-1-15*. In each vessel was determined diameter, width and thickness of the wall of the lumen [6; 7; 8]. Media cross-sectional area was calculated by the formula: 0.785 (ab-a1b1), where a, b and a1 and b1 — large and small, respectively, the outer and inner diameters of the shell. Also, in the media wall of the coronary vessels to count the number of smooth muscle cells. All digital material was subjected to statistical analysis. To determine the reliability of the data used t-test.
Results of the study
The results showed that the presence of maternal edematous forms preeclampsia neonatal noted a slight decrease in heart weight, on average to 23.4 ± 1.3 g. (rate of 26.6 ± 1.5 g.) of ventricular wall thickening due to edema endocardium, pericardial and myocardial interstitium. Hypertensive form of preeclampsia was accompanied by a narrowing of the lumen of the coronary vessels,
increase in heart weight (29.8 ± 1.72 g.) due to compaction and low ventricular hypertrophy infarction. The increase in heart weight was associated with vascular infarction area pronounced changes. What confirmed the data of counting the number of vessels on the standard cut-off area, attesting to the fact that their number increased from 6.2 ± 0.3 to 8.7 ± 0.4 (r < 0.001).
The results are set morphometric study showed, that the wall thickness of the coronary arteries we selected all calibres increased that increasing combined cross-sectional area tunica vessel walls (see table). In particular, in the SA and Ar is increased by 1.7 times compared to control values in MaA — 1.2 times, MiA — 1.3 times, respectively. It was found that the number of smooth muscle cells (SMC) in medium-sectional area of SA increased from 4.6 ± 0.3 to 6.5 ± 0.4 (p < 0.05), the area of their nuclei decreased from 20.4 ± 0.7 to 18. 9 ± 0.6 mcm 2, and the volume — with 36.7 ± 3.4 to 33.4 ± 2.7 mcm 3 (p < 0.05), indicating pycnosis both nuclei and cytoplasm SMC due to interstitial edema vascular walls. In contrast to the wall thickness of the shell and medium-
The results of the morphological study of arterial wall based on caliber vessels showed that all satellites represented by cell wall fiber components and layers. Thus, the endothelial layer is in one place only a few hyperchromatic cells. Basal membrane is not determined SMC have several rows, which are scattered into separate beams and elongate and are composed of spindle-shaped cells (Fig. 2a). Adventitia edematous, it loosened and decomposed fiber, has a unit pyknotic
sectional area, the amount of data vascular lumen changed differently. Thus, in MaA and MiA it was increased, and SA and Ar it was decreased. The latter was accompanied by the strengthening of the internal elastic membrane folding and rounding of endothelial cells of the intima, which in the form of a picket fence lined the lumen of blood vessels, indicating their compression narrowing due to edema of perivascular adventitia (Fig. 1a). Along with the above described modifications of the circular muscle of arteries in the heart newborns to mothers with preeclampsia in the arterial wall bundle SMC arranged unevenly in one end wall of the vessel they are flattened, in other thick with rounded nuclei (Fig. 1b), wherein in the control material indicated uniform the location of the SMC. Thus in some arterial vessels, these cells in the inner shell housed in several rows (Fig. 1c), observed in other vessels, and loosening of uneven thickening of elastic fibers (Fig. 1d). Thus, it may be noted that in the arterial wall with well-developed smooth muscle cells, elastic fibers are thin and discontinuous, where the elastic fibers have a thick layer, SMC thin and spindly.
connective tissue cells. Medium type Artery somewhat expanded endothelial layer is well developed, it mostly flattened cells, only in certain areas defined desquamation. Smooth muscle layer is thick kind of densely arranged in two rows, their nuclei round and oval shapes, mostly hyperchromatic (Fig. 2b). Adventitia extended due to the accumulation of the protein in its homogeneous mass, which is apparently the result of edema and plasmorrhages. Small arteries and arterioles
Fig.1. Adaptive changes of the coronary arteries of the dead children from mothers with preeclampsia: a — the average compression narrowing artery; b — uneven thinning of the walls of small arteries; c — tonic contraction of the middle artery; d — irregular thickening of the major artery elastic membranes. Painting: a, b, c — hematoxylin and eosin; d — by Weigert. Resolution: ocular 10, objective 90
are narrowed due to the disorganization of the fibrous structures of the inner layers ofcells hypertrophy and adventitial edema. Wall SA is represented by two endothelial cells thick basement membrane and a
layer ofSMC, and edematous adventitia (Fig. 2c). Especially narrowed arterioles due to hypertrophy and endothelial hyperchromasia, SMC and pronounced swelling of the adventitia (Fig. 2d).
Fig. 2. Pathological changes of the coronary arteries of all sizes of children born to mothers with preeclampsia: a — endothelial desquamation, loosening SMC major artery; b — the expansion of the lumen, the average plasmorrhages adventitia artery; c — the narrowing of the lumen of small arteries; d — a spasm of arteriolar lumen. Painting: hematoxylin and eosin. Resolution: ocular 10, objective 90
Conclusions
Edematous form accompanied by a decrease in preeclampsia, hypertensive form — an increase in heart mass due to ventricular hypertrophy, in which the part vessels mentioned increase in the number of them in a standard cut-off area.
Morphometric parameters of middle membrane walls of small arteries and arterioles increased by 1.7 times, a major artery — 1.2 times, the average artery — in 1.3 times in comparison with the control values.
The wall thickness and sectional area ofthe middle shell, the size of the lumen of the coronary arteries of all sizes have changed neod-notipno. Thus, in MaA and MiA increased, and SA and Ar decreased.
Preeclampsia mother accompanied by the development of pathological changes in the coronary arteries of all sizes: in the MaA noted desquamation endothelial loosening MMC; in MiA endothelial hypertrophy and MMC, as well as plasmorrhages adventitia; in SA and Ar narrowing by a hypertrophy of the cells and adventitial edema.
References:
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3. Бородина Г. Н. Органометрические изменения сердца при формировании его структур на поздних этапах пренатального и всех этапах постнатального онтогенеза//Современный мир, природа и человек: межвузовский сборник науч. работ с материалами трудов участников V Международной конф. - Томск, 2011. - Т. 2, № 1. - С. 71-72.
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8. Косоуров А. К., Матюшечкин С. В. Посмертное и прижизненное изучение сердца человека в пренатальном онтогенезе//Мор-фология. - 2002. -Т. 122, № 6. - С. 31-34.
9. Лузин В. И., Шутов В. Ю., Шутова Е. В. Методика морфометрии сердца лабораторных животных//Украшський морфолопчний альманах. - 2013. - Т. 11, № 3. - С. 56-58.
Kayumov Abdurakhman Abdumavlyanovich, Ph. D.,
Karimov Khamid Yakubovich, MD, professor,
Boboev Kadirzhon Tuhtabaevich, MD, Research Institute of Hematology and Blood Transfusion of the Ministry of Health of Uzbekistan E-mail: atabek2004@mail.ru
Role of polymorphism RS1800629 gene proinflammatory cytokine TNF-a in the development and clinical course of leukemia
Abstract: To evaluate the significance of genotypic variants of the poly-morphism rs1800629 gene pro-inflammatory cytokine TNF-a in the development of leukemia and associating them with complications of viral infections Epstein-Barr. Thus, we found statistically significant differences in the prevalence of genotypes of rs1800629 polymorphic variant in a gene TNFa between subgroups of the study sample. Not been identified genotype demonstrated significantly adverse effect with respect to the risk of EBV. Studies have shown that heterozygous polymorphism was more frequent (p = 0.01) in patients with hematological malignancies.
Keywords: leukemia, polymorphism 308 G/A gene TNF-a, Epstein-Barr virus.
Relevance
It is known that functional polymorphisms in the gene for pro-inflammatory cytokine TNF-a can significantly affect their production and therefore, the severity and chronicity of infection with EBV. There are many studies about role of polymorphisms of genes INF-y, TNF-alpha, IL-1 RA. in various diseases. The main mediator of inflammation is a TNF-a, stimulating immune system in many of its links, controls the expression of many cytokines and growth factors. An increased TNF-alpha production by B-lympho-cytes in response to the action ofEBV [1; 3]. M. S. Wu et al. studies, showed the presence of significant association of allele A at position — rs1800629 gene of EBV-associated gastric carcinoma [2; 4].
Increased secretion of inflammatory factors associated with latent Epstein-Barr virus (EBV) infection and pathology of EBV-associated diseases; However, knowledge of the inflammatory response and its biological significance for EBV lytic cycle remains elusive [4; 7]. BZLF1 the Early activator of proinflammatory transcription factor inhibits tumor necrosis factor alpha (TNF-alpha) by binding to the TNF-alpha promoter, and preventing the activation of NF-kV. BZLF1A207-210 deletion mutant 4 amino acids (aa) in the binding of protein-protein domain was not capable of inhibiting proinflammatory factors TNF-a and interferon-gamma (IFN-y) and reduced viral DNA replication with full transcriptional activity during lytic gene expression of EBV. Depletion of TNF-a restored virus replication mediated BZLF1A207-210. Furthermore, the combination BETA-a- and y-IFN neutralizing antibodies recovered BZLF1A207-210-mediated replication of the virus, indicating that the antiviral response is attenuated BZLF1 aid optimal lytic replication primarily by inhibiting TNF-alpha and IFN-y secretion in during the lytic cycle. These results indicate that EBV BZLF1 attenuates pro-inflammatory responses to facilitate viral replication [5; 6; 8].
However, information about the role of cytokine gene polymorphism in the development of leukemia and associating them with complications of viral infection Epstein -Barr virtually nonexistent.
Objective
To evaluate the significance of genotypic variants of the polymorphism rs1800629 gene pro-inflammatory cytokine TNF-a in the development of leukemia and associating them with complications of viral infections Epstein-Barr.
Materials and Methods
The object and subject of the study were patients with leukemia (CML and AL), DNA samples from patients and 110 healthy volunteers, TNF-a gene (6r21.3) nucleotide substitution G > A at position -308.
The study included 114 patients with AML and CML in age from 15 to 79 years, the median age was 37.8 ± 2.34 years, observed on the basis of clinic Institute of Hematology and Blood Transfusion of the Ministry of Health of Uzbekistan. The diagnosis of leukemia is based on a set of clinic, clinical, laboratory and instrumental data according to WHO criteria.
Isolation of DNA from nuclei of lymphocytes was carried out according to standard methods with some modifications (Sambrook et al., 1989). The concentration and purity of the isolated DNA were estimated by measuring the optical density of the DNA-containing solutions at a wavelength of 260 nm. and 280 nm. on a spectro-photometer against TE NanoDrop 2000 (USA). Genotyping polymorphism 308G > A TNF-a gene was performed by polymerase chain reaction on a programmable thermal cycler CG-1-96 «Cor-bett Research» (Australia) in 2720 and "an Applied Biosystems" (USA), with NGOs "Liteh" test systems (Russia) according to the manufacturer's instructions.
