Effect of lncRNA H19 on the apoptosis of vascular endothelial cells in arteriosclerosis obliterans via the NF-κB pathway.

OBJECTIVE: To explore the effect of long non-coding ribonucleic acid (lncRNA) H19 on the apoptosis of vascular endothelial cells in arteriosclerosis obliterans (ASO) via the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathway. PATIENTS AND METHODS: Human umbilical vein endothelial cells (HUVECs) were cultured, and lncRNA H19 was inhibited by Si-H9 and overexpressed by H19-OE. Then, the apoptosis rate was detected by flow cytometry, the target of lncRNA H19 was detected by dual luciferase reporter gene assay, and changes in the protein level were determined via Western blotting (WB). RESULTS: LncRNA H19 exhibited high expression in serum of patients with ASO, and compared with that in congeneric normal mice, the expression of lncRNA H19 in ASO mice rose. Besides, the proliferation ability of cells transfected with H19-OE was markedly strengthened, and H19-OE treatment could down-regulate the expression level of the apoptin, active cysteinyl aspartate-specific proteinase-3 (Caspase-3). In addition, lncRNA H19 bound to micro ribonucleic acid (miR)-19a in a targeted way. After lncRNA H19 was overexpressed, the expression of the NF-κB pathway key factors, p38 and p65, were notably increased, and the nuclear translocation of p65 was significantly enhanced after transfection with miR-19a. CONCLUSIONS: LncRNA H19 promotes the proliferation of vascular endothelial cells in ASO and inhibits the apoptosis of them via the NF-κB pathway.

MicroRNA-125b Affects Vascular Smooth Muscle Cell Function by Targeting Serum Response Factor.

BACKGROUND/AIMS: Increasing evidence links microRNAs to the pathogenesis of peripheral vascular disease. We recently found microRNA-125b (miR-125b) to be one of the most significantly down­regulated microRNAs in human arteries with arteriosclerosis obliterans (ASO) of the lower extremities. However, its function in the process of ASO remains unclear. This study aimed to investigate the expression, regulatory mechanisms, and functions of miR-125b in the process of ASO. METHODS: Using the tissue explants adherent method, vascular smooth muscle cells (VSMCs) were prepared for this study. A rat carotid artery balloon injury model was constructed to simulate the development of vascular neointima, and a lentiviral transduction system was used to overexpress serum response factor (SRF) or miR-125b. Quantitative real­time PCR (qRT­PCR) was used to detect the expression levels of miR­125b and SRF mRNA. Western blotting was performed to determine the expression levels of SRF and Ki67. In situ hybridization analysis was used to analyze the location and expression levels of miR-125b. CCK-8 and EdU assays were used to assess cell proliferation, and transwell and wound closure assays were performed to measure cell migration. Flow cytometry was used to evaluate cell apoptosis, and a dual-luciferase reporter assay was conducted to examine the effects of miR­125b on SRF. Immunohistochemistry and immunofluorescence analyses were performed to analyze the location and expression levels of SRF and Ki67. RESULTS: miR-125b expression was decreased in ASO arteries and platelet-derived growth factor (PDGF)-BB-stimulated VSMCs. miR-125b suppressed VSMC proliferation and migration but promoted VSMC apoptosis. SRF was determined to be a direct target of miR-125b. Exogenous miR-125b expression modulated SRF expression and inhibited vascular neointimal formation in balloon-injured rat carotid arteries. CONCLUSIONS: These findings demonstrate a specific role of the miR-125b/SRF pathway in regulating VSMC function and suggest that modulating miR-125b levels might be a novel approach for treating ASO.

Mir-22-3p Inhibits Arterial Smooth Muscle Cell Proliferation and Migration and Neointimal Hyperplasia by Targeting HMGB1 in Arteriosclerosis Obliterans.

BACKGROUND: Aberrant vascular smooth muscle cell (VSMC) proliferation and migration contribute to the development of vascular pathologies, such as atherosclerosis and post-angioplasty restenosis. The aim of this study was to determine whether miR-22-3p plays a role in regulating human artery vascular smooth muscle cell (HASMC) function and neointima formation. METHODS: Quantitative real-time PCR (qRT-PCR) and fluorescence in situ hybridization (FISH) were used to detect miR-22-3p expression in human arteries. Cell Counting Kit-8 (CCK-8) and EdU assays were performed to assess cell proliferation, and transwell and wound closure assays were performed to assess cell migration. Moreover, luciferase reporter assays were performed to identify the target genes of miR-22-3p. Finally, a rat carotid artery balloon-injury model was used to determine the role of miR-22-3p in neointima formation. RESULTS: MiR-22-3p expression was downregulated in arteriosclerosis obliterans (ASO) arteries compared with normal arteries, as well as in platelet-derived growth factor-BB (PDGF-BB)-stimulated HASMCs compared with control cells. MiR-22-3p overexpression had anti-proliferative and anti-migratory effects and dual-luciferase assay showed that high mobility group box-1 (HMGB1) is a direct target of miR-22-3p in HASMCs. Furthermore, miR-22-3p expression was negatively correlated with HMGB1 expression in ASO tissue specimens. Finally, LV-miR-22-3p-mediated miR-22-3p upregulation significantly suppressed neointimal hyperplasia specifically by reducing HMGB1 expression in vivo. CONCLUSIONS: Our results indicate that miR-22-3p is a key molecule in regulating HASMC proliferation and migration by targeting HMGB1 and that miR-22-3p and HMGB1 may be therapeutic targets in the treatment of human ASO.

The Association between Polymorphism of CARD8 rs2043211 and Susceptibility to Arteriosclerosis Obliterans in Chinese Han Male Population.

BACKGROUND AND AIMS: Cholesterol crystals have been shown to cause inflammation. As a response to cholesterol crystal accumulation, the NLRP3 inflammasome is activated to produce IL-1ß which eventually leads to atherosclerotic lesions. As a part of innate immunity, CARD8 is involved in the modulation of above mentioned inflammatory activities. The primary objective of this study was to investigate the association between polymorphism of CARD8 rs2043211 and susceptibility to arteriosclerosis obliterans (ASO) in Chinese Han male population. METHODS: 758 male arteriosclerosis obliterans patients and 793 male controls were genotyped for rs2043211 with the TaqMan allele assays. Fasting blood-glucose (FBG), total cholesterol (TC), triglycerides (TG), urea nitrogen, creatinine, Serum uric acid, high density lipoprotein, low density lipoprotein, ALT, AST, and IL-1ß in the blood were detected for all subjects. Clinical data were recorded to analyze the genotype-phenotype. Independent samples t-test was used to perform the comparisons between two groups. Odds ratios (ORs) with 95% confidence intervals (CIs) were calculated to measure the strength of relationship in the genotype distribution and allele frequencies between patients and controls. The analysis of variance was used for a genotype-phenotype analysis of the ASO patients. RESULTS: The genotypic and allelic frequencies in the ASO group were significantly different from that in the control group (P = 0.014 by genotype, P = 0.003 by allele). Those carrying the genotype TT had a higher risk for ASO than those carrying the genotype AA (OR = 1.494, 95%CI1.131-1.974, P = 0.005).The difference was also significant after the adjustment for the history of smoking, TC, LDL, fasting blood glucose, systolic blood pressure and BMI(OR = 1.525, 95%CI1.158-2.009, P = 0.003). CONCLUSION: Our finding suggests that the polymorphism of CARD8 rs2043211 is probably associated with the development of ASO in Chinese Han male population.

[PROCURING OF ІNTRAOPERATIVE HEMOSTASIS IN REVASCULARIZATION INTERVENTIONS].

Results of the hemostasis conduction in conditions of revascularization in 106 patients, оperated on for atherosclerotic affection of aorta and the main arteries of the lower extremities, were adduced. Syndrome of hypercoagulation of traumatic stage of surgical intervention in early postoperative period is developing due to thrombinemia on background of a fibrinolytic system depression. There was proved a necessity to impact on thrombin-fibrinous factor (factor ІІа) of hemocoagulant cascade by application of nonfractionized heparins immediately after conclusion of operative intervention with thromboprophylaxis prolongation, using low-molecular heparins (impact on Ха factor) in accordance to the branch standards.

[Correlation between autophagy and polarization of macrophages in atherosclerosis plaque in arteriosclerosis obliterans amputees].

This study was designed to investigate the correlation between autophagy and polarization of macrophages in atherosclerosis (AS) plaque in arteriosclerosis obliterans amputees. Femoral artery specimens from arteriosclerosis obliterans amputees were performed hematoxylin and eosin (HE) staining, oil red O and immunofluorescence staining to observe the morphology of atherosclerotic plaque, phenotype of macrophages and autophagy in plaque; using real-time quantitative RT-PCR technology to detect the mRNA level of M1 and M2 type markers in arterial tissue; to analyze polarized signal pathway and autophagy protein levels in macrophages by Western blotting. Arterial specimens staining showed obvious lipid deposition and obvious infiltration of amount of foam cells and inflammatory cells. Macrophages were mainly expression M1 type in percentage in fibrous plaque. Although both M1 and M2 macrophages were upregulated in atheromatous plaque, the increase was dominant in M2 type in percentage. The level of autophagy was significantly higher in the atheromatous plaque than that of fibrous plaque. The expression of tumor necrosis factor- α (TNF-α), monocyte chemotactic protein-1 (MCP-1), inducible nitric oxide synthase (iNOS), interleukin-6 (IL-6) and interleukin-12 (IL-12) mRNA was significantly higher in fibrous plaque than that of atheromatous plaque (P < 0.01 or 0.05), and arginase-1 (Arg-1), transforming growth factor-ß (TGF-ß), CD163 and interleukin-10 (IL-10) mRNA was significantly lower than that in atheromatous plaque (P < 0.01). The levels of p-STAT1 and NF-κB were significantly increased in fibrous plaque (P < 0.01), while p-STAT6 expression was significantly increased in atheromatous plaque (P < 0.01). The level of LC3-II was significantly higher in atheromatous plaque than that in fibrous plaque (P < 0.01). Macrophages in early atherosclerotic plaque were induced to M1 type through p-STAT1/NF-κB pathway and expressed moderate levels of autophagy; while macrophages in advanced plaques were induced to polarization of M2 type through p-STAT6 pathway. M2 macrophages expressed a higher level of autophagy than M1 macrophages.

[[Impact of plestazol preparation on hyperplasia of inter vascular layer in the patients, suffering obliterating atherosclerosis of the lower extremities arteries after reconstructive operations].]

In the clinic 60 patients were examined, in whom reconstructive operations on the main arteries were performed for obliterating atherosclerosis (OA) of the lower extremities vessels. Efficacy of impact of Plestazol (in a 200 mg/day dose) on neointima hyperpla- sia was studied. Clopidogrel (75 mg/day) was administered to patients of comparative group. Effective criteria for estimation of the migration-proliferation disorders state in endothelial dysfunction are concentration of the intercellular adhesion molecules (ICAM) and the basic factor of the fibroblasts growth (FGFb); morphological disorders in hyperplastic reactions of neointima - determination of thickness of "intima-media" complex in accordance to the ultrasound duplex scanning data. There was established, that Plestazol constitutes an effective disaggregate preparation, positively impacting decelerating reaction of neointima hyperplasia, including, deceleration of the smooth- muscle cells migration into subendotelial layer in the formation zone of the femoro- popliteal shunt distal anastomosis.

[Comparison of the clinical efficacy of endovascular reconstruction versus bypass surgery for transatlantic inter-society consensus II C/D femoropopliteal artery lesion resulted from arteriosclerosis obliterans].

OBJECTIVE: To study the clinical effects of endovascular reconstruction versus bypass surgery for TASC II(trans-atlantic inter-society consensus II) C/D femoropopliteal artery lesion resulted from arteriosclerosis obliterans. METHODS: One hundred and three patients(119 limbs)accepted bypass surgery or endovascular therapy for TASCII C/D femoropopliteal artery lesion between January 2002 and December 2012 at our institution were retrospectively assessed.All the patients were diagnosed with arteriosclerosis obliterins, and all their Rutherford classifications were from 2 to 5 degrees.Among them there were 71 limbs treated by endovascular reconstruction and the other 48 limbs were treated with bypass surgery.We evaluated the short term clinical effect according to the condition when patients left the hospital, and evaluated the long term clinical effect according to the results of the patients' latest follow-up in 2014. Their clinical data before treatment, complication rates, death rates, hospital stays, short term and long term effects, reoperation rates, 1 to 10 years primary and secondary accumulative patency rates and limb salvage rates were compared. RESULTS: There was no significant difference between the bypass group and the endovascular group on the mean age and ankle brachial index before treatment [(67.1 ± 7.1) years(51 to 80 years) vs. (68.0 ± 9.4) years (49 to 91 years), P=0.561;(0.41 ± 0.23) vs. (0.40 ± 0.26), P=0.928]. There were more TASCII D patients in the bypass group than those in the endovascular group (P<0.001), and the rutherford classification was higher in the endovascular group than that in the bypass group. The difference in the mean follow-up between the bypass group and the endovascular group was not significant [(41.7 ± 23.6) months vs. (59.5 ± 41.6) months, P=0.065]. Five peri-operative complication cases occurred in the bypass group, including 2 cases of acute thrombosis,1 case of infection and 2 cases of heart failure, and only 1 complication case occurred in the endovascular group that was heart failure.The complication rate was higher in the bypass group than that in the endovascular group [10.4% vs. 1.4%, P=0.039]. And there was no death in both the groups.Compared with the endovascular group, the bypass group had a longer hospital stays [(13.2 ± 4.7) d vs.(6.5 ± 3.1) d, P<0.001], a higher reoperation rate (58.3% vs.31.0%,P=0.003), a better short term, obvious, and effective rate (25.0% vs. 9.9%, P=0.027), a worse long term deterioration rate (37.5% vs. 18.3%, P=0.019) and higher 1 to 10 years primary and secondary accumulative patency rates(P=0.001, P=0.001).There was no significant difference between the two groups on the increase of ankle brachial index [(0.34 ± .28) vs. (0.31 ± 0.23), P=0.371], and short term and long term total effective rates (89.6% vs.84.5%, P=0.426; 45.8% vs. 56.3%, P=0.260), and limb salvage rate (83.3% vs.94.4%, P=0.051). CONCLUSION: Endovascular therapy is a safe, effective and minimally invasive therapy for TASCII C/D femoropopliteal artery lesion resulted from arteriosclerosis obliterans.

Investigating the Role of the Posttranscriptional Gene Regulator MiR-24- 3p in the Proliferation, Migration and Apoptosis of Human Arterial Smooth Muscle Cells in Arteriosclerosis Obliterans.

AIMS: To explore the expression of miR-24-3p in human arteries with arteriosclerosis obliterans (ASO) as well as the role of miR-24-3p in the pathogenesis of ASO. METHODS: We used quantitative real-time PCR (qRT-PCR) and in situ hybridization to monitor miR-24-3p expression in human arteries. To investigate the effect of miR-24-3p on human arterial smooth muscle cells (HASMCs), we applied cell counting and EdU assays to monitor proliferation and transwell and wound healing assays to investigate migration and flow cytometry to investigate apoptosis. Furthermore, we applied 3'-untranslated region (3'-UTR) luciferase assays to investigate the role of miR-24-3p in targeting platelet-derived growth factor receptor B (PDGFRB) and c-Myc. RESULTS: MiR-24-3p was mainly located in the media of arteries and was downregulated in ASO arteries compared with normal arteries. Platelet-derived growth factor BB (PDGF-BB) treatment reduced the expression of miR-24-3p in primary cultured HASMCs. MiR-24-3p mimic oligos inhibited the proliferation and migration, and promotes apoptosis of HASMCs. Our 3'-UTR luciferase assays confirmed that PDGFRB and c-Myc were targets of miR-24-3p. CONCLUSION: The results suggest that miR-24-3p regulates the proliferation and migration of HASMCs by targeting PDGFRB and c-Myc. The PDGF/miR-24-3p/PDGFRB and PDGF/miR-24-3p/c-Myc pathways may play critical roles in the pathogenesis of ASO. These findings highlight the potential for new therapeutic targets for ASO.

Netrin-1 with stem cells promote angiogenesis in limb ischemic rats.

BACKGROUND: Recent findings have elucidated that netrin-1 has ability of promoting angiogenesis besides the functions in nervous system. Autologous mesenchymal stem cells (MSCs) transplantation is now proved to be an effective method to treat peripheral arterial disease. However there are still many patients who cannot complete full treatments. Therefore it is necessary to improve the effectiveness. This study estimated the curative effects in chronic limb ischemia when MSCs allied with netrin-1. MATERIALS AND METHODS: Thirty-six rats were made into chronic limb ischemia models. They were randomly assigned to four groups, netrin-1 + MSCs group (treated with netrin-1 and MSCs derived from peripheral blood), MSCs group (treated with MSCs individually), netrin-1 group (treated with netrin-1 individually), and control group (treated with saline). Measurements of murine behaviors, vascular endothelial growth factor expression, and capillary density in ischemia limb were performed on days 7, 14, and 28 after treatments; measurements of contraction force in ischemia limb was performed on day 28 after treatments to compare differences among the groups. RESULTS: Netrin-1 allied with MSCs significantly increased Tarlov score, vascular endothelial growth factor expression, capillary density, and muscular strength in ischemia limb. CONCLUSIONS: Netrin-1 allied with MSCs derived from peripheral blood significantly promoted angiogenesis in aged rats with chronic limb ischemia. It may be a promising method of treating peripheral arterial disease in the future.

[Prophylaxis of thrombotic complications in patients after reconstructive operations on the main arteries of the lower extremities, made for arteriosclerosis obliterans in a critical ischemia stage].

Results of reconstructive operations, performed on the main arteries of the lower extremities (LE) in 63 patients, suffering obliterating atherosclerosis were analyzed with the objective to analyze the causes of thrombotic complications occurrence. There was established, that common clinical screening tests, applied for control of the hemostasis system state, do not permit completely to reveal thrombophylic changes in early postoperative period timely and to prevent the occurrence of the reconstructed segments thrombosis. Direct correlation connection between the ischemia stage of the LE tissues, the reperfusion changes signs and hyperaggregation severity, occurring due to deficiency of the blood serum natural anticoagulants in patients, suffering obliterating atherosclerosis, was established.

A clinicopathologic study of immunoglobulin G4-related disease of the femoral and popliteal arteries in the spectrum of immunoglobulin G4-related periarteritis.

BACKGROUND: Immunoglobulin (Ig) G4-related disease has recently been recognized to occur in the cardiovascular system in the aorta and main branching arteries, often manifesting as aneurysms and arteritis/periarteritis. Peripheral arteries (the femoral and popliteal arteries) are frequent sites of arteriosclerosis obliterans (ASO) and occasionally show aneurysms or arteritis. This study re-examined peripheral arterial lesions from the standpoint of IgG4-related disease. METHODS: The study comprised 104 patients who underwent surgical treatment of peripheral arterial lesions, including 30 patients with peripheral arterial aneurysms (PAAs) and 74 with ASO. IgG4-related disease was identified on the basis of diffuse infiltration of numerous IgG4-positive plasmacytes as revealed by immunohistochemical examination. Clinicopathologic features were compared between IgG4-related and IgG4-unrelated lesions. RESULTS: IgG4-related disease was found in four of the 30 patients with PAAs (13.3%; two in the deep femoral artery, two in the popliteal artery) but not in any patients with ASO. IgG4-related PAA displayed clinicopathologic features resembling those of other IgG4-related diseases and a characteristic saccular appearance (P = .002). CONCLUSIONS: IgG4-related disease was detected in PAA patients but not in ASO patients. IgG4-related disease thus represents one potential etiology of aneurysm in the peripheral arteries.

[Proteomics analysis of distinct proteins in human atherosclerosis obliterans: identification and verification].

OBJECTIVE: To identify distinct proteins involved in human atherosclerosis obliterans (ASO) by a differential proteomic approach. METHODS: Eight atherosclerotic femoral arteries with a mean age of 68.6 years (6 male and 2 female) and 5 normal femoral arteries with a mean age of 44.2 years (3 male and 2 female) were obtained from high amputation patients. Then the first 2-dimensional maps of the proteome of human femoral arteries was plotted to compare ASO and control specimens. Proteomic profiling was to differentiate and identify histological proteins that were associated with ASO. The differentially expressed proteins were sequenced by matrix assisted laser desorption/ionization mass spectrometry (MALDI-TOF-MS). The result was verified by immunohistochemistry (IHC) and Western blot. RESULTS: ASO was associated with distinct patterns of protein expression in the femoral arteries. A total of 25 distinct spots corresponding to 13 different proteins were identified by MALDI-TOF-MS using the NCBI and IPI databases. These proteins were mainly involved in the pathogenetic mechanisms such as inflammation, oxidative stress, proliferation and transformation of SMCs. The low level of heat shock protein 27 (HSP27) in ASO was verified by IHC and western-blot in accord with the result of MS. CONCLUSION: Proteomic analysis can be used to investigate differentially expressed proteins, which may provide new insights into ASO pathogenesis, such as HSP27.

[Ultrastructural changes of the capillary endotheliocytes in the muscle tissue of patients with chronic ischemia of the extremities after transplantation of the progenitor fetal liver cells].

Taking into account impossibility of reconstruction-restoration operations performance in cases of the distal arterial bed affection, it is necessary to find out and elaborate the methods of indirect revascularization. The cells transplantation performance for stimulation of reparation and angiogenesis in the affected extremity is considered a perspective direction of treatment. Essential stimulation of angiogenesis occurs after transplantation of progenitor stem cells of a fetal liver according to the data, obtained in experiment on laboratory animals. Later, transplantation of the cells was accomplished in patients with chronic ischemia of the extremities. Using method of electron microscopy of endotheliocvtes of the muscular tissue capillaries there was proved, that the cells transplantation causes essential stimulation of angiogenesis in patients, suffering chronic ischemia and constitutes a perspective method of indirect revascularization.

Immunohistochemical properties in the patients with Buerger's disease--possible role of plasminogen activator inhibitor-1 for preservation of vessel wall architecture.

BACKGROUND: The architecture of the arterial wall affected with Buerger's disease has been known to be preserved in all three layers, while the one affected by arteriosclerosis obliterans (ASO) is degenerated and destroyed. We analyzed affected arteries with immunohistochemical methods to clarify the differences between Buerger's disease and ASO. MATERIALS AND METHODS: Crural arteries obtained from 13 patients with Buerger's disease and 6 patients with ASO at our institute were studied. In addition, we examined seven specimens from six patients who were thought to be normal (without Buerger's disease or ASO) as negative control. Immunohistochemical studies were performed on paraffin-embedded tissues. The primary antibodies were urokinase-type plasminogen activator (uPA) and matrix metalloproteinase-3 (MMP-3). Both are known to play an important role of extracellular proteolysis and to activate each other. Additionally, plasminogen activator inhibitor-1(PAI-1) was also examined. RESULTS: In Buerger's disease, PAI-1 was well expressed along the internal elastic lamina. Urokinase-type plasminogen activator and MMP-3 were slightly positive in intima and media. In ASO, a slight amount of PAI-1 was recognized on vessel walls, and both uPA and MMP-3 were strongly positive in media. In addition, in the control group, PAI-1, uPA, and MMP-3 were well expressed in media. CONCLUSION: In Buerger's disease, PAI-1 was strongly expressed around the internal elastic lamina, while both uPA and MMP-3 were slightly recognized on vessel walls. These findings could be one of the reasons the general architecture of vessel walls in Buerger's disease is preserved.

[Electrical pulse therapy for the treatment of the patients with obliterative atherosclerosis of the vessels in the lower extremities].

The authors report the results of the application of electrical pulses to the region of lumbar ganglia for the treatment of patients with obliterative atherosclerosis of the blood vessels in the lower extremities. It was shown that the temporary blockade of sympathetic regulation of the lower limb arteries promotes reduction of vascular tone in the distal segments of the lower extremities, stimulates collateral blood flow, and improves microcirculation in ischemic tissues(specifically, following reconstructive surgery on the lower limb arteries).

[Ultrastructural changes of vascular endothelium in patients with chronic ischemia of the extremities after conduction of multipotent stromal cells from adipose tissue transplantation].

Taking into account the impossibility of performance in some situations of reconstructive operative interventions on arteries, it is necessary to look for new methods of indirect revascularization for the extremities ischemia. Adipose tissue constitutes an accessible and sufficient source of multipotent stromal cells (MSC). Experimental investigations were made in a frame of preclinical trial on laboratory animals with the extremity ischemia simulation, and there was proved the essential stimulation of angiogenesis processes after transplantation performance of stromal-vascular fraction of adipose tissue. The work objective was to study the influence of own adipose tissue MSC transplantation on vascular endothelium changes in patients, suffering chronic ischemia of the extremities. Using electron microscopy method there was proved on microstructural level, that in clinical environment the patients, suffering chronic ischemia of the extremities of various etiology, gain undoubted effect of MSC autotransplantation performed with the objective to stimulate the processes of angiogenesis in the ischemic affection region.

[Assessing the prognostic significance of morphometric parameters of vascular wall inflammation for remote results of reconstructive operations in the aortoiliac zone in patients with atherosclerosis obliterans].

The study was aimed at assessing the relationship between the activity (including the inflammatory one) of the atherosclerotic process in the zone ofarterial reconstruction in patients under-going surgery on the aortoiliac arterial segment and long-term thrombotic reocclusions. The study comprised a total offorty-nine patients, with the postoperative follow-up period amounting to 5 years. We carried out morphological studies of the aortic wall in the zone of the proximal anastomosis and the walls of the common femoral arteries in the zone of distal anastomoses. It was determined that the presence of morphometric sign of inflammation and atherosclerotic deformity in the preparations of the aortic and arterial walls was accompanied and followed by increased incidence of long-term thrombotic complications in the reconstruction zone with more pronounced progression of the thrombotic process in the arteries of the peripheral bed distal to the reconstruction site.

[New possibilities of the extremity revascularization in chronic ischemia: induction of angiogenesis by the bone marrow aspirate autotransplantation in patients with arteriosclerosis obliterans in the vessels of the lower extremities].

In 55 patients, suffering obliterating atherosclerosis and chronic arterial insufficiency, there was accomplished autotransplantation of the bone marrow aspirate (ABMA) because of impossibility of conduction of direct revascularization of the lower extremity in inoperable or operable in question affection of the distal vascular bed, as a monomethod or in simultant fashion with reconstructive operations on proximal segments of vascular bed or using the other methods of indirect revascularization. After the operation in 63.1% of patients it appeared possible to preserve the "lean on" function of the lower extremity in early period and in 52.6%--in the remote period. The ABMA method application had permitted to correct microhemodynamical disorders by stimulation of angiogenesis and development of collateral blood flow in patients, suffering chronic ischemia of lower extremities, especially in the critical ischemia stage.

[Study of the microbial spectrum of ulcerative-and-necrotic lesions in gerontological patients with lower limb chronic ischaemia].

The present work deals with a comprehensive study of the microbial spectrum of an ischaemic trophic ulcer in gerontological patients with degree IV lower limb chronic ischaemia in order to improve therapeutic outcomes by means of selecting individual antibacterial therapy for a possible prognosis of the results of treatment for an ulcerative-and-necrotic lesion of distal portions of the lower extremities depending on the spectrum of the microflora vegetating in the wound. Based on examining a total of 130 patients aged 70 years and older suffering from lower limb chronic critical ischaemia, we revealed that the pathogen of secondary wound infection isolated in trophic ulcers of the lower extremities influences the total outcomes of surgical management. A conclusion was made on the necessity of a compulsory dynamic scrutiny of the microbial flora of the lower-limb atherosclerotic ulcer, which makes it possible to carefully select individual antibacterial bactericidal therapy with due regard for microbial sensitivity to bactericidal agents.