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In order to establish signaling mechanisms of platelet dysfunction among patients with acute gastroduodenal ulcer bleeding the assessment of agonist-induced platelet aggregation was performed by means of the spectrophotometric method and inhibitory method at the time of hospitalization of patients and the third day after. It has been shown that on the first day of hospitalization the level of collagen- and ADP- induced platelet aggregation was decreased among patients with acute gastroduodenal ulcer bleeding in comparison with the controlgroup. In cases of medium/high level of platelet aggregation, the reverse aggregation graph was recorded that was associated with the risk of recurrent bleeding. On the third day after hospitalization, the rise of ADP-induced platelet aggregation was found on account of PKA becomes a positive regulator of platelet intracellular signaling system. The assessment of induced platelet aggregation among patients with acute gastroduodenal ulcer bleeding compared with the control group allowed to discover a double decreased platelet aggregation to ADP (p=0.004) and 4.5-times decreased platelet aggregation to collagen (p=0.0001). The characteristics of aggregation graphs to ADP have shown partially inverse and inverse platelet aggregation, that was widely spread among patients with medium/high level of platelet aggregation. The previous issue has been associated with reverse and partially reverse aggregation graphs to collagen. Moreover, the highest rate of recurrent bleeding was found among patients with medium/high level of platelet aggregation to collagen (p=0.02) which was featured by a long latency period. The scrutiny also has revealed the correlation between ADP and collagen-induced platelet aggregation (r=0.28; p=0.01), which indicates that platelet disfunction takes place in the intracellular signaling system. On the first day of hospitalization no effect of PK A inhibitor on ADP-induced platelet aggregation was detected (p=0.71). The examination of effect of PK C inhibitor on ADP-induced platelet aggregation also has revealed no effect (p=0.57). In addition to the level of platelet aggregation inhibitors did not influence the characteristics of aggregation graphs. The comparison of ADP- and collagen-induced platelet aggregation in dynamics (on the first and the third days of hospitalization) has shown 2-times growth of platelet aggregation to ADP (p

Edward Barinov,1 Oksana Sulaieva,1 Yuriy Lyakch,2 Vitaliy Guryanov,2 Petr Kondratenko,3 Yevgeniy Radenko3 1Department of Histology, Cytology, and Embryology, 2Department of Medical, Biological Physics, Medical Informatics, and Biostatistics, 3Department of Surgery and Endoscopy, M Gorky Donetsk National Medical University, Donetsk, Ukraine Background: The purpose of this study was to identify factors associated with the risk of unsustainable hemostasis in patients with gastric and duodenal ulcer bleeding by in vitro assessment of platelet reactivity using artificial neural networks. Methods: Patients with gastroduodenal ulcers complicated by bleeding were studied. Platelet aggregation was measured using aggregometry with adenosine diphosphate 5 µM, epinephrine 2.5 µM, 5-hydroxytryptophan 10 µM, collagen 1 µM, and thrombin 0.06 NIH Unit/mL as agonists. Multiple logistic regression was used to evaluate the independent relationship between demographic, clinical, endoscopic, and laboratory data and in vitro assessment of platelet reactivity and local parameters of hemostasis in patients with ulcer bleeding. Results: Analysis of platelet aggregation in patients with gastroduodenal ulcer bleeding allowed the variability of platelet response to different agonists used in effective concentration which induces 50% platelet aggregation (EC50) to be established. The relationship between platelet aggregation and the spatial-temporal characteristics of ulcers complicated by bleeding was demonstrated. Adrenoreactivity of platelets was associated with time elapsed since the start of ulcer bleeding and degree of hemorrhage. The lowest platelet response to collagen and thrombin was detected in patients with active bleeding (P< 0.001) and unsustainable recent bleeding (P < 0.01). Decreased adenosine diphosphate-induced platelet aggregation in patients with ulcer bleeding was correlated with the platelet response to thrombin (r = 0.714, P < 0.001) and collagen (r = 0.584, P < 0.01). Conclusion: Estimation of platelet reactivity in vitro indicates the key mechanisms of failure of hemostasis in patients with ulcer bleeding. In addition to gender, an important determinant of unsustainable hemostasis was a decreased platelet response to thrombin and adenosine diphosphate. Keywords: ulcer, hemostasis, blood platelets

Background. Gastroduodenal ulcer bleeding is one of the main causes of morbidity, mortality and high medical care expenses. It is unclear why regardless of the optimization of antisecretory therapy among the patients with peptic ulcer the frequency of bleeding remains as high. Objective. We suggest that acute bleeding development is related with hyperstimulation of acute inflammatory response due to macrophages dysfunction. Methods. To test this hypothesis we assessed characteristics of inflammatory process in different zones of the gastroduodenal area under acute bleeding in 46 patients. The number and distribution of neutrophils, eosinophils, plasma cells, mast cells, macrophages (CD68+), T- (CD3+) and B-lymphocytes (CD20+) were evaluated. Results. The comparison of morphological changes in ulcer margin and intact gastric mucosa has revealed that the development of ulcer bleeding is associated with acute inflammation. High recruitment of neutrophils in ulcer margin was associated with edema and alteration of covering epithelium. CD68-positive cells prevailed in subepithelial region. However, in the 2nd group number of macrophages (p

Current development of medicine determines the necessity to revise the content of the lessons and teaching tools in fundamental sciences including histology. In this paper the following issues are considered: 1. Use of the problembased education to stimulate clinical motivation and real interest of students to basic sciences including histology. 2. Reorganization of stuff administration to prepare highly qualified young teaches on histology. 3. Stimulation of associative and logic memory during histology studying. 4. Development of the positive educational milieu, including psychological comfort and satisfaction of the learning process and outcomes, as well as personalization of learning process. Citation: Sulaieva ON. [What factors determine the efficacy of histology learning in medical university?]. Morphologia. 2015;9(3):127-9. Russian.