Репозитарій

УДК:616.127-005.8 : 616.831-018-036].001.36

Актуальність. Гострі порушення мозкового кровообігу захворювання, які вважаються одними з найбільш складних за перебігом та важкістю ураження центральної нервової системи. Тканина мозку при гострій ішемії спочатку зазнає оборотнього, а в подальшому необоротнього пошкодження. Пенумбра при гіпоперфузії мозку може зазнати некрозу, або відновити нормальну життєдіяльність.Мета дослідження –вивчення особливостей патоморфологічних змін тканини мозку у перифокальній зоні в різні терміни від початку ішемічного інсульту. Методи.Проаналізували матеріал (аутопсія) 25 пацієнтів з ішемічним інфарктом віком від 45 до 81 років. Опрацювали історії хвороб, клінічні дані, супутні та фо-нові захворювання. Матеріалзгрупували за класифікацією стадій перебігу інфаркту мозку Mena H et al.у три фази: І –фазагострого нейронального пошкодження (1-3 день від розвитку інфаркту), ІІ –фаза гост-рої організації (4 –7 день з початкузахворювання), і ІІІ –фаза хронічної організації (через 7 днів від по-чатку захворювання).Для гістологічного дослідження забирали шматочки тканини мозку (1,5 х1,5 см) в зоні прилеглій до ішемічного інфаркту.Виготовляли препарати за стандартною методикою та фарбувализрізи гематоксиліном і еозином. Результати.На летальне завершення хворобивпливали одне, або часті-ше поєднання кількох захворювань у одного пацієнта. У найгострішу фазу захворювання у більшості випадків в перифокальній зоні зустрічались нейрони з коагуляцій ним некрозом. Підсумок.При прогре-суванні захворювання, у ІІІ фазі, в пенумбрі частіше одночасно виявлялись «червоні» і «тіні» нейронів. У І фазі навколо ядра некрозу зʼявлялися нейтрофіли та активована мікроглія, у фазу гострої та хронічної організації виявлялись лімфоцити та макрофаги. Початкова організація з наявністю поодиноких гемісто-цитарних астроцитів та тонкостінних капілярів спочатку виявлялась у зоні найбільш прилеглій до некро-зу у І фазі, а з часом, у ІІ і ІІІ фазі інфаркту мозку поширювалась вглиб пенумбри.

The aim: The study is to research the resolution of perifocal brain tissue at various type strokes using immunomorphology
Materials and methods: The immunohistochemical study of perifocal brain tissue in 21 cases of various strokes types was condacted
Results: When comparing the GFAP + astrocytes detection area at IS, HS and IS with HT, no significant difference was found. At the 1st degree of GFAP + astrocytes were in the border around the necrosis nucleus at IS and IS with HT, and at HS GFAP + astrocytes accumulated along the hematoma edge. CD34 + cells were found in most cases of strokes. 
Over time, cases with a larger CD34 + cells detection area increased (Kendal’s Tau = 0.512, p = 0.001) in all groups. The capillary network at HS was around the hematoma and formed a gliomesodermal capsule with microglia and inflammation. 1st degree τ-protein accumulation was detected in 2/3 of cases (66.7%) of all strokes without significant difference. If compared in different stroke periods, τ-protein detection frequency increased and accumulated in brain structures – Kendal’s Tau = 0.359; p = 0.023.
Conclusions: With the development of the disease, the number of cases with a larger area of detection of GFAP + astrocytes and CD34 + cells increased in strokes of various types. Ʈ-protein was detected in neurons in all variants of ACVA in the first period.

Many nano/microparticles (n/µP), to which our body is exposed, have no physiological way of removal. Our immune system sense these “small particulate objects”, and tries to decrease their harmfulness. Since oxidation, phagocytosis and other methods of degradation do not work with small, chemically resistant, and hydrophobic nanoparticles (nP). This applies to soot from air pollution, nano-diamonds from cosmic impact, polishing and related machines, synthetic polymers, and dietary n/µP. Our body tries to separate these from the surrounding tissue using aggregates from neutrophil extracellular traps (NETs). This effectively works in soft tissues where n/µP are entrapped into granuloma-like structures and isolated. The interactions of hydrophobic nanocrystals with circulating or ductal patrolling neutrophils and the consequent formation of occlusive aggregated NETs (aggNETs) are prone to obstruct capillaries, bile ducts in gallbladder and liver, and many more tubular structures. This may cause serious health problems and often fatality. Here we describe how specific size and surface properties of n/µP can activate neutrophils and lead to aggregation-related pathologies. We discuss “natural” sources of n/µP and those tightly connected to unhealthy diets. 

Introduction. An essential point in the pathogenesis of COVID-19 is endothelial dysfunction with the development of thrombosis and 
microangiopathy of pulmonary vessels, which is one of the causes of high mortality. At the same time, electron microscopic examination of 
the pulmonary vascular bed in COVID-19 coronavirus infection is rarely performed.
Objective: To investigate ultrastructural changes in the pulmonary microcirculatory bed by determining the features of endothelial damage 
and the role of vascular disorders in the pathogenesis of severe COVID19 coronavirus infection.
Methods. The material was collected at autopsy, no later than 2 hours after the fact of death of patients, fixed in Millonig's fixative with 
pH 7.36. Dehydration was carried out in increasing-strength ethanol, transferred to propylene oxide, and tarred in a mixture of Araldite. 
Ultrathin sections with a thickness of 60 nμ were made using an LKB 2188 Ultrotome NOVA ultramicrotome. According to Reynolds, sections were mounted on support grids and contrasted with uranyl acetate and lead citrate. The obtained samples were viewed in a transmission electron microscope TEM 100-01, and photofixation was carried out using a KAPPA Image Base digital camera.
Results. Significant structural changes in type 2 pneumocytes were observed with the development of degeneration and reactive hyperplasia, 
the formation of syncytial elements, dyscirculatory disorders with endothelial alteration, pronounced hyperemia and stasis, coagulopathy, 
and thrombosis. In the lumen of the alveoli, in addition to the deposition of fine-grained masses of fibrin hyaline membranes, fibrinous exudate, 
desquamated type 2 pneumocytes, macrophages, lymphocytes, plasma cells, single neutrophils, and erythrocytes were detected.
Individual type 2 pneumocytes were characterized by the appearance of “giant lamellar bodies” measuring 2-4 μm, which occupied a
significant part of the cytoplasm. Hyperplasia of type 2 pneumocytes was observed in some areas of the lung tissue. The proliferation of 
fibroblasts and collagen fibrils was detected in the interstitium of the interalveolar septa.
Conclusions. As a result of transmission electron microscopy of the lungs of patients who died due to severe COVID-19 coronavirus infection, pronounced dyscirculatory changes were found in the vessels of the microcirculatory bed, characterized by the development of hyperemia, stasis, and microthrombosis with pronounced degenerative, necrotic changes in the endothelium and the development of endotheliitis.

UDC 611.24:616.16]-092:578.834.1]-076.4  

Damage to the endothelium of pulmonary microcirculatory vessels and the development of coagulopathy are considered important elements of the pathogenesis of coronavirus infection. The purpose of the study was to determine the ultrastructural changes of the microcirculatory bed of the lungs of patients who died due to respiratory failure during the coronavirus infection, using transmission electron microscopy. In the vessels of the microcirculatory bed of the lungs of patients who died on the 14th, 20th, 22nd, and 40th days of the disease, dyscirculatory processes of varying severity were observed in the form of severe hyperemia, stasis, microthrombi, and alternative changes in the endothelium. Damage to the vessels of the microcirculatory bed was accompanied by pronounced coagulopathy and endotheliitis, which are key aspects of the pathogenesis and thanatogenesis of coronavirus infection.