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.

UDC 616.24-056.52-056.83]-018-092.9 

The influence of obesity (with and without passive smoking) on the formation of pathomorphological changes in the lungs was studied in 4 groups of sexually mature male rats: the control group (CL), the group with isolated alimentary obesity (O), the group exposed to isolated exposure to tobacco smoke (S), the group with combined dietary obesity and exposure to tobacco smoke (OS) after 4 months of the experiment. The morphological changes found in the CL group were insignificant. In group S, the presence of changes characteristic of chronic bronchitis and focal emphysema was established. Pathomorphological changes typical for the chronic obstructive pulmonary disease were found in group O: chronic bronchitis, initial manifestations of
bronchiectasis formation, pulmonary emphysema, focal pneumosclerosis, and initial manifestations of pulmonary hypertension.
In the OS group, the changes were not qualitatively different from those in the O group. It was found that the changes characteristic of chronic obstructive pulmonary disease developed in rats with simulated obesity, regardless of whether the smoking model was used

UDC 616.831-005.1 : 616.5-003.42-036-092-018. 001.36 

Pathomorphological research changes in brain tissue in the perihematomal zone of 28 autopsies of patients with hemorrhagic stroke was examinated. It has been established that the combination of acute and chronic lesions of the vascular wall is the cause of premature death in stage I. Coagulation necrosis is a common variant of neuronal death. Hemistocytic astrocytes is significantly predominate in stages II and III. The intensity of regeneration is less pronounced and significantly increases among patients who died after 7 days after the disease. The demarcation inflammation zone in most researches reveals itself in period of early and late subacute hematoma, with the gliomesodermal capsule that forms over time.