The presence of coronavirus-associated myocarditis remains controversial despite elevations in cardiac troponin and natriuretic peptide in many patients.Aim. To assess the morphological changes in the myocardium of patients who died due to coronavirus disease 2019 (COVID-19) and compare them with the intravital level of cardiac biomarkers.Material and methods. A total of 420 hospital charts and 77 autopsies of those who died from COVID-19 were analyzed. In 15 of 77 cases (19%) with histologically suspected myocarditis, an immunohistochemical examination of the myocardium with antibodies to CD3, CD45, CD8, CD68, CD34, Ang1, VWF, VEGF, HLA-DR, MHC1, C1q, VP1 of enteroviruses was performed, and in 8 patients with immunohistochemically confirmed myocarditis (10%) — polymerase chain reaction for SARS-CoV-2.Results. Hemorrhage, intramural thrombosis, necrosis of non-coronary origin, myocardial infarction and lymphocytic myocarditis were detected in 43%, 10%, 17%, 19% and 10% of cases, respectively, without coronavirus N and E gene sequences in the myocardium. Dysplasia, hyperplasia and hypertrophy of the vascular endothelium, expression of Ang1, VWF, VEGF, MHC1, C1q, VP1 of enteroviruses were determined in 100, 100, 87, 100, 75 and 62% of cases of myocarditis, respectively. There were no significant correlations between inflammatory biomarkers and myocarditis.Conclusion. The main morphological manifestation of COVID-19 in the myocardium is the so-called endotheliitis with dysplasia and endothelial activation, leading to hemorrhages, intramural thrombosis and necrosis. There is no convincing evidence of a direct involvement of coronavirus in myocarditis induction.

The prognosis of glioblastoma (GLB) is poor: the 5-year survival rate is less than 10%. Almost all patients relapse after surgery according to the standard of treatment: resection, radiation therapy, and temozolomide. T reatment options today for relapse are limited, and no amount of therapy prolongs patients' lives. The development of resistance to therapy is associated with the microenvironment and tumor stem cells. Objective: to study the expression of stem cell markers, transcription factors and PD-L1 in malignant gliomas. A retrospective study included 17 patients with high-grade gliomas who underwent surgery. All patients underwent traditional histological examination, immunohistochemical analysis with antibodies to IDH1R132H, BRAF V600E, Ki-67, GFAP, NANOG, Nestin, CD133, SALL4, OCT4, SOX2, CD38, PD-L1, FOXM1, morphometric analysis with calculation of the average ratio cells with antigen expression to the number of all tumor cells. Expression of NANOG was observed in 47% of cases, Nestin - in 88%, CD133 - in 71%, SOX2 - in 100%, CD38 and FOXM1 - in 65%. None of the tumors expressed SALL4, only one OCT4. PD-L1 expression was detected only in 2 cases. Correlation analysis established the presence of significant associations between the expression of Nestin and CD133; FOXM1 and NANOG; Nestin and CD38; Ki-67 and SOX2. The presence of expression of stem cell markers and transcription factors NANOG, Nestin, CD133, CD38, SOX2, FOXM1 in malignant gliomas, in our opinion, dictates further targeted study of these markers on a larger sample and opens up new potential targets for targeted therapy.

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