We studied the effect of a single session of hyperbaric oxygenation on the size of risk, ischemic, and necrotic zones in rat myocardium after irreversible occlusion of the coronary artery and excessive oxygen pressure of 0.02 and 0.1 MPa. Myocardium infarction was reproduced by ligation of the left coronary artery. The size of the risk, ischemic, and necrotic zones was planimetrically evaluated. Hyperbaric oxygenation (60-min session) was performed 3 h after artery occlusion at excessive oxygen pressure of 0.02 and 0.1 MPa. In rats not exposed to hyperbaric oxygenation, the risk zone median was 31.7% of the left ventricle weight, while after the session it did not exceed 25%. In spontaneous course of myocardium infarction, the ischemia to necrosis zone ratio was 1.7:1, while under conditions of hyperbaric oxygenation at oxygen pressure of 0.1 and 0.02 MPa, the these values were 0.6:1 and 2:1, respectively. Excessive oxygen pressure of 0.02 mPa is better than traditionally used 0.1 MPa, because it promotes redistribution of the ischemic and necrotic areas in the risk zone: the area of necrotic zone decreased at the expense of the ischemic zone. Hyperbaric oxygenation produces a positive effect on the myocardium under conditions of total occlusion of the coronary artery.

The advanced analysis of immune parameters describing differentiation profile, activation and exhaustion of lymphocytes, monocytes and granulocytes of patients with moderate and severe/critical COVID-19 pneumonia was performed.

При коронавирусной инфекции COVID-19 у части пациентов, преимущественно требующих вентиляционной поддержки, развивается цитокиновый шторм, который приводит к системному воспалительному ответу и полиорганной недостаточности. Одной из стратегий терапии цитокинового шторма является использование гуманизированных моноклональных антител к рецептору интерлейкина-6 (ИЛ-6), в частности препарата тоцилизумаб. Висследование включен 131 госпитализированный пациент с инфекцией COVID-19, получивший препарат тоцилизумаб в дозе 8 мг/кг через 10 [9; 12] суток после начала заболевания. Пациенты были разделены на 2 группы в зависимости от достижения конечной точки: выписка пациента из стационара (95 пациентов, группа 1) или смерть (36 пациентов, группа 2). Неблагоприятные клинические исходы при использовании препарата тоцилизумаб для лечения инфекции COVID-19 связаны с более старшим возрастом пациентов (57 [48; 62] лет в группе 1 против 63 [52; 69] лет в группе 2 (p<0,011); тяжестью поражения легких (тяжелое поражение по данным компьютерной томографии было у 37 (38,9%) пациентов группы 1 и 28 (77,8%) пациентов группы 2 (р<0,001); большей потребностью в О2 при спонтанном дыхании (7 [5,0; 10,0] л/мин в группе 1 против 12 [9,0; 15,0] л/мин в группе 2 (р<0,001); необходимостью проведения искусственной вентиляции легких (ИВЛ), более высоким уровнем ИЛ-6 (в группе 1 уровень ИЛ-6 составил 67,4 [36,4; 90,3] пг/мл против 127,0 [81,7; 339,1] пг/мл в группе 2 (р=0,002)). Через 6 суток после введения препарата тоцилизумаб по результатам рутинных лабораторных тестов (уровень лейкоцитов, лимфоцитов, соотношение нейтрофилы/лимфоциты, С-реактивный белок, креатинфосфокиназа, лактатдегидрогеназа) можно прогнозировать исход заболевания. A certain number of COVID-19 patients develops cytokine storm, which leads to the systemic inflammatory response and multiple organ failure. One of the strategies for this cytokine storm management is using of humanized monoclonal antibodies to interleukin-6 (IL-6) receptor, tocilizumab. The study included 131 hospitalized patients with COVID-19 infection, who received tocilizumab (8 mg/kg) 10 [9; 12] days after the onset of disease. Patients were divided into 2 groups, depending on the outcome: discharge from the hospital (95 patients, group 1) or death (36 patients, group 2). Adverse clinical outcomes when using Tocilizumab for the COVID-19 infection are associated with older age of patient (57 [48; 62] years in the group 1 versus 63 [52; 69] years in group 2 (p<0.011). 37 (38.9%) patients in the group 1 had severe lung damage according to computer tomography versus 28 (77.8%) patients in the group 2 (p<0.001). In the 1st group, the need for O2 was lower: the flow during spontaneous breathing was 7 [5.0; 10.0] l/min versus 12 [9.0; 15.0] l/min in the 2nd group (p<0,001); and the need for mechanical ventilation was lower too. Patients in the 1st group had lower level of IL-6 - 67.4 [36.4; 90.3] pg/ml versus 127.0 [81.7; 339.1] pg/ml in the 2nd group (p=0.002). In 6 days after tocilizumab administration, according to the results of routine laboratory tests (leukocyte, lymphocyte count, neutrophil/lymphocyte ratio, C-reactive protein, creatine kinase, lactate dehydrogenase), the outcome of the disease can be predicted.

The prevalence of asthma and allergic airway diseases has increased since the 1960s. The use of dishwasher and household detergents showed a similar trend, leading us to hypothesize that increased exposure to detergents might contribute to development of allergic diseases. The goal of this project was to test this hypothesis by using in vitro and in vivo models. METHODS: We exposed normal human bronchial epithelial (NHBE) cells that overexpress the IL-33 gene to sodium dodecyl benzene sulfonate (SDBS) as a model for detergent. Various pharmacologic agents were used to dissect the mechanisms for IL-33 release. SDBS was also administered intranasally (i.n.) to na€ ıve BALB/c mice. RESULTS: Exposure to SDBS induced IL-33 release from NHBE cells. The dose-response curve was bell-shaped, and the maximum effect was observed at a 3-fold lower concentration (i.e. 50 mg/ml) than the critical micelle concentration for SDBS. At this concentration, more than 90% of NHBE cells were alive, released ATP extracellularly and showed increase in intracellular calcium concentration. IL-33 release was abolished by treating the cells with purinergic receptor antagonists or oxygen radical scavengers or by chelating extracellular calcium. Moreover, the levels of type 2 cytokines in lung homogenates were increased in mice exposed to SDBS in vivo. CONCLUSIONS: Exposure of airway epithelial cells to a low concentration of detergents induces active release of IL-33 likely through the pathway(s) involved in cellular stress responses. Detergents may dysregulate the homeostasis of epithelium and promote development of type 2 immune responses to environmental allergens.

Data from the Coronavirus-19 disease (COVID-19) pandemic suggests asthma is not a risk factor for severe disease in adults; it is unclear if this applies to pediatric patients. This study was undertaken to determine if pediatric patients with asthma or atopic disease had altered risk for severe disease when hospitalized with COVID-19. METHODS: A retrospective chart review was performed of SARS-CoV-2 positive patients admitted to Nationwide Children's Hospital from March 1 to July 31. Charts were evaluated for history of asthma or atopic disease (including asthma) and surrogate markers of COVID-19 severity, including ICU admission, supplemental oxygen requirement, and intubation. RESULTS: 49 patients were identified as positive for SARS-CoV-2, 22 of whom were admitted for COVID-19 related symptoms. Of the admitted patients, six patients (12%) had asthma and 18 (37%) atopic disease (including those with asthma). ICU admission rate for asthma versus nonasthma was 17% versus 12% (p50.78) and for atopic versus non-atopic was 17% versus 6.4% (p50.32), while supplemental oxygen rates were 17% versus 16% asthma versus non-asthma (p50.98) and 22% versus 13% atopic versus non-atopic (p50.43). Only two patients required intubation and both had atopic dermatitis. Two patients had Multisystem Inflammatory Syndrome in Children -one with allergic rhinitis and atopic dermatitis, the other without any atopic disease. CONCLUSIONS: Markers of COVID-19 disease severity do not differ based on asthma or atopic status in pediatric patients. In children, like adults, the presence of asthma or atopy does not appear to alter the risk of severe COVID-19.248 COVID-19 pandemia: Atopy and prospective analysis of the clinical evolution of patients infected with the SARS-CoV-2 virus