Bats are potential natural reservoirs for emerging viruses, causing deadly human diseases, such as COVID-19, MERS, SARS, Nipah, Hendra, and Ebola infections. The fundamental mechanisms by which bats are considered “living bioreactors” for emerging viruses are not fully understood. Some studies suggest that tolerance to viruses is linked to suppressing antiviral immune and inflammatory responses due to DNA damage by energy generated to fly. Our study reveals that bats' gut bacteria could also be involved in the host and its microbiota's DNA damage. We performed screening of lactic acid bacteria and bacilli isolated from bats' feces for mutagenic and oxidative activity by lux-biosensors. The pro-mutagenic activity was determined when expression of recA increased with the appearance of double-strand breaks in the cell DNA, while an increase of katG expression in the presence of hydroxyl radicals indicated antioxidant activity. We identified that most of the isolated bacteria have pro-mutagenic and antioxidant properties at the same time. This study reveals new insights into bat gut microbiota's potential involvement in antiviral response and opens new frontiers in preventing emerging diseases originating from bats.

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Background: Current assessment methods of penile cavernous fibrosis in animal models have limitations due to the inability to provide complex and volume analysis of fibrotic alterations. Objective:The aim was to evaluate micro-computed tomography for assessment of cavernous fibrosis and compare it with histological, histochemical, immunohistochemical, and RT-PCR analysis. Materials and methods:A controlled trial was performed involving 25 New Zealand male rabbits with induced testosterone deficiency by orchidectomy. Penile samples were obtained before and after 7, 14, 21, and 84 days from orchidectomy. We consistently performed (a) gray value analysis of corpora cavernosa 3D models reconstructed after micro-computed tomography, (b) morphometry of smooth muscles/connective tissue ratio, collagen type I/III ratio, and area of TGF-beta-1 expression in corpora cavernosa, and (c) RT-PCR of TGF-beta-1 expression.Results: Micro-computed tomography allowed visualization of penile structures at a resolution comparable to light microscopy. Gray values of corpora cavernosa decreased from 1673 (1512-1773) on the initial day to 1184 (1089-1232) on the 21st day (p < 0.005). However, on the 84th day, it increased to 1610 (1551-1768). On 21st and 84th days, there was observed a significant decrease in smooth muscle/connective tissue ratio and a significant increase in collagen type I/III ratio (p < 0.05). TGF-beta1 expression increased on the 84th day according to immunohistochemistry (p < 0.005).RT-PCR was impossible to conduct due to the absence of RNA in obtained samples after micro-CT.Discussion and conclusions: Micro-computed tomography provided 3D visualization of entire corpora cavernosa and assessment of radiodensity alterations by gray value

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Цель: определить распространённость мутации c.1934dupG в гене ASXL1 и мутации R882H в гене DNMT3A при миелодиспластическом синдроме и их влияние на значимые клинические характеристики. Материалы и методы: в исследование были включены 33 мужчины и 17 женщин с медианным возрастом 57 лет (18-83) и верифицированным диагнозом миелодиспластического синдрома. В качестве контроля были взяты 22 добровольца без гематологической патологии, (8 мужчин, 14 женщин, от 22 до 65 лет). Во всех исследуемых группах было проведено ПЦР-исследование венозной крови с целью детекции мутаций c.1934dupG и R882H с помощью адаптированных способов анализа эффективности амплификации и рестрикционной аллель-специфической ПЦР с референсным секвенированием по Сенгеру. результаты: мутация R882H не была обнаружена ни в одной из исследуемых групп. Мутация c.1934dupG не была обнаружена у лиц без гематологической патологии. Из-за недостатка концентрации выделенной ДНК из клеток венозной крови не удалось произвести анализа эффективности амплификации у 7 пациентов. Мутация c.1934dupG была обнаружена у 46% пациентов и встречается во всех группах риска по шкале IPSS-R, WPSS и MDS-CI. Не найдено различий при анализе выживаемости при наличии и отсутствии мутации c.1934dupG. Выводы: исследование показало, что разработанный способ по детекции мутации c.1934dupG в клетках венозной крови позволяет совершить оптимизацию молекулярно-генетической диагностики. Ограничением для проведения адаптированных анализов эффективности амплификации и рестрикционного анализа являлась степень лейкопении крови. Не было обнаружено влияния мутации c.1934dupG на клиническое течение миелодиспластического синдрома при сравнении некоторых твёрдых и суррогатных конечных точек исследования.