Aim. To determine the level of SARS-CoV-2 seroprevalence among the Novosibirsk Region population against the background of the COVID-19 pandemic.Material and methods. The work was carried out in 2 phases: 1) a cross-sectional cohort study performed 28.06– 15.07.2020; 2) longitudinal cohort 3-stage seromonitoring: 1st stage 28.06–15.07.2020; 2nd 14.09–04.10.2020; 3rd 10–30.12.2020 The work was carried out according to a unified methodology developed by Rospotrebnadzor with the participation of St-Petersburg Pasteur Institute, taking into account the recommendations of the WHO. IgG antibodies to the SARS-CoV-2 nucleocapsid protein were detected by ELISA using a kit of reagents produced by the SRCMSB (Obolensk) according to the manufacturer’s instructions. Statistical analysis was performed using Microsoft Excel 2010 and other programs.Results. The seroprevalence in the region’s population was 9.1% (95% CI 8.0–10.2): maximum in children 14–17 years old (17.6%, 95% CI 12.3–23.9) and persons over 75 years (14.8%, 95% CI 11.4–18.8), minimum among persons 30–39 years old (4.9%, 95% CI 3.0–8.0). Increased rate was noted among the unemployed (15.4%, 95% CI 9.9–17.1) and other individuals (13.0%, 95% CI 8.6–18.5). Seroprevalence was 33.3% (95% CI 16.3–59.0) in COVID-19 convalescents and 19.0% (95% CI 13.9-25.0) in contact persons. More than 94.7% (95% CI 91.2–97.2) of seropositive individuals were asymptomatic. During the serological monitoring, seroprevalence increased from 7.4% (95% CI 6.2–8.9) at 1st stage 1 to 12.4% (95% CI 10.6–14.3) at 2nd , and 31% (95% CI 28.8–33.3) at 3rd stage.Conclusion. SARS-CoV-2 herd immunity has not reached the threshold level, this does not exclude exacerbation of the epidemic process.
ЦЕЛЬ: оценить ассоциации носительства полиморфных локусов генов энергетического обмена с массой тела (МТ) и пищевым поведением (ПП) детей раннего возраста. МАТЕРИАЛЫ И МЕТОДЫ: в ходе поперечного обсервационного исследования обследовано 106 детей раннего возраста. Возраст − 24 (23−26) месяца жизни, масса − 13,0 (11,2−14,5) кг. Определяли варианты (ге- нотипы и аллели) генов инсулина (INS), лептина (LEP), рецептора лептина (LEPR), рецептора активации про- лиферации пероксисом (PPARG2), липопротеинлипазы (LPL), адипонектина (ADIPOQ) и интерлейкина-6 (IL-6). Расчет и оценка показателей физического развития проведены с использованием программы ВОЗ Anthro. ПП оценивали с помощью опросника для родителей CEBQ, состоящего из 8 шкал, разделенных на 2 груп- пы − «пищевого подхода» (эмоциональное переедание (ЭП), удовольствие от еды (УЕ), реакция на еду (РЕ), желание пить (ЖП)) и «избегания пищи» (эмоциональное недоедание (ЭН), реакция насыщения, ощущение сытости (ОС), избирательность в еде (ИЕ), медлительность при приеме пищи (МЕ)). Статистическую обра- ботку данных проводили, используя пакеты прикладных программ Statistica, SPSS. РЕЗУЛЬТАТЫ: частота алелля A гена LEP в группе детей раннего возраста с избыточной МТ и ожирени- ем была статистически значимо выше (40 (54,0%)), чем у детей контрольной группы – 52 (37,7%), ОШ 1,95 (95 ДИ 1,44–2,63), χ2=4,99, р=0,022. Ассоциации с МТ при рождении установлены для генотипа GG гена IL-6 в группах маловесных и нормовесных к сроку гестации (Н=6,00; р=0,050, z1-2=2,44; р=0,043 и Н=6,51; р=0,039, z1-3=2,45; р=0,043). Частота генотипов и аллелей других изученных генов энергетического обмена среди обследованных детей с учетом соответствия МТ при рождении гестационному возрасту не различалась. Анализ шкал опросника CEBQ показал значимые различия по показателям, способствующим развитию избыточной МТ и ожирения. Носители генотипа AA гена INS имели достоверно более высокие баллы по критерию ЖП – 2,3 (1,7–3,3) баллов против 1,7 (1,3–3,0) при генотипе AT, 2,3 (2,0–3,0) баллов при генотипе TT (Н=6,82, р=0,033; z1-2=2,53, р=0,034). Шкала эмоциональное недоедание у носителей генотипа AA гена INS была 3,3 (2,8–3,8) балла, генотипа AT – 3,0 (2,3–3,5), генотипа TT – 3,8 (3,0–4,0) баллов (Н=5,89, р=0,053). Параметр группы «избегания пищи» реакция насыщения, ощущение сытости (ОС), имеющих генотип GC гена IL-6, составил 3,4 (3,1–3,8) балла, GG – 3,4 (3,0–3,8), CC – 3,8 (3,4–4,0) баллов, Н=6,18, р=0,046, z1-3=2,40; р=0,049. Показатель ЭН у обладателей генотипа GC гена IL-6 – 2,8 (2,0–3,5), GG – 3,3 (2,5–3,8), CC – 3,5 (3,0–3,8) баллов (Н=10,02, р=0,007, z2-3=3,04; р=0,007). Значимые различия установлены по критерию эмоциональное переедание для гена LEPR (генотип GG – 1,5 (1,0–1,8), генотип AG – 1,0 (1,0–1,3), генотип AA – 1,3 (1,0–1,8) баллов, Н=6,19, р=0,045). ВЫВОДЫ: установлены значимые различия при сравнении распределения частот аллелей гена LEP у детей с избыточной МТ и ожирением по сравнению с группой контроля. Выявлена ассоциация с МТ при рождении у детей по локусу rs1137101 гена IL-6. Варианты rs689 в интроне 1 гена INS, rs1800795 в промото- ре гена IL-6, rs1137101 в экзоне 6 гена LEPR ассоциированы с особенностями пищевого поведения у детей раннего возраста, оцененного с использованием опросника CEBQ.
Background:Methotrexate (MT) is a first-line drug in the treatment of rheumatoid arthritis (RA). The effectiveness and tolerability of the use of MT largely determines the prognosis of the course of the disease, the speed of achieving remission The development of hepatotoxicity (HT) is the most common adverse reaction, it is noted in 5-12.5% of cases and often requires the abolition of MT. In this regard, predicting the development of HT seems to be an important area of research.Objectives:to study genetic predictors of HT development in patients with RA using MT.Methods:44 patients with a reliable diagnosis of RA were included in study. All of the patients used MT at a dose of 15.0 (12.5-17.5) mg/week in combination with folic acid 3-5 mg / day outside of MT. The average age was 46.7 ± 12.3 years; females- 81.8% (n = 36); mail 18.2% (n = 8). The duration of RA is 5.3 ± 2.2 months. All patients were divided into two groups: the first study group (n = 17) included patients with RA who developed a HT reaction to MT, which required the abolition of MT; in the second- (n = 27) - comparison group - patients with good efficacy and tolerability of MT.Genotypes for polymorphic alleles were analyzed in all patients: C677T (rs1801133) and A1298C (rs1801131) of the methylenetetrahydrofolate reductase gene (MTHFR); 347C> G single-nucleotide polymorphism of the gene of aminoimidazole-carboxamidoriboside transformylase / inosine monophosphate cyclohydrolase (ATIC); c.80G> A locus of the SLC19A1 gene encoding the folate transporter membrane carrier protein.Groups were compared according to possible inheritance models: dominant, recessive, codominant. Statistical data processing was carried out using the SATISTICA 10.0 software package using descriptive and nonparametric statistics methods.Results:The frequency of occurrence of various mutations in genes that affect the metabolism of MT among patients with RA in the study and comparison groups are presented in table 1Table 1.The frequency of occurrence of various mutations in genes that affect the metabolism of MTGenetic optionStudy groupГТ+, n=17Comparison groupГТ <<->>, n=27MTHFR-A1298CCC56CA28AA1013MTHFR -C677TCC79CT817TT21347C>G ATICCC96CG619GG22SLC19A1c80A>GAA1122AG64GG00ГТ- hepatotoxicityWhen analyzing inheritance models, it was found that differences in hepatotoxicity for comparing genotypes (MTHFR-A1298C, MTHFR-C677T, SLC19A1c80A> G) were not statistically significant. A statistically significant increase in the risk of hepatotoxicity was found for dominant (2.18 (1.06-4.47), x2 = 4.38, p = 0.03) and codominant (0.42 (0.19-0.92), x2 = 5.23, p = 0.02) models for the 347C> G ATIC gene.Conclusion:Thus, an increase in the risk of hepatotoxicity for the dominant and codominant models for the 347C>G ATIC gene allows recommending genotyping of the alleles of this gene before MT administration in order to reduce the risk of hepatotoxic reactions.Disclosure of Interests:Natalia Martusevich Shareholder of: k, E. Aksenova: None declared, Katsiarina Gudkevich: None declared
Aims:The aim of this study was to investigate the effect of p62 on miR-NAs expression profile in exosomes derived from AML and the effect of exosomes derived from AML cells on angiogenesis. Methods: Electron microscopy and Western blot(WB) were used to confirm the exosomes derived from U937 cells, the controls and the cells knockdown p62. The Exiqon v19.0 microRNA MicroArray was used for profiling of miRNAs in exosomes derived from our specimens. The miRCURYÔ Hy3Ô/Hy5Ô Power labeling kit was used for miR-NA labelling. Then the Hy3Ô-labeled samples were hybridized on the miRCURYTM LNA Array (v.19.0). The gene ontology(GO) and Kyoto Encyclopedia of Genes and Genomes(KEGG) databases were used to predict the biological functions and potential mechanisms of the differentially expressed miRNAs in AML exosomes. Quantitative real-time polymerase chain reaction(qRT-PCR) was used to confirm the results of two downregulated microRNAs of exosomes. Then endothelial cell tube formation assays were used to investigate the effect of the angiogenesis of HUVECs which added exosomes derived from cells. Results: We demonstrated that 2080 miRNAs were expressed in exosomes derived from U937 cells with knockdown p62 and the controls, of which 215 miRNAs were upregulated and 208 miRNAs were downregulated in U937 cells with knockdown p62(Fold Change≥2.0, P < 0.05). The results revealed miR-3064-3p and miR-339-5p were downregulated in U937 cells with knockdown p62 by qRT-PCR and consistent with microarray profile. GO pathway analysis indicated that the highest enrichment was intercellular part by miRNA. There were 1460 biological processes in downregulated transcripts and there were 19 pathways related with vesicle and 1515 pathways in upregulated transcripts and 8 pathways about vesicle by BP analysis. MF analysis inducted protein binding, transcription regulator activity and DNA binding transcription factor activity were enriched (P < 0.05). Pathway analysis indicated that 84 pathways corresponded to upregulated transcripts and 55 pathways corresponded to downregulated transcripts (P < 0.05). Then we found that exosomes deviated from U937 cells can promote the angiogenesis of HUVECs Summary/Conclusion: Our data suggested that miRNA in exosomes may play an important role in the pathogenesis of AML, and knockdown p62 may treat AML by the miRNAs in exosomes as reducing angiogenesis.
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