28 research outputs found

    Phytoplankton light absorption in the deep chlorophyll maximum layer of the Black Sea

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    © The Author(s), 2019. This article is distributed under the terms of the Creative Commons Attribution License. The definitive version was published in Churilova, T., Suslin, V., Sosik, H. M., Efimova, T., Moiseeva, N., Moncheva, S., Mukhanov, V., Rylkova, O., & Krivenko, O. Phytoplankton light absorption in the deep chlorophyll maximum layer of the Black Sea. European Journal of Remote Sensing, 52, (2019): 123-136, doi: 10.1080/22797254.2018.1533389.Bio-optical data, obtained during six cruises in the Black Sea carried out during periods of seasonal stratification in years between 1996 and 2016, have been used to parametrize phytoplankton light absorption (aph(λ)) in the deep chlorophyll maximum (DCM) layer located near the bottom of euphotic zone. Relationships between aph(λ) and the sum of chlorophyll-a and phaeopigment concentrations (Chl-a) differed from those for the summertime upper mixed layer (UML). Notably, chlorophyll a specific absorption coefficients (a∗ph(λ)) were lower in the DCM and more comparable with a∗ph(λ) values typical for winter phytoplankton in the Black Sea. The aph(λ) spectral shapes in the DCM differed markedly from those in winter and in the summer UML, due to a shoulder at ~490 nm and a local maximum at ~550 nm corresponding to the absorption bands of phycourobilin and phycoerythrobilin. Light absorbing properties of phytoplankton in the DCM (amplitude and spectral shape of a∗ph(λ)) reflected physiological acclimation to local conditions on the cellular level and population shifts leading to changes in the biomass-dominant species, with Synechococcus spp. domination in the DCM. The parameterization of phytoplankton absorption in the DCM will enable refined spectral models of the downwelling radiance and primary production in the Black Sea.RAS funded this research [grant numbers АААА-А18-118020890112-1, АААА-А18-118020790229-7 and АААА-18-118012690119-7]. This work was partly supported by the Russian Foundation for Basic Research, projects [numbers 17-05-00113 and 18-45-920070]

    ПОВЫШЕНИЕ УРОВНЯ ПРОВОСПАЛИТЕЛЬНЫХ ЦИТОКИНОВ В ПЛАЗМЕ КРОВИ У ПАЦИЕНТОВ С ХРОНИЧЕСКОЙ ТРОМБОЭМБОЛИЧЕСКОЙ ЛЕГОЧНОЙ ГИПЕРТЕНЗИЕЙ

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    HighlightsIL-8 and MCP-1 have a significant role in the CTEPH pathogenesis, which indicates the importance of nonspecific immunity in the formation and progression of CTEPH. The coupling between cytokines and hemodynamic parameters, cardiac structural changes and plasma biochemical parameters were determined. AbstractBackground. Chronic thromboembolic pulmonary hypertension (CTEPH) pathogenesis is complex and not fully understood. Particular attention to the microvascular damage genesis in CTEPH is given to aseptic inflammation, which in turn could be mediated through various molecular mechanisms. According to the conflicting and incomplete data on changes in the profile of factors controlling inflammation in CTEPH, research in this field would identify new therapeutic targets for the prevention and treatment of CTEPH.Aim. To study the profile of plasma proinflammatory cytokines in patients with chronic thromboembolic pulmonary hypertension (CTEPH) and evaluate the coupling of these cytokines with the main morphofunctional and laboratory values of the disease severity.Methods. 34 patients with CTEPH were included in this study. To characterize the group, the following methods were used: echocardiographic examination, catheterization of the right cardiac chambers. Biomarkers of heart failure, systemic inflammation, as well as erythropoiesis and iron metabolism were assessed in all patients. The control group included 10 donors. To study the proinflammatory cytokine profile in plasma, interleukins (IL) 6, 8, 18, monocyte chemoattractant protein-1 (MCP-1) and matrix metalloproteinase 9 were determined using standard enzyme-linked immunosorbent assay (ELISA) kits.Results. Hemodynamic and morphofunctional changes in the pulmonary circulation specific to pulmonary hypertension were determined with catheterization of the right cardiac chambers and echocardiography. During plasma proinflammatory cytokines analysis, a significant increase in the level of IL-8 (p = 0.030) and MCP-1 (p = 0.031) in CTEPH group compared to the control group was observed. No significant differences for other analyzed markers were found. In the elaboration of the correlation analysis, moderate inverse coupling between proinflammatory markers and hemodynamic parameters characterizing the CTEPH severity were revealed, as well as positive correlations with parameters of remodeling of the right cardiac chambers and iron metabolism.Conclusion. The increased levels of IL-8 and MCP-1 in patients with CTEPH identified in the present study indicate a significant role of nonspecific immunity in the formation and progression of CTEPH. The coupling between cytokines and hemodynamic parameters, structural cardiac changes and plasma biochemical parameters were determined. Based on the obtained data, it is possible to develop new medicinal substances, targeting towards proinflammatory cytokines, their receptors and signaling pathways.Основные положенияИЛ-8 и MCP-1 играют существенную роль в патогенезе хронической тромбоэмболической легочной гипертензии, что указывает на важное значение неспецифического иммунитета в формировании и прогрессировании данного заболевания. Определена связь цитокинов с показателями гемодинамики, структурными изменениями сердца и биохимическими показателями плазмы крови. РезюмеАктуальность. Патогенез хронической тромбоэмболической легочной гипертензии (ХТЭЛГ) сложен и до конца не изучен. Особое внимание в генезе микрососудистого поражения при ХТЭЛГ уделяют асептическому воспалению, которое в свою очередь может быть опосредовано различными молекулярными механизмами. Учитывая противоречивые и неполные данные об изменении профиля факторов, контролирующих воспаление при ХТЭЛГ, исследования в этой области позволят определить новые терапевтические мишени для профилактики и лечения ХТЭЛГ.Цель. Изучить профиль провоспалительных цитокинов в плазме крови у пациентов с ХТЭЛГ и оценить связь этих цитокинов с основными морфофункциональными и лабораторными показателями тяжести течения заболевания.Материалы и методы. В исследование включены 34 пациента с верифицированным диагнозом ХТЭЛГ. Для характеризации группы использованы эхокардиографическое исследование и катетеризация правых камер сердца. У всех больных оценены биомаркеры сердечной недостаточности, системного воспаления, а также эритропоэза и обмена железа. В группу контроля вошли 10 человек-доноров. Для изучения профиля провоспалительных цитокинов в плазме крови определены интерлейкины (ИЛ) 6, 8, 18, моноцитарный хемоаттрактантный белкок 1 (MCP-1) и матриксная металлопротеиназа 9 с помощью стандартных наборов для иммуноферментного анализа.Результаты. По данным катетеризации правых камер сердца и эхокардиографии определены гемодинамические и морфофункциональные изменения малого круга кровообращения, характерные для легочной гипертензии. При анализе уровня провоспалительных цитокинов в плазме крови в группе ХТЭЛГ по сравнению с группой контроля отмечено значимое повышение ИЛ-8 (p = 0,030) и MCP-1 (p = 0,031). По другим проанализированным маркерам значимых различий не получено. В результате корреляционного анализа выявлены умеренные обратные взаимосвязи провоспалительных маркеров с гемодинамическими параметрами, характеризующими тяжесть ХТЭЛГ, а также положительные корреляционные связи с показателями ремоделирования правых камер сердца и обмена железа.Заключение. Установленное в настоящем исследовании повышение уровней ИЛ-8 и MCP-1 у пациентов с ХТЭЛГ указывает на значительную роль неспецифического иммунитета в формировании и прогрессировании ХТЭЛГ. Определены взаимосвязи цитокинов с показателями гемодинамики, структурными изменениями сердца и биохимическими показателями плазмы крови. На основе полученных данных возможна разработка новых лекарственных субстанций, мишенями для которых будут провоспалительные цитокины, их рецепторы и сигнальные пути

    Molecular structure, conformation, potential to internal rotation, and ideal gas thermodynamic properties of 3-fluoroanisole and 3,5-difluoroanisole as studied by gas-phase electron diffraction and quantum chemical calculations

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    Dorofeeva OV, Vishnevskiy YV, Rykov AN, et al. Molecular structure, conformation, potential to internal rotation, and ideal gas thermodynamic properties of 3-fluoroanisole and 3,5-difluoroanisole as studied by gas-phase electron diffraction and quantum chemical calculations. Journal of Molecular Structure. 2006;789(1-3):100-111

    Unusual Oligomeric Laccase-like Oxidases from Ascomycete <i>Curvularia geniculata</i> VKM F-3561 Polymerizing Phenylpropanoids and Phenolic Compounds under Neutral Environmental Conditions

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    The unique oligomeric alkaliphilic laccase-like oxidases of the ascomycete C. geniculata VKM F-3561 (with molecular masses about 1035 and 870 kDa) were purified and characterized for the first time. The ability of the enzymes to oxidize phenylpropanoids and phenolic compounds under neutral environmental conditions with the formation of previously unknown di-, tri-, and tetrameric products of transformation was shown. The possibility to obtain industrially valuable compounds (dihydroxybenzyl alcohol and hydroxytyrosol) from caffeic acid using laccase-like oxidases of C. geniculata VKM F-3561 has been shown. Complete nucleotide sequence of the laccase gene, which is expressed at the peak of alkaliphilic laccase activity of the fungus, and its promoter region were determined. Based on the phylogenetic analysis of the nucleotide sequence, the nearest relationship of the isolated laccase gene with similar genes of fungi of the genera Alternaria, Bipolaris, and Cochliobolus was shown. Homologous model of the laccase structure was predicted and a proton channel was found, which was presumably responsible for the accumulation and transport of protons to T2/T3-copper center in the alkaliphilic laccase molecule and providing the functional activity of the enzyme in the neutral alkaline environment conditions

    Conversion of 2-Fluoromuconate to cis-Dienelactone by Purified Enzymes of Rhodococcus opacus 1cp

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    The present study describes the (19)F nuclear magnetic resonance analysis of the conversion of 3-halocatechols to lactones by purified chlorocatechol 1,2-dioxygenase (ClcA2), chloromuconate cycloisomerase (ClcB2), and chloromuconolactone dehalogenase (ClcF) from Rhodococcus opacus 1cp grown on 2-chlorophenol. The 3-halocatechol substrates were produced from the corresponding 2-halophenols by either phenol hydroxylase from Trichosporon cutaneum or 2-hydroxybiphenyl 3-mono-oxygenase from Pseudomonas azelaica. Several fluoromuconates resulting from intradiol ring cleavage by ClcA2 were identified. ClcB2 converted 2-fluoromuconate to 5-fluoromuconolactone and 2-chloro-4-fluoromuconate to 2-chloro-4-fluoromuconolactone. Especially the cycloisomerization of 2-fluoromuconate is a new observation. ClcF catalyzed the dehalogenation of 5-fluoromuconolactone to cis-dienelactone. The ClcB2 and ClcF-mediated reactions are in line with the recent finding of a second cluster of chlorocatechol catabolic genes in R. opacus 1cp which provides a new route for the microbial dehalogenation of 3-chlorocatechol

    Inhibition of JAK1,2 Prevents Fibrotic Remodeling of Pulmonary Vascular Bed and Improves Outcomes in the Rat Model of Chronic Thromboembolic Pulmonary Hypertension

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    Chronic thromboembolic pulmonary hypertension (CTEPH) is a rare complication of acute pulmonary embolism with poor clinical outcomes. Therapeutic approaches to prevention of fibrotic remodeling of the pulmonary vascular bed in CTEPH are limited. In this work, we tested the hypothesis that Janus kinase 1/2 (JAK1/2) inhibition with ruxolitinib might prevent and attenuate CTEPH in a rat model. CTEPH was induced by repeated embolization of the pulmonary artery with partially biodegradable 180 ± 30 μm alginate microspheres. Two weeks after the last injection of microspheres, ruxolitinib was administered orally at doses of 0.86, 2.58, and 4.28 mg/kg per day for 4 weeks. Prednisolone (1.475 mg/kg, i.m.) was used as a reference drug. Ruxolitinib in all doses as well as prednisolone reduced pulmonary vascular wall hypertrophy. Ruxolitinib at a dose of 2.58 mg/kg and prednisolone reduced vascular wall fibrosis. Prednisolone treatment resulted in decreased right ventricular systolic pressure. Pulmonary vascular resistance was lower in the prednisolone and ruxolitinib (4.28 mg/kg) groups in comparison with the placebo group. The plasma level of brain natriuretic peptide was lower in groups receiving ruxolitinib at doses of 2.58 and 4.28 mg/kg versus placebo. This study demonstrated that JAK1/2 inhibitor ruxolitinib dose-dependently reduced pulmonary vascular remodeling, thereby preventing CTEPH formation in rats

    Simple Predictors for Cardiac Fibrosis in Patients with Type 2 Diabetes Mellitus: The Role of Circulating Biomarkers and Pulse Wave Velocity

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    Cardiac fibrosis is the basis of structural and functional disorders in patients with diabetes mellitus (T2DM). A wide range of laboratory and instrumental methods is used for its prediction. The study aimed to identify simple predictors of cardiac fibrosis in patients with T2DM based on the analysis of circulating fibrosis biomarkers and arterial stiffness. The study included patients with T2DM (n = 37) and cardiovascular risk factors (RF, n = 27) who underwent ECHO, cardiac magnetic resonance imaging (MRI), pulse wave analysis (PWV), reactive hyperemia (RH), peripheral arterial tonometry, carotid ultrasonography, and assessment of serum fibrosis biomarkers. As a control group, 15 healthy subjects were examined. Left ventricular concentric hypertrophy was accompanied by an increased serum galectin-3 level in T2DM patients. There was a relationship between the PICP and HbA1c levels in both main groups (R2 = 0.309; p = 0.014). A negative correlation between PICP level and the global longitudinal strain (GLS) was found (r = &minus;0.467; p = 0.004). The RH index had a negative correlation with the duration of diabetes (r = &minus;0.356; p = 0.03), the carotid-femoral PWV (r = &minus;0.371; p = 0.024), and the carotid intima-media thickness (r = &minus;0.622; p &lt; 0.001). The late gadolinium-enhanced (LGE) cardiac MRI was detected in 22 (59.5%) T2DM and in 4 (14.85%) RF patients. Diabetes, its baseline treatment with metformin, HbA1c and serum TIMP-1 levels, and left ventricle hypertrophy had moderate positive correlations with LGE findings (p &lt; 0.05). Using the multivariate regression analysis, increased TIMP-1 level was identified as an independent factor associated with cardiac fibrosis

    Sympathetic Denervation and Pharmacological Stimulation of Parasympathetic Nervous System Prevent Pulmonary Vascular Bed Remodeling in Rat Model of Chronic Thromboembolic Pulmonary Hypertension

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    Chronic thromboembolic pulmonary hypertension (CTEPH) develops in 1.5&ndash;2.0% of patients experiencing pulmonary embolism (PE) and is characterized by stable pulmonary artery obstruction, heart failure, and poor prognosis. Little is known about involvement of autonomic nervous system (ANS) in the mechanisms of CTEPH. This study was aimed at evaluation of the effect of vagal and sympathetic denervation, as well as stimulation of the parasympathetic nervous system, on the outcomes of CTEPH in rats. CTEPH was induced by multiple intravenous injections of alginate microspheres. Sympathetic and vagal denervation was performed using unilateral surgical ablation of the stellate ganglion and vagotomy, respectively. Stimulation of the parasympathetic nervous system was carried out by administering pyridostigmine. The effect of neuromodulatory effects was assessed in terms of hemodynamics, histology, and gene expression. The results demonstrated the key role of ANS in the development of CTEPH. Sympathetic denervation as well as parasympathetic stimulation resulted in attenuated pulmonary vascular remodeling. These salutary changes were associated with altered MMP2 and TIMP1 expression in the lung and decreased FGFb level in the blood. Unilateral vagotomy had no effect on physiological and morphological outcomes of the study. The data obtained contribute to the identification of new therapeutic targets for CTEPH treatment
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