Micro-Raman study of crichtonite group minerals enclosed into mantle garnet

We report the first comprehensive micro-Raman study of crichtonite group minerals (CGM) as inclusions in pyropic garnet grains from peridotite and pyroxenite mantle xenoliths of the Yakutian kimberlites as well as in garnet xenocrysts from the Aldan shield lamprophyres (Russia). The CGM form (i) morphologically oriented needles, lamellae, and short prisms and (ii) optically unoriented subhedral to euhedral grains, either single or intergrown with other minerals. We considered common mantle-derived CGM species (like loveringite, lindsleyite, and their analogues), with Ca, Ba, or Sr dominating in the dodecahedral A site and Zr or Fe in the octahedral B site. The Raman bands at the region of 600–830 cm−1 are indicative of CGM and their crystal-chemical distinction, although the intensity and shape of the bands appear to be dependent on laser beam power and wavelength. The factor-group analysis based on the loveringite crystal structure showed the octahedral and tetrahedral cation groups with 18f and 6c Wyckoff positions, namely, dominantly TiO6 and to a lower extent CrO6, MgO4, and FeO4 groups, to be the major contributors to the Raman spectral features. The ionic groups with dodecahedral (M0) and octahedral (M1) coordination are inactive for Raman scattering while active in infrared absorption. A number of observed Raman modes in the CGM spectra are several times lower than that predicted by the factor group analysis. The noticed broadening of modes in the CGM Raman spectra may result from a combining of bands at the narrow frequency shift regions. Solid solution behavior, luminescence, and partial metamictization of the CGM may exert additional influence on the Raman band shape. The Raman spectral features showed CGM to be accurately identified and distinguished from other Ti-, Fe-, Cr-, and Zr-containing oxides (e.g., ilmenite or those of spinel and magnetoplumbite groups) occurring as accessory mantle minerals. © 2020 The Authors. Journal of Raman Spectroscopy published by John Wiley & Sons LtdRussian Science Foundation, RSF: 18‐77‐10062Council on grants of the President of the Russian FederationThis study was supported by the Russian Science Foundation (Grant 18‐77‐10062). The equipment of the Ural Center for Shared Use «Modern Nanotechnology», Ural Federal University, and the Analytical Center for Multi‐elemental and Isotope Research, IGM, was used. Sampling was supported by the Russian Federation state assignment project of IGM. We are grateful to Nikolai V. Sobolev for Samples O‐173, O‐39, and O‐264. Vladimir N. Korolyuk, Elena N. Nigmatulina (IGM), and Allan Patchen (UT) are highly appreciated for the help with EMP analyses. We express our sincere thanks to F. Nestola and an anonymous reviewer for their thorough reviews and helpful suggestions, and to C. Marshall for regardful editorial handling of the manuscript on every stage of its revision

Neuroinflammation, Mast Cells, and Glia: Dangerous Liaisons

The perspective of neuroinflammation as an epiphenomenon following neuron damage is being replaced by the awareness of glia and their importance in neural functions and disorders. Systemic inflammation generates signals that communicate with the brain and leads to changes in metabolism and behavior, with microglia assuming a pro-inflammatory phenotype. Identification of potential peripheral-to-central cellular links is thus a critical step in designing effective therapeutics. Mast cells may fulfill such a role. These resident immune cells are found close to and within peripheral nerves and in brain parenchyma/meninges, where they exercise a key role in orchestrating the inflammatory process from initiation through chronic activation. Mast cells and glia engage in crosstalk that contributes to accelerate disease progression; such interactions become exaggerated with aging and increased cell sensitivity to stress. Emerging evidence for oligodendrocytes, independent of myelin and support of axonal integrity, points to their having strong immune functions, innate immune receptor expression, and production/response to chemokines and cytokines that modulate immune responses in the central nervous system while engaging in crosstalk with microglia and astrocytes. In this review, we summarize the findings related to our understanding of the biology and cellular signaling mechanisms of neuroinflammation, with emphasis on mast cell-glia interactions

An oribatid mite (Arachnida: Acari) from the Oxford Clay (Jurassic: Upper Callovian) of South Cave Station Quarry, Yorkshire, UK

A single specimen of a new species of oribatid mite belonging to the genus Jureremus Krivolutsky, in Krivolutsky and Krassilov 1977, previously described from the Upper Jurassic of the Russian Far East, is described as J. phippsi sp. nov. The mite is preserved by iron pyrite replacement, and was recovered by sieving from the Oxford Clay Formation (Jurassic: Upper Callovian) of South Cave, Yorkshire. It is the first record of a pre-Pleistocene mite, and the second species record of the family Cymbaeremaeidae, from the British Isles; also, it is only the third record of Acari from the Jurassic Period. The presence of a terrestrial mite in a sedimentary sequence of open marine origin is noteworthy, and suggestions for its mode of transport to the site of deposition are discussed

P2 purinergic receptor modulation of cytokine production

Cytokines serve important functions in controlling host immunity. Cells involved in the synthesis of these polypeptide mediators have evolved highly regulated processes to ensure that production is carefully balanced. In inflammatory and immune disorders, however, mis-regulation of the production and/or activity of cytokines is recognized as a major contributor to the disease process, and therapeutics that target individual cytokines are providing very effective treatment options in the clinic. Leukocytes are the principle producers of a number of key cytokines, and these cells also express numerous members of the purinergic P2 receptor family. Studies in several cellular systems have provided evidence that P2 receptor modulation can affect cytokine production, and mechanistic features of this regulation have emerged. This review highlights three separate examples corresponding to (1) P2Y6 receptor mediated impact on interleukin (IL)-8 production, (2) P2Y11 receptor-mediated affects on IL-12/23 output, and (3) P2X7 receptor mediated IL-1β posttranslational processing. These examples demonstrate important roles of purinergic receptors in the modulation of cytokine production. Extension of these cellular observations to in vivo situations may lead to new therapeutic strategies for treating cytokine-mediated diseases

Purinergic signalling and immune cells

This review article provides a historical perspective on the role of purinergic signalling in the regulation of various subsets of immune cells from early discoveries to current understanding. It is now recognised that adenosine 5'-triphosphate (ATP) and other nucleotides are released from cells following stress or injury. They can act on virtually all subsets of immune cells through a spectrum of P2X ligand-gated ion channels and G protein-coupled P2Y receptors. Furthermore, ATP is rapidly degraded into adenosine by ectonucleotidases such as CD39 and CD73, and adenosine exerts additional regulatory effects through its own receptors. The resulting effect ranges from stimulation to tolerance depending on the amount and time courses of nucleotides released, and the balance between ATP and adenosine. This review identifies the various receptors involved in the different subsets of immune cells and their effects on the function of these cells

Субпопуляции моноцитов крови у больных с генерализованной гипоксией

The aim of the work is to establish general regularities and features of differentiation of blood monocytes into 4 subpopulations in diseases associated with circulatory and respiratory hypoxia.Materials and methods. 18 patients with ischemic heart disease (IHD), 12 patients with ischemic cardiomyopathy (ICMP), 14 patients with chronic obstructive pulmonary disease (COPD), 15 patients with newly diagnosed infiltrative pulmonary tuberculosis (PTB) and 12 healthy donors were examined. In whole blood, we determined the relative number of different subpopulations of monocytes by flow cytometry. The results were analyzed by statistical methods.Results. It is shown that an increase in the number of classical (80.56 [77.60; 83.55]%) and the deficit of intermediate (10.38 [9.36; 11.26]%), non-classical (6.03 [5.24; 6.77]%) and transitional (2.14 [1.41; 3.92] %) monocytes in the blood is determined in patients with COPD when compared with the group of healthy donors (p < 0.05). In groups of patients with PTB and IHD, an increase in the number of intermediate monocytes (26.24 respectively [22.38; 42.88] % and 25.27 [15.78; 31.39]%) and the lack of transitional cells (1.77 [1.36; 3.74]% and 2.68 [2.63; 4.0]%) at the normal content of classical and non-classical forms of monocytes (p < 0.05) is detected. In patients with ICMP, a decrease in the number of non-classical monocytes (up to 5.05 [4.08; 6.58]%) is combined with the normal cell content of other subpopulations (p < 0.05). The interrelation between the number of classical and intermediate monocytes in patients with COPD (r = –0.63; p < 0.05), PTB (r = –0.72; p < 0.01), IHD (r = –0.59; p < 0.05), ICMP (r = –0.58; p < 0.05) was established.Conclusion. In COPD associated with generalized hypoxia, an increase in the number of classical monocytes is combined with a deficiency of their other subpopulations in the blood. In PTB and IHD, antigenic stimulation of the immune system mediates accelerated differentiation of monocytes from classical to intermediate forms with a decrease in the number of transitional cells regardless of the etiology of the disease (infectious or non-infectious) and the type of hypoxia (respiratory or circulatory).Цель работы – установить общие закономерности и особенности дифференцировки моноцитов крови на четыре субпопуляции (классические (CD14hiCD16-), промежуточные (CD14hiCD16lo), неклассические (CD14loCD16lo) и переходные (CD14loCD16-)) при заболеваниях, ассоциированных с циркуляторной и дыхательной гипоксией.Материалы и методы. Обследованы 18 больных ишемической болезнью сердца (ИБС), 12 больных ишемической кардиомиопатией (ИКМП), 14 больных с хронической обструктивной болезнью легких (ХОБЛ), 15 больных с впервые выявленным инфильтративным туберкулезом легких (ТБЛ) и 12 здоровых доноров. В цельной крови определяли относительное количество различных субпопуляций моноцитов методом проточной цитометрии. Полученные результаты анализировали статистическими методами.Результаты. Показано, что у больных ХОБЛ определяется увеличение доли классических (80,56 [77,60; 83,55]%) и дефицит промежуточных (10,38 [9,36; 11,26]%), неклассических (6,03 [5,24; 6,77]%) и переходных (2,14 [1,41; 3,92]%) моноцитов в крови по сравнению с группой здоровых доноров (р < 0,05). В группах больных с ТБЛ и ИБС обнаруживается повышение количества промежуточных моноцитов (соответственно 26,24 [22,38; 42,88]% и 25,27 [15,78; 31,39]%) на фоне дефицита переходных клеток (1,77 [1,36; 3,74]% и 2,68 [2,63; 4,0]%) при нормальном содержании классических и неклассических форм моноцитов (р < 0,05). У больных ИКМП снижение численности неклассических моноцитов (до 5,05 [4,08; 6,58]%) сочетается с нормальным содержанием клеток остальных субпопуляций (р < 0,05). Установлена взаимосвязь между численностью классических и промежуточных моноцитов у больных ХОБЛ (r = –0,63; p < 0,05), ТБЛ (r = –0,72; p < 0,01), ИБС (r = –0,59; p < 0,05), ИКМП (r = –0,58; p < 0,05).Заключение. При ХОБЛ, ассоциированной с генерализованной гипоксией, увеличение числа классических моноцитов сочетается с дефицитом остальных их субпопуляций в крови. При ТБЛ и ИБС антигенная стимуляция иммунной системы опосредует ускоренную дифференцировку моноцитов из классических в промежуточные формы при снижении числа переходных клеток вне зависимости от этиологии заболевания (инфекционная или неинфекционная) и вида гипоксии (дыхательная или циркуляторная)

Purinergic signalling links mechanical breath profile and alveolar mechanics with the pro-inflammatory innate immune response causing ventilation-induced lung injury

Severe pulmonary infection or vigorous cyclic deformation of the alveolar epithelial type I (AT I) cells by mechanical ventilation leads to massive extracellular ATP release. High levels of extracellular ATP saturate the ATP hydrolysis enzymes CD39 and CD73 resulting in persistent high ATP levels despite the conversion to adenosine. Above a certain level, extracellular ATP molecules act as danger-associated molecular patterns (DAMPs) and activate the pro-inflammatory response of the innate immunity through purinergic receptors on the surface of the immune cells. This results in lung tissue inflammation, capillary leakage, interstitial and alveolar oedema and lung injury reducing the production of surfactant by the damaged AT II cells and deactivating the surfactant function by the concomitant extravasated serum proteins through capillary leakage followed by a substantial increase in alveolar surface tension and alveolar collapse. The resulting inhomogeneous ventilation of the lungs is an important mechanism in the development of ventilation-induced lung injury. The high levels of extracellular ATP and the upregulation of ecto-enzymes and soluble enzymes that hydrolyse ATP to adenosine (CD39 and CD73) increase the extracellular adenosine levels that inhibit the innate and adaptive immune responses rendering the host susceptible to infection by invading microorganisms. Moreover, high levels of extracellular adenosine increase the expression, the production and the activation of pro-fibrotic proteins (such as TGF-β, α-SMA, etc.) followed by the establishment of lung fibrosis

3D scanning probe nanotomography of tissue spheroid fibroblasts interacting with electrospun polyurethane scaffold

We present a 3D study of nanostructural features of a bioprinted tissue spheroid interacting with polyurethane dual-scale biocompatible scaffold manufactured by three-dimensional printing and electrospinning. Three-dimensional analysis of fibroblasts interacting with electrospun polyurethane fibers was conducted using scanning probe nanotomography with an experimental setup combining ultramicrotome and a scanning probe microscope. Three-dimensional reconstruction demonstrates direct visualization of cell membrane protrusions and coherent cell-fiber interfaces, the formation of which is a prerequisite for an efficient tissue engineered implant. Analysis of obtained 3D data allows for quantitative calculation of the important morphological parameters of adhered cells, scaffolds, and cell-scaffold interfaces. The proposed method may be successfully applied to investigate 3D cell-scaffold constructs at nanoscale