Application of Mössbauer Spectroscopy for Identification of Iron-Containing Components in Upper Silesian Topsoil Being under Industrial Anthropopressure

The main objective of the presented preliminary study was the identification of iron-containing phases. Iron-containing phases had accumulated in organic topsoil horizons collected from an area that has long been affected by the steel industry and emissions from power plants. X-ray diffraction and Mössbauer spectroscopy methods were used for the determination of the iron-containing mineral phases in topsoil subsamples which, after two-staged separation, varied in terms of magnetic susceptibility and granulometry. The Mössbauer spectra were recorded using paramagnetic and magnetic components, although the latter occurred only in the strongly magnetic fraction. The central part of spectra was fitted by two doublets (D1 and D2), which were identified as aluminosilicates. Simultaneously, the experimental spectra were described using several Zeeman sextets (Z1, Z2, and Z3) corresponding to the occurrence of hematite and magnetite-like phases with iron in tetrahedral and octahedral sites. Identification of magnetic phases in the tested material, including hematite, led to the conclusion that soil contamination in the studied area was presumably caused by emissions from a nearby power plant. Magnetite-like phases with a different iron content detected in topsoil samples could be related to metallurgical and coking processes, reflecting the specificity of the industrial area from which the samples were taken. The specific composition of the iron-containing aluminosilicates also illustrated the intense and long-lasting impact of the steel and coking industries on the studied area.     

Influence of the Selected Physical Modifier on the Dynamical Behavior of the Polymer Composites Used in the Aviation Industry

In this research, an analysis of polymer composite with the matrix of L285-cured hardener H286 and six reinforcement layers of carbon fabric GG 280 T was provided. It involved a comparison of the dynamical behavior responses for three cases of composite structures in the context of the presence of the mass share modifier. The samples with the addition of a physical modifier with varying mass percentages were investigated by being subjected to dynamic tests with specific parameters, i.e., constant excitation amplitude and vibration frequency in the vicinity of the base resonance zone. The analysis allowed for indicating the relationship between the composition of the prepared composites and their dynamic response via stiffness characteristics. In addition, the investigation resulted in determining the range of harmful dynamical operating conditions, which may contribute to damage to the composite structures.     

Same host,same lagoon,different transmission pathways: effects of exogenous factors on larval emergence in two marine digenean parasites

Due to their shallow and confined nature, lagoons provide excellent conditions for the transmission of digenean trematode parasites that require two or more intermediate hosts for the completion of their complex life cycles. However, these unstable environments are characterised by an internal heterogeneity and a large variation of a range of abiotic variables. We conducted a series of experiments in a comparative framework to assess the effect of a number of exogenous factors known to exhibit marked fluctuations in the lagoonal environment, i.e. temperature, salinity, water level and photoperiod, on larval emergence of two sympatric parasites, Cainocreadium labracis and Macvicaria obovata, which share the snail intermediate host, Gibbula adansonii, and a sit-and-wait downstream host-finding strategy. Our results demonstrated contrasting patterns and rates of larval emergence indicating an overall differential response of the two species to the variation of the environmental factors. Cercariae of M. obovata exhibited increased emergence rates at elevated temperature (with a sharp increase at 15 °C), decreased salinity (35–25 practical salinity units (psu)) and low water levels, whereas larval emergence of C. labracis was unaffected by the experimental variation in temperature and water level and showed decreased rates at decreased salinity levels (35–25 psu). The differential impact of the variable environmental conditions indicates the complexity of the patterns of exogenous control modifying parasite transmission and abundance in the lagoonal environment. Most importantly, the contrasting rhythms of larval emergence indicate endogenous control associated with the different transmission pathways of the two opecoelid digeneans.     

A risk of essential thrombocythemia in carriers of constitutional CHEK2 gene mutations

Germline mutations of the CHEK2 gene have been reported in some myeloid and lymphoid malignancies, but their impact on development of essential thrombocythemia has not been studied. In 16 out of 106 (15.1%) consecutive patients, newly diagnosed with essential thrombocythemia, we found one of four analyzed CHEK2 mutations: I157T, 1100delC, IVS2+1G>A or del5395. They were associated with the increased risk of disease (OR=3.8; P=0.002). The median age at ET diagnosis among CHEK2+/JAK2V617F+ patients was seven years lower than that among CHEK2-/JAK2V617F+ (52 vs. 59 years; P=0.04), whereas there was no difference in the medians of hematologic parameters between these groups. The results obtained suggest that CHEK2 mutations could potentially contribute to the susceptibility to essential thrombocythemia. The germline inactivation of CHEK2, as it seems, has no direct impact on the development of disease, but it could cause disruption of cell cycle checkpoints and initiate or support the cancerogenic process of essential thrombocythemia at a younger age.     

Immunopathology of exercise-induced bronchoconstriction in athletes — A new modified inflammatory hypothesis

Elite athletes have a higher prevalence of exercise-induced bronchoconstriction than the general population. The pathogenesis of exercise-induced bronchoconstriction is not fully elucidated. Increasing evidence suggests that airway inflammation plays a major role in the immunopathogenesis of exercise-induced bronchoconstriction. The aim of our review is to discuss existing evidence and to present a new, modified inflammatory hypothesis of exercise-induced bronchoconstriction. Exercise alters the number and function of circulating immune cells. Episodes of upper respiratory symptoms in elite athletes do not follow the usual seasonal patterns. Moreover, they have an unusual short-term duration, which suggests a non-infectious etiology. If the pro-inflammatory response to exercise has the potential to induce symptoms that mimic respiratory tract infection, it definitely up-regulates pro-inflammatory cytokine expression in the airways. We can conclude that exercise up-regulates airway cytokine expression in a way that favors inflammation and allergic reactions in bronchi and lowers the threshold for bronchoconstriction to different stimuli like cool, dry air, allergens, and pollutants.     

Probing nanoparticle translocation across the permeable endothelium in experimental atherosclerosis

Therapeutic and diagnostic nanomaterials are being intensely studied for several diseases, including cancer and atherosclerosis. However, the exact mechanism by which nanomedicines accumulate at targeted sites remains a topic of investigation, especially in the context of atherosclerotic disease. Models to accurately predict transvascular permeation of nanomedicines are needed to aid in design optimization. Here we show that an endothelialized microchip with controllable permeability can be used to probe nanoparticle translocation across an endothelial cell layer. To validate our in vitro model, we studied nanoparticle translocation in an in vivo rabbit model of atherosclerosis using a variety of preclinical and clinical imaging methods. Our results reveal that the translocation of lipid–polymer hybrid nanoparticles across the atherosclerotic endothelium is dependent on microvascular permeability. These results were mimicked with our microfluidic chip, demonstrating the potential utility of the model system.Improving the design of nanomedicines is key for their success and ultimate clinical application (1). The accumulation of such therapeutic or diagnostic nanomaterials primarily relies on enhanced endothelial permeability of the microvasculature in diseased tissue (2). This holds true for a wide range of pathological conditions, including inflammation, atherosclerosis, and most notably, oncological disease (3–6). Although attributed to the enhanced permeability and retention (EPR) effect, the exact mechanism by which nanoparticles accumulate in tumors continues to be a topic of research (7, 8). The “leaky” vasculature of tumors, which facilitates the extravasation of nanoparticles from microvessels (9), is a heterogeneous phenomenon that varies between different tumor models and even more so in patients. Moreover, the exploitation of nanomedicines in other conditions with enhanced microvessel permeability has only recently begun to be studied in detail. For example, in the last 5 y, a small but increasing number of preclinical studies that apply nanoparticle therapy in atherosclerosis models has surfaced (10). Although several targeting mechanisms have been proposed (4), the exact mechanism by which nanoparticles accumulate in atherosclerotic plaques remains to be investigated, but is likely facilitated by highly permeable neovessels that penetrate into the plaque from the vasa vasorum (Fig. 1A), a network of microvessels that supplies the wall of larger vessels (11).Open in a separate windowFig. 1.Development of an endothelialized microfluidic device to probe nanoparticle translocation over a permeable microvessel. (A) Schematics of continuous normal capillaries surrounding the vessel wall as well as permeable capillaries that penetrate into the atherosclerotic plaque from the vasa vasorum. (B) Schematic of an endothelialized microfluidic device that consists of two-layer microfluidic channels that are separated by a porous membrane (3 μm pore) on which ECs are grown. (C) TEER was dynamically measured across the endothelial layer on the membrane between the upper and lower channels. (D) A well-established monolayer of the microvascular endothelium is formed at TEER ∼400 (Ω·cm²). (E) The monolayer becomes highly permeable when stimulated with the inflammatory mediator, TNF-α, as well as with shear stress, with disruption of intercellular junctional structures (i.e., adherens junctions) between ECs, as evidenced by patchy expression of VE–cadherin (green) in the image on the right versus the left. Blue depicts nuclei stained with DAPI. (Scale bar, 20 μm.) (F) FITC–albumin translocation through the endothelial monolayer increases when the chip is treated with TNF-α. (G) The chip with endothelium cultured in different culture media [base, +FBS, +growth factors (GFs)] for 6 h shows a decrease in TEER with increased FITC–albumin translocation. No cell indicates the membrane only. TEER was normalized to the level with no cells (membrane only). (H) Schematic and TEM image of PEGylated lipid-coated nanoparticles encapsulating PLGA-conjugated AuNCs and Cy5.5. The average size was 69.7 ± 14 nm, which was measured from TEM images. (Scale bar, 100 nm.) Details on labeling, synthesis, characterization, and large-scale production procedures can be found in Materials and Methods and Fig. S2.Advances in biomedical imaging allow the study of plaque-targeting nanoparticles in a dynamic fashion with exceptional detail (12, 13). Microchip technology has the potential to monitor nanoparticle behavior at the (sub)cellular level. Microfluidic chips in which endothelial cells (ECs) are grown in the channels can serve as unique in vitro test systems to study microvascular function and associated disorders (14–18). They allow the isolation of specific biological hallmarks relevant to nanoparticle accumulation, such as the leaky endothelium. In the current study, we validate the potential utility of our microchip technology to study nanoparticle translocation over the endothelium and combine this with in vivo and ex vivo multimodality imaging studies on a rabbit model to better understand nanoparticle targeting of atherosclerotic plaques.     

A single nucleotide polymorphism −35 kb T > C (rs9264942) is strongly associated with psoriasis vulgaris depending on HLA-Cw06

HLA class I molecules play a role both in viral infection control and in autoimmune diseases development. rs9264942T > C polymorphism in HLA-C gene was found to impact on HLA-C surface expression level and to be associated with HIV-1 control. It was found that these HLA alleles which protect against AIDS are associated with autoimmune disease e.g. psoriasis vulgaris (PsV). Whether rs9264942 SNP is associated with PsV was investigated here. rs9264942T > C was genotyped in 292 PsV patients, and 254 controls using TaqMan Genotyping Assay.