Cyclic swelling of clays

Changes in free swelling and swelling pressure of different types of clays in response to varying cycles of wetting and drying have been studied. It can be shown that cyclic tests lead to a gradual destruction of the durable contacts in the clay structure and their transformation into less durable ones. At the same time, a reconstruction of the structure of the clays takes place, manifested by the destruction of large micro-aggregates and by disorientation of structural elements. All these phenomena result in great swelling with increase in the number of wetting cycles. Between cycles 3 and 20 the expansibility is at its maximum and may be 1.3–10 times as much as that after one wetting cycle. Cyclic swelling leads to an overall equilibrium in the system, when the internal energy of the clay is minimal and the bound water content is at its maximum. Clay in this state exhibits its maximum moisture uptake (W′_s), the meaning of which is of thermodynamic character and depends neither on the initial soil density and moisture, nor on the scheme of cyclic tests adopted.     

Can Forest Trees Cope with Climate Change?—Effects of DNA Methylation on Gene Expression and Adaptation to Environmental Change

Epigenetic modifications, including chromatin modifications and DNA methylation, play key roles in regulating gene expression in both plants and animals. Transmission of epigenetic markers is important for some genes to maintain specific expression patterns and preserve the status quo of the cell. This article provides a review of existing research and the current state of knowledge about DNA methylation in trees in the context of global climate change, along with references to the potential of epigenome editing tools and the possibility of their use for forest tree research. Epigenetic modifications, including DNA methylation, are involved in evolutionary processes, developmental processes, and environmental interactions. Thus, the implications of epigenetics are important for adaptation and phenotypic plasticity because they provide the potential for tree conservation in forest ecosystems exposed to adverse conditions resulting from global warming and regional climate fluctuations.     

Cytoskeleton Reorganization in EndMT—The Role in Cancer and Fibrotic Diseases

Chronic inflammation promotes endothelial plasticity, leading to the development of several diseases, including fibrosis and cancer in numerous organs. The basis of those processes is a phenomenon called the endothelial–mesenchymal transition (EndMT), which results in the delamination of tightly connected endothelial cells that acquire a mesenchymal phenotype. EndMT-derived cells, known as the myofibroblasts or cancer-associated fibroblasts (CAFs), are characterized by the loss of cell–cell junctions, loss of endothelial markers, and gain in mesenchymal ones. As a result, the endothelium ceases its primary ability to maintain patent and functional capillaries and induce new blood vessels. At the same time, it acquires the migration and invasion potential typical of mesenchymal cells. The observed modulation of cell shape, increasedcell movement, and invasion abilities are connected with cytoskeleton reorganization. This paper focuses on the review of current knowledge about the molecular pathways involved in the modulation of each cytoskeleton element (microfilaments, microtubule, and intermediate filaments) during EndMT and their role as the potential targets for cancer and fibrosis treatment.     

Alteration of the Early Development Environment by Maternal Diet and the Occurrence of Autistic-like Phenotypes in Rat Offspring

Epidemiological and preclinical studies suggest that maternal obesity increases the risk of autism spectrum disorder (ASD) in offspring. Here, we assessed the effects of exposure to modified maternal diets limited to pregnancy and lactation on brain development and behavior in rat offspring of both sexes. Among the studied diets, a maternal high-fat diet (HFD) disturbed the expression of ASD-related genes (Cacna1d, Nlgn3, and Shank1) and proteins (SHANK1 and TAOK2) in the prefrontal cortex of male offspring during adolescence. In addition, a maternal high-fat diet induced epigenetic changes by increasing cortical global DNA methylation and the expression of miR-423 and miR-494. As well as the molecular changes, behavioral studies have shown male-specific disturbances in social interaction and an increase in repetitive behavior during adolescence. Most of the observed changes disappeared in adulthood. In conclusion, we demonstrated the contribution of a maternal HFD to the predisposition to an ASD-like phenotype in male adolescent offspring, while a protective effect occurred in females.     

De Novo ACTG1 Variant Expands the Phenotype and Genotype of Partial Deafness and Baraitser–Winter Syndrome

Actin molecules are fundamental for embryonic structural and functional differentiation; γ-actin is specifically required for the maintenance and function of cytoskeletal structures in the ear, resulting in hearing. Baraitser–Winter Syndrome (B-WS, OMIM #243310, #614583) is a rare, multiple-anomaly genetic disorder caused by mutations in either cytoplasmically expressed actin gene, ACTB (β-actin) or ACTG1 (γ-actin). The resulting actinopathies cause characteristic cerebrofrontofacial and developmental traits, including progressive sensorineural deafness. Both ACTG1-related non-syndromic A20/A26 deafness and B-WS diagnoses are characterized by hypervariable penetrance in phenotype. Here, we identify a 28th patient worldwide carrying a mutated γ-actin ACTG1 allele, with mildly manifested cerebrofrontofacial B-WS traits, hypervariable penetrance of developmental traits and sensorineural hearing loss. This patient also displays brachycephaly and a complete absence of speech faculty, previously unreported for ACTG1-related B-WS or DFNA20/26 deafness, representing phenotypic expansion. The patient’s exome sequence analyses (ES) confirms a de novo ACTG1 variant previously unlinked to the pathology. Additional microarray analysis uncover no further mutational basis for dual molecular diagnosis in our patient. We conclude that γ-actin c.542C > T, p.Ala181Val is a dominant pathogenic variant, associated with mildly manifested facial and cerebral traits typical of B-WS, hypervariable penetrance of developmental traits and sensorineural deafness. We further posit and present argument and evidence suggesting ACTG1-related non-syndromic DFNA20/A26 deafness is a manifestation of undiagnosed ACTG1-related B-WS.     

Innate Immune System Response to Burn Damage—Focus on Cytokine Alteration

In the literature, burns are understood as traumatic events accompanied by increased morbidity and mortality among affected patients. Their characteristic feature is the formation of swelling and redness at the site of the burn, which indicates the development of inflammation. This reaction is not only important in the healing process of wounds but is also responsible for stimulating the patient’s innate immune system. As a result of the loss of the protective ability of the epidermis, microbes which include bacteria, fungi, and viruses have easier access to the system, which can result in infections. However, the patient is still able to overcome the infections that occur through a cascade of cytokines and growth factors stimulated by inflammation. Long-term inflammation also has negative consequences for the body, which may result in multi-organ failure or lead to fibrosis and scarring of the skin. The innate immune response to burns is not only immediate, but also severe and prolonged, and some people with burn shock may also experience immunosuppression accompanied by an increased susceptibility to fatal infections. This immunosuppression includes apoptosis-induced lymphopenia, decreased interleukin 2 (IL-2) secretion, neutrophil storm, impaired phagocytosis, and decreased monocyte human leukocyte antigen-DR. This is why it is important to understand how the immune system works in people with burns and during infections of wounds by microorganisms. The aim of this study was to characterize the molecular pathways of cell signaling of the immune system of people affected by burns, taking into account the role of microbial infections.     

Caffeic Acid/Eu(III) Complexes: Solution Equilibrium Studies,Structure Characterization and Biological Activity

Caffeic acid (CFA) is one of the various natural antioxidants and chemoprotective agents occurring in the human diet. In addition, its metal complexes play fundamental roles in biological systems. Nevertheless, research on the properties of CFA with lanthanide metals is very scarce, and little to no chemical or biological information is known about these particular systems. Most of their properties, including their biological activity and environmental impact, strictly depend on their structure, stability, and solution behaviour. In this work, a multi-analytical-technique approach was used to study these relationships for the Eu(III)/CFA complex. The synthesized metal complex was studied by FT-IR, FT-Raman, elemental, and thermal (TGA) analysis. In order to examine the chemical speciation of the Eu(III)/CFA system in an aqueous solution, several independent potentiometric and spectrophotometric UV-Vis titrations were performed at different M:L (metal:ligand) and pH ratios. The general molecular formula of the synthesized metal complex in the solid state was [Eu(CFA)₃(H₂O)₃]∙2H₂O (M:L ratio 1:3), while in aqueous solution the 1:1 species were observed at the optimum pH of 6 ≤ pH ≤ 10, ([Eu(CFA)] and [Eu(CFA)(OH)]⁻). These results were confirmed by ¹H-NMR experiments and electrospray-ionization mass spectrometry (ESI-MS). To evaluate the interaction of Eu(III)/CFA and CFA alone with cell membranes, electrophoretic mobility assays were used. Various antioxidant tests have shown that Eu(III)/CFA exhibits lower antioxidant activity than the free CFA ligand. In addition, the antimicrobial properties of Eu(III)/CFA and CFA against Escherichia coli, Bacillus subtilis and Candida albicans were investigated by evaluation of the minimum inhibitory concentration (MIC). Eu(III)/CFA shows higher antibacterial activity against bacteria compared to CFA, which can be explained by the highly probable increased lipophilicity of the Eu(III) complex.     

Silencing of Sphingosine kinase 1 Affects Maturation Pathways in Mouse Neonatal Cardiomyocytes

Sphingosine kinase-1 (Sphk1) and its product, sphingosine-1-phosphate (S1P) are important regulators of cardiac growth and function. Numerous studies have reported that Sphk1/S1P signaling is essential for embryonic cardiac development and promotes pathological cardiac hypertrophy in adulthood. However, no studies have addressed the role of Sphk1 in postnatal cardiomyocyte (CM) development so far. The present study aimed to assess the molecular mechanism(s) by which Sphk1 silencing might influence CMs development and hypertrophy in vitro. Neonatal mouse CMs were transfected with siRNA against Sphk1 or negative control, and subsequently treated with 1 µM angiotensin II (AngII) or a control buffer for 24 h. The results of RNASeq analysis revealed that diminished expression of Sphk1 significantly accelerated neonatal CM maturation by inhibiting cell proliferation and inducing developmental pathways in the stress (AngII-induced) conditions. Importantly, similar effects were observed in the control conditions. Enhanced maturation of Sphk1-lacking CMs was further confirmed by the upregulation of the physiological hypertrophy-related signaling pathway involving Akt and downstream glycogen synthase kinase 3 beta (Gsk3β) downregulation. In summary, we demonstrated that the Sphk1 silencing in neonatal mouse CMs facilitated their postnatal maturation in both physiological and stress conditions.