The Impact of Biochar Used in Repairs to Historical Buildings on Public Health.

The subject matter of this manuscript concerns the analysis and identification of microorganisms that pose a threat to human health and, in particular, mold fungi occurring in historical buildings. Surfaces infected by fungal spores pose a threat to the structure and the health of both visitors to historical buildings and professionals working in them. Research was undertaken to fill in the defects in building partitions with a supplementary layer of biochar in order to eliminate, or partially reduce, the possibility of contamination with and development of harmful mold fungi. In the designed cement mixture, biochar was used as a filler, the task of which was to eliminate the causes that lead to the development of harmful mold fungi. Microbiological analyses of the surface of walls and air in selected buildings were carried out before and after the application of supplementary biochar layers. The inhibitory properties of the material used against the presence and growth of mold fungi were observed. The average number of microorganisms isolated on the tested partitions decreased by between 70 and 100%. As a consequence, the use of this material significantly influenced the air quality of the rooms, which is important for protecting the health of people at work, as well as those visiting historical buildings.

Cytokines and Neurodegeneration in Epileptogenesis.

Epilepsy is a common brain disorder characterized by a heterogenous etiology. Its main features are recurrent seizures. Despite many clinical studies, about 30% of cases are refractory to treatment. Recent studies suggested the important role of immune-system elements in its pathogenesis. It was suggested that a deregulated inflammatory process may lead to aberrant neural connectivity and the hyperexcitability of the neuronal network. The aim of our study was the analysis of the expression of inflammatory mediators in a mouse model of epilepsy and their impact on the neurodegeneration process located in the brain. We used the KA-induced model of epilepsy in SJL/J mice and performed the analysis of gene expression and protein levels. We observed the upregulation of IL1ß and CXCL12 in the early phase of KA-induced epilepsy and elevated levels of CCL5 at a later time point, compared with control animals. The most important result obtained in our study is the elevation of CXCL2 expression at both studied time points and its correlation with the neurodegeneration observed in mouse brain. Increasing experimental and clinical data suggest the influence of peripheral inflammation on epileptogenesis. Thus, studies focused on the molecular markers of neuroinflammation are of great value and may help deepen our knowledge about epilepsy, leading to the discovery of new drugs.

CCR6 blockade on regulatory T cells ameliorates experimental model of multiple sclerosis.

Regulatory T cells (Tregs) play a significant role in limiting damage of tissue affected by autoimmune process, which has been demonstrated in various experimental models for multiple sclerosis (MS) (mostly experimental autoimmune encephalomyelitis - EAE), rheumatoid arthritis, and type 1 diabetes. In this study, we demonstrated that Tregs increasingly migrate to central nervous system (CNS) during subsequent phases of EAE (preclinical, initial attack, and remission). In contrast, in peripheral tissues (blood, lymph nodes, and spleen), a significant accumulation of Tregs is mostly present during EAE remission. Moreover, an increased expression of CCR6 on Tregs in the CNS, blood, lymph nodes, and spleen in all phases of EAE was observed. The highest expression of CCR6 on Tregs from the CNS, lymph nodes, and spleen was noted during the initial attack of EAE, whereas in the blood, the peak expression of CCR6 was detected during the preclinical phase. The presence of Tregs in the CNS during EAE was confirmed by immunohistochemistry. To analyze additional functional significance of CCR6 expression on Tregs for EAE pathology, we modulated the clinical course of this MS model using Tregs with blocked CCR6. EAE mice, which received CCR6-deficient Tregs showed significant amelioration of disease severity. This observation suggests that CCR6 on Tregs may be a potential target for future therapeutic interventions in MS.

Prediction of Carbonation Progress in Concrete Containing Calcareous Fly Ash Co-Binder.

According to the European Standards (EN 450-1, EN 206), it is not permissible to use calcareous fly ash as an additive to concrete. However, other standards (for example, the American and Canadian ones) allow the use of high-calcium fly ash (type C) in concrete. As a result of brown coal combustion, a large amount of this type of fly ash is produced, and considerations on their use in concrete are in progress. Research into the influence of high-calcium fly ash on concrete durability is fundamental for dealing with that issue. The aim of the present research was to develop a new model of carbonation over time, also including calcareous fly ash content in the binder. The self-terminating model of carbonation is new, and not developed by other authors. In the current research, the former simplest model (a function of w/c ratio and time) is expanded with the calcareous fly ash to cement ratio. The basis is a statistically planned experiment with a large scope of two material variables (w/c ratio and fly ash to cement ratio). The main measured property is the carbonation depth after exposure to 4% of CO2 concentration (according to CEN/TS 12390-12). The model of carbonation obtained from this experiment is an output of the paper. Also, the idea of developing similar models for concrete families as a tool for designing concrete cover thickness for reinforced elements is described in the paper.

Central Nervous System and Peripheral Expression of CCL19, CCL21 and Their Receptor CCR7 in Experimental Model of Multiple Sclerosis.

It is well documented that inflammatory chemokines play a significant role in the development of multiple sclerosis (MS) and its model, experimental autoimmune encephalomyelitis (EAE). Recently, the involvement of homeostatic (or lymphoid) chemokines in the pathogenesis of autoimmune diseases has become an object of intensive study. In this work, quantitative analysis of CCL19, CCL21 and CCR7 expression in the central nervous system (CNS), as well as in inflammatory mononuclear cells isolated from several organs during the first attack, remission and the second attack of chronic-relapsing EAE (ChREAE), was performed. Using real-time PCR, RNAse Protection Assay and immunohistochemistry, the expression of both chemokines, as well as of their common receptor CCR7, was analyzed in the brain, spleen, lymph nodes and peripheral blood mononuclear cells. Increased expression of CCL19 and CCL21 was observed mostly in mononuclear inflammatory cells isolated from the CNS during active ChREAE. At the same time the expression of CCR7 in blood mononuclear leukocytes was reduced. This observation extends our current knowledge about the possible role of chemokines CCL19, CCL21 and their receptor CCR7 in the pathogenesis of ChREAE and, by extension, MS.

A strategy for genome-wide identification of gene based polymorphisms in rice reveals non-synonymous variation and functional genotypic markers.

The genetic diversity of plants has traditionally been employed to improve crop plants to suit human needs, and in the future feed the increasing population and protect crops from environmental stresses and climate change. Genome-wide sequencing is a reality and can be used to make association to crop traits to be utilized by high-throughput marker based selection methods. This study describes a strategy of using next generation sequencing (NGS) data from the rice genome to make comparisons to the high-quality reference genome, identify functional polymorphisms within genes that might result in function changes and be used to study correlations to traits and employed in genetic mapping. We analyzed the NGS data of Oryza sativa ssp indica cv. G4 covering 241 Mb with ∼20X coverage and compared to the reference genome of Oryza sativa ssp. japonica to describe the genome-wide distribution of gene-based single nucleotide polymorphisms (SNPs). The analysis shows that the 63% covered genome consists of 1.6 million SNPs with 6.9 SNPs/Kb, and including 80,146 insertions and 92,655 deletions (INDELs) genome-wide. There are a total of 1,139,801 intergenic SNPs, 295,136 SNPs in intronic/non-coding regions, 195,098 in coding regions, 23,242 SNPs at the five-prime (5') UTR regions and 22,686 SNPs at the three-prime (3') UTR region. SNP variation was found in 40,761 gene loci, which include 75,262 synonymous and 119,836 non-synonymous changes, and functional reading frame changes through 3,886 inducing STOP-codon (isSNP) and 729 preventing STOP-codon (psSNP) variation. There are quickly evolving 194 high SNP hotspot genes (>100 SNPs/gene), and 1,513 out of 2,458 transcription factors displaying 2,294 non-synonymous SNPs that can be a major source of phenotypic diversity within the species. All data is searchable at https://plantstress-pereira.uark.edu/oryza2. We envision that this strategy will be useful for the identification of genes for crop traits and molecular breeding of rice cultivars.

Chemokines and neurodegeneration in the early stage of experimental ischemic stroke.

Neurodegeneration is a hallmark of most of the central nervous system (CNS) disorders including stroke. Recently inflammation has been implicated in pathogenesis of neurodegeneration and neurodegenerative diseases. The aim of this study was analysis of expression of several inflammatory markers and its correlation with development of neurodegeneration during the early stage of experimental stroke. Ischemic stroke model was induced by stereotaxic intracerebral injection of vasoconstricting agent endothelin-1 (ET-1). It was observed that neurodegeneration appears very early in that model and correlates well with migration of inflammatory lymphocytes and macrophages to the brain. Although the expression of several studied chemotactic cytokines (chemokines) was significantly increased at the early phase of ET-1 induced stroke model, no clear correlation of this expression with neurodegeneration was observed. These data may indicate that chemokines do not induce neurodegeneration directly. Upregulated in the ischemic brain chemokines may be a potential target for future therapies reducing inflammatory cell migration to the brain in early stroke. Inhibition of inflammatory cell accumulation in the brain at the early stage of stroke may lead to amelioration of ischemic neurodegeneration.

Quantum chemistry in parallel with PQS.

This article describes the capabilities and performance of the latest release (version 4.0) of the Parallel Quantum Solutions (PQS) ab initio program package. The program was first released in 1998 and evolved from the TEXAS program package developed by Pulay and coworkers in the late 1970s. PQS was designed from the start to run on Linux-based clusters (which at the time were just becoming popular) with all major functionality being (a) fully parallel; and (b) capable of carrying out calculations on large-by ab initio standards-molecules, our initial aim being at least 100 atoms and 1000 basis functions with only modest memory requirements. With modern hardware and recent algorithmic developments, full accuracy, high-level calculations (DFT, MP2, CI, and Coupled-Cluster) can be performed on systems with up to several thousand basis functions on small (4-32 node) Linux clusters. We have also developed a graphical user interface with a model builder, job input preparation, parallel job submission, and post-job visualization and display.

Treatment of multiple sclerosis with methylprednisolone and mitoxantrone modulates the expression of CXC chemokine receptors in PBMC.

Chemokines and their receptors are involved in the development of multiple sclerosis (MS). Methylprednisolone (MP) and mitoxantrone (MTX) are commonly used in the treatment of MS. In this study, we analyzed the expression of chemokine receptors CXCR1, CXCR2, CXCR3, CXCR4, and CXCR5 in peripheral blood mononuclear cells (PBMC) from MS patients before and after treatment with MP or MTX. We observed a significant upregulation of expression of CXCR1 and CXCR2 in untreated MS patients. Treatment of MS with MP stimulated further increase of expression of both receptors. Therapy for MS with MTX resulted in decrease of CXCR2 expression. There was a negative correlation between the expression of CXCR1 and CXCR2 and the cumulative dose of MTX received by patients. These results suggest that CXCR1 and CXCR2 may be involved in MS pathogenesis and that treatment of this disease with MP and MTX may influence expression of those receptors.