Fugitive emissions in Moravian-Silesian Region

Import 22/07/2015Predložená práca sa zaoberá fugitívnymi emisiami na území priemyselnej aglomerácie Ostravska. Fugitívny prach predstavuje hlavnú časť atmosférických aerosólov, zvýšená pozornosť je mu venovaná kvôli významným dopadom na zmenu klímy, kvalitu ovzdušia a zdravie ľudí a ekosystémov. Hlavná časť práce je venovaná štúdiu vertikálnej distribúcie PM1 vo výške až 500 m n. m., ktorá bola sledovaná vo vybraných lokalitách Ostravy v jarnom a letnom období 2014, za použitia metódy merania balónom. Pozornosť bola venovaná závislosti koncentrácie PM1 na výške a meteorologických podmienkach. Ďalej bolo zisťované rozloženie organických látok vo vertikálnych profiloch atmosféry v najzaťaženejších miestach Ostravy použitím metódy Py-GC/MS a pomocou matematických metód boli identifikované príspevky zdrojov znečistenia.This thesis deals with the topic of fugitive emissions in the industrial agglomeration of Ostrava region. Fugitive dust is a major part of atmospheric aerosols, increased attention is given to it due to its significant impact on climate change, air quality and human health, and ecosystems. The main part is focused on the study of the vertical distribution of PM1 of up to 500 m a. s. l. which was monitored at selected locations during spring and summer seasons of 2014 using the balloon measuring method. Attention was given to influence of meteorological parameters on PM1 concentrations. Furthermore, distribution of organic matter in the vertical profiles of the atmosphere in the most exposed places was studied using the Py-GC/MS and, using the mathematical methods, contributions of the sources of pollution were identified.Prezenční546 - Institut environmentálního inženýrstvívýborn

Image_3_Serum CHI3L1 as a biomarker of interstitial lung disease in rheumatoid arthritis.tif

BackgroundInterstitial lung disease (ILD) is a relatively prevalent extra-articular manifestation of rheumatoid arthritis (RA) and contributes to significant morbidity and mortality. This study aimed to analyze the association between chitinase-3 like-protein-1(CHI3L1) and the presence of RA-ILD.MethodsA total of 239 RA patients fulfilling the American Rheumatism Association (ACR) 1987 revised criteria were enrolled and subclassified as RA-ILD and RA-nILD based on the results of high-resolution computed tomography scans (HRCT) of the chest. The disease activity of RA was assessed by Disease Activity Score for 28 joints (DAS28) and categorized as high, moderate, low, and remission. Chemiluminescence immunoassays were applied to determine the serum levels of CHI3L1. Univariate analysis was performed and the receiver operating characteristics (ROC) curves were plotted to evaluate the correlation between RA-ILD and CHI3L1.ResultsAmong the eligible RA patients studied, 60 (25.1%) patients were diagnosed with RA-ILD. Compared with RA-nILD, RA patients with ILD had significantly higher median age (median [IQR], 68.00 [62.00-71.75] vs 53.00 [40.00-63.00], pConclusionOur findings of elevated serum CHI3L1 levels in RA-ILD patients suggest its possible role as a biomarker to detect RA-ILD noninvasively.</p

Additional file 3: Figure S1. of Downregulating ANP32A rescues synapse and memory loss via chromatin remodeling in Alzheimer model

Downregulating ANP32A ameliorates tau phosphorylation in htau mice. (DOC 245 kb

Image_2_Serum CHI3L1 as a biomarker of interstitial lung disease in rheumatoid arthritis.tif

BackgroundInterstitial lung disease (ILD) is a relatively prevalent extra-articular manifestation of rheumatoid arthritis (RA) and contributes to significant morbidity and mortality. This study aimed to analyze the association between chitinase-3 like-protein-1(CHI3L1) and the presence of RA-ILD.MethodsA total of 239 RA patients fulfilling the American Rheumatism Association (ACR) 1987 revised criteria were enrolled and subclassified as RA-ILD and RA-nILD based on the results of high-resolution computed tomography scans (HRCT) of the chest. The disease activity of RA was assessed by Disease Activity Score for 28 joints (DAS28) and categorized as high, moderate, low, and remission. Chemiluminescence immunoassays were applied to determine the serum levels of CHI3L1. Univariate analysis was performed and the receiver operating characteristics (ROC) curves were plotted to evaluate the correlation between RA-ILD and CHI3L1.ResultsAmong the eligible RA patients studied, 60 (25.1%) patients were diagnosed with RA-ILD. Compared with RA-nILD, RA patients with ILD had significantly higher median age (median [IQR], 68.00 [62.00-71.75] vs 53.00 [40.00-63.00], pConclusionOur findings of elevated serum CHI3L1 levels in RA-ILD patients suggest its possible role as a biomarker to detect RA-ILD noninvasively.</p

Image_1_Serum CHI3L1 as a biomarker of interstitial lung disease in rheumatoid arthritis.tif

BackgroundInterstitial lung disease (ILD) is a relatively prevalent extra-articular manifestation of rheumatoid arthritis (RA) and contributes to significant morbidity and mortality. This study aimed to analyze the association between chitinase-3 like-protein-1(CHI3L1) and the presence of RA-ILD.MethodsA total of 239 RA patients fulfilling the American Rheumatism Association (ACR) 1987 revised criteria were enrolled and subclassified as RA-ILD and RA-nILD based on the results of high-resolution computed tomography scans (HRCT) of the chest. The disease activity of RA was assessed by Disease Activity Score for 28 joints (DAS28) and categorized as high, moderate, low, and remission. Chemiluminescence immunoassays were applied to determine the serum levels of CHI3L1. Univariate analysis was performed and the receiver operating characteristics (ROC) curves were plotted to evaluate the correlation between RA-ILD and CHI3L1.ResultsAmong the eligible RA patients studied, 60 (25.1%) patients were diagnosed with RA-ILD. Compared with RA-nILD, RA patients with ILD had significantly higher median age (median [IQR], 68.00 [62.00-71.75] vs 53.00 [40.00-63.00], pConclusionOur findings of elevated serum CHI3L1 levels in RA-ILD patients suggest its possible role as a biomarker to detect RA-ILD noninvasively.</p

High dose zinc supplementation induces BDNF-TrkB neurotrophic signaling impairment in hippocampus.

<p>(A–B) Western blotting (A) and the quantitative analysis (B) showed reduced levels of BDNF, TrkB, p-TrkB, CREB, and p-CREB in high-dose zinc supplemented mice (n = 4). (C) Western blotting (upper) and the quantitative analysis (lower) showed no change of the BDNF level in cortex of the mice (n = 4). *, <i>p</i><0.05; **, <i>p</i><0.01 vs. control group.</p

High dose zinc supplementation induces zinc deficiency in hippocampus.

<p>(A) Zinc concentrations in the serum and hemocytes were detected by atomic absorption spectrophotometry (n = 10). High-dose zinc supplemented mice showed significantly increased zinc levels both in serum and hemocytes, while low-dose zinc supplemented mice only showed a trend of zinc increase in hemocytes. (B) Zinc concentrations in the brain (n = 6). High-dose zinc supplemented mice showed decreased zinc levels in hippocampus than control mice, with no change of zinc levels in cortex and the whole brain. Low-dose zinc supplementation did not induce any change of the zinc levels in the detected brain regions. All values are mean ± SEM, *<i>p</i><0.05;** <i>p</i><0.01 vs. control group. (C)Timm Staining of the brain slices from zinc supplemented and control mice. High-dose zinc supplemented mice showed reduced zinc levels in hippocampus, especially in CA3 and DG area. Scale bar = 200 µm. (D) TSQ Staining of the brain slices. High-dose zinc supplemented mice showed dramatic loss of chelatable zinc staining both in CA3 and DG area. Scale bar = 200 µm.</p

Zinc is required for the expression of BDNF in hippocampus.

<p>Upper panel, SD rats were injected with zinc sulfate (1 mM, 3 µl) or 0.9% NaCl (3 µl) into the hippocampus, with or without intraperitoneal administration of zinc chelator CQ (50 mg/kg/48 h). Six days after the zinc injection, the rats were sacrificed and the hippocampus was homogenized for Western blotting. Lower, quantitative analysis (n = 4). **, <i>p</i><0.01 vs. control group; #, <i>p</i><0.05 vs. zinc injected group.</p

High dose zinc supplementation induces hippocampus-dependent memory impairment.

<p>(A) T-maze task for working memory assessment of zinc supplemented mice (n = 8). Compared with control mice, high-dose zinc supplemented mice exhibited working memory deficit. (B–C) Contextual discrimination test of the mice (n = 16).High-dose zinc supplemented mice showed significantly lower discrimination ratio than the other two groups across the seven days of acquisition. Low-dose zinc supplemented mice showed better discrimination than control in the last three testing days (B). Seven days later, the discrimination was recorded again, control and low-dose zinc supplemented mice could discriminate the two contexts whereas high-dose zinc supplemented mice still could not (C). (D) Contextual fear conditioning test of the mice (n = 16). There was no difference in freezing ratio among the three groups. (E–F) Open field test of the mice (n = 16). There was no difference in locomotor habituation among the three groups (E); Low-dose zinc supplemented mice showed shorter time in the center square than control, indicating increased anxiety in this group. *, <i>p</i><0.05; **, <i>p</i><0.01;***, <i>p</i><0.001 vs. control group.</p

High dose zinc supplementation induces decreased levels of synaptic receptors and scaffolding proteins and retarded spine formation in hippocampus.

<p>(A–B) Western blotting (A) and the quantitative analysis (B) showed reduced levels of NMDA-NR2A, NR2B, AMPA-GluR1, PSD93 and PSD95 in high-dose zinc supplemented mice. In contrast, expression levels of PSD93 was increased in low-dose zinc supplemented mice (n = 4). (C) The representative images for morphology of dendritic spine in hippocampal region of zinc supplemented and control mice visualized by Golgi staining. (D) Quantitive analysis of the spine density (calculated as the average number of spines per 10 µm on the dendrites) in hippocampal DG area. *, <i>p</i><0.05; **, <i>p</i><0.01;***, <i>p</i><0.001 vs. control group.</p