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

Both total tau and phosphorylated tau increase in activated microglia.

<p>Microglia in the brain slices were co-immunostained with Iba1 (green) and Tau46 (an antibody recognizing total tau) or AT8 (an antibody recognizing phosphorylated tau at Ser202/Thr205) (red). In contrast with the ramified microglia (arrow heads), ameboid microglia (arrows) showed increased total tau (A, C) and the phosphorylated tau (E, G) (Scale bar = 20 µm). The relative levels of integrated optical density (IOD) of Tau46/AT8 in microglia with different grades of fractal dimension value were shown in B, D, F, H. Data were presented as means ± S.D.. ** <i>p</i><0.01 versus microglia with fractal dimension value <1.1.</p

Activation of microglia in the brains of rats and mice with aging.

<p>Microglia in the cortex of 4- and 14-month-old SD rats (A), 3- and 12-month-old C57BL/6 mice (D) were immunostained by Iba1, a marker of microglia (Scale bar = 100 µm). The fractal dimension value analysis was used to evaluate the activation of microglia in the brains of different group of animals. Lower fractal dimension value indicates higher activity of microglia. We divided the fractal dimension value of the microglia into four grades (>1.3, 1.2–1.3, 1.1–1.2, <1.1), and the percentages of microglia with different grades were shown in B and E, the differences of the same grade between the different age of animals were shown in C and F (n>43 cells/group). Data were presented as means ± S.D.. * <i>p</i><0.05, ** <i>p</i><0.01 versus 4-month-old SD rats/3-month-old C57BL/6 mice.</p

Intraperitoneal supplementation of magnesium rescues ICV-STZ-induced learning and memory deficits with elevation of brain magnesium level.

<p>The experiments were designed as shown in panel A. Rats were divided into six groups, i.e., sham-operated control (Con), sham-operated plus 100 mg/kg magnesium control (Mg), STZ ICV (STZ), STZ ICV plus 50 mg/kg magnesium (STZ+Mg50), STZ ICV plus 100 mg/kg magnesium (STZ+Mg100) and STZ ICV plus 200 mg/kg magnesium (STZ+Mg200) groups, as described in the <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0108645#s2" target="_blank">Methods</a>. During the 3^rd week after ICV-STZ treatment, the rats were trained in Morris watwe maze for six consecutive days to measure the learning capacity, and memory was tested on the 7^th day via removal of the hidden platform. The escape latencies to find the hidden platform were recorded daily (B). For the memory test, the time spent in the target quadrant (C), the swimming tracks (D) and numbers of crossings (E) in the target quadrant were calculated. The rats were sacrificed after the behavioral tests, and the magnesium levels in the cerebral cortex (F) and hippocampus (G) were measured. Data were presented as means ± SD. *<i>P</i><0.05 versus the control group, <i>#P</i><0.05 versus the STZ group.</p

Expression of tau40 induces membranous accumulation of phosphorylated tau, simultaneously with inhibition of PP2A and activation of ERK and GSK-3β.

<p>In cultured rat microglial cells, the plasmid of human tau40-EGFP (T) or vector-EGFP (V) was transfected. 24 h later, triple immunofluorescence imaging was performed. The nucleus was stained with Hoechst (blue) and the phosphorylated tau was probed by pS396 (an antibody recognizing phosphorylated tau at Ser396) (red). Then cells were observed by confocal microscope (A) (Scale bar = 20 µm). The membranous (m) and cytoplasma (p) fractions were isolated as described in the method and the level of pS396 in the two fractions was analyzed by Western blotting (B) and quantitative analysis (C). The levels of PP2Ac, p-PP2Ac (Y307), ERK, p-ERK, GSK-3β and p-GSK-3β (S9) were probed and measured by Western blotting (D) and quantitative analysis (E). The data were representative of three independent experiments and were presented as means ± S.D.. * <i>p</i><0.05 versus vector-transfected cells.</p

Expression of tau40 promotes migration of microglia.

<p>In cultured rat microglia, the plasmid of human tau40-EGFP or vector-EGFP was transfected for 24 h. Then <i>in vitro</i> scratch assay was performed and the images of migration were captured at 0 h, 6 h, 12 h and 24 h after scratching with confocal microscope (A) (Scale bar = 100 µm). The migration rate of microglia was quantified by the distance that the EGFP positive cells moved from the edge of the scratch towards the center per hour. The average migration rates of the EGFP positive microglia in 0–6 h, 6–12 h and 12–24 h were calculated from three independent experiments (B). Data were presented as means ± S.D.. * <i>p</i><0.05, ** <i>p</i><0.01 versus vector-transfected cells.</p

1N3R-tau induces S phase arrest in HEK293 cells.

<p><b>(A)</b> The distribution of HEK293 with six tau isoforms in sub G1 phase. <b>(B)</b> The distribution of HEK293 with six tau isoforms in G1 phase. *<i>P</i> < 0.05, compared with vector. <b>(C)</b> The distribution of HEK293 with six tau isoforms in S phase. **<i>P</i> < 0.01, compared with vector. <b>(D)</b> The distribution of HEK293 with six tau isoforms in G2/M phase. *<i>P</i> < 0.05, compared with vector.</p

Magnesium reverses ICV-STZ-induced dendritic spines and synapse impairments.

<p>Rats were divided into sham-operated control (Con), sham-operated plus 100 mg/kg magnesium control (Mg), STZ ICV (STZ) or STZ ICV plus 100 mg/kg magnesium (STZ+Mg) groups and treated as shown in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0108645#pone-0108645-g001" target="_blank">Figure 1A</a>. The representative morphology alterations of neurons in the hippocampal CA1 regions were displayed by Golgi staining. Representative photomicrographs of primary dendrites in the hippocampal CA1 region were shown (A). Quantification of dendrite number (B) and mushroom-type dendrites (C) were calculated. The number of dendritic branches and mushroom percentage in the hippocampus of ICV-STZ-treated rats decreased markedly, and supplement of magnesium almost fully reversed the dendritic complexity. Data were presented as means ± SD. *<i>P</i><0.05 versus the control group, <i>#P</i><0.05 versus the STZ group.</p

Magnesium stimulates the activity of Akt and PI3K in the hippocampus of ICV-STZ-treated rats.

<p>Rats were divided into sham-operated control (Con), sham-operated plus 100 mg/kg magnesium control (Mg), STZ ICV (STZ) or STZ ICV plus 100 mg/kg magnesium (STZ+Mg) groups and treated as shown in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0108645#pone-0108645-g001" target="_blank">Figure 1A</a>. The total Akt, Akt (Thr308), Akt (Ser473), total PI3K and PI3K (Tyr458/199) levels in whole hippocampus extracts were measured using Western blotting (A, C) and quantitative analysis (B, D), respectively. The p-Akt (Ser473) and p-PI3K (Tyr458/199) levels decreased significantly in ICV-STZ-treated rats, and these changes were fully restored by magnesium supplement. There was no change in total Akt, Akt (Thr308) and PI3K. Data were presented as means ± SD. *<i>P</i><0.05 versus the control group, <i>#P</i><0.05 versus the STZ group.</p

Magnesium reverses the LTP deficiency induced by ICV-STZ.

<p>Rats were divided into sham-operated control (Con), sham-operated plus 100 mg/kg magnesium control (Mg), and STZ ICV (STZ) or STZ ICV plus 100 mg/kg magnesium (STZ+Mg) groups. During the 3^rd week after ICV-STZ treatment, the hippocampal slices were prepared and an ideographic electrophysiology recording set-up with a stimulating electrode and recording electrode were placed in the CA3 and CA1 regions (A). The representative analog traces of evoked potentials before (solid line) and after (broken line) high-frequency stimulation (HFS) were recorded (B). Normalized field excitatory postsynaptic potential (fEPSP) slopes were measured in four groups (C), and the relative ratio of fEPSP increments after HFS (D) was calculated. Data were presented as means ± SD. *<i>P</i><0.05 versus the control group, <i>#P</i><0.05 versus the STZ group.</p