Disposal and reuse of the water processing sludge

Osady powstające w procesie uzdatniania wód stanowią ważny problem ekologiczny, któremu nie poświęca się należytej uwagi. Ilość powstających osadów stale wzrasta wraz ze zwiększającą się ilością uzdatnianych wód powierzchniowych. Zagospodarowanie osadów należy zaliczyć do procesów trudnych podobnie jak wykorzystanie osadów. W artykule przedstawiono doświadczenia z zagospodarowania i unieszkodliwienia osadów pokoagulacyjnych zawierających glin, przedstawiono możliwości ich wykorzystania w celu zwiększenia zakresu ochrony środowiska.Sludge produced during processing of drinking water is a waste type which has been paid so far little attention only. The quantity of sludge has been increasing with the increasing volume of the processed surface water. This sludge is difficult to treat and its future use is rather limited. This paper deals with lessons learnt during from treatment and disposal of alumina water sludge and proposes re-use alternatives. The goal is to eliminate loading of the environment with this waste type

Hydrophobicity of Black Coal from Ostrava-Karviná Coal District (Czech Republic)

Właściwości hydrofobowe/hydrofilowe węgla znacząco wpływają na wartość wilgoci, która jest bardzo istotnym parametrem z punktu widzenia wykorzystania węgla do produkcji energii. Hydrofobowość została zbadana dzięki pomiarom kąta zwilżania. Dowiedziono, że w przypadku węgla kamiennego właściwości hydrofilowe wzrastają wraz ze wzrostem uwęglenia. Z drugiej strony, związek ten nie znalazł odbicia w przypadku niższego stopnia uwęglenia. Wartość kąta zwilżania jest warunkowana przez zawartość części lotnych i zawartość popiołu. Zależność kąta zwilżania od głębokości wydobycia surowca została również udowodniona. Wartość kąta zwilżania maleje wraz z głębokością.Hydrophobic/hydrophilic properties of coal influence significantly value of moisture which represents very important parameter from the point of utilization of coal in energy production. Hydrofobicity were studied by means of contact angle measurements. It was proved that for black coal the hydrofilic properties increase with coalification. On the contrary, this relationship was not found for coals with lower degree of coalification. The value of contact angle is influenced by content of volatile combustibles and content of ash. The dependence of contact angle on the depth of mining was also proved. The value of contact angle decreases with depth

Olomoucine II, but not purvalanol A, is transported by breast cancer resistance protein (ABCG2) and P-glycoprotein (ABCB1).

Contains fulltext : 125702.pdf (publisher's version ) (Open Access)Purine cyclin-dependent kinase inhibitors have been recognized as promising candidates for the treatment of various cancers; nevertheless, data regarding interaction of these substances with drug efflux transporters is still lacking. Recently, we have demonstrated inhibition of breast cancer resistance protein (ABCG2) by olomoucine II and purvalanol A and shown that these compounds are able to synergistically potentiate the antiproliferative effect of mitoxantrone, an ABCG2 substrate. In this follow up study, we investigated whether olomoucine II and purvalanol A are transported by ABCG2 and ABCB1 (P-glycoprotein). Using monolayers of MDCKII cells stably expressing human ABCB1 or ABCG2, we demonstrated that olomoucine II, but not purvalanol A, is a dual substrate of both ABCG2 and ABCB1. We, therefore, assume that pharmacokinetics of olomoucine II will be affected by both ABCB1 and ABCG2 transport proteins, which might potentially result in limited accumulation of the compound in tumor tissues or lead to drug-drug interactions. Pharmacokinetic behavior of purvalanol A, on the other hand, does not seem to be affected by either ABCG2 or ABCB1, theoretically favoring this drug in the potential treatment of efflux transporter-based multidrug resistant tumors. In addition, we observed intensive sulfatation of olomoucine II in MDCKII cell lines with subsequent active efflux of the metabolite out of the cells. Therefore, care should be taken when performing pharmacokinetic studies in MDCKII cells, especially if radiolabeled substrates are used; the generated sulfated conjugate may largely contaminate pharmacokinetic analysis and result in misleading interpretation. With regard to chemical structures of olomoucine II and purvalanol A, our data emphasize that even drugs with remarkable structure similarity may show different pharmacokinetic behavior such as interactions with ABC transporters or biotransformation enzymes

Inhibitory activities of MMV Pathogen Box compounds against O₂ consumption rate in <i>T</i>. <i>gondii</i> and <i>P</i>. <i>falciparum</i>.

Determination of the O2 consumption rate (OCR) inhibitory properties of the identified compounds on (A) WT RH strain T. gondii parasites, and on (B) WT 3D7 strain P. falciparum parasites, using a Seahorse XFe96 flux analyzer. T. gondii experiments were conducted on intact parasites, and P. falciparum experiments measured malate-dependent OCR in digitonin-permeabilized parasites. Data are reported as average EC50 value against OCR (EC50OCR) (μM) ± SEM from three or more independent experiments. ND = not determined.</p

Data table of the Pathogen Box screen for inhibitors of mitochondrial O₂ consumption in <i>T</i>. <i>gondii</i> parasites.

(Tab 1A-B) Plate configurations of the two Seahorse XFe96 plates used in the screen. Included are the MMV compounds that were injected into the indicated wells from Ports A-C during the first (Tab 1A) and second (Tab 1B) assays. Hit compounds are highlighted in yellow, compounds excluded from subsequent analyses because they were injected after hit compounds are highlighted in blue, compounds rescreened on the second plate are highlighted in green, background wells are highlighted in orange, and wells from a separate experiment that was included on Plate 2 are indicated in gray. Atovaquone and antimycin A was injected from Port D into all wells. (Tab 2A-B) Calculated OCR and ECAR values obtained for each well at each measurement time in Plate 1 (Tab 2A) and Plate 2 (Tab 2B). The time from the commencement of the assay at which each measurement was taken is indicated. Injection of compounds from Port A occurred between the third and fourth measurements, injection from Port B occurred between the seventh and eighth measurements, injection from Port C occurred between the 11th and 12th measurements, and injection from Port D occurred between the 15th and 16th measurements. Also indicated are the average OCR and ECAR values across all wells at each measurement point, with the average OCR value in the final measurement following atovaquone/antimycin A injection used to determine the non-mitochondrial OCR for the assay (highlighted in yellow). (Tab 3) Summary of the assay data, expressed in a table modified from the Pathogen Box plate mapping spreadsheet provided by MMV. Included are: the Pathogen Box plate and position of the test compounds; the MMV compound identification number and common name (where applicable); the Seahorse XFe96 plate well position and injection port from which the compound was injected during the assay (with compounds injected into Plate 1 indicated in green and compounds injected into Plate 2 in yellow); the mitochondrial OCR (mOCR) values immediately before and after compound injection (calculated by subtracting the non-mitochondrial OCR from the OCR values listed in Tab 2A-B; note that the post-drug values were obtained on the fourth measurement, approximately 18 min, after compound injection for all compounds except auranofin, for which we noticed a more gradual OCR decrease, and which was therefore calculated after ~40 min); the percent inhibition of mitochondrial OCR following compound injection (calculated from the difference between pre-compound injection and post-compound injection mOCR values); an indication of whether compounds met the >30% inhibition cut-off for hit compounds; and the chemical structures of all MMV compounds expressed in simplified molecular input line entry system (SMILES) notation. (Tab 4A-B) The O2 and pH values obtained during each measurement in the Seahorse XFe96 assays in plate 1 (Tab 4A) and plate 2 (Tab 4B). These values form the basis from which the OCR and ECAR values depicted in Tab 2A-B were determined. (Tab 5A-B) Calibration data for the OCR (left) and ECAR (right) assays conducted in plate 1 (Tab 5A) or plate 2 (Tab 5B). Note that the pH calibrations failed for some wells in plate 1 and we therefore did not include ECAR data in our analysis. (XLSX)</p

Identified compounds inhibit O₂ consumption in <i>T</i>. <i>gondii</i>.

(A-B) Traces depicting the changes in O2 consumption rate (OCR) over time of intact T. gondii parasites incubated with no drug (pink) or with (A) atovaquone (ATV; two fold serial dilution from highest concentration—10 μM, colored dark green—to lowest concentration—0.01 μM, colored light green) or (B) auranofin (AUR; two fold serial dilution from highest concentration—80 μM, colored dark green—to lowest concentration—0.08 μM, colored light green)). FCCP (1 μM) was injected into the well to uncouple electron transport from the proton gradient and thus elicit the maximal OCR. A range of concentrations of the test compounds were then injected and the inhibition of OCR measured over time. A final injection of an inhibitory concentration of atovaquone (ATVi; 5 μM) maximally inhibited mitochondrial OCR. Values represent the mean ± SD of two technical replicates from a single experiment and are representative of three independent experiments. Similar OCR inhibition traces were obtained for each test compound. (C-I) Dose-response curves depicting the percent of T. gondii OCR in the presence of increasing concentrations of (C) atovaquone, (D) buparvaquone, (E) auranofin, (F) trifloxystrobin, (G) azoxystrobin, (H) MMV024397 or (I) MMV688853. Values represent the percent OCR relative to the no-drug (100% OCR) and inhibitory atovaquone-treated (0% OCR) controls, and depict the mean ± SEM of three independent experiments, each conducted in duplicate; error bars that are not visible are smaller than the symbol. (J) Comparison of the EC50 values determined for T. gondii OCR (OCR EC50; this figure and Table 3) and WT T. gondii proliferation (proliferation EC50; S1 Fig and Table 1). Coloring of compounds is as in Figs 1 and 3 (atovaquone, black; buparvaquone, burgundy; auranofin, orange; trifloxystrobin, pink; azoxystrobin, light blue; MMV024397, red; and MMV688853, dark blue). (TIF)</p

Candidate parasite ETC inhibitors do not impair the proliferation of human cells, with the exception of auranofin.

(A-G). Dose-response curves depicting the proliferation of human foreskin fibroblast (HFF) cells in the presence of a range of concentrations of (A) atovaquone, (B) buparvaquone, (C) trifloxystrobin, (D) azoxystrobin, (E) MMV024397, (F) MMV688853, or (G) auranofin. Values are expressed as a percent of the average confluence of the no-drug control at the end point of the assay (after 4 days of proliferation), and represent the mean ± SEM of three independent experiments, each conducted in triplicate; error bars that are not visible are smaller than the symbol. (H) Representative images of HFF cells at the end point of the assay when grown in the absence of drug (left; no drug) or in the presence of 10,000 nM auranofin (right). (TIF)</p

Identification of selective and off-target inhibitors of the ETC in <i>T</i>. <i>gondii</i> parasites.

(A) O2 consumption rate (OCR) versus extracellular acidification rate (ECAR) of T. gondii parasites treated with either no drug (black square), atovaquone (black triangle; 10 μM), azoxystrobin (light blue; 80 μM), MMV024397 (red; 20 μM), MMV688853 (dark blue; 20 μM), trifloxystrobin (pink; 10 μM), buparvaquone (burgundy; 20 μM) or auranofin (orange; 80 μM) assessed using a Seahorse XFe96 flux analyzer. Data represent the mean OCR and ECAR ± SEM of three independent experiments, and are derived from the top concentration of inhibitor tested in S3 Fig. Statistical analyses of these data are presented in S4 Fig. (B) Viability of extracellular T. gondii parasites treated with atovaquone (black triangles, 10 μM) or auranofin (orange circles, 1–100 μM) for 35–140 minutes. Viability was assessed by flow cytometry of propidium iodide-stained parasites and normalized to a DMSO-treated vehicle control, with the gating strategy outlined in S5 Fig. Data represent the mean ± SEM of three independent experiments; error bars that are not visible are smaller than the symbol.</p

Parasites treated with 3-MB-PP1 and, to a lesser extent, MMV688853 exhibit abnormal cellular morphology.

Representative images of (A) WT or (B) TgCDPK1G128M parasites expressing tdTomato observed during intracellular proliferation assays, with tdTomato fluorescence (top) and differential interference contrast (DIC; bottom) images depicted. WT or TgCDPK1G128M parasites were cultured in the absence of drug (no drug), or the presence of MMV688853 (5 μM), 3-MB-PP1 (5 μM) or atovaquone (1 μM) for 20 h. Abnormal morphology was defined as vacuoles that contained misshapen parasites as depicted in the images of MMV688853 and 3MB-PP1. Scale bars are 2 μm. (TIF)</p