Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:A7KAX9 (grit)
 1,275 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The objective of this research was to investigate some of the potentially controlling factors influencing the atmospheric releases of volatile organic chlorinated compounds from the activated-sludge sewage treatment process. The field study was designed to evaluate the wastewater and airborne concentrations of six chlorinated compounds: hexachlorobicycloheptadiene (hex-BCH), heptachlorobicycloheptene (Hex-VCL), chlordene, chloroform (CHCl3), carbon tetrachloride (CCl4) and tetrachloroethylene (TCE). Analysis of samples consisted of saturating 5 mL aliquots with sodium chloride, extracting with an equal amount of petroleum ether (PE) and subsequent analysis using a gas chromatograph. The air samples collected on Chromsorb 102 were desorbed with 2 mL PE. The study revealed that the highest wastewater concentrations for the water-insoluble hex-BCH, hex-VCL and chlordene were found in the aeration basins, which suggests adsorption of these compounds to the biomass. The plant effluent wastewater concentrations were reduced because of airborne release and suspended solids separation in the clarifiers. In contrast, the wastewater concentrations for the more water-soluble CHCl3, CCl4 and TCE were significantly reduced in the aeration basins. This is because of aerial stripping at the grit-chamber weir. This study suggests that the water-insoluble compounds have prolonged aerial release from the aeration basins. The water-insoluble compounds adhere to the biomass, which is recycled through the plant. The aerial release of these water-insoluble compounds was enhanced by increased aeration rate but depressed by higher suspended solids concentrations.
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PMID:Worker exposure to chlorinated organic compounds from the activated-sludge wastewater treatment process. 683 35

Epithelial (E) cells were cultured on smooth tissue culture plastic (TCP), TCP-Ti, polished Ti (P), and rough grit-blasted Ti (B), acid-etched Ti (AE), and grit-blasted and acid-etchedTi (SLA) surfaces and their growth, area, adhesion, and membrane-Ti proximity assessed. Rough surfaces decreased the growth of E cells compared to smooth surfaces in cultures up to 28 days. In general rough surfaces decreased the spreading of E cells as assessed by their area with the most pronounced affect for the SLA surface. On the other hand, the strength of E cells adhesion as inferred by immunofluorescence staining of vinculin in focal adhesions indicated that E cells formed more and larger focal adhesions on the smooth P surface compared to the rougher AE surface. As this finding indicates a stronger adhesion to smooth surfaces, it is likely that E cells on rough surfaces are more susceptible to mechanical removal. An immunogold labeling method was developed to visualize focal adhesions using back-scattered electron imaging with a scanning electron microscope (SEM). On rough surfaces focal adhesions were primarily localized on to the ridges rather than the valleys and the cells tended to bridge over the valleys. Transmission electron microscopy (TEM) measurements of membrane proximity to the Ti surface indicated that average distance of cell to the Ti increased as the Ti surface roughness increased. Therefore, the size and shape of surface features are important determinants of epithelial adhesive behavior and epithelial coverage of rough surfaces would be difficult to attain if such surfaces become exposed.
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PMID:Substratum roughness alters the growth, area, and focal adhesions of epithelial cells, and their proximity to titanium surfaces. 1592 1

Implant surface topography can modulate macrophage behavior during wound healing by the production of proinflammatory cytokines. This study investigated the activation of FAK, Src, and ERK1/2 signaling intermediates of the proinflammatory ERK1/2 pathway in RAW 264.7 macrophages in response to polished (P), coarse-grit-blasted (B), acid etched (E), and grit-blasted and etched (SLA) surface topographies. In addition, the effects of these topographies on cell spreading, vinculin organization, and viability were determined. Macrophages on the SLA surface changed from predominantly well-spread cells to ones with a more spherical morphology over time. In contrast, macrophages on the P surface changed from being predominantly spherical cells to well spread. The morphological changes were associated with changes in the distribution of vinculin. The overall patterns of the pFAK, pSrc, pERK1/2 levels as well as pERK1/2 nuclear translocation associated with cell shape with greater activation being seen with a more spread morphology. These results suggest that surface topography differentially activates signaling pathways that affect cell function and raise the possibility that topographies can be designed to optimize desired cell responses.
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PMID:The effect of surface topography on cell shape and early ERK1/2 signaling in macrophages; linkage with FAK and Src. 2342 18