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A total of 486 unfertilized, aged human oocytes were exposed to ethanol, calcium ionophore A23187, phorbol ester or puromycin and examined for evidence of activation. Five per cent of control oocytes (3/58) were spontaneously activated. Of the two agents which cause the release of intracellular Ca2+ ions, Ca2+ ionophore induced activation of only 16% of unfertilized oocytes, while ethanol did not have any effect. Phorbol ester, a stimulator of protein kinase C, also resulted in limited activation (14% of oocytes). In contrast, puromycin, an inhibitor of protein synthesis, resulted in activation of 91% of the exposed oocytes. It is speculated that puromycin probably inhibits a specific cytostatic factor or factors which are responsible for maintenance of the metaphase II block. Morphologically activated oocytes usually retained the second polar body and formed subnuclei. The developmental potential of activated oocytes appeared to be reduced, with only some oocytes capable of a single division.

A total of 486 unfertilized, aged human oocytes were exposed to ethanol, calcium ionophore A23187, phorbol ester or puromycin and examined for evidence of activation. Five per cent of control oocytes (3/58) were spontaneously activated. Of the two agents which cause the release of intracellular Ca2+ ions, Ca2+ ionophore induced activation of only 16% of unfertilized oocytes, while ethanol did not have any effect. Phorbol ester, a stimulator of protein kinase C, also resulted in limited activation (14% of oocytes). In contrast, puromycin, an inhibitor of protein synthesis, resulted in activation of 91% of the exposed oocytes. It is speculated that puromycin probably inhibits a specific cytostatic factor or factors which are responsible for maintenance of the metaphase II block. Morphologically activated oocytes usually retained the second polar body and formed subnuclei. The developmental potential of activated oocytes appeared to be reduced, with only some oocytes capable of a single division.

During development of alcoholic pancreatitis, oxidative (acetaldehyde) and nonoxidative metabolites (ethyl palmitate, ethyl oleate), rather than ethanol itself, mediate toxic injury. Exposure of pancreatic acini to ethanol blocks cholecystokinin (CCK)-8-stimulated apical exocytosis and redirects exocytosis to the basolateral plasma membrane, causing interstitial pancreatitis. We examined how each ethanol metabolite contributes to these changes in exocytosis.Rat pancreatic acini were incubated with concentrations of ethanol associated with alcoholic pancreatitis (20-50 mmol/L) or ethanol metabolites (1-3 mmol/L) and then stimulated with CCK-8. We performed single zymogen granule (ZG) exocytosis assays, Ca(2+) imaging studies, ultrastructural analyses (with electron microscopy), and confocal microscopy to assess the actin cytoskeleton and track the movement of vesicle-associated membrane protein (VAMP)-8-containing ZGs. Coimmunoprecipitation assays were used to identify complexes that contain the distinct combinations of Munc18 and the soluble N-ethylmaleimide sensitive factor attachment protein receptor proteins, which mediate apical (ZG-apical plasma membrane) and basolateral exocytosis and fusion between ZGs (ZG-ZG).The ethanol metabolites acetaldehyde, ethyl palmitate, and ethyl oleate reduced CCK-8-stimulated apical exocytosis and formation of apical exocytotic complexes (between Munc18b and Syntaxin-2, synaptosomal-associated protein of 23 kilodaltons [SNAP23], and VAMP2) in rat pancreatic acini. Acetaldehyde and ethyl oleate redirected CCK-8-stimulated exocytosis to the basal and lateral plasma membranes and translocation of VAMP8-containing ZGs toward the basolateral plasma membrane. This process was mediated primarily via formation of basolateral exocytotic complexes (between Munc18c and Syntaxin-4, SNAP23, and VAMP8). Exposure of the acini to acetaldehyde and ethyl oleate followed by CCK-8 stimulation mildly perturbed the actin cytoskeleton and Ca(2+) signaling; exposure to ethyl palmitate severely affected Ca(2+) signaling. Acetaldehyde, like ethanol, promoted fusion between ZGs by the formation of ZG-ZG exocytotic complexes (between Munc18b and Syntaxin-3, SNAP23, and VAMP8), whereas ethyl palmitate and ethyl oleate reduced ZG-ZG fusion and formation of these complexes.The ethanol metabolites acetaldehyde, ethyl palmitate, and ethyl oleate perturb exocytosis processes in cultured rat pancreatic acini (apical blockade, basolateral exocytosis, and fusion between ZGs). Acetaldehyde and, to a lesser degree, ethyl oleate produce many of the same pathologic effects of ethanol on CCK-8-stimulated exocytosis in pancreatic acini.

During development of alcoholic pancreatitis, oxidative (acetaldehyde) and nonoxidative metabolites (ethyl palmitate, ethyl oleate), rather than ethanol itself, mediate toxic injury. Exposure of pancreatic acini to ethanol blocks cholecystokinin (CCK)-8-stimulated apical exocytosis and redirects exocytosis to the basolateral plasma membrane, causing interstitial pancreatitis. We examined how each ethanol metabolite contributes to these changes in exocytosis.Rat pancreatic acini were incubated with concentrations of ethanol associated with alcoholic pancreatitis (20-50 mmol/L) or ethanol metabolites (1-3 mmol/L) and then stimulated with CCK-8. We performed single zymogen granule (ZG) exocytosis assays, Ca(2+) imaging studies, ultrastructural analyses (with electron microscopy), and confocal microscopy to assess the actin cytoskeleton and track the movement of vesicle-associated membrane protein (VAMP)-8-containing ZGs. Coimmunoprecipitation assays were used to identify complexes that contain the distinct combinations of Munc18 and the soluble N-ethylmaleimide sensitive factor attachment protein receptor proteins, which mediate apical (ZG-apical plasma membrane) and basolateral exocytosis and fusion between ZGs (ZG-ZG).The ethanol metabolites acetaldehyde, ethyl palmitate, and ethyl oleate reduced CCK-8-stimulated apical exocytosis and formation of apical exocytotic complexes (between Munc18b and Syntaxin-2, synaptosomal-associated protein of 23 kilodaltons [SNAP23], and VAMP2) in rat pancreatic acini. Acetaldehyde and ethyl oleate redirected CCK-8-stimulated exocytosis to the basal and lateral plasma membranes and translocation of VAMP8-containing ZGs toward the basolateral plasma membrane. This process was mediated primarily via formation of basolateral exocytotic complexes (between Munc18c and Syntaxin-4, SNAP23, and VAMP8). Exposure of the acini to acetaldehyde and ethyl oleate followed by CCK-8 stimulation mildly perturbed the actin cytoskeleton and Ca(2+) signaling; exposure to ethyl palmitate severely affected Ca(2+) signaling. Acetaldehyde, like ethanol, promoted fusion between ZGs by the formation of ZG-ZG exocytotic complexes (between Munc18b and Syntaxin-3, SNAP23, and VAMP8), whereas ethyl palmitate and ethyl oleate reduced ZG-ZG fusion and formation of these complexes.The ethanol metabolites acetaldehyde, ethyl palmitate, and ethyl oleate perturb exocytosis processes in cultured rat pancreatic acini (apical blockade, basolateral exocytosis, and fusion between ZGs). Acetaldehyde and, to a lesser degree, ethyl oleate produce many of the same pathologic effects of ethanol on CCK-8-stimulated exocytosis in pancreatic acini.

Abstract Electrodeposition of silicon from a cryolite based electrolyte at a relatively low temperature is a promising approach to generate high purity silicon. In order to obtain fundamental data pertaining to electrowinning of silicon from cryolite–SiO 2 melts, charge transport properties of the melt such as conductivity and electronic and ionic transference numbers were measured. Each property was determined for a range of temperatures and SiO 2 contents. It was found that addition of silica to cryolite generally decreases the transport rate of charge carriers. The temperature on the other hand had a positive effect on the electronic and ionic conductivities. The variations arise from the structural changes in the melt, particularly formation of complex ions involving Na, Si, and Al.

Abstract Electrodeposition of silicon from a cryolite based electrolyte at a relatively low temperature is a promising approach to generate high purity silicon. In order to obtain fundamental data pertaining to electrowinning of silicon from cryolite–SiO 2 melts, charge transport properties of the melt such as conductivity and electronic and ionic transference numbers were measured. Each property was determined for a range of temperatures and SiO 2 contents. It was found that addition of silica to cryolite generally decreases the transport rate of charge carriers. The temperature on the other hand had a positive effect on the electronic and ionic conductivities. The variations arise from the structural changes in the melt, particularly formation of complex ions involving Na, Si, and Al.

Large quantities of carbon are stored in alpine grassland of the Tibetan Plateau, which is extremely sensitive to climate change. However, it remains unclear whether soil organic matter (SOM) in different layers responds to climate change analogously, and whether microbial communities play vital roles in SOM turnover of topsoil. In this study we measured and collected SOM turnover by the 14C method in alpine grassland to test climatic effects on SOM turnover in soil profiles. Edaphic properties and microbial communities in the northwestern Qinghai Lake were investigated to explore microbial influence on SOM turnover. SOM turnover in surface soil (0–10 cm) was more sensitive to precipitation than that in subsurface layers (10–40 cm). Precipitation also imposed stronger effects on the composition of microbial communities in the surface layer than that in deeper soil. At the 5–10 cm depth, the SOM turnover rate was positively associated with the bacteria/fungi biomass ratio and the relative abundance of Acidobacteria, both of which are related to precipitation. Partial correlation analysis suggested that increased precipitation could accelerate the SOM turnover rate in topsoil by structuring soil microbial communities. Conversely, carbon stored in deep soil would be barely affected by climate change. Our results provide valuable insights into the dynamics and storage of SOM in alpine grasslands under future climate scenarios.

Large quantities of carbon are stored in alpine grassland of the Tibetan Plateau, which is extremely sensitive to climate change. However, it remains unclear whether soil organic matter (SOM) in different layers responds to climate change analogously, and whether microbial communities play vital roles in SOM turnover of topsoil. In this study we measured and collected SOM turnover by the 14C method in alpine grassland to test climatic effects on SOM turnover in soil profiles. Edaphic properties and microbial communities in the northwestern Qinghai Lake were investigated to explore microbial influence on SOM turnover. SOM turnover in surface soil (0–10 cm) was more sensitive to precipitation than that in subsurface layers (10–40 cm). Precipitation also imposed stronger effects on the composition of microbial communities in the surface layer than that in deeper soil. At the 5–10 cm depth, the SOM turnover rate was positively associated with the bacteria/fungi biomass ratio and the relative abundance of Acidobacteria, both of which are related to precipitation. Partial correlation analysis suggested that increased precipitation could accelerate the SOM turnover rate in topsoil by structuring soil microbial communities. Conversely, carbon stored in deep soil would be barely affected by climate change. Our results provide valuable insights into the dynamics and storage of SOM in alpine grasslands under future climate scenarios.