Abstract— Time‐resolved measurements of 1270 nm singlet‐oxygen emission following pulsed‐laser excitation were made from unilamellar dimyristoyl 1‐α‐phosphatidylcholine liposomes labeled with zinc phthalocyanine. The effect of the hydrophobic quenchers, β‐carotene and ethyl β‐apo‐8′trans carotenoate, and the hydrophilic quenchers, histidine and methionine, upon the kinetics of the 1270 nm singlet‐oxygen emission was studied. Hydrophobic quenchers principally lowered the intensity of the 1270 nm emission and caused only modest changes in the lifetime of the 1270 nm emission. The decrease in 1270 nm emission caused by hydrophobic quenchers was related to the size of the liposomes. The larger the radius of the liposome, the greater the decrease in 1270 nm emission caused by a given concentration of hydrophobic quencher. In contrast, hydrophilic quenchers principally decreased the lifetime of the 1270 nm emission. The effect of hydrophilic quenchers was independent of the size of the liposomes. There was good agreement between the experimental results and the kinetics of the singlet‐oxygen emission calculated using a one dimensional model of singlet‐oxygen quenching and diffusion. The kinetics of singlet‐oxygen emission from liposomes without added hydrophobic quenchers closely approximated the theoretical kinetics of singlet oxygen in a homogeneous aqueous solution.

We measured 6P-cholesterol hydroperoxide (6P-CHP), a specific singlet-oxygen (02('Ag)) product, during irradiation of unilamellar dimyristoyl 1-a-phosphatidylcholine liposomes containing cholesterol and zinc phthalocyanine (ZnPC). The effects of liposome size, the hydrophobic (O2(lAJ) quencher, P-carotene, and hydrophilic O2(lA,) quenchers upon the amount of 6P-CHP formed were determined and interpreted in terms of a one dimensional model of O2(lA,) quenching and diffusion. The model correctly predicted (1) that the amount of 6P-CHP was increased with increasing liposome size, (2) that P-carotene was more effective at reducing 6P-CHP formation in 400 nm diameter liposomes than 100 nm diameter liposomes and (3) that the hydrophilic quencher, water, was also more effective in large liposomes than in small liposomes.The hydrophobic quencher, p-carotene, was more effective at reducing the formation of 6P-CHP than at reducing the 1270 nm OZ(lAg) emission. This difference was found to be due to the size distribution present in the liposome preparations because the difference between the 6P-CHP data and the 1270 nm emission data was much smaller in liposome preparations with a narrow size distribution. When a significant size distribution was present, the 6P-CHP data were weighted more heavily with large-diameter liposomes, while the 1270 nm emission data were weighted more heavily with small-diameter liposomes. pared using polycarbonate filters with pore diameters of 100 nm, 200 nm and 400 nm. The average diameter of liposomes prepared in this manner is roughly equal to the pore diameter of the filter, but variation in size is roughly 20-50% of the pore diameter (10).?Abbreviations: CHP, cholesterol hydroperoxide; 5a-CHP, 5a-cholesterol hydroperoxide; 6a-CHP, 6a-cholesterol hydroperoxide; 6P-CHP, 6P-cholesterol hydroperoxide; 7a/7P-CHP, 7a-cholesterol hydroperoxide and 7P-cholesterol hydroperoxide; ZnPC, zinc phthalocyanine (pyridine),.

We have compared the singlet oxygen-mediated inactivation of acetylcholinesterase (ACE) in solution with the inactivation of ACE on the surface of K562 leukemia cells. In solution, the actions of the singlet-oxygen quenchers, methionine, azide, disodium [N,N'-ethylenebis (5-sulfosalicylideneimminato)]nickelate(II) (Ni-chelate 1) and disodium [(N,N'-2,3-propionic acid)bis(5-sulfosal-icylideneimminato)] nickelate(II) (Ni-chelate 2) could be explained quantitatively by assuming their only mechanism of action was to quench singlet oxygen. The singlet oxygen quenchers, azide, Ni-chelate 1 and Ni-chelate 2, caused smaller inhibitions in the rate of singlet oxygen-mediated inactivation of ACE on K562 cells than ACE in solution. The effects of these quenchers and of deuterium oxide were interpreted using a mathematical model of singlet-oxygen quenching and diffusion to estimate the lifetime of singlet oxygen near the cell surface. The azide quenching data and the deuterium-oxide data gave lifetimes of 0.9 +/- 0.2 microsecond and 0.45 +/- 0.15 microsecond, respectively. The increases in ACE inactivation lifetime caused by the nickel chelates were anomalously large. The unexpectedly large quenching due to the nickel chelates may have been due to a nonuniform distribution of the chelates in the cytoplasm with a large concentration of the chelate near the cell membrane.

This paper looks at the problem of employee turnover, which has considerable influence on organizational productivity and healthy working environments. Using a publicly available dataset, key factors capable of predicting employee churn are identified. Six machine learning algorithms including decision trees, random forests, naïve Bayes and multi-layer perceptron are used to predict employees who are prone to churn. A good level of predictive accuracy is observed, and a comparison is made with previous findings. It is found that while the simplest correlation and regression tree (CART) algorithm gives the best accuracy or F1-score, the alternating decision tree (ADT) gives the best area under the ROC curve. Rules extracted in the if-then form enable successful identification of the probable causes of churning.