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Biomedical subjects

Jian-Hung Chen

Publications and source records attributed to Jian-Hung Chen.

2 recordsLinked to original sources
PubMed2004

Inheritable genetic algorithm for biobjective 0/1 combinatorial optimization problems and its applications.

In this paper, we formulate a special type of multiobjective optimization problems, named biobjective 0/1 combinatorial optimization problem BOCOP, and propose an inheritable genetic algorithm IGA with orthogonal array crossover (OAX) to efficiently find a complete set of nondominated solutions to BOCOP. BOCOP with n binary variables has two incommensurable and often competing objectives: minimizing the sum r of values of all binary variables and optimizing the system performance. BOCOP is NP-hard having a finite number C(n, r) of feasible solutions for a limited number r. The merits of IGA are threefold as follows: 1) OAX with the systematic reasoning ability based on orthogonal experimental design can efficiently explore the search space of C(n, r); 2) IGA can efficiently search the space of C(n, r+/-1) by inheriting a good solution in the space of C(n, r); and 3) The single-objective IGA can economically obtain a complete set of high-quality nondominated solutions in a single run. Two applications of BOCOP are used to illustrate the effectiveness of the proposed algorithm: polygonal approximation problem (PAP) and the problem of editing a minimum reference set for nearest neighbor classification (MRSP). It is shown empirically that IGA is efficient in finding complete sets of nondominated solutions to PAP and MRSP, compared with some existing methods.

Journal Article↗
PubMed2002

Possible involvement of glutathione and p53 in trichloroethylene- and perchloroethylene-induced lipid peroxidation and apoptosis in human lung cancer cells.

Trichloroethylene (TCE) and perchloroethylene (PERC) are volatile organic compounds (VOCs) that are primarily inhaled through the respiratory system. The aim of this study was to elucidate the role of glutathione (GSH) and p53 in TCE- and PERC-induced lung toxicity. Human lung adenocarcinoma cells NCI-H460 (p53-wild-type) have constitutively lower levels of GSH than NCI-H1299 (p53-null) cells. The results showed that exposure to vapor TCE and PERC produced a dose-dependent and more pronounced accumulation of H(2)O(2) in p53-WT H460 than p53-null H1299 cells. The accumulation of H(2)O(2) was accompanied by severe cellular damage, as indicated by the significant increase of lipid peroxidation and apoptosis in p53-WT H460 cells, but not p53-null H1299 cells. Cotreatment of p53-WT H460 cells with free radical scavengers, such as D-mannitol, uric acid, and sodium selenite, significantly attenuated the TCE- or PERC-induced lipid peroxidation. In contrast, depletion of GSH in p53-null H1299 cells enhanced TCE- or PERC-induced lipid peroxidation. The levels of p53 and Bax proteins were elevated, while Bcl-2 protein was downregulated in TCE- or PERC-treated p53-WT H460 cells. Activity of caspase 3, the apoptotic executioner, was also significantly enhanced in TCE- or PERC-treated cells. These data suggest that, in human lung cancer cells, GSH plays a vital role in the protection of TCE- and PERC-induced oxidative stress and apoptosis, which may be mediated through a p53-dependent pathway.

Adenocarcinoma↗