Yue dong jin shi lue : (9 juan) /

Reissued : 2 ban ; Taibei : Xin wen feng chu ban gong si, Minguo 71 [1982]

Mang Luo zhong mu yi wen : [san juan fu bu yi yi juan] /

Date from preface.

Yi du jin shi ji : si juan /

Reissued: 2 ban ; Tai bei : Xin wen feng chu ban gong si, Min'guo 71 [1982]

Shan you shi ke cong bian : Si shi juan (juan 26 - chuan 40) /

Reissued: 2 ban ; Tai bei : Xin wen feng chu ban gong si, Min'guo 71 [1982]

Ping Jin du bei ji : (8 juan fu xu 1 juan zai xu 1 juan 3 xu 2 juan) /

Originally published: Wu Xian : Zhu shi jia shu xing su cao tang, Guangxu 12 [1886]

Tian xia jin shi zhi /

Reissued: Chu ban ; Taibei : Xin wen feng chu ban gong si, Min'guo 68 [1979]

Tao zhai ji jin xu lu /

Reissued: Chu ban ; Taibei : Xin wen feng chu ban gong si, Min'guo 68 [1979]

Jining zhou jin shi : [8 juan] /

Errata page included.

Peiwenzhai jin shi pu : Juan 59 zhi 63.

Content page: Kangxi 47 nian [1708] xiu.

Xue fu ji wen

ed. by Tung Nai

The Formation and Circulation of Early Yanzi Lore, Fourth Century B.C. - Third Century A.D.

Thesis (Ph.D.)--University of Washington, 2016-06

Antioxidative function of L-FABP in L-FABP stably transfected Chang liver cells

Liver fatty acid binding protein (L-FABP) contains amino acids that are known to possess antioxidant function. In this study, we tested the hypothesis that L-FABP may serve as an effective endogenous cytoprotectant against oxidative stress. Chang liver cells were selected as the experimental model because of their undetectable L-FABP mRNA level. Full-length L-FABP cDNA was subcloned into the mammalian expression vector pcDNA3.1 (pcDNA-FABP). Chang cells were stably transfected with pc-DNA-FABP or vector (pcDNA3.1) alone. Oxidative stress was induced by incubating cells with 400 mu mol/L H2O2 or by subjecting cells to hypoxia/reoxygenation. Total cellular reactive oxygen species (ROS) was determined using the fluorescent probe DCF. Cellular damage induced by hypoxia/reoxygenation was assayed by lactate dehydrogenase (LDH) release. Expression of L-FABP was documented by regular reverse transcription polyrnerase chain reaction (RT-PCR), real-time RT-PCR, and Western blot. The pcDNA-FABP-transfected cells expressed full-length L-FABP mRNA, which was absent from vector-transfected control cells. Western blot showed expression of 14-kd L-FABP protein in pcDNA-FABP-transfected cells, but not in vector-transfected cells. Transfected cells showed decreased DCF fluorescence intensity under oxidative stress (H2O2 and hypoxia/reoxygenation) conditions versus control in inverse proportion to the level of L-FABP expression. Lower LDH release was observed in the higher L-FABP-expressed cells in hypoxia/reoxygenation experiments. In conclusion, we successfully transfected and cloned a Chang liver cell line that expressed the L-FABP gene. The L-FABP-expressing cell line had a reduced intracellular ROS level versus control. This finding implies that L-FABP has a significant role in oxidative stress.

Macrophage-specific expression of human lysosomal acid lipase corrects inflammation and pathogenic phenotypes in lal(-/-) mice

Lysosomal acid lipase (LAL) hydrolyzes cholesteryl esters and triglycerides to generate free fatty acids and cholesterol in the cell. The downstream metabolites of these compounds serve as hormonal ligands for nuclear receptors and transcription factors. Genetic ablation of the lal gene in the mouse caused malformation of macrophages and inflammation-triggered multiple pathogenic phenotypes in multiple organs. To assess the relationship between macro phages and lal(-/-) pathogenic phenotypes, a macrophage-specific doxycycline-inducible transgenic system was generated to induce human LAL (hLAL) expression in the lal(-/-) genetic background under control of the 7.2-kb c-fins promoter/intron2 regulatory sequence. Doxycycline-induced hLAL expression in macrophages significantly ameliorated aberrant gene expression, inflammatory cell (neutrophil) influx, and pathogenesis in multiple organs. These studies strongly support that neutral lipid metabolism in macrophages contributes to organ inflammation and pathogenesis.