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Changben Li

Researcher at Fudan University

Publications -  23
Citations -  580

Changben Li is an academic researcher from Fudan University. The author has contributed to research in topics: Complementary DNA & Gene. The author has an hindex of 9, co-authored 23 publications receiving 565 citations.

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Journal Article

Transgenic tumor necrosis factor (TNF)-alpha production in pancreatic islets leads to insulitis, not diabetes. Distinct patterns of inflammation in TNF-alpha and TNF-beta transgenic mice.

TL;DR: Transgenic mice produced in which the synthesis of murine TNF-alpha was directed by the rat insulin II promoter resulted in an overwhelming insulitis, suggesting that additional stimuli are necessary to initiate the process of islet destruction.
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Insulitis in transgenic mice expressing tumor necrosis factor beta (lymphotoxin) in the pancreas

TL;DR: The expression of TNF-beta in the pancreas of transgenic mice resulted in a leukocytic inflammatory infiltrate consisting primarily of B220+ IgM+ B cells and CD4+ and CD8+ T cells, reminiscent of the early stages of diabetes, though the mice did not progress to diabetes.
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Tsetse thrombin inhibitor: bloodmeal-induced expression of an anticoagulant in salivary glands and gut tissue of Glossina morsitans morsitans.

TL;DR: The tsetse thrombin inhibitor was identified from salivary gland extracts of Glossina morsitans morsitan (Diptera: Glossinidae) by using degenerate oligonucleotide probes as discussed by the authors.
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Superinfection of Laodelphax striatellus with Wolbachia from Drosophila simulans.

TL;DR: The segregation of Wolbachia from superinfected L. striatellus was observed during the spreading process, which suggests that WolbachIA could adapt to a phylogenetically distant host with increased infection frequency in the new host population; however, it would take a long time to establish a high-frequency superinfection line.
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The interaction between ADAM 22 and 14-3-3ζ: regulation of cell adhesion and spreading ☆ ☆☆

TL;DR: It is found that overexpression of the ADAM 22 cytoplasmic tail in human SGH44 cells inhibited cell adhesion and spreading and that deletion or mutation of the binding site for 14-3-3zeta within theADAM 22 Cytoplasmsic tail abolished the ability of the overexpressed cytopLasmic Tail to alter cell ad cohesion and spreading.