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Sen Li

Researcher at University of Miami

Publications -  19
Citations -  402

Sen Li is an academic researcher from University of Miami. The author has contributed to research in topics: Transplantation & Risk assessment. The author has an hindex of 9, co-authored 18 publications receiving 374 citations. Previous affiliations of Sen Li include Shanghai Ocean University.

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Interleukin-10 Delivery via Mesenchymal Stem Cells: A Novel Gene Therapy Approach to Prevent Lung Ischemia–Reperfusion Injury

TL;DR: A therapeutic strategy using vIL-10-engineered MSCs to prevent IR injury in lung transplantation seems promising and ISOL (in situ oligonucleotide ligation for DNA fragmentation detection) and caspase-3 staining demonstrated significantly (p < 0.05) fewer apoptotic cells in MSC-vIL10-treated lungs.
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Aging exacerbates neointimal formation, and increases proliferation and reduces susceptibility to apoptosis of vascular smooth muscle cells in mice

TL;DR: Age-dependent increases in PDGFR-alpha may alter VSMC proliferation, and when coupled with resistance to apoptosis could contribute to exaggerated neointima formation in aging animals.
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Long-term acceptance of composite tissue allografts through mixed chimerism and CD28 blockade.

TL;DR: The demonstration that tolerance can be achieved with minimal preconditioning provides a rationale for application to large animals and humans and suggests that although composite tissue allografts may have a significant skin component (and are therefore felt to be highly antigenic), protocols used to induce tolerance to organ transplants may be equally applicable to composite-tissue allotransplantation.
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Tregs expanded in vivo by TNFRSF25 agonists promote cardiac allograft survival

TL;DR: TNFRSF25 agonists expand Tregs in vivo and delay allograft rejection in a mouse model of fully major histocompatibility complex–mismatched ectopic heart transplants.
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Cardiac proteasome dysfunction during cold ischemic storage and reperfusion in a murine heart transplantation model.

TL;DR: It is concluded that substrate specificity of the proteasome changes during cold ischemia and that proteasomesome inhibition preserves the physiological ubiquitin-protein conjugate pool during organ preservation.