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Yulia Shandalov

Researcher at Technion – Israel Institute of Technology

Publications -  20
Citations -  1162

Yulia Shandalov is an academic researcher from Technion – Israel Institute of Technology. The author has contributed to research in topics: Translocator protein & Tissue engineering. The author has an hindex of 13, co-authored 20 publications receiving 909 citations.

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Improved vascular organization enhances functional integration of engineered skeletal muscle grafts.

TL;DR: A “relay” approach is suggested in which extended in vitro incubation, enabling the formation of a more structured vascular bed, allows for graft-host angiogenic collaboration that promotes anastomosis and vascular integration that supports enhanced muscle regeneration, maturation, and integration.
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VDAC activation by the 18 kDa translocator protein (TSPO), implications for apoptosis

TL;DR: Understanding is provided regarding the mechanisms whereby VDAC and TSPO may serve as targets to modulate apoptotic rates, which has implications for drug design to treat diseases such as neurodegeneration and cancer.
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Textured soy protein scaffolds enable the generation of three-dimensional bovine skeletal muscle tissue for cell-based meat

TL;DR: The use of textured soy protein—an edible porous protein-based biomaterial—as a novel CBM scaffold that can support cell attachment and proliferation to create a 3D engineered bovine muscle tissue is demonstrated.
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An engineered muscle flap for reconstruction of large soft tissue defects

TL;DR: The described engineered muscle flap, equipped with an autologous vascular pedicle, constitutes an effective tool for reconstruction of large defects, thereby circumventing the need for both harvesting autologously flaps and postoperative scarification.
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Ligands of the mitochondrial 18 kDa translocator protein attenuate apoptosis of human glioblastoma cells exposed to erucylphosphohomocholine

TL;DR: This study shows that PK 11195 and Ro5 4864 inhibit the pro-apoptotic function of ErPC3 by blocking its capacity to cause a collapse of the mitochondrial membrane potential.