3 results about "Graft survival" patented technology

The disclosure provides a method for treating and / or preventing graft rejection with A Disintegrin And Metalloproteinase with Thrombospondin type 1 motif, member-13 (ADAMT S13). The disclosure provides a method for increasing ADAMTS13-mediated von Willebrand factor (VWF) cleavage in a subject that received a graft by administering ADAMTS13. The disclosure also provides a method of determining the likelihood that a subject will rejection a graft.

The utility model discloses a grafting knife device for magnolia grafting belongs to grafting knife technical field, the device includes handle and blade, is equipped with the medicine storage jar, spray pump and battery and button on handle, and spray pump is connected with spray head through spray pipe, and the blade is connected with the limiting block, and the spray head is connected with the limiting block. The utility model integrates the cutting function of cutter and the spraying function of protective liquid, and the operator can spray the protective liquid immediately after completing the cutting action, forms the protective layer at the cutting surface, thereby effectively slows down the oxidation process, improves the tissue healing rate between the scion and the stock, and significantly improves the grafting survival rate. The structure is compact, the operation is simple, and it is suitable for field operation or nursery use. Compared with the traditional spraying treatment mode, spraying is more timely. The spray head can switch work on both sides of the blade. The left and right switching not only meets the spraying needs of the inner and outer sides of the grafting knife, but also can adapt to both hands when holding the grafting knife, greatly facilitating the operator to use.

This invention provides an engineered platelet and its application in the preparation of anti-injury drugs for liver transplantation. This engineered platelet utilizes the natural liver tropism of platelets; upon reaching the site of liver injury, PLT-aCCL2 is specifically activated under local microenvironment stimulation, releasing loaded small-sized antibody fragments or active ingredients. This effectively penetrates deep into the liver parenchyma, overcoming the problem of poor tissue penetration of large-molecule protein drugs. Through this targeted delivery strategy, aCCL2 can efficiently and specifically block the physiological function of the chemokine CCL2, inhibiting the infiltration of peripheral monocytes into the liver, thereby blocking the initiation and amplification of the inflammatory cascade. Ultimately, this strategy significantly inhibits T-cell-mediated adaptive immune responses and acute rejection, effectively reducing graft injury and prolonging graft survival.