In CRCLM, we believe that nonanatomic hepatectomy with narrow margin is indicated, and optimal treatment would include functional preservation of as much of the remnant liver as possible.
Recipient cells migrating into the transplantation site of an allograft recognize histocompatibility antigens on the grafts and are cytotoxic against the grafts. Although the alloreactive immune response is predominantly directed at the major histocompatibility complex (major histocompatibility complex [MHC]; H‐2 in mice) class I molecules, the basic mechanisms of allograft rejection (e.g., ligand‐receptor interaction) remain unclear, because of the polymorphism and complexity of the MHC. To examine the role of MHC class I molecules in allograft rejection, Dd, Kd or DdKd‐transgenic skin or tumor cells we established on a C57BL/6 (DbKb) background and transplanted into C57BL/6 mice. Skin grafts from allogeneic (i.e., BALB/c, B10.D2, and BDF1) strains of mice were rejected from C57BL/6 mice on days 12–14 after grafting, whereas isografts were tolerated by these mice. Unexpectedly, skin grafts from Dd‐, Kd‐, and DdKd‐transgenic C57BL/6 mice were rejected on days 12–14 in a transgene expression rate‐independent manner from 9/19 (47%), 20/39 (51%), and 12/17 (71%) of C57BL/6 mice, respectively. Similarly, intradermally transplanted allogeneic (i.e., Meth A), but not syngeneic (i.e., EL‐4), tumor cells were rejected from C57BL/6 mice; the growth of Dd‐ or Kd‐transfected EL‐4 cells was delayed by 10–13 days; and 4/10 (40%) of DdKd‐transfected tumor cells were rejected from C57BL/6 mice.
These results indicate that Dd and Kd genes are equivalent as allogeneic MHC class I genes and that C57BL/6 (DbKb) mice reject Dd‐, Kd‐, or DdKd‐transgened skin or tumor cells in a transgene number‐dependent, gene expression rate‐independent manner.
In small bowel adenocarcinoma, location, size, and TNM stage of the tumors were the independent prognostic factors after curative resections. Partial resection with mural lymphadenectomy may be recommended as optimal surgery for small bowel adenocarcinoma.
Background:Allogeneic skin grafts onto C57BL/6 mice are rejected, and the rejected skin is replaced by surrounding skin with black hair. In contrast, syngeneic skin grafts are tolerated, and gray hair grows on the grafts.Methods:To explore the mechanism of gray hair growing on the tolerated skin grafts, we prepared full-thickness skin (2-cm square) autografts, 2 (2 cm + 2 cm) horizontal or vertical parallel incisions, and U-shaped (2 cm × 2 cm × 2 cm) flaps with or without pedicle vessels. The grafts, incisions, and flaps were fixed by suturing with string and protected by a transparent bandage. On day 14 after the operation, the bandages were removed to observe the color of the hair growing on the skin.Results:Skin autografts from wild-type or hepatocyte growth factor-transgenic (Tg) C57BL/6 mice survived with gray hair, whereas those from steel factor (Kitl)-Tg C57BL/6 mice survived with black hair. In addition, U-shaped flaps lacking both of the 2 main feeding vessels of wild-type mice had gray hair at the tip of the flaps. Light microscopy after staining with hematoxylin and eosin or dihydroxyphenylalanine showed that the formation of melanin pigment in the follicles, but not in the interadnexal skin, was susceptible to the blood supply.Conclusions:Melanin pigment formation in the hair bulb melanocytes appeared to be susceptible to the blood supply, and melanocytosis was promoted in the follicles and in the epidermis of Kitl-Tg C57BL/6 mice.
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