インスタントブラッドとは何ですか？
Instant Blood インスタントブラッド - This instant blood-mediated inflammatory reaction (IBMIR) activates the coagulation and complement cascades and leads to the destruction of 25% of all transplanted islets within minutes, contributing to the need, in most patients, for islets from more than 1 donor. [1] The culture of liver NK cells isolated from naive mice with TNF-α, IFN-γ, and IL-lβ, mimicking instant blood-mediated inflammatory reaction, led to significantly increased DX5− NK cell percentage among total liver NK cells. [2] Unfortunately, the procedure is hampered by the instant blood-mediated inflammatory reaction, (IBMIR), a thromboinflammatory response elicited by the vascular innate immune system, causing activation of the coagulation and complement systems and clearance of transplanted cells. [3] This review first describes the 3 major pathways of rejection: hyperacute rejection mediated by preformed natural antibodies and complement, instant blood-mediated inflammatory reactions, and acute cell-mediated rejection. [4] However, many hurdles have yet to be crossed, such as instant blood-mediated inflammatory reaction, immune reactions, side effects of immunosuppressant drugs, lack of donors, islet quality variability, and others. [5] However, donor shortage and host rejection via instant blood-mediated inflammatory reactions are worrisome. [6] Given that host immune rejection and an instant blood-mediated inflammatory reaction (IBMIR) are the primary factors detrimental to islet engraftment and survival, often resulting in rapid cell loss and graft failure, CS-PEG surface engineering provides an "easy-to-adopt" approach for cell surface engineering that could potentially improve the clinical efficacy of islet transplantation and other types of cell therapies. [7] Their instant blood glucose levels were 2. [8] Different MSC products display varying levels of highly procoagulant tissue factor (TF) and may adversely trigger the instant blood-mediated inflammatory reaction (IBMIR). [9] ABSTRACT Instant Blood-Mediated Inflammatory Reaction (IBMIR) is a major cause of graft loss during pancreatic islet transplantation, leading to a low efficiency of this treatment method and significantly limiting its broader clinical use. [10] In this regard, macro/microencapsulation, surface camouflage, and surface modification with immune-privileged cells have been performed to protect the transplanted islets against instant blood-mediated inflammatory reactions or immune reactions. [11] We review the potential causes for graft death, including the instant blood-mediated inflammatory reaction, exposure to immunosuppressive agents, and low oxygen tension. [12] Some even describe a dual activation of both the coagulation and the complement pathway, called Instant Blood-Mediated Inflammatory Reaction (IBMIR), explaining the disappointing results and low engraftment rates in clinical trials. [13] However, long-term function of transplanted hepatocytes following infusion has not been achieved due to insufficient numbers of hepatocytes reaching the liver cell plates caused by activation of the instant blood-mediated inflammatory reaction (IBMIR). [14] Static protocol is based on determining insulin infusion according to an instant blood glycaemia (BG) level at a given time. [15]この瞬間的な血液媒介炎症反応（IBMIR）は、凝固と補体カスケードを活性化し、移植されたすべての膵島の25％を数分以内に破壊し、ほとんどの患者で1人以上のドナーからの膵島の必要性に貢献します。 [1] TNF-α、IFN-γ、およびIL-1βを用いてナイーブマウスから単離された肝臓NK細胞の培養は、即時の血液媒介炎症反応を模倣し、全肝臓NK細胞の中でDX5-NK細胞の割合を有意に増加させました。 [2] nan [3] nan [4] nan [5] nan [6] nan [7] nan [8] nan [9] nan [10] nan [11] nan [12] nan [13] nan [14] 静的プロトコルは、特定の時間における瞬間血糖（BG）レベルに従ってインスリン注入を決定することに基づいています。 [15]
mediated inflammatory reaction 媒介炎症反応
This instant blood-mediated inflammatory reaction (IBMIR) activates the coagulation and complement cascades and leads to the destruction of 25% of all transplanted islets within minutes, contributing to the need, in most patients, for islets from more than 1 donor. [1] The culture of liver NK cells isolated from naive mice with TNF-α, IFN-γ, and IL-lβ, mimicking instant blood-mediated inflammatory reaction, led to significantly increased DX5− NK cell percentage among total liver NK cells. [2] Unfortunately, the procedure is hampered by the instant blood-mediated inflammatory reaction, (IBMIR), a thromboinflammatory response elicited by the vascular innate immune system, causing activation of the coagulation and complement systems and clearance of transplanted cells. [3] This review first describes the 3 major pathways of rejection: hyperacute rejection mediated by preformed natural antibodies and complement, instant blood-mediated inflammatory reactions, and acute cell-mediated rejection. [4] However, many hurdles have yet to be crossed, such as instant blood-mediated inflammatory reaction, immune reactions, side effects of immunosuppressant drugs, lack of donors, islet quality variability, and others. [5] However, donor shortage and host rejection via instant blood-mediated inflammatory reactions are worrisome. [6] Given that host immune rejection and an instant blood-mediated inflammatory reaction (IBMIR) are the primary factors detrimental to islet engraftment and survival, often resulting in rapid cell loss and graft failure, CS-PEG surface engineering provides an "easy-to-adopt" approach for cell surface engineering that could potentially improve the clinical efficacy of islet transplantation and other types of cell therapies. [7] Different MSC products display varying levels of highly procoagulant tissue factor (TF) and may adversely trigger the instant blood-mediated inflammatory reaction (IBMIR). [8] ABSTRACT Instant Blood-Mediated Inflammatory Reaction (IBMIR) is a major cause of graft loss during pancreatic islet transplantation, leading to a low efficiency of this treatment method and significantly limiting its broader clinical use. [9] In this regard, macro/microencapsulation, surface camouflage, and surface modification with immune-privileged cells have been performed to protect the transplanted islets against instant blood-mediated inflammatory reactions or immune reactions. [10] We review the potential causes for graft death, including the instant blood-mediated inflammatory reaction, exposure to immunosuppressive agents, and low oxygen tension. [11] Some even describe a dual activation of both the coagulation and the complement pathway, called Instant Blood-Mediated Inflammatory Reaction (IBMIR), explaining the disappointing results and low engraftment rates in clinical trials. [12] However, long-term function of transplanted hepatocytes following infusion has not been achieved due to insufficient numbers of hepatocytes reaching the liver cell plates caused by activation of the instant blood-mediated inflammatory reaction (IBMIR). [13]この瞬間的な血液媒介炎症反応（IBMIR）は、凝固と補体カスケードを活性化し、移植されたすべての膵島の25％を数分以内に破壊し、ほとんどの患者で1人以上のドナーからの膵島の必要性に貢献します。 [1] TNF-α、IFN-γ、およびIL-1βを用いてナイーブマウスから単離された肝臓NK細胞の培養は、即時の血液媒介炎症反応を模倣し、全肝臓NK細胞の中でDX5-NK細胞の割合を有意に増加させました。 [2] nan [3] nan [4] nan [5] nan [6] nan [7] nan [8] nan [9] nan [10] nan [11] nan [12] nan [13]