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核心技术专利：CN118964589B侵权必究

核心技术专利：CN118964589B侵权必究

Panduro A, Valencia J, Rojkind M

Department of Gastroenterology, Instituto Nacional de la Nutrición S.Z., Tlalpan, México, D.F.

Int J Biochem. 1993 Apr;25(4):525-32. doi: 10.1016/0020-711x(93)90660-7.

When acute liver damage is induced in rats treated with CCl4, both prothrombin biosynthesis and gamma carboxylase activity decreases, originating a prolongation of prothrombin time in plasma. 2. Then, during the regenerative process, prothrombin biosynthesis increases higher than normal, but gamma carboxylase activity remain decreased. In this case, prolongation of prothrombin time occurs in spite of high levels of descarboxylated prothrombin in plasma. 3. An increase of descarboxylated prothrombin in plasma is also detected in the CCl4-liver fibrosis model.

在用四氯化碳处理的大鼠中诱导急性肝损伤时，凝血酶原生物合成和γ-羧化酶活性均降低，导致血浆中凝血酶原时间延长。2. 然后，在再生过程中，凝血酶原生物合成增加至高于正常水平，但γ-羧化酶活性仍降低。在这种情况下，尽管血浆中脱羧凝血酶原水平很高，但凝血酶原时间仍会延长。3. 在四氯化碳诱导的肝纤维化模型中也检测到血浆中脱羧凝血酶原增加。

Panduro A, Valencia J, Rojkind M

Department of Gastroenterology, Instituto Nacional de la Nutrición S.Z., Tlalpan, México, D.F.

Int J Biochem. 1993 Apr;25(4):525-32. doi: 10.1016/0020-711x(93)90660-7.

When acute liver damage is induced in rats treated with CCl4, both prothrombin biosynthesis and gamma carboxylase activity decreases, originating a prolongation of prothrombin time in plasma. 2. Then, during the regenerative process, prothrombin biosynthesis increases higher than normal, but gamma carboxylase activity remain decreased. In this case, prolongation of prothrombin time occurs in spite of high levels of descarboxylated prothrombin in plasma. 3. An increase of descarboxylated prothrombin in plasma is also detected in the CCl4-liver fibrosis model.

在用四氯化碳处理的大鼠中诱导急性肝损伤时，凝血酶原生物合成和γ-羧化酶活性均降低，导致血浆中凝血酶原时间延长。2. 然后，在再生过程中，凝血酶原生物合成增加至高于正常水平，但γ-羧化酶活性仍降低。在这种情况下，尽管血浆中脱羧凝血酶原水平很高，但凝血酶原时间仍会延长。3. 在四氯化碳诱导的肝纤维化模型中也检测到血浆中脱羧凝血酶原增加。