论商品价值“质的决定”与“量的决定”的辩证关系——马克思劳动价值论视阈中的“价值决定”辨析

由于马克思在《资本论》及其手稿中多个层面地论述了商品的“价值决定”问题,“价值决定”因而包含了多重含义。如果说,价值与“人类一般劳动”之间的关系是一个商品价值“质的决定”的问题;那么,价值与“社会必要劳动时间”之间的关系就是一个商品价值“量的决定”的问题。人们往往看不清商品价值“质的决定”与“量的决定”之间的这种区别,把两个“社会必要劳动时间”与价值“质”的决定联系起来,要么是从坚持和发展劳动价值论走向消解和否定劳动价值论,要么是无视马克思的有关原典论述,拒斥第二种含义的社会必要劳动时间与价值决定的内在关联,从而陷入一种“二律背反”的理论“尴尬”境地而不能自拔。

STAT3 deficiency prevents hepatocarcinogenesis and promotes biliary proliferation in thioacetamide-induced liver injury

AIM To elucidate the role of STAT3 in hepatocarcinogenesis and biliary ductular proliferation following chronic liver injury. METHODS We investigated thioacetamide(TAA)-induced liver injury, compensatory hepatocyte proliferation, and hepatocellular carcinoma(HCC) development in hepatic STAT3-deficient mice. In addition, we evaluated TAAinduced biliary ductular proliferation and analyzed the activation of sex determining region Y-box9(SOX9) and Yes-associated protein(YAP), which regulate the transdifferentiation of hepatocytes to cholangiocytes.RESULTS Both compensatory hepatocyte proliferation and HCC formation were significantly decreased in hepatic STAT3-deficient mice as compared with control mice. STAT3 deficiency resulted in augmentation of hepatic necrosis and fibrosis. On the other hand, biliary ductular proliferation increased in hepatic STAT3-deficient livers as compared with control livers. SOX9 and YAP were upregulated in hepatic STAT3-deficient hepatocytes.CONCLUSION STAT3 may regulate hepatocyte proliferation as well as transdifferentiation into cholangiocytes and serve as a therapeutic target for HCC inhibition and biliary regeneration.