We found that the expression of galectin-1 and galectin-3 was significantly up-regulated in hepatic stellate cells (HSCs) both in the course of their transdifferentiation into myofibroblasts, a process of "self-activation," and in the fibrosis of liver tissues. Recombinant galectin-1 and galectin-3 stimulated the proliferation of cultured HSCs via the MEK1/2-ERK1/2 signaling pathway. However, galectin-3 utilized protein kinases C and A to induce this process, whereas galectin-1 did not. We also found that thiodigalactoside, a potent inhibitor of ␤-galactoside binding, attenuated the effects of both galectins. In addition, galectin-1, but not galectin-3, promoted the migration of HSCs. Thus, it appears that galectin-1 and galectin-3, generated by activated HSCs, could participate in ␤-galactoside binding and induce different intracellular signaling pathways leading to the proliferation of HSCs.

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We retrospectively compared the outcome of 13 patients at our institution and that of 163 reported cases of pedunculated hepatocellular carcinoma (HCC) with that of conventional HCC subdivided by tumor diameter (group A: less than 2 cm; group B: 2–5 cm, group C: more than 5 cm). The survival of patients with pedunculated HCC in the 163 reported cases was no different from that of group B, but less favorable than in group A (p < 0.01) and more favorable than in group C (p < 0.01). Among the 163 patients with pedunculated HCC, the 113 cases of surgically treated patients had higher survival than the 21 patients treated with transcatheter arterial embolization (n = 16) or transcatheter arterial infusion chemotherapy (n = 5) (p < 0.01) and than 29 conservatively treated patients (p < 0.001). A total of 70 patients out of 163 (42%) died within 1 year after diagnosis. Additionally, almost all cases of pedunculated HCC showed histologically moderately or poorly differentiated characteristics according to Edmondson and Stainer’s classification or the WHO classification. These results suggest that pedunculated HCC has not a favorable prognosis if appropriate surgical resection has not been performed very early within a few months because of its rapid progressive nature.

Abstract. C++ Exceptions provide a useful way for dealing with abnormal program behavior, but often lead to irregular interprocedural control flow that complicates compiler optimizations and static analysis. In this paper, we present an interprocedural exception analysis and transformation framework for C++ that captures the control-flow induced by exceptions and transforms it into an exception-free program that is amenable for precise static analysis. Control-flow induced by exceptions is captured in a modular interprocedural exception control-flow graph (IECFG). The IECFG is further refined using a novel interprocedural dataflow analysis algorithm based on a compact representation for a set of types called the Signed-TypeSet domain. The results of the interprocedural analysis are used by a lowering transformation to generate an exception-free C++ program. The lowering transformations do not affect the precision and accuracy of any subsequent program analysis. Our framework handles all the features of synchronous C++ exception handling and all exception sub-typing rules from the C++0x standard. We demonstrate two applications of our framework: (a) automatic inference of exception specifications for C++ functions for documentation, and (b) checking the "no-throw" and "no-leak" exception-safety properties.