Annexin (AX) constitutes a new family of Ca2+-dependent membrane-binding proteins; 13 of them have been described. Among these, annexin-1 (AX-I) has displayed many biological functions in vitro. Its actual role in vivo, however, remains unknown. We already reported that AX-I was expressed in proliferating (regenerating) hepatocytes at both protein and messenger RNA (mRNA) levels. The role of AX-I in human hepatocellular carcinoma (HCC) remains obscure. In this study, the amounts of AX-I at protein and mRNA levels, as well as its localization, have been determined in the normal human liver, chronic hepatitis liver, and nontumorous and tumorous portions of HCC. AX-I was rarely found in normal and chronic liver tissues, whereas it is overexpressed at both the transcriptional and translational levels in tumorous and nontumorous regions of HCC. In addition, more AX-I was expressed in the tumorous portion than the nontumorous portion of HCC. AX-I was present in the hepatocytes and HCC cells, localized mainly in the cytoplasm. AX-I was expressed in poorly differentiated cancer cells. Furthermore, AX-I was tyrosine-phosphorylated in HCC. We also found that some of the AX-I- positive hepatocytes in the nontumorous tissues were derived from a particular subset of parenchymal cells (stem or oval cells). These results indicate that AX-I plays an important role in the malignant transformation process leading to HCC and that it is closely related to the histological grade of HCC. HCC would offer a novel tool with which to study the function of AX-I in malignant transformation.
Recently various real-time communication protocols have been proposed. In this paper, first, we propose a timed I/O automaton model so that we can simply specify such real-time protocols. The proposed model can handle not only time but also data values. Then, we propose a conformance testing method for the model. In order to trace a test sequence (I/O sequence) on the timed I/O automaton model, we need to execute each I/O action in the test sequence at an adequate execution timing which satisfies all timing constraints in the test sequence. However, since outputs are given from IUTs and uncontrollable, we cannot designate their output timing in advance. Also their output timing affects the executable timing for the succeeding I/O actions in the test sequence. Therefore, in general, the executable timing of each input action in a test sequence can be specified by a function of the execution time of the preceding I/O actions. In this paper, we propose an algorithm to decide efficiently whether a given test sequence is executable. We also give an algorithm to derive such a function from an executable test sequence automatically using a technique for solving linear programming problems, and propose a conformance testing method using those algorithms.
Cytosolic sulfotransferases (SULTs) are phase II drug-metabolizing enzymes that catalyze the transfer of a sulfonate group from 3Ј-phosphoadenosine 5Ј-phosphosulfate (PAPS) to molecules possessing phenols, enols, alcohols or amines. Sulfo-conjugation confers greater polarity and water solubility on the parent molecules, thereby facilitating biliary or urinary excretion and detoxification.
In this paper, we present a protocol for dynamically maintaining a degree-bounded delay sensitive spanning tree in a decentralized way on overlay networks. The protocol aims at repairing the spanning tree autonomously even if multiple nodes' leave operations or failures (disappearances) occur simultaneously or continuously in a specified period. It also aims at maintaining the diameter (maximum delay) of the tree as small as possible. The simulation results using ns-2 have shown that the protocol could keep reasonable diameters compared with the existing centralized static algorithm even if many nodes' participations and disappearances occur frequently.
To determine the safest method of hepatic vascular clamping associated with the least ischemiareperfusion injury of the liver during liver surgery. Setting: University laboratories. Subjects: Sixty-five adult male Wistar rats. Methods: The hilar area of the left lateral and median lobes of rat liver was clamped for 10 minutes (group 1), 15 minutes (group 2), or 20 minutes (group 3) followed by 5 minutes of reperfusion. The procedure was repeated for a total period of ischemia of 60 minutes in each group. Control rats underwent laparotomy without vascular clamping. In addition to histological examination, we determined calpain µ activity, a marker of liver injury, by Western blotting using specific antibodies against the intermediate (activated) and proactivated forms of calpain µ. Measurements were performed at the end of ischemia and after 2 hours of reperfusion. We also determined the degradation of talin, an intracellular substrate of calpain µ, by Western blotting. Results: The level of adenosine triphosphate and energy charge at 2 hours after reperfusion did not change after ischemia-reperfusion irrespective of the duration of ischemic cycle. After 60 minutes of intermittent ischemia followed by 2 hours of reperfusion, cell membrane bleb formation, calpain µ activation, and talin degradation were detected in groups 2 and 3 but not in group 1. Conclusion: The safest method of hepatic vascular clamping that produces a minimum or no ischemiareperfusion injury is 60 minutes of 6 cycles of 10minute vascular clamping interrupted by 5 minutes of reperfusion.
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