This paper presents a multi-core SoC architecture for consumer multimedia applications. The comprehensive functionality of such multimedia systems is described using the example of a hybrid TV application. The successful usage of a heterogeneous multi-core SoC platform is presented and it is shown how specific challenges such as inter-processor communication and real-time performance guarantees in physically centralized memory systems are addressed.

Objectives. To estimate the total cost of diabetes mellitus in Sweden in 1994 and to compare the cost structure with a former Swedish study and with American studies. The study also aims to investigate how the total cost is distributed between control of and complications of the disease. Design. In order to estimate the economic burden of diabetes mellitus in Sweden in 1994, the cost-of-illness method, based on the human capital theory, has been used. Both direct and indirect costs have been estimated using a prevalence approach and a 'topdown' method. Results. The economic burden of diabetes mellitus is estimated at 5746 MSEK (1US$ ϭ 7.50 SEK) in Sweden in 1994. The direct costs are estimated at 2455 MSEK and constitute about 43% of the total cost. The indirect costs (production loss due to morbidity and premature mortality) were the dominant costs and amounted to 3291 MSEK, or 57% of total cost. Comparisons with a previous Swedish study from 1978 show some interesting results. Firstly, the distribution of direct and indirect costs is identical between the two studies. Secondly, the distribution of costs between management/control of the disease and complications was about the same, comparing the situation 16 years apart. Four American studies show a cost structure similar to the cost structure presented in this study. Conclusions. The overall conclusion must be that very little has changed in the cost structure of diabetes in Sweden between 1978 and 1994.

Abstract. c-Met is a receptor tyrosine kinase that has been implicated in the pathogenesis and growth of a wide variety of human malignancies, including CRC, but its role in metastasis is largely unknown. We compared c-Met expression in primary human colorectal carcinomas and distant metastases from the same patients. Formalin-fixed paraffin-embedded tissue samples from 69 colorectal cancer patients were obtained. The protein expression of c-Met was evaluated immunohistochemically using a commercial antibody. The difference in expression between primary tumors and their corresponding distant metastases was analyzed using the Wilcoxon signedrank test. c-Met expression was statistically significantly lower in the distant metastases compared to their corresponding primary tumors (p<0.001), whereas no difference was found between lymph node metastases and their corresponding primary tumors (p=0.957). The degree of c-Met expression was not related to clinicopathological characteristics such as tumor grade and Dukes' stage at the time of primary tumor diagnosis, or to the location of the distant metastases. We demonstrated that c-Met expression is often reduced in distant metastases compared to their corresponding primary colorectal tumors. Additional studies of c-Met activation and signal transduction will increase our knowledge about the role of c-Met in colorectal cancer metastasis. IntroductionColorectal cancer (CRC) is the third leading cause of death in the western world with an overall 5-year survival of <60%. Succumbing to CRC is usually due to distant metastatic spread, with the liver being the most common site. Once distant metastases have been established, the chances of long-term survival are very low. Therefore, achieving an understanding of the molecular mechanisms contributing to the metastatic ability of a colorectal carcinoma is critical to the development of effective treatments.c-Met is a receptor tyrosine kinase that has been implicated in the pathogenesis and growth of a wide variety of human malignancies (1-3), including CRC (4-6). c-Met expression in colonic cells increases during the progression towards malignancy (7), and a higher c-Met expression has been observed in colorectal tumors compared with corresponding normal colon mucosa (8).The heterodimeric c-Met protein (9) is activated by hepatocyte growth factor (HGF), also known as scatter factor (SF) (9). The binding of HGF/SF to c-Met is known to promote motility, morphogenesis and mitogenesis in epithelial cell lines of various origins (10,11), causing colon cancer cells to form crypt-like structures (10) and inducing angiogenesis in endothelial cells (5).The c-Met signaling pathway is believed to stimulate tumor invasion and metastasis. The Madkin-Darby canine kidney (MDCK) cell line responds to HGF/SF by colony dispersal and epithelial-to-mesenchymal transition (EMT), increasing cell motility and the invasion of collagen matrices (12). c-Met stimulation by HGF/SF from stromal cells has been suggested to facilitate local invasion of epith...

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